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1,421 terms

ALL Pharm cards for Final Review

STUDY
PLAY
what is the cause of heart failure?
heart is unable to pump blood in sufficient amounts from the ventricles to meet the body's metabolic needs
Drugs commonly used for heart failure?
ACE inhibitors (vasodilators)
Angiotensin receptor blockers
diuretics
spironolactone
beta blockers
cardiac glycosides
phosphodiasterase inhibitors
b-type natriuretic peptides
what does inotropic mean?
force or energy of muscular contractions
definition of chronotropic
rate of the heartbeat
definition of dromotropic
the conduction of electrical impulses
How do ACE inhibitors help wtih decreased cardiac output?
vasodilator- get more blood out

decrease the after load, increase cardiac output
how do ARBs help with heart failure?
same as ACE inhibitors
decrease afterload, increase cardiac output
how do diuretics treat heart failre?
decrease volume around heart
what effect do beta blockers have on contractility of the heart? Why is this good for heart failure?
-decrease contractility
-beta blockers are cardioprotective against catecholamines
Spironolactone is what kind of diuretic?
potassium sparing diuretic
what effect does aldosterone have on the heart?
remodeling
why is spironolactone good for heart failure?
decreases chance of remodeling from occuring
what are the 2 major side effects of spironolactone?
hyperkalemia and gynecomastia
what is another name for Cardiac Glycosides?
Digoxin, digitalis
Is digoxin used to prolong life?
No, improves quality of life
what effect does digoxin have on the heart?
-increase in force of myocardial contraction without an increase in oxygen consumption
-reduced heart rate
-decreases automaticity at SA node, decreases AV nodal conduction
In other words digoxin does what?
-increased stroke volume and cardiac output
-pseudodiuretic- improved renal perfusion
digoxin adverse effects
colored vision (green, yellow, purple), seeing halos
nausea, vomiting, anorexia
dysrhythmias, bradycardia
therapeutic range for digoxin?
very narrow, 1-2ng/ml
what increases risk of toxicity in digoxin?
hypokalemia
what should be monitored prior digoxin dose?
potassium levels, heart rate (hold dose: <60, >120 bpm)
What food should be avoided with digoxin?
high fiber foods
what effect do phosphodiesterase inhibitors have on heart?
vasodilation=decrease after load, increase cardiac output
positive inotropic response= increase heart rate
common inodilators?
"rinone"
-inamrinone (Inocor)
-milrinone (Primacor)
When should phosphodiesterase inhibitors be used?
When patient has not responded to treatment of digoxin, diuretics, and/or vasodilators
How long should phosphodiesterase inhibitors be used?
short term
Adverse effects of Phosphodiesterase inhibitors
-thrombocytopenia
-elevated liver enzymes
-dysrhythmias
B-type natriuretic peptide (BNP)
nesiritide (Natrecor)
What effect does nesiritide (Natrecor) have on heart?
vasodilation=decreased after load, increased cardiac output
When should b-type natriuretic peptides be used?
Last resort
How is nesiritide (Natrecor) administered?
IV, in IC unit
What causes angina?
when the supply of oxygen int he blood is insufficient to meet the demands of hte heart, the heart muscle "aches"
what are the main objectives in treating angina?
1.increase blood flow to heart muscle
2. decrease myocardial oxygen demand
Main drug classes to treat angina
-nitrates
-beta blockers
-calcium channel blockers
routes of administration for nitrates?
sublingual, buccal, oral, chewable tablets, iv, ointments, transdermal patches, translingual sprays
nitrates MOA
-cause relaxation of smooth muscles of blood vessels leading to vasodilation
-potent dilating effect especially on coronary arteries
Result of nitrates
increase oxygen to myocardial tissues
nitrates can also help what symptom?
alleviate coronary artery spasms
Do rapid acting forms of nitrates treat or prevent angina? What about long-acting forms?
-rapid acting-treat acute anginal attacks (sublingual tablets, intravenous infusion)
-long acting- prevent episodes
adverse effects of nitrates
-headache
-tachycardia, postural hypotension
-tolerance
When does tolerance of nitrates occur?
patients taking around the clock or with long acting forms
how to prevent tolerance
allow regular nitrate free period

transdermal patch-remove at bedtime for 8 hrs, apply new patch in morning
when do you take prn nitrates?
first hint of anginal pain
what is the proper technique for sublingual NTG for anginal pain?
Take 1 SL tab, wait 5 min, if no relief call 911
how many SL tabs can patient take?
up to 3
is burning sensation with SL tabs normal?
yes, indicates drug is still potent
when should NTG be replenished?
potency is lost in 3 months after bottle has been opened
Which drug should nitrate patients avoid?
"afil" drugs
sildenafil (viagra)
cause additive hypotension effect, potentially dangerous
Beta Blockers MOA
Beta receptors on heart blocked
Effect of Beta Blockers
DECREASE: HR, myocardial contractility, myocardial oxygen demand
How are beta blockers cardioprotective?
block harmful effects of caetcholamines, improving survival afterr MI
adverse effects of BB?
bradycardia, hypotension, altered glucose and lipid metabolism, wheezing and dyspnea
common beta blockers?
atenolol (Tenormin)
metoprolol (Lopressor)
nadolol (Corgard)-nonselective
propranolol (Inderal)- nonselective
what should be monitored on beta blockers?
pulse rate daily- lower than 60 bpm needs to be reported
what may happen if drugs discontinued abruptly?
risk of rebound hypertensive crisis
are beta blockers used for immediate relief or long term prevention of anginas?
long term prevention
Calcium Channel Blockers MOA
cause coronary artery vasodilation
effects of CCBs
decrease myocardial contractility: decreased myocardial oxygen demand
adverse effects of CCBs
acceptable s.e
hypotension, palpitations, tachycardia, bradycardia, CONSTIPATION, nausea
Name three classes of CCBs
Benzothiazepines-diltiazem (Cardiazem, Dilacor)
Phenylalkamine- verapamil (Calan, Isoptin)
Dihydropyridines- "dipines"
how can patients help decrease risk of constipation?
adequate fluids and eat high fiber foods
should patients be warned about postural hypotension?
yes, need to change positions slowly
what should be avoided or cautioned of using when on antianginal drugs?
alcohol consumption, hot baths, hot tubs, whirlpools, saunas
may cause vasodilation, hypotension, and possibility of fainting
4 stages of hypertension
normal <120/<80
prehyper 120-139/80-89
stage 1 140-159/90-99
stage 2 >160/>100
first line drug therapy without other "compelling" indicators
Thiazide diuretics
Compelling indicators
post-MI, high cardiovascular risk, heart failure, diabetes mellitus, chronic kidney disease, previous stroke
Drugs more effective in white patients
beta blockers and ACE inhibitors
Drugs more effective in african americans
CCBs and diuretics
Drugs to tx hypertension
diuretics
adrenergic agents
ACE inhibitors
Angiotensin II Receptor Blockers
Calcium Channel Blockers
Vasodilators
Direct Renin Inhibitors
Diuretics do what?
decrease fluid volume
decrease: preload, cardiac output, total peripheral resistance, workload of heart, BP
Most common diuretic used for BP?
Thiazide
How do alpha 1 antagonists lower BP?
vasodilate

"osin"
How do alpha 2 agonists lower BP?
inhibit norepinephrine, dilate blood vessels
Common alpha 2 agonists?
clonidine (Catapress)
methyldopa (Aldomet)
How do Beta Blockers decrease BP?
reduce heart rate through beta1 blockade
cause reduced secretion of renin
What does antiotensin do?
potent vasoconstrictor
what does ACE do?
converts angiotensin I to angiotensin II
What does angiotensin II do?
potent vasoconstricor
causes aldosterone secretion from adrenals
ACE inhibitors do what?
block ACE
"pril"
ACE inhibitors are beneficial to who?
diabetics
slows progression of renal disease in hypertensive diabetics with renal diseases
Adverse effects of ACE inhibitors
dry unproductive cough
hyperkalemia
angioedema-rare but potentially fatal
What do you need to check before administering ACE inhibitor?
BP
K level
Pregnant or not
Angiotensin II Receptor Blockers (ARBs)
MOA?
allow angiotensin I to be converted to angiotensin II but BLOCK receptors that receive angiotensin II
Block vasoconstriction and release of aldosterone
Common ARB side effect
URI and HA
does NOT cause cough or significant hyperkalemia
ARB suffix?
sartan
CCB MOA?
cause smooth muscle relaxation by blocking the binding of calcium to the receptors, preventing muscle contraction
Decreased BP
indications for CCB?
angina, hypertension, dysrhythmias
CCB adverse effects
hypotension, palpations, tachycardia
CONSTIPATION
Benzothiazepines
diltiazem (Cardizem, Dilacor)
hypertension, angina, dysrhythmia
Phenylalkamines
verapamil (Calan, Isoptin)
hypertension, angina, dysrhythmia
Dihydropridines
"dipine"
hypertension and angina
amlodipine (Norvasc)
nimodipine (Nimotop)
used for vasospasms following subarachnoid hemorrhage
Direct-Acting vasodilators MOA?
directly relax smooth muscle walls of blood vessels

lowerr peripheral resistance and BP
HR increased
Common vasodilators
diazoxide (Hyperstat)
hydralazine (Apresoline)
minoxidil (Loniten)
sodium nitroprusside (Nipride)-used for hypertensive crisis
Direct Renin Inhibitors MOA?
inhibit renin and blocks conversion of angiotensinogen to angiotensin I
ultimately decreases level of angiotensin II
What must be corrected before direct renin inhibitors can be started?
correct hypovolemia and monitor fluid volume closely
Should antihypertensive drugs be stopped abruptly?
NO- may cause rebound hypertensive crisis, may lead to stroke
What must you monitor during therapy?
BP
Is medication only thing patient can do to treat hypertension?
No- watch diet, stress level, weight and alcohol intake
Can patients experience postural hypotension with antihypertensives?
yes-change positions slowly
What should men be aware of that may cause compliance issues?
impotence
What should patients avoid or use with caution when on drug therapy?
hot tubs, hot weather, prolonged sitting or standing, alcohol ingestion.

may lead to fainting and injury
What are pharmacodynamics
What the drug does to the body
What are pharmacokinetics
What the body does to the drug
Absorbtion
movement from the site of administration into the bloodstream
What factors influence absorbtion?
1. route of administration
2. rate of dissolution
3. surface area
4. blood flow to area
5. lipid solubility
6. first pass effect
Distribution
When the drug reaches the target site from bloodstream
Metabolism
breakdown of dug by liver
excretion
elimination of drug from body
Bioavailability
quantifies drug absorption
What does it mean if drug is highly protein bound?
There is less "free" drug to be distributed to tissue which will increase the duration of action
What will happen if a patient takes 2 drugs that are both highly protein bound?
The 2 drugs will compete for binding sites on the protein. One will win and the other will have more "free" drug in the bloodstream which will shorten its expected duration of action and increase the chance of toxicity
Why is hyopalbumenia dangerous for patients taking highly protein bound drugs?
The risk of toxicity will be increased because the lack of available protein will result in more "free" drug in circulation than expected.
What are the 6 rights of drug administration?
1. Right Patient
2. Right Drug
3. Right Dose
4. Right Route
5. Right Time
6. Right Documentation

Mneumonic: Patients Do Drugs Round The Day
In laymans terms what does the PSNS do?
Rest & Digest
What are the 2 divisions of the ANS
1. Parasympathetic
2. Sympathetic
What is the primary neurotransmitter for the PSNS?
Acetyl Choline (ACh)
What are the indicated uses of cholinergic agonists?
1. urinary Retention
2. myasthenia gravis
3. alzheimers disease
4. xerostomia
5. glaucoma
What are the contraidications for cholinergic agonists?
1. drug allergy
2. bowel obstruction
3. bradycardia
4. hypotension
5. COPD
6. peptic ulcers
What are the signs and symptoms of cholinergic crisis?
1. hypotension
2. shock
3. salivation
how do you treat cholinergic crisis?
with an anticholinergic
What does SLUDGE stand for?
S=Salivation
L=Lacrimation
U=Urinary incontenence
D=Diarrhea
G=GI Motility & Secretions
E=Emisis

Used to describe the actions of cholinergic agonists
What happens when cholinergic receptors are activated?
1. Miosis
2. decreased heart rate & contractility
3. bronchial contriction & increased secretions
4. increased GI motility & secretions
5. emptying of bladder and bowel
6. vasodilation
7. sex organ = erect
How do direct acting cholinergic agonists work?
They bind to cholinergc receptors and activate them
How do indirect acting cholinergic agonists work?
They inhibit the action of cholinesterase
What are the types of cholinergic receptors?
1. muscarinic
2. nicotinic
In laymans terms what does the SNS do?
Fight or Flight
What is the primary neurotransmitter of the SNS
norepinephrine
What are the principal actions of the SNS?
1. mydriasis
2. increased heart rate & contractility
3. bronchdilation
4. decrease GI motility & secretions
5. urinary retention
6. constipation
7. vasoconstriction
What is a saying to describe the actions of the SNS?
Can't See, Can't Pee, Can't Spit, Can't ****
What are the receptors of the SNS
1. alpha 1 & 2
2. beta 1 & 2
3. dopamine
What are the effects of alpha 1 activation?
1. vasoconstriction
2. increased BP
3. mydriasis
4. urinary retention
What are the effects of alpha 2 activation?
1. inhibition of norepinephrine
2. vasodilation
3. decreased BP
What are the effects of beta 1 activation?
1. increased heart rate
2. increased contractility (positive inotropic effect)
3. increased renin secretion
What are the effects of beta 2 activation?
1. bronchodilation
2. uterine relaxation
What are the effects of dopaminergic receptor activation?
improved renal perfusion r/t dilation of renal blood vessels
What is the prototype cholinergic direct acting muscarinic agonist?
bethanechol (Urecholine)
What is the MOA for bethanechol (Urecholine)?
relaxes the bladder sphincter
What is bethanechol (Urecholine) used for?
urinary retention, commonly given post-op and/or post partum
What are the S/E of bethanechol (Urecholine)?
* S/E rare by PO, more common by SC *
1. hypotension
2. bradycardia
3. diarrhea
What is the indirect-acting cholinergic agonist prototype:
pyridostigmine (Mestinon)
What is the MOA for pyridostigmine (Mestinon)?
1. inhibits cholinesterase
2. increases force of muscular contractions
What is the primary indication for pyridostigmine (Mestinon)?
myasthenia gravis
What is/are the S/E of pyridostigmine (Mestinon)?
* S/E Rare but Serious *
cholinergic crisis
What are the contraindications of pyridostigmine (Mestinon)?
1. GI obstruction
2. Urinary Obstruction
What is the anticholinergic prototype?
Atropine
What is the MOA of Atropine?
Competes with ACh for binding and inhibits nerve tranmission at those receptors
What are the effects of Atropine?
1. Decreases in salivary, bronchial, GI, and seat gland secretions
2. mydriasis
3. increased HR
4 bronchodilation
5. decreased bladder tone
6. decreased GI Motility
What is Atropine used for?
1. CPR
2. perioperative to decrease GI secretions and motility
What should you watch for when giving Atropine?
overdose
What is the nocotinic prototype drug?
succinylcholine (Anectine)
What is the MOA of succinylcholine (Anectine)?
It is a NMBA so it blocks the nicotinic M receptors, very short acting
What is succinylcholine (Anectine) used for?
1. endotracheal intubation (primary use)
2. mechanical ventilation
3. procedures in which muscle relaxation/para;yzation is necessary
What are the advers S/E of succinylcholine (Anectine)?
malignant hyperthermia
What is the nonselective adrenergic prototype?
epinephrine
What is the MOA of epinephrine?
It is a catecholamine so it produces a sympathomimetic repsonse by positive inotropic and chronotropic effects (B1), increased BP (A1), and bronchodilation (B2)
What is epinephrine used for?
1. anaphylaxis
2. asthama
3. CPR
4. simple glaucoma
What are the S/E of epinephrine?
1. increased BP
2. angina
3. cerebral hemorrhage
4. increased blood glucose
5. necrosis
6. dysrhythmias
What is the alpha 1 selective prototype drug?
phenylephrine (Neosynephrine)
What is the MOA of phenylephrine (Neosynephrine)?
stimulation of A1 receptors = vasconstriction
What is phenylephrine (Neosynephrine) used for?
1. nasal congestion
2. mydriasis for eye exams
What are the S/E phenylephrine (Neosynephrine)?
increased BP
What is the alpha 2 selective prototype drug?
clonidine(Catapres)
What are the effects of clonidine(Catapres)?
vasodilation which decreases BP & HR
What is clonidine(Catapres) used for?
antihypertensive (given secondary)
What is the beta nonselective prototype drug?
isoproterenol (Isuprel)
What are the effects of isoproterenol (Isuprel)?
B1 = +inotropic, +chronotropic
B2 = bronchodilation, glycogenolysis
Results if increased cardiac output
What is isoproterenol (Isuprel) used for?
1. shock
2. cardiac arrest
3. CHF
What the adverse S/E of isoproterenol (Isuprel)?
1. tachydysrythmias
2. angina
3. hyperglycemia
What is the beta 1 selective prototype drug?
dobutamine (Dobutrex)
What are the effects of dobutamine (Dobutrex)?
+inotropic effects with increased oxygen consumption. Leads to increased cardac output.
What is dobutamine (Dobutrex) used for?
heart failure
What are the S/E of dobutamine (Dobutrex)?
tachycardia
What is the beta 2 selective prototype drug?
albuterol (Proventil)
What are the effects of albuterol (Proventil)?
bronchodilation
What is albuterol (Proventil) used for?
asthma
What is the dopaminic receptor prototype drug?
dopamine (Intropin)
What does dopamine (Intropin) do?
1. increases renal perfusion
2. stimulates dopamine, A1, and B1 receptors (which one depends on dosage)
What is dopamine (Intropin) used for?
1. shock
2. heart failure
3. renal failure
What are the 2 type of chemotherapy agents
1. cell cycle specific
2. non cell cycle specific
True or False:
Chemotherapy drugs are more effective to cells that have a high growth fraction (rapid proliferation)

Is this a good thing or a bod thing?
True
Sounds like a good thing but really means it is hard to get ahead of the growth
What is the implication to chemotherapy drugs having a low therapeutic index?
The low therapeutic index is does limiting. This means there is a fine line between therapeutic levels and toxic levels.
What is Nadir
the lowest level of WBC follwoing chemo treatment
When does Nadir occur
10-28 days after chemo dosing
What percentage of malignant cells must be killed for a cancer to be 'cured'
100%
Why is there a poor response to chemo from solid tumors
They typically have a low growth fraction and so are less responsive to cytotoxic drugs
What precaution should be taken by providers when administering cytotoxic drugs
Wear gloves when handling the drug
What the obstacles to successful chemotherapy
1. Toxicity to normal cells
2. Nadir - can require interupption to scheduled chemotherapy
3. Cure requires 100% of malignant cells be killed
4. Abscence of early detection
5. Poor response of solid tumors
6. Drug Resistance
What are the general toxicities of chemotherapy
1. Bone marrow suppression
2. Digestive tract injury
3. Alopecia
4. Reproductive toxicity
5. Hyperuricemia (increased blood uric acid)
6. Local injury from extravasation
What are the results of bone marrow suppression
1. neutropenia
2. thrombocytopenia
3. anemia
What digetive tract injuries are caused by chemotherapy
1. stomatitis - inflammation of the stoma[oral cavity(mouth)]
2. diarrhea
3. N/V
What is Methotrexate? What is the antidote for it?
1. A common cell cycle-specific antineoplastic drug
2. leucovorin
What is a critical administration issue for Vincristine
it must never be given intrathecally (directly into spinal canal)
What type of drug is paclitaxel (Taxol)
It is a chemo drug
What is a nursing consideration for cisplatin (platinol)? Why?
Requires extensive hydration to minimize risk of nephrotoxicity
What is a nursing consideration for cyclophosphamide (cytoxan)? Why?
Requires extensive hydration for minimize risk of hemorrhagic cystitis.
What would you want to monitor in a patient who is taking cisplatin (platinol) or cyclophosphamide (cytoxan)?
BUN and creatnine levels
What are cytotoxic antibiotics used for?
To Tx cancer NOT infections
What is a concern for a patient taking doxorubicin (adriamycin)?
cardiotoxicity
Is doxorubicin (adriamycin) related cardiotoxicity going to acute or delayed?
Both
What is doxorubicin (adriamycin) realted cardiotoxicty related to? Why?
The total cumulative dose. There is a lifetime max on this drug.
What should you be sure to tell a patient who is taking doxorrubicin (adriamycin)?
Urine may turn a reddish color for a few days.
What precaution should a nurse take who is administering a cytotoxic antobiotic?
Wear gloves.
What are the primary indications for immunosuppresants
1. Prevention of organ rejection in transplant clients
2. Treatment of autoimmune disorders (eg rheumatoid arthritis, SLE, MS)
What are the primary concerns with immunosuppressants
1. increased risk of infection
2. increased risk of neoplasms
What effect can immunosuppressants have on vaccines
reduce their effectiveness
What are the special considerations for administration of immunosuppressants
1. Don't take on an empty stomach to avoid GI upset
2. Don't mix oral solutions in a styrofoam cup because meds can adhere to sides
What special instructions should be given to female patients receiving immunosuppressants
Use contraceptive during treatment and for up to 12 weeks after therapy ends
Name 5 immunosuppressants
1. cyclosporine
2. azathioprine (Imuran)
3. mycophenolate mofetil (Cell Cept)
4. glatiramer acetate (Copaxone)
5. muromonab-Cd3 (Orthoclone OKT3)
What is an allogenic transplant
A transplant between genetically nonidentical individuals of the same species
What is the drug of coice for preventing organ rejection following allogenic transplantation
cyclosporine
What drug is often given in conjuction with cyclsporines and why
glucocorticoids because they are also immunosuppressants so you are doubling up
What is a very common concern with cyclosporines? How can you monitor for it? What can you do if it happens?
1. nephrotoxicity
2. Monitor BUN & creatnine levels
3. it is usually reversible following dosage reduction
How is cyclosporine administered
oral or IV
Why should a patient starting cycloesporine have a baseline oral assessment performed
it can cause gingival hyperplasia
What effect can grapefruit juice have on cyclosporine
It can inhibit metabolism of cyclosporine and which will raise the serum levels and increase the risk of toxicity
What is a primary indication for CellCept
MS
What is the route of administration for CellCept
SC
What is unique about orthoclone OKT3
It is used for reversal and prevention of graft rejection. It is the only drug available for reversal
What is a major A/E of orthoclone OKT3? What do you do to monitor for it?
1. pulmonary edema
2. get a chest X-Ray within 24 hours of starting treatment
What must be done prior to starting orthoclone OTK3
you must get a baseline weight to monitor for heart and lung issues
What are the general S/E of antifungals?
1. hepatotoxicity
2. nephrotoxcity
What must be monitored in patients taking antifungals
1. BUN
2. creatnine
3. liver enzymes
What are the common antifungal drugs
1. amphotericin B (Fungizone)
2. fluconazole (Diflucan)
3. nystatin (Mycostatin)
4. caspofungin (Cacidas)
5. voriconazole (VFEND)
What is amphotericin used to treat
progressive and potentially fatal systemc fungal infections
What condition in a patient would indicate caution should be used in Rx amphotericin B? Why?
1. renal impairment
2. nephrotoxicity is a serious A/E that occurs in 80+% of patients receiving amphotercin B IV
What are the "other" common S/E of amphotericin B? What can be done to decrease the effects?
1. HA
2. Chills
3. Fever
4. Hypotension
5. N/V

1. Premedicate with hydrocortisone or ibuprofen
2. Slow administration
What must you monitor the IV site of amphotericin B for?
Extravasation
What is fluconazole (Diflucan) the DOC for?
supress vulvovaginal candidiasis
What is special about fluconazole (Diflucan)? What does that make it effective in treating?
1. it can penetrate the CSF
2. cryptomeningitis
What is nystatin (Mycostatin) used to Tx and how is it administered
1. thrush = Oral (swish and swallow)
2. diaper rash = topically
3. yeast infection = intravaginally
If a patient is NPO how would you administer nystatin?
dip a spongette in the nystatin and treat the mouth
What drug(s) is/are used to Tx Aspergillus
1. caspofungin (Cacidas)
2. voriconazole (VFEND)
A patient has just been admitted to the hospital and has been prescribed an antibiotic. What is the first thing a the nurse should do?
Obtain a culture BEFORE starting the antibiotics. Cultures obtained after antibiotics are started will be inaccurate. Once the culture has been collected start the antibiotics.
Define Empiric Therapy
Giving an antibiotic BEFORE a culture has identified a specific causitive organsim
Define Definitive Therapy
Giving antibiotics after a culture has grown and the specific causitive organism has been identified.
What is a superinfection/suprainfection
A side effect of antibiotic therapy wher the antibiotics reduce or eliminate normal bacterial flora allowing other bacteria or fungus to take over and cause infection.
If a patient on antibiotics gets diarrhea what should the nurse be aware of?
The patient could develop a C. dif infection
What are the 2 main factors contributing to antibiotic reistance
1. Overprescribing of antibiotics
2. Patients not completing the entire course of prescribed antibiotics
What are the different categories of antibiotics
1. Beta-lactam antibiotics
2. Macrolides
3. Tetracyclines
4. Sulfonamides
5. Aminoglycosides
6. Quinolones or fluoroquinolones
7. Misc.
What are the categories of beta-lactam antibiotics
1. penicillins
2. cephalosporins
3. carbapenems
4. monobactams
What is beta lactamase
An ezyme that makes bacteria resistant to antibiotics
What is the most common cause of drug allergy
Penicillin
Is penicillin a bacterialcidal or bacterialstatic? What is it most effectice against?
1. bacteriocidal
2. gram positive organisms
What does penicillin have cross reactivity to?
cephalosporins
Does a penecillin allergy contraindicate the use of a cephalosporin?
Not unless anaphylaxis was involved.
Name the beta lactamase inhibitors
1. clavulanic acid
2. tazoactam
3. sulbactam
What is clavulanic acid
a beta lactamase inhibitor
What is tazoactam
a beta lactamase inhibitor
What is sulbactum
a beta lactamase inhibitor
What is important to remember about nafcillin
is it extremely irritating to veins
How many generations of cephalosprins are there
5
What change from one generation to the next
As you progress from first generation to later generations you get:

1. increased effectiveness against gram negative organisms
2. increase resistance to destruction by beta-lactamases
3. increased ability to cross the blood brain barrier
When a client is going to be taking a cephalosporin what should you tell them regarding drinking alcohol
It depends. Some cephalosporins can cause a reaction with alcohol so you should check the specific one they will be taking and if there is a reaction teach about it.
What generation of cephalorsporins starts to cross the blood brain barrier
third generation
Are carbapenems bacterialcidal or bacterialstatic
bacteriocidal
With carbapenems there is an increased risk for what?
drug induced seizures
Name the carbapenems
1. imipenem/cilastatin (Primaxin)
2. meropenem (Merrem)
Which carabepenem has the highest risk of seizure
imipenem/cilastatin (Primax)
Are tetracyclines bacteriocidal or bacteriostatic
bacteriostatic
What is the effect of administering tetracyclines with antacids
It decreases aborption. The same is true for milk and calcium
What can happen to children younger than 8 years old who are administered tetracyclines
Their teeth can be discolored
What is a common S/E of tetracycline
photosensitivity
Are sulfonamides bacteriocidal or bacteriostatic
bacteriostatic
Where do sulfonamides achecive a high concentration and what are they used to treat?
1. The kidneys
2. UTIs
What are the nursing considerations for sulfonamides
1. Allergic reations are common
2. Photosensitivity is common
3. Delayed reactions are common
4. You must encourage increased fluid intake to avoid crystalluria
Are aminglycosides bacteriocidal or bacteriostatic
bacteriocidal
What should be monitored in a patient taking an aminoglycoside and why
1. Hearing (tinnitus, feelingof fullness in ears) because ototoxicity is an A/E
2. BUN and Creatnine levels because nephrotoxicity is an A/E
How good is the bioavailability of quinolones?
Excellant, almost as good orally as parenterally
What is the generic suffix for quinolones?
flaxacin
What are the side effects of quinolones?
1. prolonged QT/cardiac dysrhythmias
2. joint upture/tendonitis
Name the misc antibiotics
1. clindamycin (Cleocin)
2. linezolid (Zyvox)
3. nitrofurantoin (Macrodantin)
4. vancomycin (Vancocin)
What should you monitor in patients taking clindamycin (Cleocin)?
1. CBC
2. What for C. Dif
What is linezolid (Zyvox) used to treat?
VRE
What is a special consideration for metronidazole (Flagyl)?
It can cause acute alcohol intolerance when taken with alocholic beverages
What is nitrofurantoin (Macrodantin) commonly used for?
UTIs
What are the general considerations for antibiotics
1.Give on time
2. Don't give with antacids, milk, or calcium as these will decrease absorbtion
3. Hypersensitivity reaction may be delayed
4. Oral contraceptives may be ineffective
What is the most common use for antimalarials in the USA?
For prophylaxis for people traveling to high risk regions
What is the prevention protocol for antimalarial drugs?
Varies from med to med but...
1. Commonly starts 2 weeks before exposure and continues for several weeks
2. May be taken one time/week
3. Take with at least 6-8 ounces of water
Which type of organism does metronidazole (Flagyl) have especially good activity against? Give examples...
1. anaerobic organsims
2. Peptostreptococcus spp., Eubacterium spp., Bacteroides spp., Clostridium spp.
What is metronidazole (Flagyl) widely used to treat?
intraabdominal and gynecologic infections
Besides intraabdominal and gynecologic infections what is metronidazole (Flagyl) used to treat?
protozoal infections such as amebiasis and trichomoniasis
What is the route of administration when when metronidazole (Flagyl) is used to treat antibiotic related colitis?
oral
When is metronidazole (Flagyl) contraindicated?
in the case of drug allergy
What are the available routes of administration for metronidazole (Flagyl)?
There are oral and injectable forms
What pregnancy category is metronidazole (Flagyl)?
category B but is not recommened in the first trimester
What are the A/E of metronidazole (Flagyl)?
1. dizziness
2. headache
3. gastrointestinal discomfort
4. nasal congestion
5. reversible neutropenia
6. reversible thrombocytopenia
What should you teach a patient who is about to start taking metronidazole (Flagyl) regarding alcohol?
Alcohol should not be taken for 24 hours before and 36 hour after taking metronidazole (Flagyl) because it can cause acute alcohol intolerance
Metronidazole (Flagyl) may increase the toxicity of which drugs?
1. lithium
2. benzodiazapines
3. cyclosporines
4. CCBs
5. various antidepressants
6. warfarin
7. others
Which drugs may decrease the effectiveness of metronidazole (Flagyl)?
1. phenytoin
2. phenobarbital
Why might an NSAID be used in conjuction with an opioid?
Because when used together there is often an opioid sparing effect allowing less opiods to be used.
What does it mean that NSAIDs show a 'ceiling effect' that limits their effectiveness?
At a certain point any further increase in dosage will increase the risk for adverse effects without a corresponding increase in therapeutic effect.
If a patients comes to the hospital with a Vitamin K definciency are NSAIDs an appropriate drug? Why or why not...
No. NSAIDs are contraindicated when there are conditions for putting the patient at risk for bleeding such as rhinitis, Vit K deficiency, and peptic ulcers
What pregnancy category are NSAIDs?
Category C in the first 2 trimesters and category d in the third trimester.
What would you tell new mother who wants to know why she can't just take Advil for her pain?
Because NSAIDs are excreted in mothers milk.
How long before elective surgery should a client stop taking NSAIDs and why?
1 week becuase of the potential for increased bleeding.
What is the most common and severe adverse affect of NSAIDs on the gastrointestinal lining and how can it be avoided?
Gastrointestinal bleeding. it can be avoided with the use of misoprostol (Cytotec).
Why would NSAIDs be contraindicated for dehydrated patients?
The can increase the chance of acute renal failure occurring.
What are the 3 major functions of COX1
1. Protects gastric mucosa
2. Supports renal function
3. promotes platelet aggregation
What does COX2 do?
Enhances inflammation and perception of pain
Why would you administer a dosage of 80-325mg qd of aspirin?
To inhibit platelet aggregation
Why would you administer a dosage of 325-650 mg q4-6h of aspirin?
For its antiinflammatory effects
If a child is diagnosed with a viral disease is aspirin a good choice for pain relief? Why or why not...
They are not because use of aspirin in children with viral diseases is linked to an increased incidence of Reye's syndrome.
Name 2 instances when aspirin would be indicated for use by children
1. Rheumatoid arthritis
2. Kawasaki Disease
If a client, who takes aspirin, calls and complains of ringing in her/his ears what should you do? Why?
They should be referred to their physician immediately because tinnitus is a sign of aspirin toxicity
How does tylenol help with inflammation?
It has not anitiinflammatory action
What does ketorolac do? How long can it be used for?
It is an antiinflammatory with the analgesic properties equivalent to opioids but WITHOUT respiratory depression or addiction. It should be taken for maximum of 5 days.
If an infant has patent ductus arteriosis what drug might be administered to try to close it?
indomethacin (Indocin)
What is the only COX2 inhibtor still on the market and what is the FDA monitoring it for?
celecoxib (Celebrex).

cardiovascular effects
What are the primary indications for use of Celebrex?
1. osteoarthritis
2. rheumatoid arthritis
How do COX2 inhibitors benefit the heart?
They don't.
Name 3 antigout medications
1. allopurinol (Zyloprim)
2. Colchicine
3. probenecid (Benemid)
A patient taking a steroids after receiving an organ transplant asks if they can continue taking Echinacea, how do you respond?
The steroids are being taken as an immunosupressant and Echinacea is taken to stimulate the immune system so the Echinacea would be contraindicated.
Would a patient suffering from dementia benefit from taking Gingko?
No. Gingko will improve blood flow to the brain and periperally but will not help if dementia is already present.
How does Gingko effect platelet aggregation? How will this impact the use of anticoagulants and antiplatelet drugs?
Gingko inhibits platelet aggregation and will potentiate the effects of anticoagulants and antiplatelet drugs.
What is Saw Palmetto used for?
To relieve the symptoms of BPH.
If a women does not have a uterus which HRT will she most likely be given? If she does have a uterus? What risk does this pose?
1. Estrogen only therapy because the increased risk of endometrial cancer does not apply and if progestin were given with estrogen it would increase her chances of developing breast cancer.

2. Estrogen and Progestin. The progestin removes the increased risk of endometrial cancer but increases the risk of breast cancer.
What advice would you give a women who takes SERMs and is about to take a long flight?
Stop using the SERM 72 hours before the flight to reduce the risk of thromboembolism and resume taking SERM once fully ambulatory again.
What is the common suffix for the generic name of bisphosphonates?
dronate
What is the longest a women should take a bisphosphonate? What happend after this time?
5 years. After 5 years there is an increase in the number of fractures of "cortical bones" - femur, humerus, etc.
What are the adverse affects of progestins?
breakthrough bleeding
spotting
amenorrhea
breast tenderness
increased risk of breast cancer
What are the risks of HRT therapy?
1. Heart disease
2. Stroke
3. Blood clots
4. Endometrial cancer
5. Breast cancer
6. Dementia
7. Chlosma (brown macular spots on the face)
What special consideration should be given when administering bisphosphonates?
It should be taken first thing in the morning with a full glass of water and the patient must remain upright for 30 minutes to avoid esophogeal erosion.
What is the special consideration for Calitonin?
It is derived from salmon so be aware of salmon allergies.
What is the common suffix for erectile dysfunction drugs?
asfil
Should a patient taking a nitrate take viagra? Why?
No, it can lead to a dangerous drop in BP.
What are the common side effects of erectile drugs?
headache
flushing
dyspepsia
What should a man who has taken a drug for erectile dysfunction do if he has an erection lasting longer than 4 hours?
He should seek immediate care as this is considered to be a medical emergency.
What class of drugs has a suffix of osin? What mens health issue are they used for?What else are these drugs used for? What should be monitored when using these drugs?
1. alpha 1 adrenergic blockers
2. BPH
3. hypertension
4. BP
What special precaution should a woman take when handling finasteride (Proscar)? Why?
She should wear gloves because finasteride is potentially teratogenic.
What is the primary therapeutic use of Growth Hormone?
To tx hyperpituitary dwarfism
What is the route for growth hormone administration? Frequency?
3 times per week via injection
What are the common side effects of growth hormones?
1. hyperglycemia
2. inflammation at the injetion site
What is a growth hormone antagonist used to Tx?
Acromegaly
How are growth hormone antagonists administered?
parenterally
What is ADH and what does it do?
AntiDiuretic Hormone
It decreases urine output
What are the primary uses of ADH?
1. To Tx diabetes insipidus
2. To Tx nocturnal enuresis (bedwetting)
3. Control of hemmorage (esp. vasopressin a vasoconstrictor)
4. To Tx hemophilia A (esp. desmopressin)
What is the common suffix for ADH
pressin
Why are thyroid hormones not cardioprotective?
They increase the sensitivity of the heart to catecholamines
What are the signs/symptoms of hyperthyroidism?
1. palpitations
2. nervousness
3. tachycardia
4. dysrhythmias
When and how should thyroid agents for hypothyroidism be administered?
30 minutes ac breakfast
What are the 2 ways thyroid agents for hyperthyroidism work?
1. Interfere with formation of thyroid hormone
2. Destroy part of the thyroid gland (I-131)
What are the advantages of I-131
1. Avoid surgery
2. Low cost
3. No reported deaths
4. Only thyroid tissue is destroyed
What are the disadvantages of I-131
1. Effect is delayed
2. It is common for to much thyroid gland to be destroyed giving the client life long hypothyroidism
Define glucocorticoid
A major class of corticosteroid hormones that regulate carbohydrate, protein, and lipid metabolism and inhibit the release of corticotropin
Define mineralocorticoid
A major group of corticosteroid hormones that regulate electrolyte and water balance; in humans the primary mineralocorticoid is aldosterone
If a patient has a cerebral edema what glucocorticoid would you anticipate administering?
dexamethaone (Decadron)
What glucocorticoid is commonly used to Tx COPD?
Prednisone
Why is long term use of glucocorticoids avoided in children?
It can cause growth retardation
What are the nursing care points for Growth Hormone?
1. injection only
2. Monitor gluose levels
3. contraindicated in anyone who has stopped growing.
What are the nursing care points for ACTH (adrenocorticotropic hormone)?
1. monitor for allergic response
2. given by injection
What are the nursing care points for ADH?
1. contraindicated in cardiac disease
2. monitor vital signs and I/O
3. Assess weight changes
4. Assess for signs of hyponatermia
Name 3 things to do/no do when taking I-131
1. Wait 7 days for contact with children and pregnant women
2. Wash eating utensils
3. avoid oral contact (kissing)
Myxedma
Hypothyroidism marked by dry skin and swelloing around lips and nose as well as mental deterioration
Enuresis
bedwetting
Epitaxis
Nosebleed
Golytely
Hyperosmotic Laxative
Lactulose
Hyperosmotic Laxative
Glycerin
Hyperosmotic Laxative
Bisacodyl
Stimulant Laxative
Somatropin
Growth Hormone (GH)
Sandostatin
Growth Hormone Antagonist
Somavert
Growth Hormone Antagonist
Corticotropin
ACTH
Cosyntropin
ACTH
Vasopressin
Antidiuretic Hormone
Desmopressin
Antidiuretic Hormone
"asteride"
5-alpha reductase inhibitor
"Afil" or "Adil"
E.D. Drugs
"Osin"
Alpha-1 blocker
Provera
Progestin
Depo Provera
Progestin
Megace
Progestin
Estradiol
Estrogen
Calitonin
Anti-osteoporosis
Tamoxifen
SERM
Raloxifene
SERM
"Dronate"
Bisphosphonates
Garlic
Herbal Remedy-antiplatelet/antihypertensive/antilipid
Ginger
Herbal Remedy-n/v
Kava
Herbal Remedy-anxiety
Valerian
Herbal Remedy-anxiety
Black Cohosh
Herbal Remedy-menopause/PMS
Flax
Herbal Remedy-hypercholesterolemia
Soy
Herbal Remedy-menopause
Ginseng
Herbal Remedy-physical endurance
Saw Palmetto
Herbal Remedy-BPH
Aloe
Herbal Remedy-burns, constipation
Echinacea
Herbal Remedy-immunity
Ginkgo
Herbal Remedy-memory/brain
Feverfew
Herbal Remedy-fever
St. John's Wort
Herbal Remedy-depression
Allopurino
Anti-gout med
Colchicine
Anti-gout med
Probenecid
Anti-gout med
"oxicam"
Enolic Acid NSAID
Mefanamic acid
NSAID
Voltaren
NSAID
Ibuprofen
NSAID
Relafen
NSAID
Celebrex
Cox-2 selective NSAID
Acetaminophen
NSAID
Indomethacin
NSAID
Aspirin
NSAID
Misoprostol
Take it with NSAIDS
Ketorolac
NSAID
Colace
Stool softener
Milk of Magnesia
Saline Laxative
Bentyl
for IBS
Lomotil
Opioid antidiarrheal
Immodium
Opioid antidiarrheal
Kaopectate
antidiarrheal
Pepto Bismol
adsorbent antidiarrheal
Lantus
long-acting insulin
Levemir
long-acting insulin
NPH
intermediate-acting insulin
Humalog
rapid-acting insulin
Novalog
rapid-acting insulin
Apidra
rapid-acting insulin
Metamucil
bulk-forming laxative
Citrucel
bulk-forming laxative
Belladonna
anticholinergic antidiarrheal
Humulin-R
short-acting insulin
Levothyroxine
Hypothyroid drug
PTU
Hyperthyroid drug
Tapazole
Hyperthyroid drug
Iodine
Hyperthyroid drug
Type 1 Diabetes
Beta cells of the pancreas destroyed-- no insulin is produced. Primarily affects children and adolescents.
Type 2 Diabetes
Most prevalent form of diabetes, usually begins in middle age. Decreased insulin secretion & increased insulin resistance.
Metabolic Syndrome/Syndrome X
The collective group of comorbid conditions that are associated with type 2 diabetes.
Gestational Diabetes is characterized by?
High insulin resistance
Normal Hemoglobin A1c=?
4.0-6.0
Desired Hemoglobin A1c for Diabetics=?
<7.0
Who receives insulin?
All type 1 Diabetics, some long term type 2 diabetics, and some short term type 2 diabetics when caused by illness, pregnancy, steroid use, etc.
Rapid Acting Insulin (Humalog, Novolog, Apidra)- onset of action, duration, route of administration, and color of solution?
Onset=5-15 minutes Duration= 3-5 or 6 hours
Route=SC Color=Clear
Short Acting Insulin (Humulin R)- onset of action, duration, route of administration, and color of solution?
Onset=30-60 minutes Duration= 6-10 hours
Route=IV or IM Color=Clear
Intermediate Acting Insulin (NPH)- onset of action, duration, route of administration, and color of solution?
Onset=1-2 hours Duration= 10-18 hours
Route=SC Color=Cloudy (roll to mix solution)
Long Acting Insulin (Lantus, Levemir)-route of administration, color of solution, able to mix with other insulins in same syringe?
Route=SC Color=Clear
*Able to Mix=No, do not mix with other insulins in the same syringe
Sliding Scale Insulin Dosing
Short or Rapid Acting insulin doses adjusted according to blood glucose test results.
Who receives oral antidiabetic agents?
Type 2 diabetics
Biguanide (metformin (Glucophage))- major adverse effect? contraindications? when to hold?
*Adverse Effect-Lactic Acidosis
*Contraindications-renal disease, liver disease, alcoholics
*Hold if patient is to undergo studies w/ contrast dye
Sulfonylureas- MOA? Adverse effects? Precaution?
*MOA-Stimulate pancreas to produce more insulin
*Adverse effects-Hypoglycemia & weight gain
*Precaution: Do not use alcohol w/ med
Glinides- MOA? Adverse effects?
*MOA-Stimulate pancreas to produce more insulin (same effect but shorter duration than sulfonylureas)
*Adverse effects- Hypoglycemia & weight gain
Glitazones- MOA? Adverse effects? Contraindications?
*MOA- Decrease insulin resistance
*Adverse effects- edema and hepatotoxicity
*Contraindications- Liver disease, heart disease, heart failure
Alpha-Glucosidase Inhibitors- MOA? Adverse effects? Time to take?
*MOA-slows absorption of carbs in intestines
Adverse effects- flatulence, cramps, diarrhea, hepatotoxicity @ high doses. Take w/ first bite of food at all meals.
Gliptin- MOA? Adverse effect?
*MOA- Incretin mimetic- enhances action of incretin by inhibiting enzymes that break incretin down
*Adverse effect- pancreatitis
exenatide (Byetta) & liraglutide (Victoza)- MOA? Route? Who can use? Adverse effect?
*MOA- Incretin mimetic- Activate incretin receptors directly
Route-SC Only for Type 2 Diabetics
*Adverse effect- Risk of pancreatitis
pramlintide (Symlin)- Effects? Who can use? Route? Adverse effects?
Effects- Slows gastric emptying & decreases postprandial glucose levels. Can be used by Type 1 and Type 2 Diabetics
Route-SC Adverse effects- Nausea, vomiting
Hypoglycemia blood glucose levels=?
<50-70 mg/dl
Early symptoms of hypoglycemia
headache, confusion, irritability, tremor, fatigue, sweating, drowsiness
Late symptoms of hypoglycemia
seizures, coma, death
Treatment for hypoglycemia
Give oral glucose tabs, D50W (50% Dextrose), Glucagon
Humulin 70/30 should be given how long before a meal?
30 minutes
Humalog 75/25 should be given how long before a meal?
5-15 minutes
insulin lispro (Humalog)
rapid acting insulin
insulin aspart (Novolog)
rapid acting insulin
insulin glulisine (Apidra)
rapid acting insulin
Humulin R
regular insulin
NPH insulin
intermediate acting insulin
glargine (Lantus)
long acting insulin
detemir (Levemir)
long acting insulin
bulk-forming laxatives
psyllium (Metamucil)
methylcellulose (Citrucel)
emollient or surfactant laxatives
docusate sodium (Colace)
mineral oil
stimulant laxatives
bisacodyl (correctol, Dulcolax)
bowel-cleansing solution
polyethylene glycol 3350 (GoLytely)
opioid antidiarrheals
diphenoxylate (Lomotil)
loperamide (Imodium)
anticholinergic antidiarrheal
belladonna (Donnatal)
miscellaneous antidiarrheals that are not opioid or anticholinergic
bismuth subsalicylate (pepto bismol)
attapulgite (kaopectate)
HRT
estrogen
estrogen + progestin
progestins
Provera
Depo-Provera
Megace
SERMs
tamoxifen (Nolvadex)
raloxifene (Evista)
bisphosphonates
alendronate (Foxamax)
risedronate (Actonel)
ibandronate (Boniva)
Calitonin
calcitonin (Miacalcin)
classes of drugs appropriate for tx of osteoporosis
SERMs (selective estrogen receptor modulators)
bisphosphonates
calitonin
erectile dysfunction drugs
slidenafil (Viagra)
vardenafil (Levitra)
tadalafil (Cialis)
alprostadil (Muse)
nonselective anti-inflammatory drugs
ibuprofen
aspirin
naprosyn
ketorolac (Toradol)
indomethacin (Indocin)
the only COX 2 selective inhibitor still on the market
celecoxib (Celebrex)
antigout medications
allopurinol (Zyloprim)
colchicine
probenecid (Benemid)
CLASSES of drugs appropriate to treat BPH
alpha-1 blockers
androgen inhibitors
alpha-1 blockers to treat BPH
doxazosin (Cardura)
tamsulosin (Flomax)
terazosin (Hytrin)
androgen inhibitors
finasteride (Proscar)
dutasteride (Avodart)
growth hormone drugs
somatrem (Protropin)
somatropin (Humatrope)
growth hormone antagonist
octreotide acetate (Sandostatin)
antidiuretic hormone (ADH) drugs
vasopressin (Pitressin)
desmopressin (DDAVP)
hypothyroid tx drug
levothyroxine (Synthroid)
hyperthyroid tx drugs
methimazole (Tapazole)
propylthiouracil (PTU)
I-131
CLASSES of drugs considered adrenal cortex agents
glucocorticoids
mineralcorticoids
glucocorticoids
dexamethasone (Decadron)
prednisone
mineralcorticoids
fludrocortisone (Florinef)
name the three zones of the stomach
cardiac zone
gastric zone
pyloric zone
in the gastric zone, what are the three types of cells, their (main) associated secretions, and the reasons for those secretions?
parietal cells secrete hydrochloric acid to help break down food;
chief cells secrete pepsinogin that also helps break down substances;
mucous cells secrete mucus that serve as a protective coating against the digestive ation of the hydrochloric acid and digestive enzymes
if these three neurotransmitters make connection to their receptor sites, acid production increases, which is why, if we have blockers for any one of these, we effectively reduce acid production
acetylocholine, histamine, gastrin
________ is the last step in acid production, most effective drugs we have for suppressing gastric acid production
proton pump
________ don't bind with any of the receptor sites and don't work with the proton pump to reduce acid
antacids
explain how giving an alkaline compound, such as an antacid, doesn't alter your blood pH
because antacids are generally poorly absorbed, they only work in the stomach, not systemically. Therefore, they don't alter systemic pH
What Antacids will you find constipation a common side effect?
aluminum and calcium based
what antacids will you find diarrhea a common side effect?
magnesium based antacids
antacids are used in treatment of what two conditions?
Peptic Ulcer Disease
GERD
with calcium-based antacids, what is a unique (common) problem in pts once they stop taking it?
hyperacidity; those that take it for a prolonged time, once they stop taking it, they can have a rebound hyperacidity
histamine blockers (H2RAs) suppress secretion of gastric acid by _____
blocking histamine receptor on parietal cell
H2RAs typically end in
-tidine
what is a lifestyle activity that decreases the effectiveness of H2RAs?
smoking
when administering H2RAs and the pt is taking other antacids, when do you want to give it?
1 hour before other antacids
what was the prototype H2RA
cimetidine (Tagamet)
is cimetidine (Tagamet) selective or non-selective?
H2 selective (so it has minimal effect on h1 (allergy) symptoms)
how can cimetidine (Tagamet) be administered?
orally, IM, IV
what is different about cimetidine (Tagamet) when compared to other H2RA's
it CAN cross the BBB, so it can cause confusion, hallucinations, lethargy, etc
(also gynoclamastia, male impotence, decreased libido in men)
this type of drug makes pts achlorhydric
proton pump inhibitors
achlorhydric
without acid
proton pump inhibitors have a new FDA warning about in increased risk of ___
fractures
PPIs are indicated for GERD and what kind of ulcers?
gastric and duodenal ulcers
prototype PPI
omeprazole
PPI typically end in
-prazole
when do you take PPI?
before meals
what are the two classes of drugs that REDUCE ACID (not neutralize existing acid)
H2 blockers, and PPIs
sucralfate (Carafate) - what's different about this drug?
it doesn't neutralize acid and doesn't reduce acid production; it promotes HEALING by creating a protective barrier against acid and pepsin
When to administer sucralfate (Carafate)?
2 hours apart from other drugs (and it has a short half life, so it's given often)
major s/e of sucralfate (Carafate)
constipation
if you have a pt that has to take NSAIDs often due to arthritis, what would you give them and why?
misoprostol (Cytotec). This drug is approved for preventing gastric ulcers caused by long-term NSAID use.
drug approved for preventing gastric ulcers caused by long-term NSAID use
misoprostol (Cytotec)
why do we TYPICALLY not like to use anti-cholinergic drugs as an antacid (although they would decrease GI secretions?)
they would also have yucky side effects (can't see, can't pee, can't sit, can't s*^t)
what is an anti-cholinergic drug that we would consider using, because it's a muscarinic selective antagonist and only works on the muscarinic receptors in the stomach that regulate gastric acid secretion (and thus, would have very little other side effects)
pirenzepine (gastroezepine)
antiemetics are drugs used for
nausea
where is the vomiting center located?
medulla oblongata
what receptors are important in the emetic response?
serotonin, dopamine, ACh, histamine
these drug classes are most effective drugs available for n/v caused by chemo
serotonin receptor antagonists
serotonin receptor antagonists end in
-setron
serotonin receptor antagonists can be combined with ______ (a steroid) for increased effects
dexamethasone (Decadron)
this serotonin receptor antagonist is the BIG chemo drug given for n/v
ondansetron (Zofran)
Serotonin Receptor Antagonists can be administered via
IV or oral
meclizine (Antivert), dimenhydrinate (Dramamine), diphenhyramine (Benadryl) are all what class of drugs being used to treat emesis/vertigo in this case?
antihistamines (h1 receptor blockers)
h1 receptor blockers, when used as an antiemesis, are used most commonly to treat
motion sickness
what is the most common side effect of antihistamines?
drowsiness, but can have anticholinergic effects, as well.
t/f: anticholinergics can be used for antiemesis
true
prokinetic agents
increase the tone and motility of GI tract
what is prokinetic agent prototype?
metoclopramide (Reglan)
common side effect of prokinetic
diarrhea
tetrahydrocannabinoids
dronabinol (Marinol) - related to marijuana - approved for stimulation of appetite and antiemesis
when is dronabinol (Marinol) contraindicated?
psychiatric disorders
Neuroleptics - how do they work?
block the dopamine receptors in the CTZ
why would you not want to give promethazine (Phenergan) or prochlorperazine (Compazine), both neuroleptics, via IV, if at all possible
can cause massive tissue necrosis if leaked out.
normal BP measurements
<120/<80
prehypertesnion
120-139/80-89
stage 1 hypertension
140-159 / 90-99
stage 2 hypertension
=>160 / => 100
as long as there are no other "compelling" indicators, what is first-line therapy for hypertension?
thiazide diuretics (**there is new documentation questioning this, but as of now, this is the standard)
what are compelling indicators?
-post-MI
-high cardiovascular risk
-heart failure
- diabetes mellitus
- chronic kidney disease
- previous stroke
T/F: may pt will require >1 medication to control BP
true
what classes of drugs would be appropriate for a pt with hypertension and stable angina?
beta blocker or calcium channel blocker
what classes of drugs would be appropriate for a pt with hypertension and unstable angina/MI?
beta blocker or ACE inhibitor
what classes of drugs would be appropriate for a pt with asymptomatic heart failure and hypertension?
ACE inhibitor or beta blocker
what classes of drugs would be appropriate for a pt with hypertension and symptomatic heart failure
ACE inhibitor, Beta blocker, ARBs, or aldosterone blocker along with loop diuretic
what classes of drugs would be appropriate for a pt with hypertension and diabetes
2 or more durgs: thiazides, beta blockers, ACE inhibitors, ARBs, CCBs can be used. ACE inhib and ARbs slow progression of kidney disease (if we can use something that can help a patient with hypertension AND that can be reno-protective, it's smart for us to do so)
what two classes of drugs are more effective in whites than in african-americans?
ace inhibitors and beta blockers
what two classes of drugs are typically more effective in blacks than whites?
CCBs, and diuretcs
T/F diuretcs are highly effective antihypertensive agents because they increase fluid volume
False. They are highly effective antihypertensive agents because they DECREASE fluid volume
explain how a diuretic decreases fluid volume and thus decreases BP
a diuretic decreases preload -> which decreases cardiac output -> decreases total peripheral resistance -> decreases workload of heart = lowered BP
Drug Classes Used to Treat Hypertension
-Diuretics
-Adrenergic Agents
-ACE Inhibitors
-Angiotensin II Receptor -Blockers
-Calcium Channel Blockers
-Vasodilators
-Direct Renin Inhibitors
how do alpha 2 agonists lower BP
alpha 2 agonists reduce brainstem vasomotor center-mediated CNS activation; used as antihypertensives to lower BP
What are the adrenergic agents that reduce BP?
alpha 1 antagonists (alpha 1 blockers), alpha 2 agonists, and beta blockers
ACE inhibitors do what to BP
REDUCE bp - but watch for hypotension!
what is a large group of "safe" and effective drugs and used as first-line drugs for heart failure and hypertension?
ACE inhibitors
when are ACE Inhibitors contraindicated?
2nd and 3rd trimesters of pregnancy (but generally stay away during all of pregnancy)
ACE adverse effects
hyperkalemia
ANGIODEMA
dry nonproductive cough
ARB stands for ?
angiotensin II receptor blockers
ARBs MOA
allows the conversion of angiotensin I to angiotensin II but blocks the actual receptor that receives the angiotensin II
benefit of ARB over ACE?
does not cause cough or significant hyperkalemia
contraindication of ARBs?
pregancny
ARBs typically end in
-sartan
when do you typically use calcium channel blockers? (CCB)
angina
hypertension
dysrhythmias
PRIMARY side effect of calcium channel blocker?
constipation
other side effects, besides constipation, of calcium channel blockers
Hypotension, palpitations, tachycardia, nausea,
Rash, flushing, edema, dermatitis
calcium channel blockers typically end in:
-ipine
direct-acting vasodilators lower BP by doing what?
irectly relaxing the smooth muscle walls of blood vessels and thereby lowering peripheral resistance and BP.
direct renin inhibitors work by inhibiting renin and blocking what?
blocking the conversion of angiotensiogen to angiotensin 1 (the precurser)
what should you watch for before starting direct renin inhibitors?
correct hypovolemia before starting and monitor fluid volume closely in patients taking concurrent diuretics
Nursing implications related to hypertension
1. monitor BP during therapy (keep a log)
2. don't stop drugs abruptly- this could cause a rebound hypertensive crisis and lead to stroke
3. teach pts that drugs are only PART of the solution - diet, stress level, weight and ETOH intake can all affect BP as well.
4. encourage pts to avoid smoking and eating foods high in sodium
5. encourage supervised exercise
6. watch for orthostatic hypotension
what additional complications can men encounter while on hypertensive meds?
impotence
why should we care if pts enjoy a hot tub, want to partake in exercise or vacation to bermuda while on antihypertensive meds?
hot tubs, showers, or baths; hot weather; prolonged sitting or standing; physical exercise; and alcohol ingestion may aggravate low blood pressurel, leading to fainting and injury. patients should sit or lie down until symptoms subside.
Nitrates
This group of drugs are antihypertension agents. Patients typically complain of a bad headaches at first but it decrease with time
Nitroglicerin
This drug is a SL form - burning sensation good
No viagra (hypotension risk)
Beta Blockers
This group of drugs are used to treat angina, dysrhythmias, MI, hypertension and more. They are considered "cardioprotective"
Calcium Channel Blockers.
This group of drugs are used to treat Angina, hypertension, & dysrhythmias. They are especially effective for vasospastic angina. Constipation is big problem
diltiazem
This drug is a Calcium Channel Blocker
verapamil
This drug is a Calcium Channel Blocker in the Phenylalkylamine class
adenosine (Adenocard)
This drug is an unclassified antidysrhythmic. Asystole for a period of seconds is normal side effect
thiazide diuretics
This group of drugs are antihypertension agents that are considered the first line therapy for hypertension without "compelling" indicators
Normal BP
<120 / <80
Prehypertension
120-139 / 80-89
Stage 1 hypertension
140-159 / 90-99
Stage 2 hypertension
> 160 / > 100
Alpha-1 Blockers
This group of drugs are antihypertensive agents they may cause orthostatic hypotension when first starting. It is recommended they be taken at night
methyldopa (Aldomet)
This drug is an antihypertensive agent used to treat hypertension during pregnancy
ACE inhibitors
This group of drugs are antihypertensive agents that are commonly called "renoprotective." Serious side effects are hyperkalemia and angioedema - rare but potentially fatal
"nitrate"
Nitrates
"osin"
Alpha-1 Blockers
"lol"
B-Blockers
"dipines"
Calcium Channel Blockers
"sartan"
Angiotensin II Receptor Blockers
"pril"
ACE inhibitors
"tidine"
H2 antagonists
"tropium"
Anticholinergics Bronchodilators
"terol"
Beta-Agonists (Sympathomimetics)
nimodipine
This drug is a Calcium Channel Blocker used to prevent vasospasms after subarachnoid hemmorrhage
Direct-Acting Vasodilators
This group of drugs are antihypertensive agents. May cause HR to increase reflexively due to the vasodilation. Must correct hypovolemia prior to starting
diazoxide and sodium nitroprusside
This drug is a Direct-Acting Vasodilators used to treat emergency hypertension
minoxidil (loniten)
This drug is a Direct-Acting Vasodilator that can cause hair growth. Used in male baldness now as well
BiDil
This drug is a combo drug (hydralazine and isosorbide dinitrate) used to treat hypertension in African American
Dramamine
This drug is an antihistamines usedfor motion sickness
Antivert
This drug is an antihistamine used for vertigo
azelastine (Astelin)
This drug is a 1st generation antihistamine that is available intranasally. This form causes less sedation because it is applied topically
fexofenadine (Allegra)
This drug is a 2nd generation antihistamine. The D form contains pseudoephedrine (drug used to make meth). It also has decreased abosorption with grapefruit and other juices
loratadine (Claritin)
This drug is a 2nd generation antihistamine. The D form contains pseudoephedrine
Topical adrenergics
This group of drugs are potents decongestants with a prompt onset. They can't be used for more than 3-5 days b/c of rebound congestion
Antitussives
This group of drugs are generally used only for nonproductive coughs
dextromethorphan
This drug is the most frequently used nonopioid antitussive.
guaifenesin (Mucinex)
This drug is an expectorant and the actual clinical effectiveness is questionable
Beta-Agonists (Sympathomimetics)
This group of drugs are bronchodilator agents. Short-acting form commonly called "rescue agents". Long-acting form NOT to abort an acute asthma attack.
albuterol
This drug is a beta-2 agonist that is commonly called a "rescue drug" because it treats acute asthma attacks
ipratropium bromide (Atrovent)
This drug is the Anticholinergics Bronchodilator prototype and is contraindicated in clients who are allergic to peanuts.
theophylline
This drug is the Xanthines prototype. The therapeutic range is 10-15 or 20. Concurrent tobacco use ↓ serum levels. & St. John's wort also ↓ serum levels.
Inhaled Corticosteroid
This group of drugs are antiinflammatory agents that have been known to cause oral fungal infections. Abrupt stopping of the oral form can cause adrenal crisis.
Antileukotrienes
This group of drugs are antiinflammatory agents that have been known to cause Liver dysfunction.
terbutaline
This drug is a beta II agonist that was recently banned for use in stopping preterm labor
Xanthines
This group of drugs are bronchodialator agents with a narrow margin of safety and many drug interactions
what is the main adverse effect of anticoagulants (specifically heparin)?
bleeding
what lab value will you monitor when a pt is on heparin?
ptt
what is the normal ptt value of a patient who is NOT on heparin?
25-35 seconds
what is the ptt lab value that we WANT to see of a pt that is on heparin?
1.5 - 2.5x normal ptt times (between 35-70 seconds)
via what route can heparin be administered?
parenteral - SC or IV
what is the antidote for overdose of heparin?
protamine sulfate
what is HIT/HAT?
heparin induced/heparin associated thrombocytopenia. It is NOT the same as heparin toxicity; it is when your platelets bottom out/get too low because you are on heparin.
what is the treatment for a patient with HIT/HAT
argatroban (most common!) or lepirudin
do anticoagulants work on existing clots?
NO- only work to prevent clots from happening, OR to prevent existing clots from growing LARGER.
Name the 3 most common anticoagulants
Heparin
Low molecular weight heparins (I know- sneaky, but they are different!)
warfarin (Coumadin)
How is warfarin (Coumadin) administered?
orally
Name the four major events that anticoagulants are used to PREVENT
1. MI
2. stroke
3. DVT
4. PE
anticoagulants are also used to prevent clot formations in certain settings where clot formations are likely. Name 3 of the 5 given in class.
1. MI
2. Unstable angina
3. atrial fibrillation
4. indwelling devices, such as mechanical heart valves (**note - this is one area in which ptt values may go a bit higher than the 2.5-3.5xs normal)
5. major orthopedic surgery
Does heparin have a short half life, or long half life, in comparison to warfarin?
much shorter half-life: 1-2 hours
What do the 3 low-molecular weigh heparins that are currently available end in (regarding their names) that give us a clue that they are Low-Molecular weight Heparins?
-parin (enoxaparin, daltexparin, and tinzaparin)
what are the 2 MAJOR benefits of low molecular weight heparins over regular heparin?
1. it's given subcutaneously, so it can be done on an outpatient basis at home
2. because it's given subcutaneously, we don't have to monitor daily ptt values
do you aspirate LMWH? (low molecular weight heparin?)
no
what kind of needle do we use to administer regular heparin?
TB syringe
lmwh comes in a predrawn syringe. what else do we know that is different about this?
we DON'T want to get rid of the air bubble in this syringe!
how does warfarin (Coumadin) suppress coagulation?
antagonizing vitamin K (think of it this way - warfarin declares "WAR" on vitamin K and keeps it moving so nothing/noone clumps together!)
what is the antidote of there is warfarin toxicity?
vitamin K
what lab values do we care about if a pt of ours is on warfarin?
prothrombin time (PT or "pro time"), and INR
is warfarin a short-term drug, or long term drug?
long term. (remember that wars drag on for a loooong time)
what is the purpose of an antiplatelet drug?
to prevent platelet adhesion or aggregation
what are some major things we use antiplatelet drugs for?
to prevent MI, reinfarction, strokes, etc
what is THE MOST COMMON antiplatelet drug?
aspirin. usually given around 81-325 mg/day
thrombolytics are different from anticoagulants in what way?
they break down, or lyse, preformed clots (whereas anticoagulants can't break down existing clots - only keep them from forming in the first place)
thrombolytics prevent tissue destruction by ...?
reestablishing blood flow to the tissue by breaking up the clot
thrombolytics are used in what acute care settings?
MI (though less frequently now thanks to cardiac cath labs)
CVA
PE
what common ending do thrombolytic drugs typically have?
-ase (eminase, activase, streptokinase, retavase, etc)
what are the adverse effects of thrombolytics?
BLEEDING! (internal, intracranial, superficial)
n/v
hypotension
anaphylactoid reactions
cardiac dysrhythmias
4 important patient teaching points for pt on thrombolytics
1. importance of regular lab testing
2. signs of abnormal bleeding
3. measures to prevent bruising, bleeding, tissue injury
4. importance of wearing med bracelet
3 important nursing implications for thrombolytics
1. following strict manufacturers guidelines for prep and administration
2. monitor IV sites for pain, redness & bleeding
3. monitor for excessive bleeding (anything from bleeding gums and heavier-than-normal menstrual periods to vomiting blood, decreased BP and increased pulse)
Name the 5 most pharm ways of lowering lipids
1. statins
2. bile acid sequestrants
3. fibric acid derivatives (aka fibrates)
4. cholesterol absorption inhibitor
5. niacin
lipids is another word for
fats
how do lipids transport in the blood?
they bind to protein
this type of lipoprotein is produced by the liver and transports endogenous lipids to the cells
very-low-density lipoprotein (VLDL)
this lipoprotein is most closely correlated with heart disease
low-density lipoprotein (LDL)
this lipoprotein is responsible for cholesterol removal and is known as the "good" cholesterol
high-density lipoprotein (HDL)
the risk of CHD in pt with cholesterol levels of ____ mg/dl is 3-4 times greater than in pateinets with levels less than ____ mg/dl
300 mg/dl ; 200 mg/dl
what should be done before antilipemic drug therapy is used?
all reasonable non-drug means of controlling blood cholesterol levels, such as diet and exercise should be tried for at least 6 months and found to fail before drug therapy is considered. Even then, antilipemic drugs are used as an adjunct to diet therapy and is based on the specific lipid profile of the pt.
Statins are used for pts with what kind of cholesterol problem?
High LDL. (Statins are potent LDL reducers and basically decrease the rate of cholesterol production)
Statin drugs (which treat for pts with high LDL) typically end in what?
-statin (lovastatin, pravastatin, simvastatin, vastatin)
what are the 2 MAJOR adverse effects of statins?
1. MYOPATHY (muscle pain) --> could lead to rhabdomyolysis
2. elevation in LIVER ENZYMES or LIVER DISEASE
When are statins contraindicated?
1. known drug allergy
2. pregnancy
3. liver disease
___________ are used as second or third line therapy, often combined with a statin, and prevent resorption of bile acids from small intestine
bile acid sequestrants
primary side effect of bile acid sequestrants
constipation
when a pt is given a bile acid sequestrant, when should other meds be given?
either 1 hour before or 4 hours after
which antilipemic is appropriate for a pt with a high triglyceride level?
fibric acid derivative (fibrates)
fibrates increase HDL levels by ___% and lower LDL slightly.
25%
explain how fibrates work
fibrates work by activating lipase. the lipase (ASE=enzyme) breaks down cholesterol and inhibits the creation of triglycerides in the liver, and increase secretion of cholesterol into bile.
2 common fibrate drugs
gemfibrozil (Lopid) and fenofibrate (Tricor)
what are side effects/adverse reactions to gemfibrozil (Lopid), a fibric acid derivative?
gi upset
increased risk of gallstones
hepatotoxicity
T/F: cholesterol absorption inhibitors reduce total cholesterol, LDL, triglycerides, and increase HDL levels
true
Give an example of a cholesterol absorption inhibitor
ezetimibe (Zetia)
What vitamin in Niacin also known as?
B3
Name 3 adverse effects of Niacin
1. flushing
2. pruritus
3. gi distress
What is ANGINA PECTORIS?
Chest Pain. The heart requires a large supply of oxygen to meet the demands placed on it. When the supply of oxygen in the blood is insufficient to meet the demands of the heart, the heart muscle "aches"
What are the therapeutic Objectives in the Treatment of Angina?
Increase blood flow to heart muscle and/or Decrease myocardial oxygen demand. Minimize the frequency of attacks and decrease the duration and intensity of anginal pain. Improve the patient's functional capacity with as few adverse effects as possible. Prevent or delay the worst possible outcome, MI
What are the Major drug classes used to treat angina?
Nitrates, Beta Blockers, Calcium Channel Blockers
What forms of Nitrates are used to treat angina?
Sublingual, Buccal, Intravenous solutions, Ointments, Transdermal patches, Translingual sprays (all six bypass 1st-pass effect), Chewable tablets, Oral capsules/tablets
What is the MOA of Nitrates?
Cause relaxation of smooth muscles of the blood vessels which leads to vasodilation. Potent dilating effect especially on coronary arteries. Result: ↑ oxygen to myocardial tissue.

IMPORTANT - Nitrates also alleviate coronary artery spasms. Used for prevention and treatment of angina
Why do they use both rapid-acting and Long-acting Nitrates?
Rapid-acting forms Used to TREAT acute anginal attacks. Sublingual tablets; intravenous infusion.

Long-acting forms Used to PREVENT anginal episodes. All other forms
What are the adverse effects of Nitrates?
Headaches-Usually diminish in intensity and frequency with continued use, Tachycardia, postural hypotension, Tolerance may develop
How do they prevent Nitrates tolerance from developing?
Occurs in patients taking nitrates around the clock or with long-acting forms. Prevented by allowing a regular nitrate-free period to allow enzyme pathways to replenish. Transdermal forms: remove patch at bedtime for 8 hours, then apply a new patch in the morning
How to remember Nitrate names
nitroglycerin others have "nitrate" in name
Nitroglycerin—Nursing Implications: When do you call 911?
Take 1 SL tab, wait 5 minutes, if no relief, call 911 and take another. Take third dose in 5 more minutes and hopefully the ambulance is there and you are still alive.
Name 7 Nursing Instructions to give a patient taking Nitroglcerin at home
1. Instruct patients to take prn nitrates at the first hint of anginal pain
2. Instruct patients in proper technique and guidelines for taking sublingual NTG for anginal pain
3. Instruct patients never to chew or swallow the SL form.
4. Instruct patients that a burning sensation felt with SL forms indicates that the drug is still potent
5. Instruct patients to keep a fresh supply of NTG on hand; potency is lost in about 3 months after the bottle has been opened 6. Medications should be stored in an airtight, dark glass bottle with a metal cap and no cotton filler to preserve potency
7. Instruct patients in the proper application of nitrate topical ointments and transdermal forms, including site rotation and removal of old medication
Name 4 nursing considerations when giving nitroglycerin inpatient
1. Monitor VS frequently during acute exacerbations of angina and during IV administration.
2. If experiencing chest pain, the patient taking SL NTG should be lying down to prevent or decrease dizziness and fainting that may occur due to hypotension
3. IV forms of NTG must be given with special non-PVC tubing and bags
4. Discard parenteral solution that is blue, green, or dark red
Name an important drug interaction that the client should be aware of when taking Nitroglycerin
sildenafil (Viagra) should not be taken within 24 hours of nitrates. The two together can cause an additive hypotensive effect which can be potentially dangerous
Beta Blockers MOA Review. Tell me why you think they should be used after MI
CARDIOPROTECTIVE. B1-receptors on the heart are blocked. Remember...when this happens, the correct answer is "decrease" in terms of effects on the heart. Decreased HR, Decreased myocardial contractility , Decreased myocardial oxygen demand.

After an MI, a high level of circulating catecholamines irritate the heart, causing an imbalance in supply and demand ratio and even leading to life-threatening dysrhythmias. B-blockers block the harmful effects of catecholamines, thus improving survival after an MI. β blockers sometimes called cardioprotective for this purpose
What are β Blockers Adverse Effects?
Bradycardia, hypotension, altered glucose and lipid metabolism, wheezing and dyspnea if nonselective
Name 4 things to teach a patient taking beta blockers at home
1. Patients taking b-blockers should monitor pulse rate daily and report any rate lower than 60 beats per minute
2. Dizziness or fainting should also be reported
3. These medications should never be abruptly discontinued due to risk of rebound hypertensive crisis
4. Inform patients that these medications are for long-term prevention of angina, not for immediate relief
Describe the MOA of Calcium Channel Blockers.
Cause coronary artery vasodilation. Decrease myocardial contractility. Result: decreased myocardial oxygen demand.

IMPORTANT - Especially effective for treatment of vasospastic angina
What are the adverse effects of Calcium Channel Blockers?
Very acceptable adverse effect and safety profile. May cause hypotension, palpitations, tachycardia or bradycardia, constipation, nausea, dyspnea
What are the three Calcium Channel Blockers used for angina?
diltiazem (Cardizem, Dilacor)
verapamil (Calan, Isoptin)
several "dipines"
What is the most common side effect of calcium channel blockers? What instructions should a nurse give a patient who is taking them?
Constipation is a common problem; instruct patients to take in adequate fluids and eat high-fiber foods.
What are 3 general nursing implications for antianginals?
1. Alcohol consumption and hot baths or spending time in whirlpools, hot tubs, or saunas will result in vasodilation, hypotension, and the possibility of fainting
2. Teach patients to change positions slowly to avoid postural BP changes
3. Encourage patients to keep a record of their anginal attacks, including precipitating factors, number of pills taken, and therapeutic effects
CHAP 24 Antianginal Agents REVIEW
The use of Nitrates, Beta Blockers, & Calcium Channel Blockers to control angina and prevent MI.

DRUGS
Nitrates - nitroglycerin (all others have "nitrate" in name

B-Blockers - all end in "lol"

Calcium Channel Blockers - diltiazem (Cardizem, Dilacor)
verapamil (Calan, Isoptin)
several "dipine"
What do the terms Dysrhythmia and Antidysrhythmics mean?
Dysrythmia is any deviation from the normal rhythm of the heart. Antidysrhythmics are Drugs used for the treatment and prevention of disturbances in cardiac rhythm.
Name the six Common Dysrhythmias
1. Supraventricular dysrhythmias
2. Ventricular dysrhythmias
3. Ectopic foci
4. Conduction blocks
5. Bradydysrhythmia
6. Tachydysrhythmia
What is Vaughan Williams Classification?
Classification of dysrythmias.
Class I, A, B, C
Class II
Class III
Class IV
Miscellaneous
Tell about Class 1--Sodium Channel Blockers
1. Block the fast sodium channels
2. All are prodysrhythmic
3. Similar in structure to local anesthetic properties
4. Adverse effects vary with individual drug but In general: bradycardia, hypotension
However, some have significant anticholinergic effects (dry mouth, constipation, urinary retention)
Name four Class 1a drugs
1. procainamide (Pronestyl, Procan SR)
2. quinidine sulfate (Quinidex)
3. quinidine gluconate
4. disopyramide (Norpace)
Tell about MOA, usages, and adverse effects of the Class 1a drug procainamide (Pronestyl, Procan SR)
Blocks fast sodium channels, slows impulse conduction, delays repolarization, prolongs refractory period. Inhibit formation of ectopic foci in atria and ventricle

Can be used for both atrial and ventricular dysrhythmias

Adverse effects are
Prodysrhythmic
Hypotension
Bradycardia
Lupus-like syndrome
You are administering oral procainamide to a client. What do you want to know before you give the drug? What will you watch for after administration?
...
What is the MOA and usage of Class 1b drugs
Block sodium channels. Shorten refractory period. Little effect on conduction velocity. Minimal effects on ECG

Used for ventricular dysrhythmias
Class 1b drugs
lidocaine (Xylocaine)
mexiletine (Mexitil)
phenytoin (Dilantin)
What are 5 important points to remember about Class IB--lidocaine (Xylocaine)
1. No anticholinergic properties
2. Administered IV for acute ventricular dysrhythmias
3. Not effective with atrial dysrhythmias
4. Serum lidocaine levels may be monitored
5. First signs of toxicity involve the CNS: confusion, anxiety, tremors, paresthesias
Tell about the MOA and usage of Class 1c drugs
Block sodium channels. Profoundly decreases conduction velocity. ECG intervals often prolonged

Generally used for life-threatening dysrhythmias—atrial predominately. Pronouned prodysrhymic effects
Name 2 Class Ic drugs
flecainide (Tambocor)
propafenone (Rhythmol)
Name the four important points to remember about Class IC--flecainide (Tambocor)
1. CAST—p. 360
2. Generates new ventricular dysrhythmias in about 10% of patients
3. Use is limited to life-threatening ventricular dysrhythmias
4. Serum levels generally monitored
Tell about MOA and usage of Class II--Beta Blockers
Block SNS stimulation. Slow the heart rate (- chronotropic)

Many uses as an antidysrhythmic. Tx of atrial dysrhythmias associated with heart failure. Decrease likelihood of sudden death due to fatal dysrhythmias in post-MI clients. Tx of tachydysrhythmias
Name the two types of Class II—Beta blockers
Cardioselective and nonselective.
All end in LOL
Tell about the MOA and usage of Class III—Potassium channel blockers
Repolarization of the heart depends on removal of potassium from the cell. Class III drugs block the potassium channels in myocardial cells. This causes a delay of repolarization and prolongs the refractory period.
ECG: increase QT interval, bradycardia

Limited use due to potentially serious toxicity
Name three important things to remember about Class III--amiodarone (Cordarone)
1. Effective in both atrial and ventricular dysrhythmias.
2. Adverse effects common!
Corneal microdeposits
Hypo- or hyperthyroidism
Pulmonary toxicity
Prodysrhythmic
3. Exceptionally long half-life!
Your patient has been receiving amiodarone for several months. What are your assessment priorities?
...
Tell about the MOA and usage of Class IV--Calcium Channel Blockers
Inhibit the slow channels or the calcium-dependent channels. Slows impulse conduction and heart rate

Used to treat atrial dysrhythimias
Generally well tolerated; monitor for bradycardia and hypotension
Name two Class IV - Calcium Channel Blockers
verapamil (Calan)
diltiazem (Cardizem)
Name the two Unclassified Antidysrhythmics
adenosine (Adenocard)
digoxin (Lanoxin)
Name 4 important points about adenosine (Adenocard)
1. Terminates tachycardia
2. Given as rapid IV bolus for the conversion of PSVT to NSR
3. Very short half-life
4. IMPORTANT - Asystole for a period of seconds is normal side effect
digoxin (Lanoxin)
1. Sometimes used as an antidysrhythmic
2. Primarily used for Afib/Aflutter
3. Negative inotropic, chronotropic, and dromotropic effects
Five Nursing Considerations with a patient on antidysrhythmics
1. Frequent measurement of serum drug levels, serum electrolytes, heart rate and BP
2. Patients taking -blockers, digoxin, etc., should be taught how to take their own radial pulse for 1 full minute, and to notify their physician if the pulse is less than 60 beats/minute before taking the next dose of medication
3. For class I drugs, monitor ECG for QT intervals prolonged more than 50%
4. IV infusions should be administered with an IV pump
5. Solutions of lidocaine that contain epinephrine should not be given IV—they are to be used ONLY as local anesthetics
What are two reasons a patient taking antidysrhythmics should be instructed to call the doc?
1. Any worsening of dysrhythmia
2. Toxic effects - Shortness of breath, Edema, Dizziness, Syncope, Chest pain, GI distress, Blurred vision, Edema
What two mechanisms determine BP?
cardiac output and peripheral vascular resistance
What is JNC VII
Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC-7) May 2003. JNC VIII (8) Panel appointed August 2008, Expected release date is Spring 2011
What are the Four stages of hypertension based on BP measurements? She want this memorized
Normal--<120 / <80
Prehypertension—120-139 / 80-89
Stage 1 hypertension—140-159 / 90-99
Stage 2 hypertension--> 160 / > 100
What is generally the first line therapy for patients with hypertension but without other "compelling" indicators?
thiazide diuretics according to JNC VII but has recently been questioned. Many patients will require >1 medication to control BP
What are "Compelling indicators" for hypertension?
Post-MI, High cardiovascular risk, Heart failure, Diabetes mellitus, Chronic kidney disease, Previous stroke
Which hypertensive medications work better for African Americans? Which work better for caucasion?
Better for African American: CCBs and diuretics

Better for Caucasion:
B-blockers and ACE inhibitors
What are the 7 Drug Classes Used to Treat Hypertension?
Diuretics
Adrenergic Agents
ACE Inhibitors
Angiotensin II Receptor Blockers
Calcium Channel Blockers
Vasodilators
Direct Renin Inhibitors
Why are Diuretics highly effective antihypertensive agents? What type of diuretics are most commonly used for BP?
Decreases fluid volume
↓ preload
↓ cardiac output
↓ total peripheral resistance
↓ workload of heart
↓ BP
Exert effects in different areas of the renal tubules

Thiazides are used most commonly for BP control and are listed in JNC 7 guidelines
How do alpha-1 antagonists lower BP?
vasodilation
Alpha-1 Blockers
"osin"
prazosin (Minipress)
doxazosin (Cardura)
terazosin (Hytrin)

Remember causes orthostatic hypotension when first starting.... take at night
How do alpha-2 agonists lower BP?
inhibit secretion of norepinephrine
methyldopa (Aldomet)
commonly used to treat hypertension during pregnancy
How do Beta Blockers
Reduce BP?
by reducing heart rate through B1-blockade. reduced secretion of renin
Things to remember when taking B-Blocker
1. don't stop abruptly
2. watch for orthostatic hypotension
3. take pulse rate at home. Call if less than 60
4. Also watch systolic blood pressure, hold if it is less than 90-100.
Name 2 b blockers used as antihypertensives
atenolol (Tenormin)
nebivolol (Bystolic)
What letters do alpha/beta blockers end in?
still end in lol if it is alpha and beta blocker - she will tell us if it is an alpha/beta blocker on test
Who is ACE and why do we want to inhibit him?
ACE inhibitors come from the venom of a Brazilian pit viper in the Brazilian rain forest. Well known that pit viper bites lead to rapid hypotension. Now used therapeutically to treat hypertension
Angiotensin: What does it do?
"Tenses" your "angios"!! →vasoconstriction

Renin-Angiotensin-Aldosterone System (RAS)
Angiotensin-converting enzyme (ACE) is responsible for converting angiotensin I (through the action of renin) to angiotensin II. Angiotensin II is a potent vasoconstrictor and causes aldosterone secretion from the adrenals.

Watch for hyperkalemia - lose sodium and water and hold potassium on ACE drugs
Why would a hypertensive diabetic benefit especially from ACE inhibitors?
"renoprotective" Slows progression of renal disease in hypertensive diabetics with renal disease
What letters do ACE inhibitors all end in?
"pril"
ACE Inhibitors are generally considered safe(ish). When would it NOT be safe at all for a person with hypertension to take an ACE Inhibitor?
If you are pregnant. All ACE inhibitors are contraindicated in the 2nd and 3rd trimesters of pregnancy
ACE inhibitors side effects
dry nonproductive cough
hypokalemia
angioedema - rare but potentially fatal
What is the MOA of Angiotensin II Receptor Blockers (ARBs)?
Allow angiotensin I to be converted to angiotensin II, but block the receptors that receive angiotensin II. Block vasoconstriction and release of aldosterone
How do Angiotensin II Receptor Blockers compare to ACE Inhibitors?
Both contraindicated in pregnancy

ARBs Do not cause cough or significant hyperkalemia but can cause upper respiratory infection and headache.
What letters do all ARBs end in?
"sartan"
What is the MOA of Calcium Channel Blockers?
Cause smooth muscle relaxation by blocking the binding of calcium to its receptors, preventing muscle contraction.
This causes decreased peripheral smooth muscle tone and decreased systemic vascular resistance.
Result: decreased blood pressure
What conditions are calcium chanel blockers used to treat?
Angina, hypertension, dysrhythmias
What are the adverse effects of calcium channel blockers?
Causes major constipation problems!!!! Hypotension, palpitations, tachycardia, Constipation, nausea
Rash, flushing, peripheral edema, dermatitis
What are the Calcium Channel Blocker drugs used for hypertension?
diltiazem and verapamil are used to treat hypertension, angina, and dysrhythmias

All of the other ones end in "dipine" These are used to treat hypertension and angina, but NOT dysrhythmias.

nimodipine - solely used to prevent vasospasms after subarachnoid hemmorrhage
What do you check before giving an ACE inhibitor?
potassium and bp
What is the MOA of Direct-Acting Vasodilators?
Directly relax the smooth muscle walls of blood vessels thereby lowering peripheral resistance and BP. HR is often increased reflexively due to the vasodilation.

diazoxide and sodium nitroprusside used to treat emergency hypertension

minoxidil (loniten) can cause hair growth. Used in male baldness now as well

BiDil- combo drug (hydralazine and isosorbide dinitrate) used for African American
What is the MOA of Direct Renin Inhibitors?
Inhibits renin and blocks the conversion of angiotensinogen to angiotensin I.
Ultimately decreases the level of angiotensin II and suppresses activation of the RAS.
What should you monitor for when a patient is on this med?
Must correct hypovolemia prior to starting and monitor fluid volume closely in patients taking concurrent diuretics.
What is a Combination antihypertensive?
There are many available. Now actually combining three separate medications into one pill
8 Nursing Implications related to hypertension
1. Monitor BP during therapy; instruct patients to keep a journal of regular BP checks
2. Instruct patients that these drugs should not be stopped abruptly because this may cause a rebound hypertensive crisis, and perhaps lead to stroke
3. Remind patients that medication is only part of therapy. Encourage patients to watch their diet, stress level, weight, and alcohol intake
4. Patients should avoid smoking and eating foods high in sodium
5. Encourage supervised exercise.
6. Instruct patients to change positions slowly to avoid syncope from postural hypotension
7. Men taking these drugs may not be aware that impotence is an expected effect of many medications. This may influence compliance with drug therapy
8. Hot tubs, showers, or baths; hot weather; prolonged sitting or standing; physical exercise; and alcohol ingestion may aggravate low blood pressure, leading to fainting and injury. Patients should sit or lie down until symptoms subside.
What are the DRUGS AFFECTING THE UPPER RESPIRATORY SYSTEM?
Antihistamines, Decongestants, Antitussives, and Expectorants
What is the MOA of Antihistamines?
Drugs that directly compete with histamine for specific receptor sites
What are the two histamine receptors
H1 (histamine1), H2 (histamine2)
What are H1 blockers or antagonists used for?
What are H2 blockers or antagonists used for?
H1 antagonists are commonly referred to as antihistamines and are used for respiratory disorders

H2 blockers or H2 antagonists
Used to reduce gastric acid in peptic ulcer disease
What letters do H2 antagonists all end in?
"tidine"
Common trade names are Tagamet, Zantac, Pepcid, and Axid
What does H1 do? (why would we need to take H1 blockers?)
Bronchoconstriction
Increase in body secretions—especially mucus
Vasodilation→↓ BP
Fluid movement out of the blood vessels and into tissues leading to edema
Stimulation of nerve endings causing itching
What does H2 do? (why would we need to take H2 blockers?)
Secretion of gastric acid
What percentage of the population needs to take Antihistamines for environmental allergies?
10% to 20% of general population is sensitive to various environmental allergies.
Name 7 common disorders antihistamines are used to treat.
1. Histamine-mediated disorders
2. Allergic rhinitis (hay fever, mold, and dust allergies)
3. Anaphylaxis
4. Angioneurotic edema
5. Drug fevers
6. Insect bite reactions
7. Urticaria (itching)

Also used for motion sickness, insomnia, vertigo. May be used to treat colds and influenza—palliative, not curative

IMPORTANT -
Dramamine for motion sickness
Antivert for vertigo
Why is it important to administer antihistamines promptly?
Work by inhibiting the action of histamine (H1)—not by preventing its release
Do not "push off" histamine that is already bound to a receptor, but competes with histamine for unoccupied receptors.

So take it before you go around a known allergen
What are antihistamine beneficial effects?
Produces the opposite effect of histamine causing relaxation of bronchial tree, DECREASES secretions, itching, flushing, & edema. Cause vasoconstriction,

Older antihistamines also cause mild CNS depression→sedative effect
What are antihistamine Adverse effects?
Anticholinergic (drying) effects, most common: Dry mouth, Difficulty urinating, Constipation,
Changes in vision.
Drowsiness - Mild drowsiness to deep sleep
What are the Two Types of Antihistamines?
Traditional—1st generation

Nonsedating/peripherally acting—2nd generation
Tell about Traditional antihistamines—1st generation
Older. Work both peripherally and centrally. Have anticholinergic effects, making them more effective (more drying of secretions) than nonsedating drugs in some cases.

diphenhydramine (Benadryl)
chlorpheniramine (Chlor-Trimeton)
Nonsedating/peripherally acting—2nd generation
Developed to eliminate unwanted adverse effects, mainly sedation. Work peripherally to block the actions of histamine; thus, fewer CNS adverse effects. Longer duration of action (increases compliance)

fexofenadine (Allegra)
loratadine (Claritin)
cetirizine (Zyrtec)
What is the myth about first generation drugs and sedation?
Benedryl causes significant sedation but many first generation drugs are actually comparable to 2nd. First gen efficacy is higher as well.
How are most 1st Generation Antihistamines administered?
Most given orally
When people just say antihistamine, are they talking about H1, H2, or both?
H1
How is the intranasally form of azelastine (Astelin) - a 1st generation antihistamine - different from oral meds?
azelastine (Astelin) is available intranasally. Just as effective as oral meds. Less sedation because it is applied topically
Tell about fexofenadine (Allegra) a 2nd generation antihistamine
Approved in 1996. Long duration of action. Can dose 1-2 times/day. Administered orally.
Allegra-D—contains pseudoephedrine (drug used to make meth).
Drug/food interactions - Decreased abosorption with grapefruit and other juices
Tell about loratadine (Claritin) a 2nd generation antihistamine
Can dose 1-2 times/day. Administered orally
Claritin-D contains pseudoephedrine

Two others:
cetirizine (Zyrtec)
levocetirizine (Xyzal)
What are 5 things a nurse should teach a patient taking antihistamines?
1. Instruct patients to report excessive sedation, confusion, or hypotension
2. Instruct patients to avoid driving or operating heavy machinery; advise against consuming alcohol or other CNS depressants
3. Instruct patients to not take these medications with other prescribed or OTC medications without checking with prescriber
4. Best tolerated when taken with meals—reduces GI upset
5. If dry mouth occurs, teach patient to perform frequent mouth care, chew gum, or suck on hard candy (preferably sugarless) to ease discomfort
What are the three main types of Decongestants?
Three main types are used
1. Adrenergics - Largest group, Sympathomimetics

2. Corticosteroids - Topical, intranasal steroids

3. Anticholinergics - Less commonly used, Parasympatholytics
What are the two dosage forms of decongestants?
1. Oral
2. Inhaled/topically applied to the nasal membranes
What is the MOA of Adrenergics?
Adrenergics (sympathomimetics)
Site of action: blood vessels surrounding nasal sinuses
Constrict small blood vessels that supply
URI structures—(α1 agonist)
As a result these tissues shrink, and nasal secretions in the swollen mucous membranes are better able to drain
Nasal stuffiness is relieved
What is the MOA of Nasal steroids?
Nasal steroids
Site of action: blood vessels surrounding nasal sinuses.
Antiinflammatory effect.
Work to turn off the immune system cells involved in the inflammatory response.
Decreased inflammation results in decreased congestion.
Nasal stuffiness is relieved
What is the MOA of Anticholinergics?
Anticholinergic
Ipratropium (Atrovent)
↓ nasal secretions
What are the benefits of using Topical adrenergics?
Prompt onset
Potent

phenylephrine (Neo-Synephrine)
How long should a patient use topical adrenergics?
Sustained use over several days causes rebound congestion, making the condition worse. Should not be used longer than 3-5 days
What do you teach a patient who has become addicted to adrenergic nasal spray?
To stop Cold Turkey.... it may take a week or longer for rebound congestion to subside.
Or Stop one side at a time.
What are the benefits of using topical Intranasal steroids?
Do not cause rebound congestion
beclomethasone (Beconase)
flunisolide (Nasalide)
fluticasone (Flonase)
How do oral decongestants compare to topical?
Prolonged decongestant effects,
but delayed onset.
Effect less potent than topical.
No rebound congestion.
More systemic side effects.
Exclusively adrenergics.
Example: pseudoephedrine (Sudafed)
What are 3 things a nurse should teach a patient taking decongestants?
1. Patients on medication therapy for hypertension should check with their physician before taking OTC decongestants
2. Patients should avoid caffeine and caffeine-containing products
3. Report a fever, cough, or other symptoms lasting longer than a week
What are Antitussives?
Drugs used to stop or reduce coughing. Most of the time, coughing is beneficial because it removes excessive secretions and potentially harmful foreign substances. In some situations, coughing can be harmful, such as after hernia repair surgery. Or can be used for dry cough.

IMPORTANT-
Generally used only for nonproductive coughs!
What are the 2 types of antitussives?
Opiods and nonopiods
What is the MOA of Opiod Antitussives?
Suppress the cough reflex by direct action on the cough center in the medulla
Examples:
codeine (Robitussin A-C, Dimetane-DC)
hydrocodone
What is the MOA of Nonopiod Antitussives?
Suppress the cough reflex directly or numbs the stretch receptors in the respiratory tract and prevents the cough reflex from being stimulated
Examples:
benzonatate (Tessalon Perles)
dextromethorphan (Vicks Formula 44,
Robitussin-DM)
dextromethorphan
Most frequently used and most effective nonopioid antitussive.
Considered as effective as codeine.
Minimal risk of dependence.
Widely available OTC in capsules, lozenges, syrups, suspensions, and chewable tablets.
Adverse effects are rare, but include N/V, drowsiness, dizziness, restlessness.
Generally recommended for a persistent, nonproductive cough
What are 3 things a nurse should teach a patient taking antitussives?
1. Instruct patients to avoid driving or operating heavy equipment
2. Patients taking chewable tablets or lozenges should not drink liquids for 30 to 35 minutes afterward
3. Report a persistent cough to the caregiver
What are Expectorants?
Drugs that aid in the expectoration (removal) of mucus.
Reduce the viscosity of secretions.
Disintegrate and thin secretions.
Tell about guaifenesin (Mucinex)
guaifenesin reduces the adhesiveness and surface tension of bronchial secretions; thus, making them easier to "cough up". Actual clinical effectiveness in reducing acute cold symptoms questionable. Look at pg 559. Often found in combination with other OTC cold/flu medications. Few adverse effects
What should a nurse teach a patient who is taking an expectorant?
1. Patients taking expectorants should receive more fluids, if permitted, to help loosen and liquefy secretions
2. Report a fever, cough, or other symptoms lasting longer than a week
What are the Drugs that Affect the Lower Respiratory System
Bronchodilators and Antiinflammatory Agents
Tell about Pulmonary Inhalers
Metered-dose inhaler (MDI) - old type not environmentally friendly and patients don't like new type. Using them without spacers causes user errors because people put them too close to their mouth and the dose goes to the roof of mouth instead of lungs

Dry powder inhaler (DPI)
Nebulizer
What are the three types of bronchodialators?
Beta-Agonists, Anticholinergics, and Xanthines
Beta-Agonists (Sympathomimetics)
For the desired effects on the lungs, would want a beta-2 stimulant→broncho-dilation
Most are administered orally or by inhalation.

Short-acting: Inhaled, Used to terminate an acute asthma attack
IMPORTANT - Sometimes referred to as rescue agents

Long-acting: NOT indicated to abort an acute asthma attack.
Inhaled or oral
albuterol (ProAir, Proventil)
A moderately selective beta-2 agonist. Available orally and by inhalation (MDI). Inhaled IMPORTANT - albuterol is referred to as a "rescue drug". Adverse effects more common with oral administration—tachycardia, palpitations, anxiety, tremors, HA, insomnia.

There are others - all end in "terol"
salmeterol (Serevent) - Black box warning use with caution
What is the MOA of Anticholinergics as Bronchodilators?
Acetylcholine (ACh) causes bronchial constriction and narrowing of the airways
Anticholinergics bind to the ACh receptors, preventing ACh from binding
Result: bronchoconstriction is prevented, airways dilate
Generally administered via inhalation—oral or nasal

Anticholinergics Bronchodilators end in "tropium"
Tell about ipratropium bromide (Atrovent) Anticholinergics Bronchodilator Prototype
A muscarinic antagonist
Contraindicated in clients who are allergic to peanuts.
S.e. rare as little is absorbed systemically—cough, throat irritation

Similar drug:
tiotropium (Spiriva)
Longer onset and duration
DPI

Another option
albuterol/ipratropium (Combivent)—MDI or (DuoNeb)—inhalation solution
Tell about Xanthines
Once the treatment of choice for asthma and bronchospasm.
Relatively narrow margin of safety and many drug interactions. Consequently, no longer widely used.
Chemically related to caffeine and have a similar stimulant effect
theophylline
Xanthine Prototype. Relaxes bronchial smooth muscle→ bronchodilation. Suppresses airway responsiveness to stimuli that promote bronchospasm.
Therapeutic range is 10-15 or 20
Adverse effects directly related to serum levels: N/V, HA, irritability, insomnia, dysrhythmias, hypotension, tachycardia, seizures.

IMPORTANT - Concurrent tobacco use ↓ serum levels; St. John's wort does as well. Concurrent caffeine use leads to ↑ CNS stimulation
What are the three antiinflammatory agents?
Corticosteroids, Antileukotrienes, and Mast Cell Stabilizers
What is the MOA of corticosteroids?
MOA—Inhibit release of inflammatory mediators (histamine, leukotriene, cytokines, etc.)
Tell about Corticosteroid usage to treat asthma
The most effective anti-inflammatory drugs available. Inhaled steroids used both for prevention of asthmatic attacks and management of chronic asthma—fixed schedule, not prn. Oral steroids reserved for short-term tx of acute exacerbations. Used cautiously in anyone with an active infection.
Adverse effects limited with the inhaled route—pharyngeal irritation, cough, dry mouth, and

IMPORTANT-
- oral fungal infections - always rinse mouth after use to help prevent.
- Steroids are NOT used to abort an acute asthma attack
Corticosteroid Prototype—beclomethasone (Beconase)
Administered via inhalation for asthma (Qvar)

Similar medications
triamcinolone acetonide (Azmacort)
fluticasone (Flovent, Flonase)
Note the spelling of the generic names!
What are 3 thing a nurse should teach a patient who is taking corticosteroids?
1. If switching from oral to inhaled steroids, must taper doses. When taking oral, adrenal glands stop producing the steroid. If you switch abruptly to inhaled form (which doesn't have a lot of systemic effect) you can cause adrenal crisis because your adrenal glands have not begun to produce the steroid again. This can be fatal. It can take up to a year for the adrenal gland to fully function after longterm steroid use.
2. Teach patients to gargle and rinse the mouth with lukewarm water afterward to prevent the development of oral fungal infections
3. If a β-agonist bronchodilator and corticosteroid inhaler are both ordered, the bronchodilator should be used several minutes before the corticosteroid to provide bronchodilation before administration of the corticosteroid
What are Antileukotriene Agents, and what is the MOA?
Also called leukotriene receptor antagonists (LTRAs). Leukotrienes are substances released when a trigger, such as cat hair or dust, starts a series of chemical reactions in the body.
Leukotrienes cause inflammation, bronchoconstriction, and mucus production. LTRAs prevent leukotrienes from attaching to receptors within the lungs which blocks inflammation in the lungs.
Not used for an acute attack; may be used for prophylaxis and long-term maintenance.
Antileukotrienes: Adverse Effects
HA, nausea
IMPORTANT - Liver dysfunction.
Assess liver function before beginning therapy and periodically throughout.
montelukast (Singulair) has not been associated with liver dysfunction
What are Mast Cell Stabilizers and what is the MOA?
Mast cells contain inflammatory granules such as histamine. When released, these granules initiate the inflammatory response.

Available medications
cromolyn (Intal)—MDI
nedocromil (Tilade)—has a very bitter taste (MDI)
When would you use Mast Cell Stabilizers to treat asthma?
Used to treat asthma when steroids are not effective or are contraindicated.
Not for an acute attack.
Must take on a regular basis to maintain benefit if used because of histamine related asthma.
If used for exercise-induced asthma, take 15-30 minutes before exercise
Some things to read in book
Pharmaco Bridge of Nitrate on page 376.

How to correctly apply ointments pg 377

Dig Babies and children pg 342

Xanthine and elderly - pg. 576
tributaline (beta II agonist)
no longer used to stop preterm labor
What is a recent change in the treatment of asthma?
Recently the focus has switched from using bronchodilators to using more antiinflamatory meds.
Kayexalate
treatment for hyperkalemia
Aldosterone
causes the retension of water and sodium and excretion of potassium
Glaucoma
the primary therapeutic use of carbonic anhydrase inhibitors
Lasix
the main loop diuretic
spironolactone (Aldactone)
Now commonly used in the treatment of heart failure—evidence based practice!
Protects the heart from ventricular remodeling after a MI.
Mannitol
Osmotic Diuretics prototype. Can only be given parenterally. May crystallize when exposed to low temperatures
Acetazolamide
is used in the management of edema secondary to heart failure when other diuretics are not effective
phenobarbital
prototype of barbiturates
Valium (diazepam)
benzodiazepine
Lorazepam (Ativan)
Benzo antianxiety, habbit forming, only use for short time
hydroxyzine (Vistaril)
Antihistimine for anxiety causes significant sedation
valproic acid (Depakote)
abticonvulsant drug is also used to treat anxiety
buspirone (BuSpar).
Miscellaneous axiolytic. Exact MOA not known. Anxiolytic effects develop slowly—not appropriate for prn use
Lithium
Antimanic drug is the prototype
chlorpromazine (Thorazine)
Phenothiazine antipsychotic. many anticholinergic adverse effects
fluphenazine (Prolixin)
Phenothiazine antipsychotic. many anticholinergic adverse effects
clozapine (Clozaril—1989)
Atypical antipsychotic. increased risk of agranulocytosis and need lab work weekly (WBCs)
olanzapine (Zyprexa--1996)
Atypical antipsychotic
aripiprazole (Abilify—2002)
Atypical antipsychotic
bupropion (Wellbutrin)—Zyban
Miscellaneous Antideppressant - is a sustained release form that is also used as first-line therapy for smoking cessation. it does not cause sexual dysfunction or weight gain. In fact, it can increase libido and cause weight loss! However, it can also cause seizures.
trazodone (Desyrel)
Miscellaneous antidepressant. is commonly used for insomnia
imipramine (Tofranil)
TCA is also used to treat enuresis (or bedwetting)
ENSAM
a new selegiline transdermal patch. It is selective MAOI Type B inhibitor —can be used without the dietary restrictions at its lowest dose (6 mg over 24 hrs).
amphetamine (Adderall)
Drugs used in Treatment of attention deficit hyperactivity disorder (ADHD)
methylphenidate (Concerta, Ritalin)
Drugs used in Treatment of attention deficit hyperactivity disorder (ADHD)
atomoxetine (Strattera)
used in Treatment of (ADHD). It is not addictive, but the FDA issued a warning in 2005 describing cases of suicidal thinking in recipients
modafinil (Provigil)
the CNS Stimulant drug used to treat narcolepsy
sumatriptan (Imitrex),
drugs used for Treatment of migraine headaches. abortive drugs and not preventative
zolmitriptan (Zomig)
drugs used for Treatment of migraine headaches . abortive drugs and not preventative
Sodium Oxybate (Xyrem)
Is misused as a "date rape" drug. Approved to treat cataplexy which is a condition characterized by acute attacks of muscle weakness and often associated with epilepsy. Only available through restricted dispensing programs Schedule III drug. Technically a CNS depressant
phentermine (Ionamin)
Appetite suppressants (anorexiant)
sibutramine (Meridia)
Appetite suppressants (anorexiant)
orlistat (Xenical)
not actually a CNS Stimulant it is a Lipase inhibitor. Used as anorexiant
Diazepam
Benzodiazipine drug that can be given IV or rectally and is commonly used to treat epilepsy.
Phenytoin
antiepileptic. tightly protien bound and it induces hepatic enzymes. It can cause gingival hyperplasia with prolonged use
fosphenytoin
phenytoin precursor
carbemazepine (Tegretol)
Antiepileptic. Carbamazepine undergoes autoinduction. Levels may need to e adjusted for the first few months, but then it should level out
PHENOBARBITAL
A barbiturate. LONG half-life 2-3 weeks. Drowsiness is common side effect, but tolerance usually develops, Some children experience paradoxical excitability
VALPROIC ACID (Depakene) an Antiepileptic
Used for tx of seizures, bipolar disorder, and migraine prevention. Serious side effects are rare but include liver toxicity and pancreatitis. Several drug interactions but it is NOT an inducer
Sinemet
The cornerstone of levodopa therapy. Some advantages over levodopa alone are:
1. Dose reduction
2. Don't need to limit pyridoxine
3. Less on-off
amantadine (Symmetrel)
Another common drug used for PD. Stimulates the release of dopamine from nerve endings in the CNS or may block the reuptake of dopamine. Most effective in earlier stages. Usually effective for only 6-12 months. It is actually an anti-viral drug used for influenza
tolcapone (Tasmar)
COMT inhibitors. has been associated with severe liver failure and is not used as much
entacapone (Comtan)
COMT inhibitors
Stalevo
entacapone, carbidopa, and levodopa all in one pill
selegiline (Eldepryl)
A selective inhibitor of type B monoamine oxidase (MAO-B). This enzyme inactivates dopamine so inhibition of this enzyme is good. Does not have the food interactions of MAOI-As. May actually slow the progression of PD. Can delay the need for levodopa when used early in treatment.
Apomorphine (Apokyn)
Ordered in mL instead of mg
Potassium content outside of cells (serum) ranges from ___ to ___ mEq/L
3.5 to 5
why are potassium levels critical to normal body function?
hypo or hyperkalemia can lead to fatal cardiac dysrhythmias
Potassium obtained from foods
Fruit and fruit juices, fish, vegetables, poultry, meats, dairy products
How would impaired kidney function effect potassium levels?
excreted via kidneys would be impaired leading to higher serum levels, possibly toxicity
Hyperkalemia:
>5.5
Hypokalemia
<3.5
What causes hyperkalemia?
Potassium supplements
ACE inhibitors
Renal failure
Potassium-sparing diuretics
What causes Hypokalemia?
Commonly caused by excessive loss as opposed to poor intake. Average daily requirement = 5-10 mEq.
Average daily diet=35-100 mEq
Causes of hypokalemia
Loop and thiazide diuretics
Malabsorption
Large amounts of licorice consumption!
Alkalosis
Corticosteroids
Crash diets
Diarrhea or vomiting
Ketoacidosis
Administration of digoxin in the presence of _______ can lead to fatal cardiac dysrhythmias!
hypokalemia
If the potassium level was 3.4 should you call physician?
Yes. Even slightly high or low levels are cause for concern
What are some side effects of potassium?
Oral preparations can cause diarrhea, vomiting, GI bleeding, ulceration
What should you remember to do if giving potassium in liquid form?
dilute first, even if giving through a feeding tube
What should you remember to do if giving potassium by IV?
ALWAYS use a pump for IV administration because it will slow the rate it is administered and reduce pain at injection site and phlebitis (inflammation of vein).
What is the treatment for hyperkalemia?
Kayexalate—can be given orally or rectally via an enema
What is the normal concentration of sodium in ecf?
135 to 145 mEq/L
How do we get sodium?
Maintained through dietary intake of sodium chloride. Salt, fish, meats, foods flavored or preserved with salt
What are hyponatremia symptoms?
Symptoms:
Lethargy, stomach cramps, hypotension, vomiting, diarrhea, seizures
What are hyponatremia causes?
Causes:
Same causes as hypokalemia; also excessive perspiration (during hot weather or physical work), prolonged diarrhea or vomiting, or renal disorders
What are Hypernatremia symptoms?
Water retention (edema), hypertension
Red, flushed skin; dry, sticky mucous membranes,
increased thirst,
elevated temperature,
decreased urine output
What are Hypernatremia causes?
Poor renal excretion stemming from kidney malfunction; inadequate water consumption and dehydration
If the sodium level is 134 should you call the physician?
No. The body can handle variations in the sodium level better than it can potassium.
Name the 5 groups of Diuretics.
1. Thiazide and Thiazide-like Diuretics
2. Loop Diuretics
3. Potassium-Sparing Diuretics
4. Osmotic Diuretics
5. Carbonic Anhydrase Inhibitors
What are Diuretic Drugs?
Drugs that accelerate the rate of urine formation. Result: removal of sodium and water
What two drugs get rid of the most H20 but don't directly work with sodium?
Osmotic Diuretics &
Carbonic Anhydrase Inhibitors
What is the parenchyma of the kidney?
Parenchyma means functioning unit.... and it is nephrons? I think????
Where do the 5 major classes of diuretics exert their action and why is this important?
...In the tubules and I forgot why that is important!!! Do you have notes on this?
Why is a patient more likely to develop hypokalemia when on loop diuretics than on thiazide diuretics?
Because loop diuretics absorb 20-25% of sodium, and Thiazides only absorb 5-10%.
How are osmotic diuretics different from thiazide or loop diuretics?
because they cause the excretion of water without directly effecting sodium. They do not cause Hypers or Hypos
If blood flow to the kidneys is decreased, how is the action of diuretics effected? What is the exception to this?
It is also decreased. The exception is Loop Diuretics. They can be effective even with low blood flow.
Identify three conditions which include diuretic therapy as a part of treatment.
heart failure
brain edema (or any edema)
Glaucoma
What are the effects of aldosterone on sodium, water, and potassium?
Aldosterone causes the retension of water and sodium and excretion of potassium
Do all potassium sparing diuretics work by antagonizing the action of aldosterone?
No
What is the primary therapeutic use of carbonic anhydrase inhibitors?
Glaucoma
Name the main loop diuretic
Lasix. There are more but we don't need to memorize.
When should diuretics be given if they are only to be administered once a day and why?
In the morning.
Why do we encourage foods high in potassium in clients on diuretics and list 3 foods high in potassium BESIDES bananas!
To prevent Hypokalemia. Foods are:
Bananas
Oranges
Cantaloupe
Dates
Raisins
Plums
Fresh Vegetables--broccoli, spinach
Potatoes (especially potato skins)
Client Assessment: Do you know what to watch for?
Muscle weakness, lethargy, irregular heart rythym
Loop Diuretics...
1. Exert their action in the ascending loop of Henle
2. Block resorption of sodium, chloride, water, as well as potassium
3. Considered potent diuretics
4. Potent diuresis and subsequent loss of fluid
Decreased fluid volume causes:
Reduced BP
Reduced pulmonary vascular resistance
Reduced systemic vascular resistance
Reduced central venous pressure
Reduced left ventricular end-diastolic pressure
Potassium and sodium depletion
3 unique facts about furosemide, a loop diuretic....
1. Risk of ototoxicity with high doses and rapid IV administration
2. Diuresis begins within 5 minutes following IV administration and within 1 hour following oral administration (She said in class that you should be able to see significant amount of urine within 5-15 minutes)
3. Sometimes referred to as a high-ceiling diuretic because it works even in the presence of diminished kidney function
Thiazide and Thiazide-like Diuretics
Thiazide diuretics - all end in "thiazide"
Thiazide-like diuretics - Don't have to memorize
Thiazide MOA is...
Inhibit resorption of sodium, chloride, and potassium ions in the distal tubule.

- Result: water, sodium, and chloride are excreted.
- Potassium is also excreted to a lesser extent.
- Less potent than loop diuretics
- hydrochlorothiazide (HCTZ) is the prototype
Thiazide and Thiazide-like Diuretics: Indications
- Hypertension (one of the most prescribed group of drugs for this)
- Edematous states
- Heart failure
- Idiopathic hypercalciuria
- Adjunct drugs in treatment of edema related to hepatic cirrhosis, corticosteroid or estrogen therapy
Thiazide and Thiazide-like Diuretics: Adverse Effects
Dehydration
Electrolyte imbalances
Potassium Sparing Diuretics
- Promote Na and H20 excretion in the distal tubule
- Potassium reabsorbed
- Weak diuresis and antihypertensive effects when used alone
- Used frequently in combination
spironolactone (Aldactone)
Now commonly used in the treatment of heart failure—evidence based practice!
Protects the heart from ventricular remodeling after a MI.
Nursing Notes on Spironolactone...
Caution when giving in combination with other potassium sparing drugs
What if you received an order to give two potassium sparing drugs? What would you do first?
Check potassium serum levels
Osmotic Diuretics
Act by increasing osmotic pressure and pulling fluid into the vascular space. This increases urine production and causes only a slight loss of electrolytes

Mannitol is the prototype. Can only be given parenterally
Osmotic Diuretics Indications:
- Reduction of intracranial pressure (cerebral edema)
- Treatment of cerebral edema

NOT indicated for peripheral edema
Mannitol Crysalization
May crystallize when exposed to low temperatures—use of a filter is required. If you see crystal discard dose and get new dose.
Carbonic Anhydrase Inhibitors
Adjunct drugs in the long-term management of open-angle glaucoma

Used with miotics to lower intraocular pressure before ocular surgery in certain cases
Acetazolamide (a CAI) is used in the management of
edema secondary to heart failure when other diuretics are not effective
CAIs are less potent or more diuretics than loop diuretics or thiazides?
LESS
What are the adverse effects to remember when taking a CAI?
metabolic acidosis and hypokalemia
Nursing Implications for Diuretics
1. Assess baseline fluid volume status, intake and output, serum electrolyte values, weight, and vital signs—especially postural BPs

2. Assess for disorders that may contraindicate or necessitate cautious use of these drugs

3. Monitor serum potassium levels during therapy.

4. Teach patients to maintain proper nutritional and fluid volume status

5. Teach patients to eat more potassium-rich foods when taking any but the potassium-sparing drugs

6. Teach patients to change positions slowly, and to rise slowly after sitting or lying to prevent dizziness and possible fainting related to orthostatic hypotension

7. Encourage patients to keep a log of their daily weight

8. Encourage patients to return for follow-up visits and labwork

9. A weight gain of 2 or more pounds a day or 5 or more pounds a week should be
reported immediately
sedative
drug which has an INHIBITORY effect on the CNS to the degree that they reduce NERVOUSNESS, EXCITABILITY or IRRITABILITY without causing sleep
hypnotics
drug which has an inhibitory effect on the cns to the degree that they reduce nervousness, excitability or irritability by causing sleep
what's the difference between a sedative and hypnotic
sedative does not cause sleep while a hypnotic does; however, a sedative can become a hypnotic if it is given in large enough doses
are barbiturates prescribed more/less/the same as benzodiazepines?
less. benzodiazepines are now considered safer
barbiturates - common info
-not prescribed as often as benzos
-many unwanted side effects
-habit forming
-narrow therapeutic range
-may see used for LONG TERM control of seizures
- do not stop abruptly
-considered a controlled substance
-prototype is phenobarbital
-ultra short acting barbs typically end in "-tal"
prototype of barbiturates
phenobarbital
what part of the brain do barbiturates work on?
brain stem (primarily); they also decrease nerve impulses to cerebral cortex
what neurotransmitter do barbiturates potentiate?
GABA (an inhibitory amino acid)
what do barbiturates do to the seizure threshold?
raise seizure threshold
barbiturate drug effects
-low doses: sedative effects
-high doses: hypnotic effects (also lowers respiratory rate)
-anticonvulsant
barbiturate therapeutic effects
-hypnotics: help insomnia
-sedatives: decrease anxiety
-anticonvulsants: prevent seizures
-surgical procedures: induction of anesthesia
barbiturates are ______, meaning they stimulate the enzymes in the liver responsible for metabolizing them
inducers
CNS side effects of barbiturates
DROWSINESS
lethargy
vertigo
mental depression
paradoxical restlessness
Respiratory side effects of barbiturates
RESPIRATORY DEPRESSION
apnea
bronchospasms
cough
GI side effects of barbiturates
nausea
vomiting
diarrhea
constipation
Sleep side effects of barbiturates
decrease REM sleep, which leads to agitation and inability to deal with normal stress
Side effects to barbiturates not related to CNS, respiratory, GI, or sleep
agranulocytosis, hypotension, and Stevens-Johnson syndrom
what are the triad of symptoms that point to barbiturate toxicity?
respiratory depression
coma
pinpoint pupils
when would you WANT to give a pt an "overdose" of barbiturates?
-to induce anesthesia
- to stop uncontrollable sz's
common barbiturates
-phenobarbital (Luminal)
-butabarbital (Butisol)
-pentobarbital (Nembutol)
-secobarbital (Seconal)
what are benzodiazepines considered better for pts than barbiturates?
-favorable side effects
-effectiveness
-safer - when taken alone as an OD, they result in little more than sedation. Also don't work on the brainstem, so they do not depress respirations
what are the classes of benzodiazepines?
-sedative-hypnotics
-anxiolytics
what part of the brain do benzodiazepines work on?
limbic system
thalamus
hypothalamus
*there is a thought that the brain contains receptors that ONLY allow benzos into to work*
benzo drug effects
-calming effect on CNS
-useful in controlling agitation and anxiety
-reduces excessive sensory stimulation, inducing sleep
-induce skeletal muscle relaxation
Valium (diazepam) is a ____
benzodiazepine
give some examples of when you would use a benzodiazepine?
-sedation
-sleep induction
-skeletal muscle relaxation
-anxiety relief
-treatment of ETOH withdrawal
-agitation
-depression
-epilepsy
-balanced anesthesia
-moderate/conscious sedation (such as a colonoscopy)
What are the Four Categories of Psychotherapeutic Drugs
Antianxiety drugs, Antimanic drugs, Antipsychotics, Antidepressants
Name 3 Types of Antianxiety drugs
Benzodiazepines, Antihistamines, Miscellaneous anxiolytic medications
What is commonly used as the first-line treatment for anxiety?
Benzodiazepines
Lorazepam (Ativan)
Benzo antianxiety, habbit forming, only use for short time
What is occasionally used to treat anxiety?
Antihistamines.

hydroxyzine (Vistaril) causes significant sedation
What abticonvulsant drug is also used to treat anxiety?
valproic acid (Depakote)
What are miscellaneous anxiolytic medications?
buspirone (BuSpar). Exact MOA not known. Anxiolytic effects develop slowly—not appropriate for prn use
Which antianxiety med causes significant sedation?
Antihistamines. hydroxyzine (Vistaril).
Which antianxiety catagory medications are NOT habbit forming, do NOT cause sedation and do NOT depress the CNS
miscellaneous anxiolytic medications
Which Antimanic drug is the prototype?
Lithium, a mood-stabilizing drug
Lithium has a wide or narrow therapeutic range?
Narrow. Normally want to keep it between 0.6-1.2 mEq/l. For acute mania the level is 1-1.5
When taking lithium, what is important to monitor?
serum sodium levels
What are early symptoms of lithium toxicity?
diarrhea, vomiting, and motor tremors. Clients should drink at least 2 liters of water daily and maintain a stable amount of sodium in their diet.
All Antipsychotics can cause what?
extrapyramidal symptoms (EPS) symptoms that arise adjacent to the pyramaidal portions of the brain - symptoms are various motion disorders similar to Parkinson's Disease. p. 260 in book
Memorize the 5 antipsychotics!!!!
Phenothiazines are largest group, but have many anticholinergic adverse effects.
1. chlorpromazine (Thorazine)
2. fluphenazine (Prolixin)

Atypical antipsychotics
1.clozapine (Clozaril—1989) increased risk of agranulocytosis and need lab work weekly (WBCs)
2.olanzapine (Zyprexa--1996)
3.aripiprazole (Abilify—2002)
What are 2 types of antipsychotics?
Phenothiazines & Atypical
What are largest group of antipsychotics
Phenothiazines.
1. chlorpromazine (Thorazine) &
2. fluphenazine (Prolixin) are examples.
Which antipsychotics have many anticholinergic adverse effects?
Phenothiazines
What are the risks of clozapine (Clozaril) an Atypical antpsychotic?
increased risk of agranulocytosis and need lab work weekly (WBCs). The two other antipychotics in the Atypical group are olanzapine (Zyprexa--1996)
aripiprazole (Abilify—2002)
Name 4 types of Antidepressants
1. Selective Serotonin Reuptake Inhibitors (SSRIs)
2. Miscellaneous antidepressants
3. Tricyclic Antidepressants (TCAs)
4. Monoamine Oxidase Inhibitors (MAOIs)
What drugs are Commonly used as first-line therapy for depression?
Selective Serotonin Reuptake Inhibitors (SSRIs).
Newer SSRIs are also targeting norephinephrine.
The therapeutic effects of SSRI antidepressants may not occur for...
several weeks
As the name suggests, SSRIs selectively inhibit serotonin reuptake causing...
increased concentrations of serotonin at nerve endings in the CNS.
Adverse effects of SSRIs
Sexual dysfunction (impotence, decreased libido), weight gain, and serotonin syndrome
What are common symptoms of seratonin syndrome?
delerium, agitation, tchycardia, sweating, myoclonus (muscle spasms), hyperreflexia, shivering, coarse tremors, extensor planter muscle responses. In more severe cases - hyperthermia, seizures, rhabdomyolysis, renal failure, cardiac dysrythmias, and disseminated intravascular coagulation may occur.

Seratonin Syndrome is happening more than is being documented.
Why are SSRIs a relatively safe choice?
Little to no adverse effect on cardiac system
3.Common SSRIs
a.fluoxetine (Prozac)
b.paroxetine (Paxil)
c.sertraline (Zoloft)
d.citalopram (Celexa)
e.escitalopram (Lexapro)
f.duloxetine (Cymbalta)
bupropion (Wellbutrin)—Zyban (a Miscellaneous antidepressant)
is a sustained release form that is also used as first-line therapy for smoking cessation.
bupropion (Wellbutrin)—Zyban (a Miscellaneous antidepressant) is often classified as an Atypical Antidepressant because....
it does not cause sexual dysfunction or weight gain. In fact, it can increase libido and cause weight loss! However, it can also cause seizures.
trazodone (Desyrel) a Miscellaneous antidepressant
is commonly used for insomnia
Which antidepressants have been available for more than 40 years and are Used less commonly today due to adverse and toxic effects?
Tricyclic Antidepressants (TCAs)
Which drugs are considerably less expensive than many of the newer agents and many are available in generic form.
Tricyclic Antidepressants (TCAs)
Relief of depressive symptoms when using TCAs may take...
several weeks and consistent dosing is required; prn administration is inappropriate. Therapeutic effects are often not realized for 10-21 days.
Adverse effects of TCAs
Sedation, impotence, orthostatic hypotension, tachycardia, dysrhythmias, weight gain. The client may develop some tolerance to some of these, but they usually do not disappear completely.
Toxicity of Tricyclic Antidepressants (TCAs)
TCA overdoses are notoriously lethal. The lethal dose is only 8 times the average daily dose. Estimates suggest that 70-80% of patients who die of TCA overdose do so before reaching the hospital. The CNS and cardiovascular system are the primary systems affected and clients generally die either from seizures or dysrhythmias. There is no specific antidote for TCA poisoning. Activated charcoal may be administered.
imipramine (Tofranil) a TCA is also used to treat....
enuresis (or bedwetting)
Why are Monoamine Oxidase Inhibitors (MAOIs) typically used as second-line therapy?
Because, even though they are highly effective antidepressants, there is a risk of hypertensive crisis caused by tyramine interaction.
How do Monoamine Oxidase Inhibitors (MAOIs) work?
by inhibiting the enzyme MAO. Iinhibition of this enzyme results in accumulation of neurotransmitters.
Adverse effects of Monoamine Oxidase Inhibitors (MAOIs)
Very few serious side effects in the absence of tyramine. Can cause orthostatic hypotension.
Food Interactions with Monoamine Oxidase Inhibitors (MAOIs)
Food containing the amino acid tyramine is the primary culprit and a hypertensive crisis is the result. Foods that MUST be avoided are aged, mature cheeses (cheddar, blue, Swiss); smoked/pickled meats, fish, or poultry (herring, sausage, corned beef, salami, pepperoni); aged/fermented meats, fish, or poultry; Brewer's yeast, red wines. Important for the client to have a nutritional consult prior to beginning these meds. Some of the above foods MAY be allowed in very small portions.
Drug Interactions with Monoamine Oxidase Inhibitors (MAOIs)
Many drug interactions can occur. Clients must be instructed to avoid all medications, including OTC meds, not specifically approved by the physician.
ENSAM
a new selegiline transdermal patch. It is selective MAOI Type B inhibitor —can be used without the dietary restrictions at its lowest dose (6 mg over 24 hrs).
Why should a client be informed that the drug takes a few weeks to begin working?
Because a lack of instant success, along with sexual dysfunction and weight gain, may cause them to quit taking the meds prematurely.
Why should you check the patient's mouth if they are on a psychotherapeutic drug?
to make sure oral doses are swallowed.
What are some things you should include in your teaching about psychotherapeutic drugs?
Provide simple explanations about the drug, its effects, and the length of time before therapeutic effects can be expected
How should you stop taking a psychotherapeutic?
Abrupt withdrawal should be avoided
Why should patients to change positions slowly when on a psychotherapeutic?
to avoid postural hypotension and possible injury
Why should only small amounts of medications should be dispensed at a time?
to minimize the risk of suicide attempts
Simultaneous use of these drugs with alcohol or other CNS depressants can be fatal. True or false
True
Why is it important to monitor nutrition in a child being treated for ADHD
Because CNS stimulants decrease appetite
What should you teach a client to do when taking Drugs that can cause anticholinergic side effects:
have frequent drinks of water, sugarless hard candy, eye drops for dry eyes, checking for constipation, etc.
CNS Stimulants
Drugs that stimulate a specific area of the brain or spinal cord.
What are the therapeutic Uses of CNS Stimulants
1. Treatment of attention deficit hyperactivity disorder (ADHD)
2. Treatment of narcolepsy
3. Treatment of migraine headaches
4. Appetite suppressants (anorexiant)
Drugs used in Treatment of attention deficit hyperactivity disorder (ADHD)
1.amphetamine (Adderall, others)
2.methylphenidate (Concerta, Ritalin)
3.atomoxetine (Strattera)
What are some benefits and risks associated with atomoxetine (Strattera)?
It is not addictive, but the FDA issued a warning in 2005 describing cases of suicidal thinking in recipients
What are some Nursing Considerations when giving CNS Stimulants?
1.Should be given at least 6 hours before bedtime to reduce problems from insomnia
2. May cause dry mouth; frequent oral care is needed
3. Take on an empty stomach, 30-45 minutes before meals
4. Drug "holidays" may be ordered
5. Parents should keep a journal to note child's response to therapy
What is the drug used to treat narcolepsy
modafinil (Provigil)
2 drugs used for Treatment of migraine headaches are?
sumatriptan (Imitrex), zolmitriptan (Zomig)
Antimigraine drugs, sumatriptan (Imitrex) & zolmitriptan (Zomig) are known as
abortive drugs and not preventative because they don't prevent migraines but are used as treatment if a migraine comes on. They all end in "triptan"
Sodium Oxybate (Xyrem)
Is misused as a "date rape" drug. Approved to treat cataplexy which is a condition characterized by acute attacks of muscle weakness and often associated with epilepsy. Only available through restricted dispensing programs Schedule III drug. Technically a CNS depressant
Appetite suppressants (anorexiant)
1.sibutramine (Meridia)
2.phentermine (Ionamin)
3.orlistat (Xenical) - not actually a CNS Stimulant
Why is it significant that sibutramine (Meridia) is found in many diet medications including OTC?
Because it is linked to increased risk of stroke
Is orlistat (Xenical) a CNS stimulant?
NO. it is a Lipase inhibitor
What are the Major adverse effects of orlistat (Xenical)?
oily spotting, flatulence, steatorrhea, and fecal incontinence in 20-40% of patients and deficiency of fat soluble vitamins (A,D,E,K)
Does orlistat (Xenical) cause serious liver injury?
The FDA is investigating. 13 cases have been found in ten years
What are Analeptics (CNS stimulants) used for?
used for neonatal apnea although less frequently
What are some Adverse Effects Analeptics
1. Wide range of effects - dose related
2. Tend to "speed up" body systems
3. Palpitations, tachycardia, hypertension, angina, dysrhythmias, nervousness, restlessness, anxiety, insomnia, nausea, vomiting, diarrhea, dry mouth, increased urinary frequency, others
ANTIEPILEPTIC DRUGS (AEDs) are Also known as
anticonvulsants
Goals of therapy using antiepileptics
To control or prevent seizures while maintaining a reasonable quality of life, and To minimize adverse effects and drug-induced toxicity
How long does ANTIEPILEPTIC DRUGS (AEDs) therapy usually last?
Traditionally believed to be lifelong - recent studies are suggesting that patients who have been seizure-free on medications for 1-2 years can eventually stop taking the drugs with doctor supervision
Can a combination of drugs be used to treat epilepsy?
Yes
Many antiepileptic drugs have a narrow therapeutic range. What would you need to check before giving this med?
Check serum drug levels
What are we now seeing AEDs also used as?
mood stabilizers
What is the Mechanism of Action of AEDs
Exact mechanism of action not known, they raise seizure threshold
Diazepam is a ___ drug that can be given IV or rectally and is commonly used to treat epilepsy.
Benzodiazipine
Why does Phenytoin react with other medications?
It is tightly protien bound and it induces hepatic enzymes
Why would a nurse perform a careful assessment of a patient's oral cavity after being told they are on Phenytoin?
It can cause gingival hyperplasia with prolonged use.
What is the difference between phenytoin and fosphenytoin?
Phenytoin has to be injected very slowly, per min. Also, it is very alkaline (pH of 12) and that makes it painful to administer IV. Fosphenytoin is thought of as a pre-phenytoin because it turns into phenytoin once in the body, but is not painful to administer so a better choice for IV.
A fosphenytoin equivalent will have what on the label?
a "PE" on the label
Why do you need to monitor carbemazepine (Tegretol) when first starting it?
Carbamazepine undergoes autoinduction. Levels may need to e adjusted for the first few months, but then it should level out
Stevens-Johnson Syndrome
First sign is a big nasty red rash. The problem is it is systemic and can be very dangerous if not recognized.
If a person on phenytoin or carbamazepine develops the Stevens-Johnson Syndrome rash, what should you do?
Stop the meds and call dr.
What are some other antiepileptic Drugs
PHENOBARBITAL
VALPROIC ACID (Depakene)
Tell about PHENOBARBITAL an Antiepileptic
A barbiturate. LONG half-life 2-3 weeks. Drowsiness is common side effect, but tolerance usually develops, Some children experience paradoxical excitability
Does PHENOBARBITAL have any drug-drug interactions?
Yes, it has Many drug-drug interactions because it is an inducer of drug-metabolizing enzymes
VALPROIC ACID (Depakene) an Antiepileptic
Used for tx of seizures, bipolar disorder, and migraine prevention. Serious side effects are rare but include liver toxicity and pancreatitis. Several drug interactions but it is NOT an inducer
Other AEDs
1. gabapentin (Neurontin) Well tolerated, Commonly used for neuropathic pain.
2. ethosuximide (Zarontin), DOC for absence seizures
3. a bunch more that we don't have to memorize
Nursing Implications
1. Oral drugs - should be taken regularly, same time each day with meals to reduce GI upset. Do not crush, chew, open extended-release forms. If patient is NPO for a procedure, contact physician regarding AED dosage
2. A medical alert tag or ID should be worn
3. Driving may be impaired until drug levels stabilize
______ is a Chronic, progressive, degenerative disorder Caused by an imbalance of two neurotransmitters
Parkinson's Disease (PD)
What are the two neurotransmitters involved in PD?
Dopamine (inhibitory) - too little & Acetocholine (excititory) - too much
If PD is caused by too little Dopamine, why not just give exogenous Dopamine?
Dopamine cannot cross blood-brain barrier. As disease progresses, none of the meds work bc the functioning nerve terminals die off. 80% are already nonfunctioning before any symptoms start.
What is levodopa?
Common treatment for PD. It is the biologic precurser of dopamine. Levodopa is taken up by the dopaminergic terminals, converted into dopamine, then released as needed. As a result, the neurotransmitter imbalance is controlled in patients with early PD who still have functioning nerve terminals.
Can levodopa cross the blood/brain barrier?
Yes. Dopamine cannot, but Levodopa can. It is administerred orally.
Does levodopa require functioning nerve terminals?
Yes, without functioning nerve terminals, levadopa or dopamine cannot be utilized by the body
Does the client with PD have functioning nerve terminals?
By the time PD is diagnosed, around 80% of the terminals are nonfunctioning. When there aren't any functioning nerve terminals left the symptoms can no longer be controlled.
PD Has no cure, but levodopa can permenently control the signs and symptoms. True or False
False. As PD progresses, it becomes more and more difficult to control it with levodopa. Ultimately, levodopa no longer controls the PD, and patient is seriously debilitated
How long does levodopa therapy typically work?
5-10 years after starting the med
Considerations for the Client Receiving Levodopa
1. On-off phenomenon
2. Wearing off
3. Pyridoxine (vitamin B6)
4. Foods high in protein
5. Dyskinesias
6. Drug holiday
What is On-off phenomenon?
A common experience of patients taking medications for PD in which they experience periods of greater symptomatic control alternating with periods of lesser control
Dyskinesias
imparied ability to execute voluntary movements. Sometimes the very drugs that are meant to control this symptom can actually cause it or make it worse.
3. Pyridoxine (vitamin B6)
4. Foods high in protein
B6 enhances the effect of decarboxylase (an enzyme that breaks down lavodopa).

Foods high in protein should be eaten but since they compete with levodopa, the meds should be taken 30 minutes before meal is consumed.
What is Carbidopa???
Carbidopa is given with levodopa. Carbidopa prevents levodopa breakdown in the periphery by the enzyme decaroxylace. Carbidopa does not cross the blood-brain barrier. As a result, more levodopa crosses the blood-brain barrier, where it can be converted to dopamine
What is carbidopa-levodopa (Sinemet)?
The cornerstone of levodopa therapy. Some advantages over levodopa alone are:
1. Dose reduction
2. Don't need to limit pyridoxine
3. Less on-off
What is the difference in Sinemet and Sinemet CR?
CR is controlled release, so it is absorbed much slower. It increases the drugs "on-time"
Can Sinemet CR be crushed?
no
amantadine (Symmetrel)
Another common drug used for PD. Stimulates the release of dopamine from nerve endings in the CNS or may block the reuptake of dopamine. Most effective in earlier stages. Usually effective for only 6-12 months.
Why would a patient without PD be taking amantadine?
It is actually an anti-viral drug used for influenza
What is COMT?
Catechol Ortho-Methyltransferase Inhibitors
Why is COMT important in the treatment of PD?
They prolong the duration of action of levodopa. Fast acting effective in first dose. Benefit patients experiencing the "wearing off effect" or "on-off effect"
Two COMT inhibitors available
entacapone (Comtan)
tolcapone (Tasmar) - has been associated with severe liver failure and is not used as much
What is the most serious adverse effect caused by tolcapone (Tasmar)?
severe liver failure
What laboratory monitoring is required when taking tolcapone (Tasmar)?
liver?
Stalevo
entacapone, carbidopa, and levodopa all in one pill
What effect would a dopamine agonists have on PD?
They do not turn into dopamine, but stimulate dopamine receptors. This way you can lower the dose of levodopa reducing side effects
What are the two major categories of dopamine agonists?
1. Nonergot derivatives = Fewer side effects
2. Ergot derivatives
What is the main adverse effect of dopamine agonists?
Sleep attacks
selegiline (Eldepryl)
A selective inhibitor of type B monoamine oxidase (MAO-B). This enzyme inactivates dopamine so inhibition of this enzyme is good. Does not have the food interactions of MAOI-As. May actually slow the progression of PD. Can delay the need for levodopa when used early in treatment.
Anticholinergic Therapy
Drugs that inhibit acetylcholine
Is Acetylcholine excitatory or inhibitory?
excitatory. Overstimulation of the cholinergic excitatory pathways result in muscle tremors and rigidity
How would anticholinergic therapy be helpful?
It helps with some of the symptoms od PD - such as salivation, diarrhea, frequent urination, and muscle tremors. It Does NOT help with extremely slow movements (bradykinesia) associated with PD.
What are some anticholinergic Adverse Effects?
Dry mouth
Urinary retention
Constipation
OVERHEATING CAN BE BIG PROBLEM
What are some nursing Implications with antiparkinsonian drugs?
1. Patients should be told not to discontinue antiparkinsonian drugs suddenly
2. Teach patients about what therapeutic and adverse effects to expect with antiparkinsonian drug therapy
3. Levodopa preparations may darken the patient's urine and sweat
Apomorphine (Apokyn) should be ordered in___ instead of ___
Ordered in mL instead of mg
Analgesics
-medications that relieve pain without causing loss of of consciousness
-"painkillers"
-opioids
-acetaminophen (Tylenol)
- NSAIDs
Afferent nerves transmit impulses from the ____ to the ____
periphery; CNS
prefix "noci-" means
"to cause harm, injury or pain."
True or False: Lantus insulin does not peak.
True. Lantus insulin does NOT peak. It is a basal coverage insulin.
analgesics
medications that relieve pain without causing loss of consciousness. aka painkillers, opioids, acetaminophen (Tylenol - APAP), NSAIDs
NSAID
non-steroid anti-inflammatory
APAP
Tylenol / acetaminophen
max dose of Tylenol for healthy liver
4 grams
max dose of Tylenol for those with compromised liver
2 grams
name the 2 types of nociceptors
A-delta fibers
C fibers
A-delta fibers
1 of 2 types of nociceptors; fast traveling, myelinated fibers that respond to mechanical stimuli; they sense sharp, stinging, cutting or pinching pain that is localized
C fibers
1 of types of nociceptors.

Slower-traveling, unmyelinated fibers that respond to mechanical, chemical, or thermal stimuli

They sense dull, burning or aching pain that is generally nonlocalized
2 barriers to adequate pain management
caregiver barriers
client barriers
tolerance
a client who needs more of a drug to get the same effect.
physical dependence
strictly a physiological phenomena
addiction
a psychological problem
what would I give for someone in mild pain?
non-opioid (tylenol, NSAID - SAA, ibuprofen, etc) ATC
Parasympathetic Nervous System is also known as _____
cholinergic
Sympathetic Nervous System is also known as:
adrenergic
miosis
pupils constrict
mydriasis
pupils dilate
agonist
activates receptor (HELPS)
parasympthetic system is in charge of what in the body?
rest and digest
sympathetic system is in charge of what in the body?
fight or flight responses
_____ receptors are the most therapeutic
muscarinic
when talking about ANS receptors, these are the three type of CHOLINERGIC (PSNS) receptors:
1. muscarinic (most therapeutic)
2. nicotinic (N)
3. nicotinic (M)
when talking about ANS Receptors, these are the 5 ADRENERGIC (SNS) receptors
1. alpha 1
2. alpha 2
3. beta 1
4. beta 2
5. dopamine
____ is one of the most desirable qualities a drug can have because it can enable a drug to alter a disease process while leaving other physiologic processes largely unaffected.
selectivity
cholinergic agonists
drugs that STIMULATE the PSNS. also called parasympathomimetics
parasympathomimetics
cholinergic agonists
cholinergic blockers
anticholinergics or antimuscarinics or cholinergic antagonists or parasympatholytics
primary neurotransmitter for PSNS
Ach (acetylcholine)
cholineserase
the enzyme responsible for breaking down acetylcholine
direct-acting cholinergic agonist
binds to receptors and activates them
indirect-acting cholinergic agonists
inhibit action of cholinesterase
SLUDGE
cholinergic agonists:
S= increase Salivation
L= increase Lacrimation (tearing)
U= increase urination
D= diarrhea
G= increase GI motility/secretions
E=Emesis (vomiting)
primary uses of cholinergic agonists
-urinary retention
-myasthenia gravis
-alzheimers disease
-xerostomia
-glaucoma
can you give a cholinergic agonist for a pt when there is a possible bowel obstruction?
NO - you can cause a perforated bowel
should you give a cholinergic agonist for a pt with an ulcer?
NO - cholinergic agonists increase gastric secretions!
cholinergic crisis
occurs when a pt receives too much of a cholinergic agonist. Sx are shock, salivation, etc. Treat with an anticholinergic.
if a pt is in a cholinergic crisis, you should give him:
an anticholinergic
bethanechol (Urecholine), a direct=acting muscarinic agent
primarily used for urinary retention
what kind of drug would be used for an alzheimers pt?
an indirect-acting cholinergic agonists; they inhibit cholinesterase and allow ACh to accumulate
anticholinergics, or cholinergi antagonists, block ____ receptors and inhibit _____ neurotransmitter
muscarinic; ACh
atropine is the prototype of the _____
anticholinergics
____ is used primarily during endotracheal intubation; an extremely short acting paralysis NMBA; malignant hyperthermia is a rare and potentially fatal adverse effect
succinylcholine (Anectine)
NMBA
neuromuscular blocking agents
I am on a ventilator and am panicked, working against the machine. What drug will you give me to calm my A$$ down?
an NMBA (neuromuscular blocking agent)
I am a drug that mimics the action of the SNS and also go by the sexy name of "sympathomimetics"
adrenergic agonists
2 classifications of adrenergic agonists
catecholamines and noncatecholamines
I am a substance that can produce a sympathomimetic response; i get my name because of my super sassy similar chemical structure; I have a "short duration of action", so I need to be administered in a continuous fashion; I cannot do oral, and I do not cross the blood-brain barrier, or pass Go and collect $200. What am I?
catecholamine
nonselective adrenergic agonists stimulate both alpha and beta receptors. True or false?
true
Alpha 1 Activation does what to the body?
increases BP
Vasoconstriction
Mydriasis
Urinary retention
What good does Alpha 2 do?
decrease BP
inhibits NE release
vasodilation
beta 1 receptors are primarily found in the ___
heart.
beta 1 stimulation does what to the body?
increases heart rate
increases contractility
increases renin secretion
is considered a positive inotropic
positive inotropic effect
an increase in the force of heart contraction
positive chronotropic effect
an increase in heart RATE
positive dromotropic effect
an increase in the conduction of cardiac electrical nerve impulses through the AV node
beta 2 activation
brochodilation
uterine relaxation (GOOD USE FOR PRETERM LABOR!)
therapeutic in asthma and preterm labor

warning: cuases glycogenolysis (breakdown of glycogen) and can therefore lead to hyperglycemia in diabetics - give supportive meds
dopaminergic receptors are also _____ receptors
adrenergic
dopaminergic receptors are ONLY stimulated by
dopamine
what good is dopamine to us?
it can dilate renal blood vessels and improve renal perfusion
BPH
benign prostatic hypertrophy
what type of drug is used to treat hypertension and BPH?
alpha adrenergic antagonists
1st dose syncope
orthostatic hypotension is a common side effect, and effect is most pronounced with the 1st dose, therefore it is recommended that the 1st dose be taken at bedtime.
in what drug is the most common s.e. orthostatic hypotension?
adrenergic antagonist; alpha 1 selective
when are beta adrenergic antagonists used?
angina, hypertension, dysrhythmias
mi
heart failure
somatic pain responds well to what kind of analgesic?
NSAIDs
visceral pain often needs what kind of analgesic?
opioids
neuropathic pain, characterized by shooting, burning or stabbing pain, is often given what kind of drugs?
antiepileptics
if I'm in Moderate pain, you would typically give me what kind of analgesic?
add opioid ATC
ATC
around the clock
If I'm in severe pain, give me
strong opioid
adjuvants
drugs that typically do very little on their own, but can immensely help other drugs
is acetaminophen (tylenol) an opioid?
No. Tylenol is a nonopioid analgesic; it is not an antiinflammatory
antidote to acetaminophen toxicity
acetylcysteine; works by preventing hepatotoxic metabolites of APAP from forming; 18 oral doses over 72 hours or via IV over 20 hours
opioids
pain relievers that contain opium, durived from opiumm poppy or chemically related to opium
Opioid receptors
Mu; Kappa
Mu receptors
primarily pain blocking receptors; associated with respiratory depression, euphoria, decreased GI activity, miosis, sedation and physical dependence
Kappa receptors
associated with miosis, decreased GI motility and sedation
MOA Agonist
binds to mu and/or kappa receptors and causes response. Ex: morphine and codeine
MOA antagonist
binds strongly to mu/kappa receptors, but REVERSES the effect of the opioid. ex: naloxone (Narcan)
MOA Agonist-Antagonist
aka a partial agonist; produces analgesia when used alone; when used with a pure agonist, reverses those effects
uses for opioid analgesics
pain!!!
cough center suppression (only at correct dosages - higher dosages can actually CAUSE coughing)
treatment of diarrhea
balanced anesthesia (typically in the beginning of anesthesia for a procedure)
Contraindications of opioid analgesics
-KDA (known drug allergy)
-severe asthma or other respiratory insufficiency (Floyd said this was more of a precaution than a contraindication)
-elevated intracranial pressure (Floyd also said this was more of a precaution; it's given quite often in recovering trauma pts)
-Pregnancy
Adverse Effects of opioid analgesics
-euphoria (this is what makes them habit-forming)
-CNS depression (this is what makes respirations decrease)
-N/V (nausea/vomiting)
-urinary retention
-diphoresis (sweating) and flushing
-miosis (pupil constriction)
-constipation
-itching
codeine has (more/less) respiratory depression than morphine
less
is hydrocodone refillable?
yes. it's currently schedule III
Vicoprofen
hydrocodone + ibuprofen; available orally
most common trade name drug for oxycodone
percocet
percodan
oxycodone + aspirin
combunox
oxycodone + ibuprofen
oxycontin
oxycodone in continuous/extended release form
oxyIR
instant release oxycodone
MSIR
instant release morphine
what is morphine's maximum dose?
there is no maximum dose for morphine
if morphine was given via epidural or intrathecal, you do not have to monitor respirations if you did not give the morphine. true or false?
false. If it was given epidurally or intrathecally, respiratory depression my be delayed b/c analgesia can persist for 24 hours
in what circumstance should you NEVER give a pt a fentanyl patch? (Duragesic)
if they are opioid naive
opioid naive
pt has never, or has not recently, been given opiods
the initial onset of fentanyl when given as a Duragesic patch takes __ hours
12
important things to remember when administering the fentanyl patch to clients
-apply only on intact skin (open wounds, abrasions, or nicks from shaving could give too much of the drug to the pts bloodstream too quickly)
- you may clip hair, but do not shave
- make sure patch is adhered completely so pt can bathe or shower comfortably
- when putting on new patch, make sure you have located and removed ALL old patches
- when putting on new patch, do not put on same spot to keep skin from breaking down
why is meperidine (Demerol) not used very often anymore?
contains a byproduct that can decrease seizure threshold and increase CNS excitability, which means it can lead to seizures; it is very short lasting, and causes more euphoria than other opioids; oral doses arent recommended because it takes so much of the drug to be effective
why are opioid agonist-antagonists used?
- less respiratory depression
- less abuse
- DONT USE IF YOU HAVE A PURE AGONIST ON BOARD
naloxone HCL (Narcan)
does not have any sort of analgesia or respiratory depression because it's an ANTAGONIST - given for reversal of opioid induced respiratory depression; remember you are reversing analgesia also, so pt will be in pain
-commonly given when respirations dip below 10-12/min
PCA
patient controlled analgesia (the pain button)
PCA by proxy
when someone other than the pt pushes the button to administer analgesic (this should NOT BE DONE)
what should be done before administering analgesics to a pt?
-perform thorough history
- obtain baseline vital signs and I&O
-assess for potential contraindications and drug interactions
-perform thorough pain assessment (including COLDSPAA factors)
-be sure to include other (nonpharmacologic) interventions as well
- medicate patients before the pain becomes severe
- ensure safety measures to prevent injury
t/f: after a procedure or surgery, a patient will automatically be given pain meds
False. The patient needs to alert the nurse when he/she is hurting so adequate pain medication can be administered and monitored.
opioid analgesics (should/should not) be taken with food
should. it will minimize gastric upset
if there is a decline in pt's condition or if vital signs are abnormal, what do you do in regard to pts analgesic order?
withhold dose and contact physician; especially important if respiratory rate is less than 10-12 breaths/min
what are desired outcomes that let you know the analgesics are therapeutic?
-decreased complaints of pain
-decreased severity of pain
-increased periods of comfort
- improved activities of daily living, appetite, and sense of well-being
-decreased fever (aceteminophen)
Autonomic Nervous System:Three principal functions
1. Regulate the heart
2. Regulate secretory glands (salivary, gastric, sweat, & bronchial)
3. Regulate smooth muscles (bronchi, blood vessels, urogenital system, and GI tract)
PSNS Effects (Rest and Digest)
1. Pupils constrict (miosis)
2. Heart rate and contractility both ↓
3. Bronchi constrict & ↑ secretions
4. ↑ GI motility and secretions
5. Emptying of bladder and bowel
6. Vasodilation
7. Sex organs→erection
SNS Main Effects
SNS - Fight or Flight
1. Pupils dilate (mydriasis)
2. Heart rate and contractility increase
2. Bronchi dilate
3. Slight decrease GI motility
4. Urinary retention and possible constipation
5. Vasoconstriction
6. Uterus relaxation (B2)
7 Liver - glycogenolysis
Sympathetic
Adrenergic. Main hormone is Norepinephrine
Parasympathetic
Cholinergic - Main hormone is Acetylcholine
Parasympathomimetic
Mimics the action of the PSNS. (PSNS agonist)
Sympathomimetic
Mimics the action of the SNS. (SNS agonist)
Parasympatholytic
Blocks the normal effects of the PSNS. (PSNS antagonist)
Sympatholytic
Blocks the normal effects of the SNS. (SNS antagonist)
Sympathetic receptors
ADRENERGIC - Alpha 1 and 2, Beta 1 and 2, and Dopamine
Parasympethetic Receptors
Cholinergic - Muscarinic, Nicotinic M
Selectivity
is one of the most desirable qualities a drug can have, because a selective drug is able to alter a disease process while leaving other physiologic processes largely unaffected.
Cholinergic agonists
drugs that stimulate the PSNS. Also called parasympathomimetics
parasympathomimetics
AKA Cholinergic agonists. drugs that stimulate the PSNS
Cholinergic blockers
AKA anticholinergics or more accurately antimuscarinics. Drugs that block the action of the PSNS
anticholinergics
AKA Cholinergic blockers, cholinergic antagonist, or parasympatholytics. Drugs that block the action of the PSNS
Cholinesterase
is the enzyme responsible for breaking down acetylcholine.
Direct-acting cholinergic agonist
Bind to receptor and activate them
Indirect-acting cholinergic agonist
inhibit action of cholinesterase
SLUDGE
S=salivation (↑)
L=lacrimation (↑ tearing)
U=urination (↑)
D=diarrhea
G=GI motility/secretions (↑)
E=Emesis
Primary Uses of Cholinergic Agonists
Urinary retention, Myasthenia gravis, Alzheimer's Disease, Xerostomia, Glaucoma
General contraindications for cholinergic agonists
Drug allergy, GI or GU obstruction, Bradycardia, Hypotension, COPD, Peptic ulcers
Cholinergic crisis
Occurs when a client recieves too much of a cholinergic agonist - causes hypertension, shock, salivation, etc. Treated with an anticholinergic
bethanechol (Urecholine)
A direct-acting muscarinic agonist. Cholinergic agonists relax bladder sphincter and Primarily used for urinary retention. Commonly given post-operative or postpartum. S.E. rare with oral administration, more common with subcutaneous to treat hypertension, bradycardia, and diarrhea
cevimeline (Evoxac)
Also a direct acting muscarinic agonist. Parasympathomimetic. Limited therapeutic use, Stimulates salivation and Stimulates lacrimation. Used in Sjogren's syndrome which causes xerostomia and dry eyes
Pyridostigmine (Mestinon)
An indirect-acting cholinergic agonist. Inhibits cholinesterase--the enzyme that breaks down Ach Used primarily for myasthenia gravis, Therapeutic doses ↑ force of muscular contraction; toxic doses ↓. Absolutely contraindicated with GI obstruction and urinary tract obstruction. Cholinergic crisis most serious adverse effect. Neostigmine (Prostigmin) is a similar drug used
Drugs Used for Alzheimer's Disease
Most are indirect-acting cholinergic agonists meaning they inhibit cholinesterase and allow ACh to accumulate. donepezil (Aricept)—1996, rivastigmine (Exelon)—2000, galantamine (Razadyne)—2001, memantine (Namenda)—2003. See p. 316 for MOA of Memantine
Cholinergic Agonists Uses
Glaucoma, Urinary retention, Xerostomia (Sjogren's sndrome), Myasthenia gravis, Alzheimer's. Overdose results in cholinergic crisis and should be treated with anticholinergic
Anticholinergics (Cholinergic Antagonists)
Also known as parasympatholytics or antimuscarinics. Drugs that antagonize or block the muscarinic receptors. Basically they inhibit the action of ACh. Atropine is the prototype of this group
parasympatholytics
AKA Anticholinergenics or antimuscarinics. Drugs that antagonize or block the muscarinic receptors. Basically they inhibit the action of ACh. Atropine is the prototype of this group
ATROPINE
Competes with ACh for binding at the muscarinic receptors of the PSNS and ultimately inhibit nerve transmission at these receptors. Principle actions are: decrease in salivary, bronchial, GI, and sweat gland secretions; mydriasis; increase HR; bronchodilation. Also causes decreased bladder tone (retention) and decreased GI motility (constipation). Used commonly in CPR and preoperatively. Most serious adverse effect is overdose
Other Anticholinergics
- Scopolamine--suppresses emesis and motion sickness,
- ipratropium bromide (Atrovent)--Bronchodilator (Inhaler)
- benztropine mesylate (Cogentin)—used in Parkinson's
- tolterodine (Detrol) Urge incontinence
- dicyclomine (bentyl) IBS
- glycopyrrolate (Robinul) dries secretions is used in palliative care
Neuromuscular Blocking Agents (NMBAs)
Block Nicotinic M receptors. Given to produce muscle relaxation during surgery, endotracheal intubation, mechanical ventilation, and other procedures
succinylcholine (Anectine)
An ultra-short acting drug. Paralysis abates rapidly . Paralysis peaks about 1 minute after IV injection and fades completely within 4-10 minutes. Used primarily during endotracheal intubation. Malignant hyperthermia is a rare and potenially fatal adverse effect - genetically determined
pancuronium (Pavulon)
Intermediate-acting. Used to facilitate intubation and for muscle relaxation during surgery or mechanical ventilation
vecuronium (norcuron)
Intermediate-acting. Used to facilitate itubation and for muscle relaxation during surgery or ventilation. One of the most commonly used NMBAs
ADRENERGIC AGONISTS
Also known as sympthomimetics. Drugs that mimic the action of the SNS. Generally classified into two groups: catecholamines and noncatecholamines. Also classified according to their selectivity
sympthomimetics
AKA ADRENERGIC AGONISTS Drugs that mimic the action of the SNS. Generally classified into two groups: catecholamines and noncatecholamines. Also classified according to their selectivity
Catecholamines
Substances which can produce a sympathomimetic response. Receive their name because of their similar chemical structure. Generally have a short duration of action (often need to be administered in a continuous fashion), cannot be given orally, and do not cross the blood-brain barrier. Examples: epinephrine, dopamine
Nonselective adrenergic agonists
stimulate both alpha and beta receptors
Selective adrenergic agonists
target a specific subtype receptor. Selective drugs are used more frequently as they minimize adverse effects and maximize therapeutic effects
Alpha-1 Activation causes
Vasoconstriction, Mydriasis, Urinary retention
ALPHA-2 ACTIVATION
Inhibits NE release
BETA 1 ACTIVATION
Beta-1 receptors: primarily in the heart. Response to Beta-1 stimulation is ↑ heart rate, ↑ contractility, ↑ renin secretion
BETA 2 ACTIVATION
Activation leads to bronchodilation and uterine relaxation. Therapeutic uses: Asthma, Delay of preterm labor. Caution: Beta 2 activation causes glycogenolysis and can lead to hyperglycemia. Usually only an issue if diabetic.
Dopaminergic Receptors
Also adrenergic receptors. Stimulated by dopamine only. Clinical significance: Depending on dose, dopamine can dilate renal blood vessels and therefore improve renal perfusion
Adrenergic Agonists, Nonselective
epinephrine is the prototype. A catecholamine. Used in anaphylaxis, asthma, CPR, simple glaucoma, etc. Administered parenterally, topically, or by inhalation. Causes increased inotropic and chronotropic effects in B1, increased BP A1, and bronchodilation B2. Side effects raised BP, angina, cerebral hemorrhage, increased blood glucose, necrosis, and dysrhythmias
ADRENERGIC AGONISTS—Alpha 1 Selective
phenylephrine (Neosynephrine). Alpha 1stimulation causes vasoconstriction. Not a catecholamine, but poorly absorbed orally. Commonly given for relief of nasal congestion and to produce mydriasis for optic procedures. Side effects are raised blood pressure if given IV
ADRENERGIC AGONISTS—Alpha2 Selective (Centrally Acting)
clonidine (Catapres) is the prototype. Selective stimulation of 2 receptors, Inhibiting release of NE→vasodilation. Results in decreased BP,decreased HR. Used as an antihypertensive. Considered as secondary or supplemental and is usually not appropriate for monotherapy. Can be administered transdermally whhere the drug is released at a constant rate for 7 days
ADRENERGIC AGONISTS—Beta Nonselective
isoproterenol (Isuprel) is the prototype. +inotropic and +chronotropic effects (B1). Bronchodilation, glycogenolysis (B2). Results in increased cardiac output. Used to treat shock, cardiac arrest, CHF. Adverse effects are tachydysrhythmias, angina, hyperglycemia
ADRENERGIC AGONISTS—Beta 1 Selective
dobutamine (Dobutrex) is the prototype. A catecholamine. Available for IV use only. + inotropic effects with raised O2 consumption. Leads to increased cardiac output. Used for heart failure and chronic heart failure. Not used as much as digoxin. Major side effect is tachycadia
ADRENERGIC AGONISTS—Beta 2 Selective
Preferred bronchodilators-- produce fewer cardiac-related side effects. albuterol (Proventil) is the prototype. Commonly administered orally or by inhalation. Used in asthma. terbutaline (Brethine) mainly beta 2 agonist that is used to stop preterm labor
ADRENERGIC AGONISTS--Dopamine (Intropin)
Stimulates dopamine, a1 and b1 receptors. Receptor stimulated depends on the dose. Low doses—stimulate dopamine receptors only. Moderate doses—dopamine & beta 1. A catecholamine. Remember that dopamine improves renal perfusion. Primary uses are shock b1 and dopamine, Heart failure b1, Renal failure dopamine. Administered by continuous IV infusion
ADRENERGIC BLOCKERS
Adrenergic blockers have the opposite effect of adrenergic agonists and are therefore referred to as antagonists. They bind to adrenergic receptors, but in so doing inhibit or block stimulation of the SNS. Can also be called sympatholytics. Generally have a high degree of selectivity
Alpha Adrenergic Antagonists
Block the stimulation of alpha receptors. Clinically relevant drugs in current use block 1 receptors in the vasculature and bladder. Alpha 1 blockade leads to vasodialation and decreased bp, relaxation of bladder sphincter and micturation (urination). Uses are hypertension and BPH. The prototype is prazosin (Minipress)
ADRENERGIC ANTAGONIST- Alpha 1 Selective
prazosin (Minipress). Primarily used for hypertension. Can also be used for urinary obstruction in BPH. Most common s.e.→ orthostatic hypotension, lightheadedness, dizziness, HA, etc. Doxazosin (Cardura), terazosin (Hytrin), tramsulosin (Flaomax)-approved only for BPH, alfuzosin (Uroxatral)-approved only for BPH
Another use for alpha blockers-- phentolamine (Regitine)
Because of their potent vasodilating effects, alpha blockers can also be used to prevent skin necrosis and sloughing following extravasation.
BETA ADRENERGIC ANTAGONISTS
More commonly called beta blockers. May be selective or nonselective. Beta-1 blockers are often called cardioselective→↓ heart rate, ↓ contractility, ↓ myocardial oxygen demand. Nonselective beta blockers also cause bronchoconstriction and inhibition of glycogenolysis. Uses are agina, hypertension, dysrhythmias, MI, heart failure, others
ADRENERGIC ANTAGONISTS—Beta Nonselective
propranolol (Inderal) is the prototype. Causes decrease HR and decrease contractility leading to decrease cardiac output (β1). As cardiac output decreases, so does BP (decrease renin also). O2 demand decreases as well so can be used for angina. Adverse effects related to b2 blockade are bronchoconstriction and inhibition of glycogenolysis
ADRENERGIC ANTAGONIST—Beta 1 Selective (Cardioselective)
metoprolol (Lopressor) is the prototype. Inhibits the beta 1 effects without causing bronchoconstriction or inhibiting glycogenolysis. Used for hypertension, angina, and following a MI. Safer choice for asthmetics and diabetics. Other b1 selectives are atenolol (Tenormin) and acebutolol (sectral)
ADRENERGIC ANTAGONISTS—Nonselective Beta plus Alpha 1
carvedilol (Coreg). Also a calcium channel blocker. Also possesses antioxidant properties. Used for heart failure, hypertension, angina, post-MI. Most often given in combination with digoxin, furosemide and ACE inhibitors when used to tx heart failure
xerostomia
dry mouth
miosis
constriction of pupil
mydriasis
dialation of pupil
Which has a more dominent effect? A1 or A2
A1
Cholinergic Agonist not recommended for
COPD or GI obstruction
What drugs cure Alzheimers?
None, cholinergic agonists help some. Usually takes 6 weeks to work
Why give sedatives with NMBAs?
Paralysis can cause panic if the patient is alert
Why give catacholamines continuously through IV?
They have a short duration of action
Why might a diabetics medications need to be altered when taking a B2?
Because if hyperglucose occurs, they may need more insulin
Alpha 2 Antagonists
Not used. If a med is an alpha blocker it is referring to alpha1
micturate
urination
BPH
Benign Prostate Hypertrophy, it sometimes makes urination difficult
Alpha 1 blockers used for
antihypertention, and to help urinate
1st dose syncope
faint
Why take alpha 1 blockers at bedtime?
syncope is common especially when first starting drug. Advise patient to go slowly if getting out of bed at night.
extravasation
AKA infiltration of IV, Give phentolamine if needed
What is the first response action if infiltration occurs?
Stop IV. Some meds like dopamine can be very damaging to tissues
Do not give beta blocker if
hr below 60
Which drugs do athletes avoid?
Beta blockers because they feel it decreases their performance
Why is it important to know that B2 inhibit glycogenolysis by the liver?
Because glycogenolysis is what the liver does to counteract hypoglycemia. if patient is diabetic they have no other natural mechanism to handle the situation if hypoglycemia occurs. Can be fatal
When stopping Beta blockers remember
they should not be stopped abruptly
Other uses for Beta 1 blockers
anxiety, stage fright, migraine headaches
Memorize this quote
Beta blockers are also considered to be cardioprotective because they inhibit stimulation of the myocardium by circulating catacholamines
inotropic
An Inotropic drug influences the force of the contraction of the cardiac muscle, or heart, thereby affecting cardiac output
chronotropic
Chronotropic drugs may change the heart rate by affecting the nerves controlling the heart, or by changing the rhythm produced by the sinoatrial node
dromotropic
A dromotropic agent is one which affects the conduction speed in the AV node
glycogenolysis
the splitting up of glycogen in the liver, yielding glucose
Acetadote
antidote for acetaminophen toxicity that can be given as an intravenous injection.
pharmacokinetics
the study of what the body does to the drug
pharmacodynamics
what the drug does to the body
4 points of pharmacokinetics
absorption, distribution, metabolism, excretion
rate of absorption
determines how SOON effects will begin
amount of absorption
determines how INTENSE effects will be.
bioavailability
quantifies the extent of drug absorption
what factors affect absorption?
route of administration, rate of dissolution, surface area, blood flow to area, lipid solubility, first pass effect
common routes of medication administration
enteral, parenteral, rectal, vaginal, topical or transdermal, inhaled by nasal or oral, opthalmic, otic
enteral
oral, sublingual, buccal
parenteral
intravenous, intramuscular, subcutaneous
first pass effect
most drugs given orally are absorbed directly into portal circulation. Once in the liver, many drugs are highly metabolized causing much of the active dose to be lost before ever entering general circulation.
parenteral is generally the ___ route by which a drug can be absorbed
fastest
distribution
the delivery of a drug from the bloodstream to its site of action
primary factors that affect distribution
blood flow to tissues, ability to exit the vascular system
biotransformation
aka metabolism; liver is the most important site (the sewage treatment plant)
compliance
implementation or fulfillment of a prescriber's or caregiver's prescribed course of treatment or therapeutic plan by a patient. Also called adherence.
goals
statements that are time specific and describe generally what is to be accomplished to address a specific nursing diagnosis
medication error
any preventable adverse drug event involving inappropriate medication use by a patient or health care professional; it may or may not cause the patient harm
noncompliance
an informed decision on the part of the patient not to adhere to or follow a therapeutic plan or suggestion. Also called "nonadherence"
nursing process
an organizational framework for the practice of nursing. It encompasses all steps taken by the nurse in caring for a patient: assessment, nursing diagnoses, planning (with goals and outcome criteria), implementation of the plan (with patient teaching), and evaluation
outcome criteria
descriptions of specific patient behaviors or responses that demonstrate meeting of or achievement of goals related to each nursing diagnosis. These statements, like goals, should be verifiable, framed in behavioral terms, measurable, and time specific. Outcome criteria are considered to be specific, whereas goals are broad.
prescriber
any health care professional licensed by the appropriate regulatory board to prescribe medicine.
6 rights of drug administration
right client/pt, right med/drug, right dose, right time, right route, right documentation

(Carol May Drive To Rodeo Drive)
difference between chemical, generic, and trade names of drugs
Chemical names: actual chemical composition of drug
Generic names: nonproprietary name assigned by US Adopted Name Council Each drug only has 1 generic name and it's in all lowercase. must be bioequivalent (has same active ingredient).
TRADE: aka proprietary name or brand name. Given to drug by manufacturer; protected by trademark.
properties of an ideal drug
effectiveness (most important property a drug can have), safety (no such thing as a safe drug), selectivety (no such thing as a selective drug), other goodies: reversible action, predictability, ease of administration, freedom from drug interactions, low cost, chemical stability, and possession of a simple generic name
prototype
typical of drugs within a drug class (ex: hydrochlorothiazide is a prototype representative of thiazide diuretics)
clinical pharmacology
study of drugs in humans
therapeutics
use of drugs to diagnose, prevent, or treat disease or prevent pregnancy
Pure Food and Drug Act of 1906
1st law that helped regulate drugs and dealt with labeling
Food, Drug, and Cosmetic Act of 1938
Dealt with safety (Forgo Drug Complications Always)
Durham-Humphrey Amendment of the 1938 Act (in 1951)
Rx vs. OTC
Kefauver-Harris Amendment of the 1938 Act (in 1962)
Required drugs to be proven effective
Comprehensive Drug Abuse Prevention and Control Act of 1970
required education/labeling of what drugs can be habit-forming (p. 53 of text)
Best Pharmaceuticals for Children Act of 2002
One of the first studies that dealt with how drugs affect the pediatric population
Pediatric Research Equity Act of 2003
a legislative move that boosted pharmaceutical safety amongst the nation's children. Gives the FDA the authority to require pediatric studies of drugs to ensure they are safe for children. Many of today's drugs have only been tested on adults.
Legend Drug
Any prescription drug
new drug development process
preclinical trials -> phase 1 clinical trial -> phases 2, 3, and 4
preclinical trial
time when patent clock STARTS, time when chemicals that have therapeutic value are tested on animals to determine if they have the same effects on living tissue and any adverse effects. After extensive testing, company can submit app for an "investigational new drug" (IND)
phase 1
drug tested on small # of healthy human volunteers
phase 2
drug tested on small group of volunteers who have the disease drug is thought to treat
phase 3
drug is tested in vast clinical market
phase 4
postmarketing studies VOLUNTARILY conducted by drug companies
orphan drugs
when new/promising drugs never complete research phase due to overwhelming cost of research and development
Orphan Drug Act of 1983
government incentives designed to bring "orphan drugs" to market if proven safe
EMAR
electronic med administration record
time allowed to pass patient medication
within window of 30min before prescribed time to 30min after prescribed time.
factors influencing med administration
body weight, age (infants/elderly are especially sensitive), gender, culture, baseline data (VS, labs), whether pt is "high risk"
high risk clients
infants and elderly, pregnant patients
why are elderly high risk?
cardiovascular (decreased absorption and distribution), GI (altered absorption and delayed gastric emptying), Hepatic (decreased metabolism), renal (decreased excretion), Beers criteria
Beers criteria
list of medications inappropriate for the elderly
pregnancy category A
no evidence of risk to fetus
pregnancy category B
no risk to animal fetus; info for humans not available
pregnancy category C
adverse effects in animal fetus, info for humans not available
pregnancy category D
possible fetal risk in humans reported; consider benefit vs. risk
pregnancy category X
fetal abnormalities reported. Do NOT use!
polypharmacy
use of many medications
2 meds: risk of interaction
6%
5 meds: risk of interactions
50%
10 meds: risk of interactions
100%
contraindication
a pre-existing condition that precludes use of a particular drug under all but most desperate of circumstances
Precaution
a pre-existing condition that significantly increases the risk of an adverse reaction to a particular drug, but not to a degree that is life threatening
ADR (Adverse Drug Reaction)
any noxious, unintended and undesired effect that occurs at NORMAL drug doses
side effect
a nearly unavoidable secondary drug effect produced at therapeutic doses
allergic reaction
an IMMUNE RESPONSE
idiosyncratic effect
abnormal & unexpected response to a medication, other than an allergic reaction, that is peculiar to an individual client. No explanation for effect.
toxicity
ADR caused by EXCESSIVE DOSING, however, in practice, we will hear the term toxicity to refer to any SEVERE ADR regardless of dose that caused it.
SALAD
sound alike, look alike drugs - high alert meds (high risk for med errors)
induction/autoinduction
process of stimulating enzyme synthesis; can require increased dosages and increase the risk of drug-drug interactions
inhibitors
drugs that inhibit various classes of drug metabolizing enzymes and are called enzyme inhibitors; can lead to toxicity bc there is more free drug available (not broken down as much); requires lower dosage
excretion
elimination of drugs from the body
important organs for excretion, in order
kidneys, liver, bowel
drug-food interaction
when food can decrease the rate and extent of absorption
half-life
amount of time it takes for amount of drug in body to decrease to 1/2 of peak life
how many half-lives are necessary to remove drug from body?
4
steady state/plateau
when the administration rate equals rate of drug elimination/clearance. generally 4 half-lives.
peak level
highest blood level of drug; generally occurs within an hour or few hours after administration
trough level
lowest blood level; occurs just prior to administration of next dose
how does a drug produce a response? (3 ways)
receptor interaction, enzyme interaction, nonselective interaction
agonists
drugs that mimic the body's own regulatory molecules; activate receptors
antagonists
drugs that block the actions of endogenous regulators; receptors commonly blocked
teratogenic
capable of causing structural defects in fetus
mutagenic
capable of causing permanent changes in the genetic composition of living organisms
carcinogenic
capable of causing cancer.
plasma drug levels
direct correlation between therapeutic and toxic responses and amount of drug in plasma
MEC
minimum effective concentration; the plasma drug level below which therapuetic effects will not occur
toxicity
occurs when plasma drug levels climb too high
therapeutic range
the range between the MEC and toxicity
1000 mL --> L
1 L
1L = mL
1000
1 oz = mL = tbsp
1oz = 30 mL = 2 tbsp
1 tsp = mL
1 tsp = 5mL
what are three main mechanisms of action
receptors, enzymes, non-specific
list some drug - food interactions
grapefruit
digoxin - high fiber
tetracycline - calcium
warfarin (coumadin) - green leafy veggies/vit K
what information is included in a med profile/history?
all drug use
herbal/home remedies
ETOH, tobacco, caffeine
current and history of illegal drugs
otc
vitamins/supplements
hormonal (birth control)
past prescriptions on reg basis
family history, cultural, racial history related to meds
NANDA
North American Nursing Diagnosis Association
What are some of the commonly used NANDA approved diagnosis related to patient education?
deficient knowledge
ineffective health maintenance
ineffective self health mgmt
risk for injury
impaired memory
noncompliance
1 gr (grain) = ?mg
1 gr = 65mg
1000mg = ?g
1000mg= 1 g
1 kg = ?lb
1 kg = 2.2lb
1mg = ?mcg
1mg = 1000 mcg
1g = ?mg
1 g = 1000 mg
1k = ? g
1 k = 1000 g
1 tsp = ? mL
1 tsp = 5 mL
1 tbsp = ?mL
1 tbsp = 15mL
6 main factors you must consider when monitoring a drugs effect
THERAPEUTIC INDEX (therapeutic level to toxic. Some have very small ratio such as warfarin)
DRUG CONCENTRATION (adjust dosage if concentration too high due to complications like kidney protein)
PATIENT CONDITION (all physical and psych conditions)
TOLERANCE & DEPENDENCE (tolerance decreases effect; you want to avoid dependence where the body/mind starts to NEED the drug)
INTERACTIONS - drug/drug or drug/food
ADVERSE EFFECT - nonintended neg effect
7 types of pharmactherapeutics
Acute- drug treatment, sustain life, emergency
Maintenance- prevent progression, chronic illnesses
Supplemental- substance body needs but cannot produce ex: insulin for DM pts
Palliative- make comfortable, no cure, end-stage ex: morphine for cancer patient
Supportive- support body while recovering ex: fluid or blood products
Prophylactic- prevent illness, ex: vaccines, pre-surgery antibiotics
Empiric - probably cause of illness treated
pharmacognosy
study of drug's natural sources such as plants, animals, minerals, laboratory synthesis
what are 3 factors that can alter drugs effect on fetus?
1) gestational age; 1st trimester is most crucial
2) mothers health
3) drug chemistry & dosage

**breastfeeding can be harmful depending on drug
what characteristics do infants have that can affect dosage or drug choice?
skin is thinner and more permeable
stomach lacks acid
lungs are weaker/less of a barrier
body temperature is not as regulated
immature organs
sensitivity of receptors
rapidly developing tissues
BSA
body surface are
what are the 3 FDA recall responses?
class 1: most serious - drug carries reasonable probability of serious adverse health effects or death

class 2: less severe - may result in reversible health effects; likely not permanent

class 3: least severe; not likely to result in any significant health problems
what are the 4 levels of med errors?
level 1: no error, but risk is present for one
level 2: error occurred - no harm caused
level 3: error occurred - harm was caused
level 4: error occurred - death
What 6 elements must be present on an Rx?
patient's name
date order was written
name of drug
dosage amount and frequency
route of administration
prescriber's signature
what type of drugs given on the skin would be used for localized treatment?
ointments, gels, creams
what type of drugs given on the skin would be used for systemic treatment?
transdermal patches
prolonged absorption in the form of enteric-coated tablets is absorbed into the body through?
small intestine
Initials preceeding names of enteric coated tablets are
SR, SA, CR, XL, XT
A
ACE Inhibitors.

ACE stands for angiotesin converting enzyme, and it is responsible for converting angiotesin I to angiotesin II. Angiotesin II (A2) is a potent vasoconstrictor and it also stimulates the secretion of aldosterone, increases BP, increases sodium and water retention, increases potassium excretion.

ACE Inhibitor meds inhibit enzyme that allows for conversion and thus DECREASES BP. This is the main reason it's given as an anti-hypertensive med.

When giving ACE Inhibitors, you must monitor BP and watch for hyperkalemia (too much potassium in the blood). A persistent cough is a common side effect. Angioedema is rare but serious.

Generic names often end in "...pril" Ex: lisinopril

Refer to p 389 in text
B
Beta Adrenergic Blockers (most often referred to as "beta blockers")

Can block beta 1 receptors (heart), or beta 2 receptors (lung). If the beta blocker affects only one of these, it is a "selective beta blocker." Drugs that block beta 1 AND beta 2 receptors are called "non selective."

Effects on the heart of cardioselective (B1) blockade: decrease heart rate, slow (decrease) conduction through AV node, decrease myocardial oxygen demand, decrease myocardial contractility.

Uses: angina, hypertension dysrythmias, myocardial infarction, etc.

Commonly end in "...lol" Ex: propranolol
C
Calcium channel blockers.

Prevents calcium from entering cells. Have greatest effects on heart (decreases heart rate & contractility( and blood vessels. (smooth muscle relaxation). Used to treat hypertension, angina, and cardiac dysrhythmias.

Examples include amlodipine (Norvasc)- antihypertensive. Verapamil (Calan) - all the above, and diltiamem (Cardizem) - all of the above.

Hint
D
Digoxin (Lanoxin)

A cardiac drug that increases the myocardial contractility w/out a corresponding oxygen requirement. Slows the heart rate & improves stroke volume. Commonly used to treat heart failure. Narrow theraputic window (approx 1-2 ng/ml.

Early symptoms of toxicity: N/V & anorexia. Low serum K+ levels increase risk of toxicity. Do NOT administer w/meals high in fiber (it binds to it, rendering it ineffective).
F
furosemide (Lasix)

A loop diuretic, meaning it exerts its action (inhibits reabsorption of sodium & water) in the loop of Henle. Used to treat hypertension, heart failure, edema, etc.

Also causes excretion of K+, so must monitor serum K+ levels prior to administration.
E
Epinephrine

A NONselective adrenergic agonist commonly called Adrenalin.

A sympathomimetic. Often used to treat anaphylactic reactions. Increases contractility of the heart, increases BP & causes bronchodilation. Can increase blood glucose as well.
G
glucocorticoids

A corticosteroid or "steroid."

An immunosuppressant. Influences metabolism of carbohydrates -> increases blood glucose -> proteins -> suppress protein synthesis reducing muscle mass & delaying wound healing; and fats -> breaks down fat causing redistribution (moonface, hump back).

Also possess potent anti-inflammatory actions. MANY uses and many adverse reactions.

Must be tapered when discontinuing.

Typically ends in "one" (Prednazone, Cortisone)
H
Heparin (HIGH ALERT MED!)

An anticoagulant administered by IV or SC (subcutaneously). DOES NOT DISSOLVE CLOTS, but can prevent clots from forming. Used to treat pulmonary embolism, CVA (stroke), DVT, etc. Primary adverse reaction is hemorrhage. Protamine sulfate is the antidote for heparin overdose. Effects of heparin monitored via a blood test, PTT, usually obtained daily or more often if heparin is administered IV. Generally not necessary to monitor PTT w/SC administration.
I
I: Insulin: transports glucose into the cell. That's why diabetics (who lack endogenous insulin) have high serum blood glucose levels - because the glucose can't enter the cell. Available in many different types. Types differ in terms of onset of action, duration of action etc. Novolog insulin has a RAPID onset and is commonly used for both meal coverage and "correction" dose. (if you do a finger stick and blood sugar is high and I'm not about to eat, you would administer Novolog b/c it would be quick to bring that high glucose down. If your blood sugar is good (say, 100), but I'm about to eat, I will also need a fast acting insulin to cover the sugar I'm about to intake in a meal)). Glargine insulin (Lantus) provides basal coverage meaning it lasts approximately 24 hours and does not peak.
J
J: Januvia (trade name). Generic name is sitagliptin. An oral incretin mimetic used only for type II diabetes. MOA is to stimulate glucose-dependent release of insulin by enhancing the action of incretin hormones. Generally well tolerated. FDA currently monitoring for increased incidence of pancreatitus in in patients taking Januvia. Taken one time/day.
K
K= potassium Sparing diuretics! Includes aldosterone antagonists and nonaldosterone antagonists. Aldosterone antagonists (i.e. spironolactone [aldactone]) inhibit the effects of aldosterone. (Aldosterone causes retention of sodium and water and excretion of potassium). Nonaldosterone antagonists (i.e. triamterene [dyrenium]) acts directly on the renal tubule to suppress reabsorption of sodium and water and encourage reabsorption of potassium. Regardless, MUST MONITOR POTASSIUM LEVELS!
L
L= levothyroxine (Synthroid). A synthetic thyroid hormone used in hypothyroidism. Long half life and can be dosed one time a day BEFORE BREAKFAST (absorption is better on an empty stomach). However, can take approximately a month to reach steady state. Replacement therapy generally necessary for life. Side effects: s/s of hyperthyroidism - tachycardia, palpitations, etc.
M
M= metformin (Glucophage). An oral antidiabetic agent. Lowers blood sugar by decreasing production of glucose in the liver. Can cause lactic acidosis - primarily in those with renal insufficiency. Held prior to and following any procedure involving "dye" until kidney function is confirmed via creatine level.
N
N= NSAIDs - Nonsterioidal Anti-inflammatory Drugs. Decrease inflammation by inhibiting COX (cyclooxygenase). COX has two forms - 1 and 2. NSAIDs may be nonselective (1st generation) or COX2 selective (2nd generation). Fewer harmful effects with COX2 selective agents. Aspirin is a nonselective; Celecoxib (Celebrex) is a COX2 selective.
O
O= Opioids. Most effective pain relievers available. When classified according to receptor activity, may be a pure agonist, an agonist-antagonist, or a pure antagonist. When agonist-antagonists are given alone, they produce analgesia. When they are given in the presence of a pure agonist, they will antagonize analgesia and can precipitate withdrawal syndrome. Major adverse reactions of pure opioid agonist: respiratory depression and constipation. Antidote: a pure antagonist! Naloxone (Narcan)
Q
Q= Quinidine. A Class 1A antidysrhythmic. Common side effects: diarrhea and hypotension. Can also cause "cinchonism" which causes blurred vision, tinnitus, and GI upset. Fairly strong anticholinergic effects as well. Usually given po. Only quinidine gluconate can be given IV.
P
P= Proton pump inhibitors. Most effective drugs for suppressing secretion of stomach acid. Blocks the final step in gastric acid production. Used primarily for ulcers and GERD. Generic names commonly end in "...prazole". Prototype is omeprazol (prilosec) which is now available OTC.
R
R=Reglan. Generic name is metoclopramide. The only "prokinetic" (meaning it increases the tone and motility of the GI tract) agent currently available. Used for GERD, N/V, diabetic gastroparesis, and postoperative emesis. Major side effect: DIARRHEA!
S
S= Statins. Most commonly used class of drugs to lower acholesterol. Cause significant decrease in LDL and a more mild increase in HDL. Side effects are uncommon. However, can cause liver toxicity (liver enzymes should be monitored at least yearly) and rarely, myopathy. Use with caution in combination with fibrates. Usually administered at bedtime.
T
T= Tamoxifen (Nalvadex). A SERM (selective estrogen receptor modulator). One of the most widely prescribed drugs for breast cancer. Can inhibit cell growth by blocking estrogen receptors. Used both to treat active disease as well as to reduce occurrence of breast cancer in high risk women. Most common adverse reaction is hot flashes. Most serious is development of endometrial cancer or thromboembolism.
U
U= Ultram. Generic name is tramadol.
This is a nonopioid analgesic. Does have weak agonist activity at mu opioid receptors but causes minimal respiratory depression and is not a controlled substance. notable side effect: seizures. Avoid use in clients with or at high risk for seizures.
V
V=vancomycin (Vancocin)
Potentially toxic antibiotic used for serious infections including MRSA and C. dif. Inhibits cell wall synthesis. Effective only against Gm+ organisms. Usually given IV. Serious s.e.=ototoxicity. Must also be alert for "Red Man Syndrome" - rash, flushing, hypotension, etc., - can be minimized by slow IV administration.
W
W=Warfarin
Oral anticoagulant that antagonizes the effects of vitamin K. Peak effects take several days to develop. PT and INR are tests used to monitor effectiveness. Highly protein bound and subject to MANY drug interactions. Antidote is vit K
X
X=Xanax.
Generic name is alprazolam. A benzodiazepine. Used for anxiety, panic disorders, and occasionally for PMS. Drowsiness is a common side effect. May be habit forming. Generally not recommended for use for anxiety for longer than 4 months. Do not discontinue abruptly after long-term use.
Z
Z= zithromax. Generic name is Azithromycin.
Commonly referred to as a Z-pack. A macrolide antibiotic. Used commonly for respiratory tract infections. Administer on an empty stomach. Side effects uncommon, but can cause GI upset. Oral therapy usually consists of once a day dosing for 3-5 days.