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Pharmacology Exam 1

STUDY
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The 5 Classes of Scheduled Drugs
I - LSD, Heroin
II - Narcotic analgesics
III - Sedatives, Anabolic steroids
IV - Sedative-Hypnotics
V - Partially controlled: Lomotil
Pharmacokinetics: 4 thing that effect absorption
1. Route of administration
2. Drug solubility and concentration
3. Acid-base composition
4. Site conditions
Cytochrome P450
set of liver enzymes that metabolize drugs
First pass effect
the initial metabolism in the liver of a drug absorbed from the gastrointestinal tract before the drug reaches systemic circulation through the bloodstream
bypass the liver when absorbed
buccal, sublingual, vaginal, rectal, topical & parenteral route meds
parenteral
IV: intravenous
IM: intramuscular
Subq: subcutaneous
Intradermal
Topical
Patches
Inhalants
Pharmacokinetics: Distribution (from the blood stream to the site of action)
Depends on:
good blood supply
good blood pressure
Blood brain barrier
Protein Binding
Protein Binding
Pharmacokinetics: Biotransformation ( Metabolism or inactivating the drug)
Enzyme induction
Enzyme inhibition
First-pass effect
Note: Liver disease or failure --> an increase potential for a toxic or adverse drug effect
Enzyme induction
Increased enzyme activity by certain compounds. Drugs or chemicals have the ability to stimulate the activity of microsomal enzymes. Occurs when certain drugs are administered that have the ability to rev up the cytochrome P450 system. This causes the enzymes to work much more efficiently so the body requires more drug to receive the desired effect.
Enzyme inhibition
The decrease in hepatic enzyme activity that results in reduced metabolism of drugs
Pharmacokinetics: Excretion ( Getting the drugs out of the body)
Lungs
Intestines
Breast milk
Kidney
Note: Kidney disease or failure an increase potential for a toxic or adverse drug effect
Serum Half-Life
The time it takes for the serum concentration of a drug to decrease by 50%
Therapeutic Medication effects
Palliative
Curative
Supportive
Substitute
Chemotherapeutic
Restorative
cross tolerance
tolerance for a substance one has not taken before as a result of using another substance similar to it eg opioids such as heroin to methadone
Drug effects on the fetus
A - studies done on pregnant women
B - Animal studies
C - Animal studies
D - Evidence of human fetal risk
X - Risk outweighs any potential benefit
Assessment factors
1. ALLERGIES
2. RECREATIONAL DRUGS
3. OTC DRUGS
4. AGE
5. BODY SIZE
6. SEX (teratogenicity)
7. ETHNICITY
8. GENETICS
Pharmacogenetics
Pharmacogenomics
9. DOSE
Dosage
Depends on:
Characteristics of the drug
Characteristics of the patient
Cellular reaction to damage
Injury to cell --> arachidonic acid--> cyclooxygenase--> prostaglandins--> Activating & Sensitizing Pain Receptors

Injury to cell --> bradykinin--> Activating & Sensitizing Pain Receptors

Both cascades happen simultaneously

Vasodilitation (erythema and warmth), edema, pain receptors innervated.
bradykinins
a protein produced that acts to stimulate vasodilation and pain receptor activation. Released during tissue injury and promote pain INFLAMMATORY MEDIATOR
cyclooxygenase
Key enzyme in the prostaglandin metabolic pathway that is blocked by aspirin and other NSAIDs.
3 Categories for Pain Management
1. Opiates/Opioids or narcotics (7-10 on pain scale)
2. Nonopiates: Acetaminiphen, Salicylates (ASA), & NSAIDs (4-6 or combined with opiate, 1-3 alone)
3. Adjuvant analgesics (not known pain relief but for things that go with pain like anxiety, insomnia, nausea): Benzodiazopines, TCA, Corticosteriods
Types of Pain by Origin
Somatic "sharp, burning, throbbing, cramping" can stimulate sympathetic NS
Visceral - thoracic or abdominal, hard to localize, can stimulate parasympathetic vasovagal
Neuropathic - injury to nerves, "shooting"
opioid antagonist examples
Prototype: pentazocine (Talwin)
Stadol, Nubain
opioid agonist
bind to opiate receptors and prevent neurons from sending pain signals
opioid agonist antagonist
Medications in which an opioid antagonist (e.g., naloxone/Narcan) is added to an opioid agonist, in hopes of decreasing opioid abuse.
ADEs of opioids
Depresses CNS
Serious: Respiratory depression
Common: Sedation, dizziness
Depress GI Tract
Common: N&V, constipation
Alters psychological responses to pain
Produces euphoria
clinical uses of opiates
Relief of moderate to severe pain
Pre-op sedation
Labor and delivery
Invasive diagnostic tests
Acute Pulmonary Edema
Severe nonproductive cough
MI
Times for pain relief by route
PO 45-60 min
intramuscular 30 min
IV 5-15 min
Opiate prototype?
morphine
endogenous
from body (eg endorphines)
exogenous
from outside body (eg morphine)
Does morphine have a ceiling?
No, can increase dose indefinitely with tolerance
Opiate agonist-antagonist definition
Developed to decrease addictive qualities of drugs. For new patient will relieve pain, for addict will put into withdrawal because will block some receptors.
Opiate agonist-antagonist prototype?
pentazocine (Talwin)
Opiate antagonist prototype?
Narcan (naloxone)
Opiate antagonist description
NOT a stimulant
Given IV
knocks opiate off receptor sites
Shorter duration of action (2hrs) than opiate so may need to be given again
Drugs to treat opiate withdrawal?
Methadone
Buprenorphine (Suboxone)
Arachidonic acid produces?
Cyclooxygenase I (physiologi/protective prostaglandins) -
Cyclooxygenase II (pathological prostaglandins)
What does cyclooxygenase I do?
Physiological/Protective
GI
Renal
Regulates smooth muscle - bronchodilitation
Regulates blood clotting
What does cyclooxygenase II do?
Inflammation
Edema
Leukocytosis
Release of cytokines - increase inflammatory and pain response
What drugs interfere with arachidonic acid to cyclooxygenase I and II?
Non-selective cycclooxygenase blockers
aspirin, acetaminophen, NSAIDs
Selective cyclooxygenase II inhibitor
celecoxib (Celebrex)
Acetylsalicylic Acid
Aspirin - ASA
ASA function
Analgesic
Anti-inflammatory
Antipyretic
Anti-thrombotic
ASA effect on platelets?
ASA binds irreversibly to platelet for life of platelet (7-10 days) and platelet will not aggregate
ASA ADEs
Tinnitus
Reye's Syndrome
N/V
GI System
Bleeding - heamatoria, heamatemisis, GI bleeds, bruising, epistaxis
During Pregnancy
ASA sensitive asthma
Salisilate Poisoning
Reye's syndrome
Acute encephalitis characterized by an onset of symptoms 1 to 3 weeks following a viral infection. A complication of a viral infection. Associated with salicylate use during viral infections.
Salisilate poison
ASA overdose
if <1hr gastric lavage
if >1 hr (hyperventilation, diaphoresis, thirst, drowsiness, coma) no med to reverse, support
NSAID protoype
ibuprofen (Advil)
NSAID effects
Analgesic
Anti-inflammatory
Antipyretic
Anti-thrombotic (not like ASA, binds to platelet only as long as drug is in circulation)
NSAIDs - Adverse Effects
CNS - depresses a little, dizziness drowsiness,
Eyes - blurred vision
GI System - pain, ulceration, bleeding, N/V
Renal System
Pregnancy
Prototype: acetaminophen (Tylenol) therapeutic use
Analgesic
Antipyretic
Acetominophen ADEs
Serious: liver necrosis,hepatic or renal toxicity (large doses)
Common: rash, urticaria, nausea
Celecoxib functions
Analgesic
Anti-inflammatory
Aceitaminophen overdose
first 24 hours flu symptoms (can use mucomyst)
next 24 hours pain in upper right quadrant
in next 2 days hepatotoxiity - jaundice, elevated liver enzymes, bleeding problems, death
Celecoxib ADEs
increases platelet activity, increases clotting
MI
stroke
Anti-anxiety & Sedatives = Relaxation
Hypnotics = Sleep
The difference between the effects is dosage dependent meaning...
Large doses of anti-anxiety and sedatives = Sleep
Small doses of hypnotics = sedation
antianxiety and sedcatives are like opiates because...
both are CNS depressants
Barbiturates prototype
Phenobarbital
Anxiety action
Amygdala - store memory, associate with memory like anxiety
Hippocampus - same
Neurotransmitter Gamma-aminobutyric acid or GABA inhibition will rid anxiety
Barbiturates are not just sedative-hypnotics
also anticonvulsants
Barbiturates ADEs
no REM sleep
enzyme induction = high tolerance
addiction and abose
Anxiolytic
anti-anxiety
BENZODIAZEPINES protoype
diazapam (Valium)
adavantages to benzodiazepines over barbiturates
doesn't supress REM sleep
less enzyme induction
wider margin safety between therapeutic and toxic dosage
Benzodiazapenes ADEs
CNS depressants
mental and physical activity impairment
Barbiturates, Benzodiazepines, & Miscellaneous ADEs
Serious: Paradoxical reaction
Common: drowsiness, ataxia (lack muscle control), confusion
Barbiturates & Benzodiazepines
Abuse: Drug Synergism Effect
Overdose
Respiratory support
Nasogastric lavage
IV fluids & diuretics
Flumazenil (Romazicon)
sympathomimetic
mimcs SNS stimulation
adrenergic (alpha and beta)
parasympathomimetic
mimics PSNA stim
cholinergic
sympatholytic
blocks/prevents/inhibits SNS
antiadrenergic, alpha and beta adrenergic-blocker
parasympatholytic
blocks/prevents/inhibits PSNS
anticholinergic, cholinergic blocker
Adrenergics neurotransmitter?
9nor)epinephrine
Cholinergics neurotransmitter?
acetylcholine
ADRENERGIC EFFECTS
Heart rate UP - chronotrpoic and ianotropic
Blood vessels - peripheral constriction, UP to heart brain and large muscles
Bronchi OPEN
Pupils OPEN
Feelings TENSION
GI System SLOWS, less blood
Blood sugar UP
Fatty acids UP
Sweating UP
Blood coagulation UP
heart rate up?
positive chronotropic effect
heart rate stronger?
ianotropic
adrenergic ADEs
dysrythmias, tachy,
bronchodilitation
Adrenergic Specific receptors
Alpha
Peripherally vasoconstrict in the arms and legs
Beta 1
Cardiac
HR (chronotropic)
force of contraction (inotropic)
Beta 2
Lungs
Bronchodilation
Catecholamines prototype
epinephrine (Adrenalin)
effects all 3 receptors
Catecholamines effects
Both endogenous and exogenous
Can't be PO
are adrenergic and parasympatholytic
Emergency
Cardiac arrest
Hypotension
Shock
Bronchial asthma
Obstructive pulmonary disease
Non-catecholamines
Similar to catecholamines
Effects last longer
Effective orally
OTC medications
Adrenergic ADEs
Cardiac arrhythmias
Angina
Hypertension
Cerebral hemorrhage
Anxiety, nervousness, insomnia,
Nursing Assessment for Adrenergics
? Diabetes
IV site - can be vasoconstrictor to point of necrosis
Respiratory & cardiovascular assessment
Antiadrenergic Effects
Use for patholigical stimulation, hypertension, tachycardia etc
Blood vessels dilate peripherally
Blood pressure DOWN
Heart Rate DOWN
Bronchoconstriction
Cardiac Output DOWN - negative chronotropic and ianotropic
Weakness, lethargy
Less effective metabolism of glucose --> hypoglycemic
Antiadrenergic ADEs
Circulation to periphery
Orthostatic hypotension
Bradycardia
Resp difficulties
Fatigue
Weakness, insomnia
Hypogylcemia
Antiadrenergic Receptor effects
Alpha
Extremities, arms and legs
Dilation of peripheral arterioles and veins
Beta 1
Cardiac
Negative Chronotropic
Negative Inotropic
Beta 2
Lungs: Bronchoconstriction
alpha adrenergic blockers prototype
prozosin or mini-pres
alpha adrenergic blockers effects
BP down
heart rate can go up from contraction going down
peripheral blood flow up
urinary output out

Clinical Use
Tx of hypertension
Raynaud's, Frostbite
Prevent necrosis 2nd from IV extravasation
Tx Benign Prostatic hypertrophy

Serious ADE: first dose syncope
Beta Adrenergic Blockers prototype
propanolol (Inderal)
Beta Adrenergic Blockers
Review:
Heart Rate ( neg chronotropic)
Force of contraction ( neg inotropic)
CO at rest and w/ exercise
Slowed conduction ( neg dromotropic)
BP
Bronchoconstriction
Less effective metabolism of glucose
Weakness, insomnia
beta adrenergic blockers
Clinical Use
Tx Hypertension, Angina, MI, Tacky arrhythmias
Glaucoma
Pheochromocytoma
Migraines
Palpitations
Contraindications/ADE
Common: hypotension, bradycardia, heart block, CHF,
asthma, bronchoconstriction, and heart block
Cholinergic effects "WET"
Eye - pupil constriction
Salivary glands
Bronchi - constriction and secretion
Heart - slows, vasodilitation, BP down
GI Tract - increase secretion, pooping
Urinary Bladder - increase flow
Increased sweating
Nicotinic Receptors
in motor nerves and skeletal muscles --> muscle contraction
Muscarinic Receptors
in most internal organs --> secretions
Cholinergic Medications
Prototype: neostigmine (Prostigmine)
neostigmine uses and contraindications
Clinical Uses:
Bladder atony
Dx & Tx MG
Antidote
Glaucoma
Alzheimer's
GI Tract atony
Contraindications:
Urinary or GI tract obstruction
Asthma
Peptic Ulcer
CAD
Pregnancy