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Pharmacology Test III
Terms in this set (255)
Which offers the best delivery of topical drugs?
Topical steroids are classified according to:
What skin changes may occur w/ topical steroid use?
Atrophy & acne
When are systemic corticosteroids recommended for derm conditions?
When topical corticosteroids are ineffective.
What is the most common cause of contact dermatitis in older patients?
What antibiotic is safest for pregnant women?
Amoxicillin + clavulanate
What is clavulanate?
A B lactamase inhibitor
Which antibiotic should be reserved for the most serious skin infections?
Which is NOT indicated for treatment of psoriasis?
Which drug is LEAST LIKELY to cause an acne-like outbreak?
Which drug is highly teratogenic? (Pregnancy Category X)
What is pulse dosing?
Drug on/drug off schedules
Which antiviral drug dramatically decreases length of post herpetic neuralgia in patients w/ herpes zoster?
When prescribing oral anti fungal drugs, what lab tests need to be monitored?
Liver functions studies
Which is NOT recommended for treatment of tinea versicolor?
For which condition is systemic (rather than topical) anti fungal drugs recommended?
What is a common reason for non adherence to anti fungal drug remains?
When can topical azalea anti fungal therapy be discontinued?
1 - 2 weeks after lesions clear.
What can be done to enhance topical corticosteroid absorption?
Apply after bathing
Which topical antimicrobial agent is recommended for prophylaxis?
Antifungal powders or sprays.
Sympathetic (Adrenergic) Nervous System: (5)
1. Increases HR
2. Constricts vessels
3. Dilates airways
4. Dilates pupils
5. Mediates orgasm and ejaculation
Organs and tissues not receiving adequate blood flow (decrease oxygenation)
Inadequate blood flow secondary to hypersensitivity reaction.
Anaphylactic Shock results in. . (3)
1. dilated vessels = BP drops
2. less blood return to <3 = decreased stroke volume
3. muscles in airways tighten = bronchoconstriction
What can we give the patient w/ anaphylaxis?
An adrenergic agonist, like epinephrine!
1. dilates the bronchi
2. causes vasoconstriction
3. increases force of cardiac contraction
Epinephrine has a short half life SO..
We will start an IV with an adrenergic agonist such as norepinephrine (Levophed); a prodrug
Norepinephrine is a powerful ________.
What do we call drugs that have vasoconstrictive adrenergic effects on vessels? (5)
3. Vasopressive drugs
4. Vasoactive drugs
5. Inotropes (inotropic)
Refers to force of contraction.
Refers to <3 rate.
Refers to speed of cardiac impulse conduction.
Levophed (or any pressor) effects on BP:
Increases; monitor at least every 15 minutes
Levophed (or any pressor) effects UOP:
Decreases; monitor at least every hour
What if the IV becomes displaced?
The adrenergic agonist mimics the actions of:
Sympathetic Nervous System
How can Afrin relieve nasal congestion?
Vasoconstriction of vessels in the nose
Problems from Afrin: (2)
1. nasal dryness, easy bleeding
2. rhinitis medicamentosa (rebound congestion)
How does visine "get the red out"?
Adrenergic agonist that acts on dilated vessels in the conjunctiva by stimulating a adrenergic receptors to cause vasoconstriction.
Drugs that are adrenergic blockers:
1. decrease HR
2. dilate blood vessels
3. constrict smooth muscles in the airways
4. constrict pupils
Indications for B blocker propranolol (Inderal):
1. decreased BP
2. decreases rapid pulse
3. cardioprotective effect post- MI
4. stage fright
What happens if we give an adrenergic antagonist such as a beta blocker to someone w/ asthma?
B blockers constrict airways so it can worsen asthma
Adrenergic antagonists w/ sexual functions: (2)
1. failure to ejaculate
How would a provider discontinue a B blocker like propranolol (Inderal)?
Taper to avoid rebound hypertension & tachycardia;
The extra cardia work load can lead to angina
Parasympathetic Nervous System: (6)
1. decreases HR
2. constricts airways & increases secretions
3. increases peristalsis & increases secretions
4. increase detrusor activity & relaxes sphincter
5. miosis = constricts pupils
6. mediates arousal & erection
cholinergics (Cholinergic Agonists) indications: (5)
1. Mysathenia gravis
2. Alzheimer's Disease
3. urinary retention
4. bethanechol (Urecholine) stimulates cholinergic receptors in bladder
Cholinergic Toxicity: (6)
3. Urinary incontinence
5. GI cramping
Cholinergic Antagonists make better & make worse? <3
- can treat bradycardia
- can worsen already fast HR
Cholinergic Antagonists make better & worse? airways
-dilate airways & decrease secretions
-given pre-op to decrease secretions
-cause dry mouth
Cholinergic Antagonists make better & worse? gastro
-relaxing smooth muscles to decrease peristalsis & decrease secretions
-help control diarrhea
-relieve irritable bowel symptoms
-can cause constipation
Cholinergic Antagonists make better & worse? bladder
-decrease bladder tone & tighten urinary sphincter
- relieve bladder spasms
-decrease urinary frequency & some types of incontinence
-make bladder obstruction worse
Since cholinergic agonists increase perspiration, anticholinergic. . .
Which is dangerous for OLDER people b/c:
1.because perspiration cools the body
2. older folks already have probs w/ thermoregulation
3. puts them at risk for heat-related injury
Since cholinergic agonists have a role in sexual arousal & erectionanticholinergics:
-can cause impotence
-they may think its a "normal" part of aging when it isn't.
-educate your patients so that they can approach the prescriber about these problems; may be possible to change meds
Adrenergic drugs stimulates:
Cholinergic drugs stimulate:
When given for myasthenia graves, give drug ____ minutes prior to meal.
Hold Cholinergic Drugs IF:
3. respiratory depression
What would be the antidote for cholinergic poisoning?
Anticholinergic (usually atropine)
The root "ADREN" is used when referring to the _______ nervous system.
2 types of adrenergic receptors:
The root "CHOLINE" is used when referring to the ______ nervous system.
Sympathetic or Parasympathetic: Mydriasis?
Sympathetic or Parasympathetic: Bronchiolar dilation?
Sympathetic or Parasympathetic: Erection?
Sympathetic or Parasympathetic: Lysis of glycogen to increase glucose?
Parasympatholytics are often called anticholinergics. Can you explain why this would be appropriate?
-they destroy the parasympathetic effect so they could be called "anti-parasympathetic"
-the term cholinergic is associated w/ the parasympathetic nervous system
-therefore, a drug that is anti-parasympathetic would also be anti-parasympathetic would also be anti-cholinergic
A patient is prescribed dicyclomine (Bentyl), an anticholinergic drug. What effects would this drug have on the GI system?
Decrease GI motility & secretions.
A patient has a heart rate of 46 and is symptomatic. Which drug would you anticipate being asked to give STAT?
Atropine, an anti-cholinergic agent; b/c anticholinergic agents are parasympatholytic.
What purpose do antianginal drugs serve? (4)
1. decrease frequency of anginal attacks
2. decrease duration & intensity of anginal pain
3. prevent or delays a MI
4. improve cardiac functional capacity
What would decrease O2 supply? (2)
1. Plaque accumulation in coronary arteries
2. Spasm of coronary artery decreases
What would increase O2 demand? (4)
1. increased HR
2. increased cardiac contractility
3. increased preload- harder the <3 has to work to eject it all
4. increased afterload- harder the <3 has to work to eject blood into constricted or narrow blood vessels
Antianginal drugs work by:
1. increasing oxygen supply
-increase blood flow
-decrease coronary artery spasm
2. decreasing oxygen demand
-decrease cardiac contractility
Increase oxygen supply by dilating coronary arteries & decrease oxygen demand by relaxing smooth muscle cells in arteries & veins --> dilates blood vessels.
1. used to abort an anginal attack
2. taken before activity that causes angina to prevent an anginal attack
ie. sublingual, translingual, spray, IV
Long acting nitrates:
Used to prevent an anginal attack
ie. tablets, patches, ointment
What major side effect of nitrates would you anticipate based on decreased preload & decreased afterload?
soooo, patient should sit or lie down when taking rapid acting nitro
AND check BP before giving & every 5 minutes after. . contact prescriber if SBP <90 mm Hg systolic and/or HR <60 beats/min or greater than 100 beats/min.
Other common side effects or problems associated w/ nitrates such as nitroglycerin?
2. reflex tachycardia (body's attempt to maintain cardiac output)
What can be done to help decrease nitrate tolerance?
1. nitrate-free scheduling allows for drop in serum drug levels
ie. it is common practice to remove nitrate patch at night and replace it in the morning
Nitrate cautions & contradictions: (2)
1. additive hypotensive effects when given w/ other drugs that decrease BP
2. given w/ phosphodiesterase 5 (PD5) inhibitors erectile -dysfunction drugs such as sildenafil (Viagra) or tadalafil (Cialis)
Teaching for sublingual tablets: (5)
1. store in the original container
2. drugs lose potency when opened; must be replaced within 6 months
3. take 1 @ start of chest pain & repeat every 5 min until pain is relieved or until 3 doses are taken
4. place under toungue & do not swallow
5. should burn or tingle
How do nitrates prevent or abort anginal attacks?
1. relax coronary arteries (increase myocardial perfusion --> O2 supply to <3) & prevents coronary artery spasm (decrease Printzmetal's angina)
2. systemic vasodilation --> decrease venous return --> decrease preload (decrease cardiac workload --> O2 demand)
What common concern do Nitrates have?
Significant decrease in BP;
How do beta blockers manage angina?
1. slows HR
(negative chronotropic effect)
2. slows conduction through the AV node
(negative dromotropic effect)
3. decreases the force of myocardial contraction
(negative inotropic effect)
How do calcium channel blockers manage angina?
It has a role in the contraction of cardiac and skeletal muscle and of vascular smooth muscle cells.
-decrease calcium entry into cardiac muscle, force of cardiac contraction is decreased
-decreasing calcium entry in vascular smooth muscle, vessels dilate
-decrease conduction through the SA & AV nodes, which slow the HR
Common side effects of calcium channel blockers: (3)
2. peripheral edema
3 classes of antianginal drugs:
2. Beta Blockers
3. Calcium Channel Blockers
How to decrease BP? (3)
1. decreasing force of cardiac contraction
2. dilating vessels
3. decreasing circulatory volume
Risks of hypokalemia:
1. Thiazides, e.g. hydocholorothiazide (HCTZ)
2. GREATER RISK:
Loop diuretics, e.g. furosemide (Lasix)
Risks of hyperkalemia:
1. Potassium-sparing diuretics, e.g. spironolactone (Aldactone)
2 examples of centrally-acting a2 adrenergic agonists:
Methyldopa & clonidine.
(Methyldopa recommended for pregnant women w/ hypertension)
Cardiovascular indications for CCBs:
1. management of hypertension;
Vasodilation of peripheral vessels decrease systemic vascular resistance
2. Management of angina;
Decreased cardiac workload decreases O2 demand & for Prinzmetal's (vasospastic) angina, prevents coronary artery vasospasm
3. management of selected dysrhythmias, e.g. supra ventricular tachydysrhythmias (PSVT, afib, aflutter);
Calcium channels blocked in the SA & AV node & decreases automaticity & decreases conduction
Dilates peripheral arteries and/or veins to decrease SVR:
Examples of vasodilators:
1. diazoxide (Hyperstat)
2. hydralazine HCl (Apresoline)
3. sodium nitroprusside (Nipride)
4. minoxidil (Loniten);
male pattern baldness
Antidysrhythmic drugs classes:
Class I: Fast sodium channel blockers
Class II: Beta blockers
Class III: Increase action potential
Class IV: Calcium channel blockers
Antidysrhythmic drugs can cause. .
Some antidysrhythmics have serious toxicities:
1. Lidocaine (Xylocaine) can cause CNS toxicity w/ manifestations that range from altered mental status --> seizures
2. Amiodarone (Cordarone) can cause pulmonary toxicity which is fatal in 10% of patients
3. Procainamide (Pronestyl) can cause cardiac toxicity & dangerous dysrhythmias
A patient who has frequent premature ventricular contractions (PVCs) and runs of v-tach is given. .
What is the mechanism of action of lidocaine?
1. Decreases electrical conduction
2. Decreases automaticity
3. Increases repolarization.
Why is lidocaine indicated for short term use only?
CNS toxicity may occur;
symptoms may include: CNS depression or irritability which may progress to seizures, respiratory depression, & respiratory arrest.
What is the mechanism of action of Amiodarone (Cordarone)? (4)
1. decrease rate of depolarization
2. decreases electrical conduction
3. decreases contractility
4. decreases automaticity
Decreases contractility =
Decreases automaticity =
Decreases electrical conduction =
What changes might we expect as a result of decreased inotropy, decreased chronotropy, and decreased dromotropy? (2)
1. AV block may occur as a result of decreased dromotropy
2. <3 failure may occur
Serious adverse effect that kills about 10% of patients on amiodarone?
monitor for shortness of breath, cough, crackles. And check CXRs and compare to baseline.
Digoxin (Lanoxin) uses: (2)
1. treatment of <3 failure
2. slows ventricular response to atrial fibrillation
S/s of digoxin toxicity: (4)
1. EKG changes such as bradycardia & AV block
2. GI effects (anorexia, N/V, abdominal discomfort)
3. CNS effects (fatigue, weakness)
4. Vision effects (diplopia, blurred vision, yellow-green vision or halos around objects)
What electrolyte imbalance increases the risk of digoxin toxicity?
What does Adenocard do?
Slows conduction through the AV node; therefore, it is very useful in converting PSVT to a normal sinus rhythm
Half life of Adenocard:
sooo must be given fast IV over 1-2 seconds
Antilipemic drugs purpose:
Management of cholesterol
The liver requires HMG-CoA reductase to produce cholesterol, so decrease cholesterol production.
HMG-CoA Reductase Inhibitors (statins)
Required for the absorption of cholesterol from the small intestine; bind to bile acids rendering it useless
Bile acid sequestrant
Inhibits absorption cholesterol from the small intestines.
Cholesterol absorption inhibitor
Acts via multiple mechanism to breakdown cholesterol and triglycerides, suppress synthesis of triglycerides, and increase the secretion of cholesterol into bile.
Fabric acid derivative
Vitamin B3 MOA:
Exact mechanism of action unknown.
Which drugs might be dangerous to administer if the patient has bradycardia with AV block?
1. Digoxin- decrease HR & decrease conduction
2. Beta blockers- decrease HR & decrease conduction
3. Any other drugs that cause decrease HR (negative chronotropy) or decreases conduction (negative dromotropy)
ALWAYS verify the patient's <3 rate (pulse check will do)
Potent dilator of coronary arteries.
This class of drugs is highly effective for coronary artery spasms.
Calcium channel blockers
This drug experiences a large first-pass effect if taken orally.
Used for prevention of anginal episodes.
Most effective for the treatment of exertional angina.
Drugs that primarily cause arterial and venous dilation through blocking the SNS
Blood pressure is determined by the product of _______ and systemic vascular resistance (SVR)
Drugs in this class cause a characteristic dry, nonproductive cough
These drugs block vasoconstriction and the secretion of aldosterone.
Angiotensin II-receptor blockers
A drug that is inactive in its administered form and must be biotransformed in the liver to its active form.
An elevated systemic arterial pressure for which no cause
can be found
A common adverse effect of adrenergic drugs that involves a sudden drop in blood pressure
A common cardiac dysrhythmia involving atrial contractions.
The period during the myocardium is unable to respond to electrical stimulation.
A serious adverse effect of inamrinone.
A condition that may indicate the need for treatment with digoxin-immune Fab.
A condition that leads to an increased potential for digoxin toxicity.
Drugs that influence the rate of the heartbeat.
Drugs that influence the conduction of electrical impulses.
Drugs that influence the force of cardiac muscle contractions.
The range of drug levels in the blood that is considered beneficial as opposed to toxic.
A property of the pacemaker cells of the heart that allows self-activation.
Many respiratory drugs are given by inhalation, why?
1. Direct delivery to site of action --> rapid onset
2. Minimized systemic effects
What adverse effects are likely to occur if, instead of giving glucocorticoids by inhalation, systemic (oral or parental) glucocorticoids were given long term?
1. redistribution of adipose tissue to trunk, upper back, & face (extremities are thin in comparision)
3. ^ risk of infection
4. growth retardation in children
Which inhaled drug should be given in an acute asthma attack?
short-acting beta agonist- albuterol (Proventil)
e.g. aminophylline (Theophylline)
1. large # of drug-drug interactions & narrow therapeutic index (high toxicity)
2. smoking increases clearance of this drug so higher doses are required for smokers
3. related to caffeine; has similar side effects to high dose caffeine (nervousness, tachycardia, palpitations)
Mast Cell Stabilizers
e.g. Cromolyn & Nedocromil
1. help to prevent inflammation by preventing mast cell degranulation
2. not as effective as steroids- used if steroids are contraindicated
e.g. montelukast (Singulair)
FDA alert- tied to neuropsychiatric problems (agitation, depression, hallucinations, insomnia, suicidal thoughts and behaviors)
B comes before C (or G):
Bronchodilator comes before Corticosteroid (or Glucocorticoid)
Corticosteroid inhalers can contribute to:
Why are inhaled glucocorticoids used for long term respiratory therapy when oral glucocorticoids are not?
Less drug is absorbed systemically when administration is by inhaler, more drug is delivered to the site of action.
What is the device that delivers medication as a mist?
most often used for young children, for people who have difficulty using inhalers, & for treatment of severe asthma.
2 primary types of drugs used in the treatment of asthma:
2. anti-inflammatory agents
Which is most likely to cause nervousness, shakiness, & tachycardia or palpitations?
What is the device that is used to monitor the effectiveness of drugs when given for asthma?
A peak flow meter
What is the device that can be used if the patient has difficulty coordinating inhaler activation w/ inhalation?
Sodium retention leads to _____.
Sodium excretion promotes _______.
Mediates exchange of sodium & hydrogen in the nephron, this allows sodium to be reabsorbed by the body.
Carbonic Anhydrase Inhibitors
Carbonic Anhydrase Inhibitors effectiveness:
Act on proximal tubule, because sodium can exit the tubule & be reabsorbed by the body at a point distal to this, some diuretic effectiveness is lost.
Carbonic Anhydrase Inhibitors uses:
To decrease ocular fluid in treatment of glaucoma; used when there is resistance to other diuretics.
Blocks sodium reabsorption by the body along the nephron's loop of Henle;
also dilates blood vessels, which decreases systemic vascular resistance.
Loop diuretics effectiveness:
HIGHLY effective w/ rapid onset of action, works even when renal function is low (increases renal blood flow)
Loop diuretics main uses:
Decreases edema resulting from a variety of causes;
in <3 failure, it not only decreases edema BUT also decreases cardiac workload
Enters into the nephron, because it is hypertonic, extra fluid is pulled into the nephron and eliminated.
DOES NOT act by increasing sodium excretion.
Osmotic Diuretics uses: (3)
1. head trauma & other causes of increased intracranial pressure
2. prevention of chronic renal failure
3. edema that is not caused by sodium retention
Block aldosterone receptors or inhibit aldosterone reabsorption;
REMEMBER: aldosterone is part of the renin-angiotension-aldosterone system that maintains BP.
Where sodium goes,
water flows... so more fluid is eliminated.
Potassium-Sparing diuretics effectiveness:
Potassium-Sparing Diuretics uses:
An adjunct to other diuretics, especially those which would tend to cause potassium loss such as thiazide or loop diuretics.
Inhibits reabsorption of sodium, potassium, & chloride;
dilates blood vessels.
Thiazide diuretics effectiveness:
Moderate; not effective if renal function decreases significantly.
Thiazide diuretics uses:
has recommended 1st-choice role in management of hypertension & may be used either alone or in combination w/ other antihypertensives
Which diuretic class would NOT cause hypokalemia?
Which 2 diuretic classes are more effective & have a rapid onset of action?
1. Loop diuretics
2. Osmotic diuretics
Which diuretic class does NOT use increased sodium excretion as a mechanism for promoting diuresis?
Which diuretic class is often recommended as the drug of choice for managing hypertension?
Adverse effects of diuretics:
1. can cause hypotension (particularly orthostatic hypotension)
2. can cause fluid & electrolyte imbalance
3. can cause lightheadedness & weakness
4. can cause urinary frequency
Loop diuretics adverse effects: (7)
1. profound fluid loss
2. hypokalemia, hyponatremia, & hypocalcemia
3. may be allergic to "sulfa" drugs
4. blood glucose elevation
6. sensitivity to sunlight - increased risk of heat-related illnesses
7. hearing loss (RARE)
Osmotic diuretics adverse effects: (5)
1. high fluid loss w/ relatively little loss of electrolytes
2. can cause crystals if too cold
3. should NOT be given if there is inadequate renal function
4. should NOT be given in cardiac failure b/c transient volume overload can worsen cardiac workload
5. EXTREME caution when given to older patients who may have decreased renal, hepatic, or cardiac function
Potassium-Sparing diuretics: (2)
1. can cause hyperkalemia- increased when given with drugs such as lithium or ACE inhibitors
2. ones that bind to aldosterone receptors can cause hormonal changes such as gynecomastia
Thiazide diuretics adverse effects: (4)
1. hypokalemia, hyponatremia, & hypomagnesemia
2. allergic to "sulfa" drugs
3. can cause blood glucose elevation- especially important if patient has diabetes
4. can cause elevated uric acid levels
Which diuretic may require adjustment of anti diabetic drugs if given to patients w/ diabetes?
Loop diuretics & thiazide diuretics can cause blood glucose elevations.
Which diuretic class must be given w/ a filter in order to avoid injection of intact crystals?
Which diuretic classes can precipitate a gout attack?
Loop diuretics & thiazide diuretics can cause hyperuricemia (elevated uric acid levels).
Diuretics should be given in the morning. If order 2x a day, it is best to give the second dose early in the afternoon. Why?
Less likely to disturb sleep & in older patients, the likelihood of falls increases at night.
Some diuretics, particularly loop diuretics & thiazide diuretics, can cause hypokalemia. What sort of foods might you recommend be included in the diet to prevent this?
High potassium foods, like dried apricots, avocados, bananas, cantaloupe, oranges, raisins, beans, & potatoes w/ skin
Hypokalemia increases the risk of ________.
What distressing effects may happen to men & women taking potassium-sparing diuretics?
Hormonal effects that can cause gynecomastia in about half of men who take this drug, in women it may alter the menstrual cycles.
Antihypertensives are often paired with diuretics for improved management of blood pressure. When ACE inhibitors are needed, which diuretic pairing can result in a dangerous combination?
When given with potassium-sparing diuretic increases the likelihood of hyperkalemia, so it will be important to monitor labs.
What is unique about the way osmotic diuretics such as mannitol work?
Increase plasma osmolarity which pulls fluid into the intravascular space. It also increases the osmotic pressure in the glomerular filtrate so that less fluid is reabsorbed by the body after filtration.
What special procedural precaution should be implemented when giving mannitol?
Administered through IV, because it forms crystals at cool temps, it should be warmed between 70-98 & administered w/ a filter needle.
Concerns for all diuretics?
They can cause dehydration & electrolyte problems; also over correction of hypertension.
What do diuretics do?
They increase fluid loss by increasing urine output.
Indications for diuretics: (6)
1. lower BP
2. decrease pulmonary edema
3. reduce cerebral edema
4. promote adequate output
5. decrease localized fluid volume (glaucoma)
6. decrease generalized fluid volume (anasarca)
Interrupt processes that lead to vomiting
Is an antihistamine appropriate treatment for N/V?
How is a 1st generation antihistamine different from a 2nd generation antihistamine?
The 2nd generation antihistamines primarily decrease gastric acid.
Common side effects of antihistamines? (4)
2. paradoxical excitement
3. dry mouth
4. additive effects when taken with alcohol
When should laxatives be contraindicated?
When nausea, vomiting, and abdominal pain are present.
Which antidiarrheal drug could be given to older family members but could cause problems for Stewie?
1. Bismuth subsalicylate (Pepto Bismol)
2. Lactobacillus acidophilus
Which antidiarrheal drug causes tarry stools w/o causing GI bleeding?
1. Bismuth subsalicylate (Pepto Bismol)
2. diphenoxylate with atropine (Lomotil), an opioid + anticholinergic
Act as irritants to increase peristalsis.
How quickly do stimulant laxatives work?
For most people, within a few hours. Suppository form works in less than an hour.
Advantages of stimulant laxatives?
Fast acting & generally effective, also inexpensive & available without a prescription.
What are the disadvantages of stimulant laxatives?
1. Because they increase peristalsis, they can cause abdominal cramping.
2. Dependency with long term use.
3. Bowel urgency
Non-digestible & non-absorbable agents; they pull water into the GI tract so that stool doesn't become hard & dry.
Also, they form viscous solution that expands the bulk of the stool & softens it.
Bulk Forming Laxative
How long does it take bulk forming laxatives to work?
2-3 days, especially if patient has been constipated.
When would bulk forming laxatives be used?
Good for short-term & long-term treatment; also used when weaning patients from harsher stimulant laxatives..
ALSO, lower the risk of colon cancer & lower serum cholesterol levels
Any risks of bulk forming laxatives?
Patient MUST have adequate fluid intake, if the patient does not drink 6- 8oz glasses of fluid then opposite effect could happen.
Lower the surface tension of the stool which allows the stool to be penetrated by fluids & fats making it softer.
How long does it take stool softeners to work?
Vary greatly, time of onset is anywhere from 12-72 hours.
What are the advantages of stool softeners?
1. They can be used long term for constipation.
2. Prevent straining, so good for patients post-op or post-MI.
3. Good alternative for those who cannot or will not drink adequate fluids.
They are non-absorbable magnesium salts; b/c they are not absorbed & b/c saline attracts water, they pull into the intestine; this increases intestinal contents which stimulates peristalsis.
How long does it take saline laxatives to work?
Rapid onset of 3-12 hours. Often used for prep of GI studies.
Advantages of saline laxatives?
They don't contain a lot of foreign substances, so work well when a stool specimen is needed.
Disadvantages of saline laxatives?
They contain magnesium, which can be an issue if the patient has renal insufficiency. Also pose for dehydration.
Usually made with non-absorbable sugars, because they are not absorbed they pull water into the bowel via osmosis- this stimulates peristalsis & increases bowel content.
How fast do osmotic laxatives work?
Usually work very fast; however some types (e.g. lactulose) may take up to a couple of days. While glycerin suppositories have the least osmotic effect, they typically work quickest b/w 15 minutes to a hour.
When would osmotic laxatives be indicated?
Used for both short or long term constipation; however dehydration is a risk if used long term. Better than others if constipation is severe.
What are the advantages of osmotic laxatives?
Fast onset so they are good choices for bowel preps. And HIGHLY effective.
What are the disadvantages of osmotic laxatives?
Dehydrations, also many require prescription.
What would be the safest laxative drug to give with a sleeping pill?
Bulk forming laxatives take 48-72 hours.
Protype for the laxatives?
Psyllium mucilloid (Metamucil), a bulk forming laxative.
Are they any precautions associated w/ giving IM phenothiazine antiemetics such as the prototype prochlorperazine (Compazine)?
Prochlorperazine can be very irritating to subcutaneous tissues, therefore it should be given deep IM in a large muscle.
This can be sedating so take safety precautions.
Other than sedation, what are the side effects of phenothiazine antiemetics?
Extrapyramidal symptoms (EPS) if taken at high doses & anticholinergic effects (dry mouth, constipation, tachycardia)
Coat the GI tract then bind to bacteria or toxin causing the diarrhea; example is bismuth subsalicylate (Pepto Bismol)
Problems with adsorbents?
Can bind to drugs like they do bacteria, which decrease absorption of medication.
Side effects or adverse effects with anticholinergic antidiarrheal agents: (5)
1. dry mouth
2. possible urinary retention
3. possible increased intraocular pressure
4. possible mental status changes
5. possible constipation
Restore intestinal flora (i.e. beneficial organisms commonly found in the intestine that play important roles in colon health)
When are intestinal flora modifier preferred over another agent?
When normal flora has been largely eradicated by antibiotics.
Prototype diphenoxylate with atropine (Lomotil):
Combo opioid & anticholinergic.
Recommended scheduling for antacids when the patient is taking other medications.
2 hours before medications
Antacids that are based primarily on this component may cause diarrhea.
Antacids that are based primarily on these 2 components may cause constipation.
Calcium & aluminum.
Two formulations of antacids that should be avoided in patients who have renal failure & who have <3 failure or hypertension.
Magnesium & sodium.
Because histamine 2 receptor antagonists decrease acidity, you will want to assess for this nutritional deficiency.
These are "habits" that patients with GERD & PUD should be instructed to avoid because they increase gastric acid production, thus decreasing the effectiveness of the medications.
Smoking & alcohol intake.
These are special precautions that need to be taken because H2 receptor antagonists are available over the counter.
Educate and take a good history!
A hypersecretory condition for which proton pump inhibitors may be given at higher than usual doses for years instead of weeks.
Irreversible enzyme binding
Proton Pump Inhibitors
A reason why there are many drug reactions w/ proton pump inhibitors.
Metabolized by CYP45o system.
There is a big problem for all agents that decrease acidity but is an even greater risk for proton pump inhibitors.
A condition that can occur when gastric acid secretion is significantly decreased.
This is the reason that a proton pump inhibitor or H2 receptor antagonists is given as part of combination antibiotic therapy for PUD.
This is the minimum amount of time patients should be told that they will need to remain on antibiotic treatment of H. pylori infection.
At least 1-2 weeks (7-14 days)
This is the reason bismuth preparations such as bismuth subsalicylate (Pepto Bismol) is often added to combination antibiotic therapy for treatment of PUD.
Works as an adsorbent.
The reason why 2 or more antibiotics are often given when treating H. pylori infection.
This is the only class of drugs that truly cures the H. pylori infection that causes most ulcers.
The drug that produces a gel-like substance that coats the ulcer to protect it against further erosion, thus promoting healing.
This agent works similar to prostaglandins to inhibit gastric acid secretion & stimulate mucus production.
This complication of misoprostol (Cytotec) limits the ability to prescribe the drug to women of child-bearing age.
Pregnancy Category X
This drug, now seldom used for GERD & PUD, decreases gastric acid secretion by inhibiting autonomic nervous system receptors that promote gastric acid secretion for digestion. The reason is it seldom used now is because of side effects that occur due to ANS receptor inhibition.
These are some brief mnemonics to help remember the mechanisms of action for the miscellaneous drugs used to treat peptic ulcer disease:
1. sucralfate (Carafate)
2. misoprostol (Cytotec)
1. sucralfate (Carafate)
2. misoprostol (Cytotec)
misoPROSTol = PROSTaglandin-like
cholinergic = rest/digest
digest requires acid secretion
anticholingergic = anti-rest/digest
anti-digest less acid secretion
THIS SET IS OFTEN IN FOLDERS WITH...
Pharmacology Test 3 Skin Drugs
Pharmacology Test 3 CNS Drugs
Pharmacology Test 3 Adrenergic Blockers
Pharmacology Test 3 Cholinergic Drugs
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