Tufts Pharmacology NBDE Part II

HTN, alpha1 blocker, inhibits release of norepinephrine
HTN, acts centrally to stimulate alpha receptors
HTN, stimulates alpha2 receptors in CNS
HTN, nonselective beta blocker
HTN, selective beta1 blocker
HTN, directly acts to vasodilate vascular smooth muscle
HTN, diuretic, thiazide, when administered with digitalis, will increase penetration of digitalis into myocardium
HTN, diuretic, high-ceiling or loop acting
Ethyacrinic acid
HTN, loop or high ceiling diuretic, is associated with deafness
HTN, diuretic, potassium sparing
HTN, neuronal blockers, only for severe hypertension, prevents release and causes depletion of catecholamines taken up into storage vesicles and is released like false transmitter, does not cross blood-brain barrier
Captopril, lisinopril
HTN, ACE inhibitors
angina, increases oxygen supply to heart by direct vasodilatory action on smooth muscle in coronary arteries
angina, reduces oxygen demand by preventing chronotropic responses to endogenous epinephrine
angina, Ca2+ channel blocker, decrease oxygen demand by reducing afterload by reducing peripheral resistance via vasodilation
Lidocaine (Type 1B drugs)
arrhythmia, decrease cardiac excitability, for ventricular arrhythmias
arrhythmia, to reverse digitalis induced arrhythmias
Quinidine (Type 1A drugs)
arrhythmia, increases refractory period of cardiac muscle, for supraventricular tachyarrhythmias and atrial fibrillation
arrhythmia, for supraventricular tachyarrhythmias and paroxysmal tachycardia and atrial fibrillation
arrhythmia, decreases rate of AV conduction, for atrial fibrillation and paroxysmal tachycardia
arrhythmia, for paroxysmal tachycardia
CHF, ex: digitalis and digoxin, have positive inotropic effect, increasing force of contraction of myocardium by inhibiting Na+/K+ ATPase and thus increasing Ca2+ influx, reduces compensatory changes associated with CHF like heart size, rate, edema
CHF, ACE inhibitor
Digitalis toxicity
nausea and vomiting, yellow-green vision, extrasystole, AV conduction block
related to coadministration with chlorothiazide
Aspirin mechanisms of action
analgesic effects: inhibits synthesis of prostaglandins
antipyretic effects: inhibits synthesis of prostaglandins in hypothalamus, cutaneous vasodilation
bleeding time: inhibits thromboxane A2 synthesis and thus platelet aggregation slows
Aspirin therapeutic effects
pain relief, antipyretic effects, antirheumatic, anti-inflammatory effects
Aspirin adverse/toxic effects
occult bleeding from GI tract, tinnitus, nausea and vomiting, acid-base disturbance, metabolic acidosis, decreased tubular resorption of uric acid, salicylism, delirium, hyperventilation
no anti-inflammatory activity, is hepatotoxic, does not cause GI upset, liver toxicity esp when combined with alcohol or taking 4g/day, is choice for feverish kid, may induce methemoglobinemia at high doses
Corticosteroids (like Prednisone, Hydrocortisone, Triamcinolone)
inhibit phospholipase A2, enzymatic step that precedes prostaglandin synthetase
much less GI irritation, is anti-inflammatory, will have gastric irritation and bleeding after prolonged use
Diflunisal (Dolobid)
salicylate analgesic, longer half-life than acetaminophen and ibuprofen
mixed agonist-antagonists, has both agonistic and antagonistic activities
mixed agonist-antagonists, has both agonistic and antagonistic activites
antagonist to treat overdose of morphine
used in detox of morphine addicts, is full agonist with analgesic properties, when taken orally is not euphoric in addicts, just acts to produce tolerance and physical dependence, withdrawal is less severe because of long half-life
Morphine effects
respiratory depression, euphoria, sedation, dysphoria, analgesia, constipation, urinary retention
Morphine overdose
coma, respiratory depression, miosis
Morphine mechanism of action
binds mu receptors in CNS
causes vomiting by stimulating medullary chemoreceptor trigger zone
decrease in ventilation due to loss of sensitivity of medullary resp center to CO2
Meperidine, morphine, codeine
is the best opioid for suppressing cough reflex
Competitive muscarinic receptor blockers
atropine, scopolamine, propantheline, are sometimes used to control salivary secretions
competitive muscarinic receptor blocker
blocks vagal reflexive control of heart rate => results in tachycardia
reversible anticholinesterase, acts both centrally and peripherally, sometimes for treating xerostomia
reversible anticholinesterase, acts peripherally only, has some direct ACh-like activity at NMJ => prolongs activity of endogenous ACh, sometimes for treating xerostomia
Direct acting cholinergic agonists
pilocarpine, methacholine, may be used for xerostomia
Irreversible inhibitors of cholinesterase
organophosphates and insecticides
enzyme regenerator used in organophosphate toxicity
agonist at nicotinic receptors, depolarizing NMJ blocker subject to rapid inactivation by plasma pseudocholinesterase, used to prevent laryngospasm
paralyzing dose causes muscle stimulation
non-depolarizing neuromuscular junction blocker
Ganglionic blockers
mecamylamine and hexamethonium, produce orthostatic hypotension
alpha blocker, competitive inhibitor of postjunctional adrenergic receptors, associated with epinephrine reversal
beta blocker, competitive inhibitor of postjunctional adrenergic receptors
depletes norepinephrine by inhibiting reuptake, causes depletiong from storage sites
inhibits release of catecholamines (like norepinephrine)
Alpha methyldopa
acts centrally as false neurotransmitter which gets taken up into storage vesicles and is released with norepinephrine, decreases sympathetic activity, reduces sympathetic outflow via alpha agonist action
stimulates alpha2 receptors in CNS with resulting decrease in sympathetic outflow
causes release of stored norepinephrine and acts at receptor itself
stimulates release of stored norepinephrine and stimulates alpha receptors in CNS
norepinephrine reuptake inhibition and release
TCA antidepressant
norepinephrine reuptake inhibition
MAO inhibitors
blocks enzymatic destruction of norepinephrine
Epinephrine reversal
when epinephrine is administered in the presence of an alpha blocker (Prazosin or Chlorpromaxine), will cause decrease in BP rather than increase because beta-mediated vasodilation predominates
Vagal reflex
injection of pressor dose of norepinephrine may result in decreased heart rate due to activation of baroreceptors that stimulate vagal reflex to reduce heart rate
Alpha1 receptor stimulation
vasoconstriction, urinary retention, mydriasis
Alpha2 receptor stimulation
hypotention, reduces sympathetic outflow from CNS
Beta1 receptor stimulation
increased heart rate, increased force of contraction, positive inotropic and chronotropic actions
Beta2 receptor stimulation
bronchodilation, vasodilation, dilation of skeletal muscle
Levodopa with Carbidopa
levodopa: is a dopamine precursor that can cross the blood brain barrier
carbidopa: is a dopa decarboxylase converter blocker
used to treat Parkinson’s
nonselective alpha blocker, will cause vasodilation
rise in BP due to myocardial stimulation that increases ventricular contraction, increase in heart rate, vasoconstriction because of alpha receptor stimulation
leads to decreased heart rate because of baroreceptor reflexes, stimulates alpha and beta1 receptors
beta2 receptor stimulator
alpha1 receptor agonist
vasoconstrictor that stimulates alpha receptors
beta2 agonist for bronchodilatory effects
Physiological antagonism
two drugs produce opposite effects but don’t act on the same receptor
ex: epinephrine and histamine, epinephrine and nitroglycerin
Idiosyncratic reactions
genetically determined abnormal responses to a drug, are most unpredictable because may not be shown until drug is taken for the first time by a pt
ex: succinylcholine and atypical plasma cholinesterase
modulates the action of inhibitory neurotransmitter GABA, many form active metabolites, is most common drug group given for oral sedation
ex: diazepam, chlordiazepoxide
Benzodiazepines > barbiturates
less addiction potential, less profound CNS depression, larger therapeutic index, less resp depression
Benzodiazepine adverse effects
IV injection of diazepam can cause irritation like thrombophletbitis due to solvent (propylene glycol)
benzodiazepine, Valium, is given most commonly for oral sedation
benzodiazepine, Halcion, is ultrashort acting version
benzodiazepine, water soluble (doesn’t cause thrombophlebitis), shorter acting than valium because it doesn’t have active metabolites, has more rapid and predictable onset of action when given IM than valium
reverses effect of benzodiazepines
CNS depressants, will depress all levels of CNS, are not analgesic, will often induce excessive salivation and bronchial secretion and require use of anticholinergic drug to reduce these, are metabolized by the liver, are classified according to duration of action
action is terminated by redistribution of drug out of the chain, will enter and exit the brain rapidly, thus quick onset and short duration of action
long acting barbiturate
Barbiturate toxicity
overdose kills you because of respiratory depression
Barbiturate contraindications
intermittent porphyria: will enhance porphyrin synthesis and will aggravate the disease
undiagnosed severe pain: may make the pain worse and result in arousal, rage, delirium
Barbiturate toxicity treatment
need to maintain open airway, increase input of afferent stimuli, maintain respiration, administer CNS stimulant
1st generation antipsychotic drugs
Phenothiazine or Haloperidol, specific D2 (dopamine) receptor blocker
Side effects of 1st generation antipsychotic drugs
anticholinergic effects and anti-alpha adrenergic side effects, extrapyramidal stimulation resulting in tardive dyskinesia, may have jaundice due to allergic reaction
2nd generation antipsychotic drugs
Clozapine, block dopamine receptors and serotonin 5HT receptors, treat negative and positive symptoms, have fewer extrapyramidal side effects
mostly dopaminergic receptor blockers, are often used as antiemetic drugs
prototypic phenothiazine, used in treatment of schizophrenia
Tricycline antidepressants
Imipramine or Amitriptyline, are reuptake inhibitors for amine neurotransmitters, were most commonly used in the past, are strong anticholinergics
MAO inhibitors
Tranylcypromine or Phenylene
2nd generation antidepressant drugs
Fluoxetine or Trazadone, much more commonly used now, block amine reuptake or alterations of receptor number
Side effects of 2nd generation antidepressant drugs
anticholinergic side effects
drug of choice for manic phase of manic depression (bipolar disorder)
Corticosteroids or glucocorticoids
suppress immune system in addition to anti-inflammatory activity, so latent infection like TB may go systemic and opportunistic infections like Candidiasis may become more of a problem
Side effects of corticosteroids or glucocorticoids
gastric ulcers, immunosuppression, acute adrenal insufficiency, osteoporosis, hyperglycemia, redistribution of body fat
General anesthesia onset and rate of induction
inversely proportional to solubility of anesthetic in the blood, also influenced by pulmonary ventilation, blood supply to lungs, concentration of anesthetic in inspired mixture
associated with hepatotoxicity, may use atropine before to reduce salivation and bronchial secretions
Stages of anesthesia
I: analgesia
II: delirium
III: surgical anesthesia
IV: medullary paralysis (once you start depressing medullary centers, pt will stop breathing and die)
Ester anesthetics
procaine, tetracaine, cocaine, metabolized by esterases in the plasma and some in the liver
Amide anesthetics
lidocaine, mepivacaine, bupivacaine, prilocaine, dibucaine, metabolized in the liver
Anesthetics mechanism of action
prevent generation of nerve impulses by interfering with sodium transport into neuron, only non-ionized form can penetrate tissue membranes
because inflamed tissue has a lower than normal pH, the amount of non-ionized form available to penetrate is decreased
Short acting anesthetics
Moderate acting anesthetics
prilocaine, mepivacaine, lidocaine
Long acting anesthetics
bupivacaine, tetracaine, etidocaine
interacts with propranolol by slowing down heart via beta receptor blockade and keeping lidocaine in the circulation longer and causing toxicity and by competing for the same enzyme in the liver
can cause methemoglobinemia because of toluidine metabolite called orthotoluidine
Toxic reactions to anesthetic
mostly related to excessive blood levels arising from inadvertent intravascular injection
CNS stimulation because of inhibition of central inhibitory neurons
at higher doses, will inhibit inhibitory and excitatory neurons => generalized state of CNS depression => respiratory depression and death
Epinephrine toxicity
elevated pulse rate
in pt’s with Grave’s disease, will have heightened sympathetic activity and could result in hypertensive crisis
Anesthetics that are vasodilators
procaine, lidocaine, tetracaine, mepivacaine
AHA limit of epinephrine that pt with CV disease can have
normal pt is 0.2mg
Penicillin G
more sensitive to acid degradation, so is usually injected rather than taken orally, not really used that much anymore
best gram negative spectrum
Cross-allergenic with penicillin
cephalosporins and ampicillins are
erythromycin is not
penicillin useful against penicillinase-producing bugs (like staphylococcus)
extended spectrum, specific for Pseudomonas infections and indole-positive Proteus species
higher concentration in bone than in serum, mostly affects gram positive organisms
higher concentration in gingival fluid than in serum, pretty broad spectrum against gram positive and negative cocci and bacilli
Cephalosporins 1st gen
effective against both gram negative and gram positive organisms
Cephalosporins 3rd gen
increased activity against gram negative, greatly decreased activity against gram positive
Prophylaxis no-no’s
don’t use tetracycline because endocarditis is streptococcal infection and some are resistant to tetracyclines
Prophylaxis for prosthetic joint
Keflex 2g, take 1hr before tx
compete with PABA in folic acid synthesis so there is folic acid deficiency
Allergic reactions to penicillins
dermatitis, stomatitis, bronchoconstriction, cardiovascular collapse
Clindamycin side effects
GI upset and pseudomonas colitis
antbiotic, associated with aplastic anemia
Tetracycline adverse effects
liver damage or hepatotoxicity, esp in pregnant pts with history of renal disease, superinfection, photosensitivity, discoloration of newly forming teeth, GI symptoms, diarrhea
Erythromycin estolate
associated with allergic cholestatic hepatitis
Streptomycin adverse effects
8th nerve damage, will affect balance and healing
Amphotericin B adverse effects
nephrotoxicity and hypokalemia
Tetracycline and penicillin
cancel each other out because they ahve opposing mechanisms of action
Tetracycline interactions
will chelate with calcium, reduced by concurrent ingestion of antacids or dairy products
alters rate of renal clearance of penicillin, is a uricosuric agent that tends to enhance excretion of uric acid by reducing renal tubular transport mechanisms
Antibiotics interaction with coumarin
deplete vitK sources so will enhance coumarin anticoagulants
Antibiotics interaction with oral conctraceptives
suppress normal flora involved in active steroids from bile conjugates => more rapid excretion of steroid from body
Macrolide interactions
inhibit metabolism of drugs like seldane, digoxin
erythromycin blocks the metabolism of seldane to antihistamine metabolity => will stay unmetabolized and cause cardiac arrhythmias

What local anesthetics are Amides? All the rest Where are Esters metabolized? Plasma WE WILL WRITE A CUSTOM ESSAY SAMPLE ON ANY TOPIC SPECIFICALLY FOR YOU FOR ONLY $13.90/PAGE Write my sample Where are Amides metabolized? Liver Short acting LAs …

Neutropenia A common side effects of Interferon (INF) treatment is? TMP-SMZ Antimicrobial prophylaxis for a history of recurrent UTIs WE WILL WRITE A CUSTOM ESSAY SAMPLE ON ANY TOPIC SPECIFICALLY FOR YOU FOR ONLY $13.90/PAGE Write my sample Ceftriaxone Antimicrobial …

Anethetists often administer midazolam (Versed) during induction of anesthesia because of which of the pharmacologic actions? causes amnesia adverse effects, carbamazepine (Tegretol)? a) begin taking the drug at a low dosage Adverse effects: visual distrubances, vertigo, and ataxia can result …

Antibiotics that block cell wall synthesis by inhibition of peptidoglycan CROSS-LINKING Beta lactams. Penicillin, methicillin, ampicillin, piperacillin, cephalosporins, aztreonam, imipenem Antibiotics that block peptidoglycan SYNTHESIS bacitracin, vancomycin WE WILL WRITE A CUSTOM ESSAY SAMPLE ON ANY TOPIC SPECIFICALLY FOR YOU …

Antibiotics that block cell wall synthesis by inhibition of peptidoglycan CROSS-LINKING Beta lactams. Penicillin, methicillin, ampicillin, piperacillin, cephalosporins, aztreonam, imipenem Antibiotics that block peptidoglycan SYNTHESIS bacitracin, vancomycin WE WILL WRITE A CUSTOM ESSAY SAMPLE ON ANY TOPIC SPECIFICALLY FOR YOU …

Bioavailability The ability of a drug to reach the systemic circulation from its site of administration. Absorption The movement of a drug from its site of administration into the blood. *Rate-determines how soon effects will begin *Amount-Determine how intense effects …

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