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Rapid Review STEP 1 > General/Autonomics Pharm > Flashcards

General/Autonomics Pharm Flashcards

1
Q

Difference in competitive vs noncompetitve inhibitors?

A

competitive = decrease potency, noncompetitive = decrease efficacy. Pharmacology General

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1
Q

What is Km?

A

Inverse relation of affinity of enzyme for its substrate. Pharmacology General

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2
Q

What is Vmax?

A

Direct proportion to enzyme concentration Pharmacology General

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3
Q

What is bioavailability?

A

Fraction of administered drug that reaches systemic circulation unchanged. Pharmacology General

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4
Q

Time to steady state depends on?

A

depends on half-life. Does not depend on frequency or size of dose. Pharmacology General

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5
Q

What is rate of elimination in zero order kinetics?

A

constant amount eliminated per time. Pharmacology General

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6
Q

Give three drugs that are zero order eliminated.

A

PEA - phenytoin, Ethanol, Aspirin. Pharmacology General

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7
Q

What is the rate of elimination for first order kinetics?

A

A constant FRACTION is eliminted, variable by concentration! Pharmacology General

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8
Q

How does ionization relate to urine pH?

A

Ionzied species are trapped in urine and not resorbed. Neutral can be resorbed. Pharmacology general

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9
Q

How do you treat overdose of weak acid? Give drug examples.

A

Treat with Bicarb to make neutral. Exp: phenobarbital, methotrexate, aspirin. Pharmacology general

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10
Q

How do you treat overdose of weak base? Give drug examples.

A

Treat with ammonium chloride. exp: amphetamines. Pharmacology general

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11
Q

What is phase I drug metabolism? What pt. population loses this?

A

Reduction, Oxidation, hydrolysis with CYP450. Often gives neutral products. Geriatrics lose this phase. Pharmacology general

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12
Q

What is phase II metaboloism? What population depend on this?

A

Conjugation (Glucuronidation, Acetylation, and Sulfation.) Gives charged products. Geriatrics depend on this, old people have GAS. Pharmacology general

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13
Q

What is efficacy?

A

maximal effect a drug can produce. Pharmacology general

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14
Q

What is potency?

A

amount of drug needed for the same effect. Pharmacology general

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15
Q

What happends to efficacy when a partial agonist and full agonist are mixed?

A

DECREASED efficacy. fight for same binding site, full agonist cant exert full effect. Pharmacology general

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16
Q

What is therapetuic index?

A

LD50/ED50. Median lethal dose divded by median effective dose. Safer drugs have a higher TI. pharmacology general

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17
Q

What is a therapeutic window?

A

Minimum effective dose to minimum toxic dose. Think of it as range of use. pharmacology general

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18
Q

What are the two types of Nicotonic receptors? What kind of messenger do they use?

A
  1. Nicotinic - Ligang gated Na/K channels. Two nicotinic types: Nm(NMJ) and Nn(autonomic ganglia. 2. Muscarinic - G-proteins. 5 types, M1-M5. pharmacology general
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19
Q

Alpha-1 sympathetic receptor (G-protein class, major function)

A

q, increase: vasc. smooth muscle contraction, pupillary dilator muscle contraction, intestinal and bladder sphincter contaction. pharmacology autonomics

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20
Q

Alpha-2 sympathetic receptor(G-protein class, major function)

A

i, decrease: sympathetic outflow, insulin release, lipolysis. increase: platlet aggregation. pharmacology autonomics

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21
Q

Beta-1 sympathetic receptor(G-protein class, major function)

A

s, increase: heart rate, contractilty, renin release, lipolysis pharmacology autonomics

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22
Q

Beta-2 sympathetic receptor(G-protein class, major function)

A

s, vasodilation, brochodilation, increase: heart rate, contractility, lipolysis, insulin release, aqueous humor production. decrease: uterine tone, ciliary muscle tone. pharmacology autonomics

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23
Q

M-1 Parasymp receptor(G-protein class, major function)

A

q, CNS, enteric nervouse system. pharmacology autonomics

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24
Q

M-2 Parasymp(G-protein class, major function)

A

i, decease: heart rate, contractility of atria pharmacology autonomics

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25
Q

M-3 parasymp(G-protein class, major function)

A

increase: exocrine gland secretion (tears, gastric, etc), gut peristalsis, bladder contraction, bronchoconstriction, pupillary spinchter contraction, cilliary muscle contraction. pharmacology autonomics

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26
Q

What receptor is responsible for miosis and accomadation?

A

Parasympathetic M-3. pharmacology autonomics

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27
Q

What receptor is responsbile for mydriasis?

A

Sympathetic Alpha-1. pharmacology autonomics

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28
Q

Dopamine D-1 receptor(G-protein class, major function)

A

s, relaxes renal vascular smooth muscle pharmacology autonomics

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29
Q

Dopamine D-2 receptor(G-protein class, major function)

A

i, modulates transmitter release especially in brain. pharmacology autonomics

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30
Q

Histamine H-1 receptor(G-protein class, major function)

A

q, increase: mucus production, contraction of bronchioles, pruritus, pain. pharmacology autonomics

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31
Q

histamine H-2 receptor(G-protein class, major function)

A

a, increase gastric acid secretion pharmacology autonomics

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32
Q

vasopression V-1 receptor(G-protein class, major function)

A

q, increase: vascular smooth muscle contraction pharmacology autonomics

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33
Q

vasopression V-2 receptor(G-protein class, major function)

A

s, increase water permeability and reabsorption in kidneys. (V2 found in 2 kidneys). pharmacology autonomics

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34
Q

Which receptors work via Gq -> Phospholipase C ->Pip2->DAG + IP3?

A

H1,Alpha1,V1,M1,M3. (remember HAVe 1 M&M) pharmacology autonomics

35
Q

DAG causes activation of what?

A

Protein Kinase C. pharmacology autonomics

36
Q

IP3 causes increase in what?

A

Calcium -> smouth muscle contraction pharmacology autonomics

37
Q

Which receptors work via Gi->Adenyly cyclase ->cAMP ->Protein Kinase A?

A

M2, Alpha2, D2. (remember MAD 2’s.) pharmacology autonomics

38
Q

Which receptors work via Gs->adenylyate cyclase ->cAMP->Protein Kinase A?

A

Beta1, Beta2, D1, H2,V2. pharmacology autonomics

39
Q

What does protein kinase A do?

A

increase calcium release in heart and blocks myosin light chain kinase. pharmacology autonomics

40
Q

What are the two classes of cholinomimetics?

A
  1. direct agonsts 2. indirect agonists (anticholinesterases). pharmacology autonomics
41
Q

Bethanechol(mechanism,use,toxicity)

A

Direct cholinomimetic. Postop or neurogenic ileus, urinary retention. COPD+asthma exacerbation, peptic ulcers. pharmacology autonomics

42
Q

Carbachol(mechanism,use,toxicity)

A

Direct Cholinomimetic. Identical to Ach. Glaucoma, pupillary contraction, relief of IOP. COPD+asthma exacerbation, peptic ulcers. pharmacology autonomics

43
Q

Pilocarpine(mechanism,use,toxicity)

A

Direct Cholinomimetic. Stimulates tears, salvia, sweat. Open and closed-angle glaucoma.COPD+asthma exacerbation, peptic ulcers. pharmacology autonomics

44
Q

methacholine(mechanism,use,toxicity)

A

Direct Cholinomimetic. challenge test of asthma diagnosis. COPD+asthma exacerbation, peptic ulcers. pharmacology autonomics

45
Q

Neostigmine(mechanism,use,toxicity)

A

Indirect cholinomimetic agonist. NO cns penetration. Postop and neurogenic ileus, myasthenia gravis, reversal of NMJ block. COPD+asthma exacerbation, peptic ulcers. pharmacology autonomics

46
Q

pyridostigmine(mechanism,use,toxicity)

A

indirect cholinomimetic agonist. Long acting myasthenia gravis treatment. COPD+asthma exacerbation, peptic ulcers. pharmacology autonomics

47
Q

edrophonium(mechanism,use,toxicity)

A

indirect cholinomimetic agonist. Short acting, for myasthenia gravis diagnosis. COPD+asthma exacerbation, peptic ulcers. pharmacology autonomics

48
Q

Physostigmine(mechanism,use,toxicity)

A

indirect cholinomimetic agonist. for anti-cholinergic overdose, crosses BBB. COPD+asthma exacerbation, peptic ulcers. pharmacology autonomics

49
Q

Donepezil(mechanism,use,toxicity)

A

indirect cholinomimetic agonist. Alzheimers disease. COPD+asthma exacerbation, peptic ulcers. pharmacology autonomics

50
Q

signs of cholinesterase inhibitor poisoning. treatment.

A

DUMBBELSS (diarrhea, urination, miosis, bronchospasm, bradycardia, excitation of skeletal muscle +CNS, lacrimation, sweating, salvia.) tx: atropine + pralidoxime. pharmacology autonomics

51
Q

Parathion(mechanism, treatment)

A

Irreversible cholinesterase inhibitor, ACH overdose. Tx: atropine + pralidoxime. pharmacology autonomics

52
Q

Atropine, homatropine, tropicamide (mechanism, use, toxicity).

A

Muscarinic antagonist. produces mydriasis and cycloplegia. (Atropine also used for bradycardia). Causes hot as a hare, dry as bone, red as beet, blind as bat, mad as a hatter. pharmacology autonomics

53
Q

Benztropine(mechanism,use,toxicity)

A

Muscarinic antagoist. Parkinsons disease (park my benz). Causes hot as a hare, dry as bone, red as a beet, blind as a bat, mad as a hatter. pharmacology autonomics

54
Q

Scopolamine(mechanism,use,toxicity)

A

Muscarinic antagonist. Motion sickness. causes hot as a hare, dry as a cone, red as a beet, blind as a bat, mad as a hatter. pharmacology autonomics

55
Q

Ipratropium,tiotropium (mechanism, use, toxicity)

A

Muscarinic antagonist. COPD, Asthma. Causes hot as a hare, dry as a bone, red as a beet, blind as a bat, mad as a hatter. pharmacology autonomics

56
Q

Oxybutynin(mechanism,use,toxicity)

A

Muscarinic anatagonist. reduces urgency in mild cystitis and reduce bladder spasms. causes hot as a hare, dry as a bone, red as a beet, blind as a bat, mad as a hatter.

57
Q

Glycopyrrolate(mechanism,use,toxicity)

A

Muscarinic anatagonist. IP: given in preop to reduce airway secretions. oral:reduce drooling, peptic ulcer. Can cause hot as a hare, dry as a bone red as a beet, blind as a bat, mad as a hatter. pharmacology autonomics

58
Q

Jimson Weed(mechanism, toxicity)

A

muscarinic antagonist, causes gardner’s pupil (mydriasis). pharmacology autonomics

59
Q

Epinephrine(Mechanism, receptors bound, use, toxicity)

A

Direct Sympathomemetic. A1,A2,B1,B2. Anaphylaxis, open angle glaucoma, asthma, hypotension. pharmacology autonomics

60
Q

Norepinephine(Mechanism, receptors bound, use, toxicity)

A

direct sympathomemetic. A1,A2, some B1. used in hypotension but it decrease renal perfusion. pharmacology autonomics

61
Q

Isoproterenol(Mechanism, receptors bound, use, toxicity)

A

Direct sympathomemetic. B1, B2. Used in Torsade de pointe and bradyarryhmia. Can cause tachycardia and worsen cardiac ischemia. pharmacology autonomics

62
Q

dopamine(Mechanism, receptors bound, use, toxicity)

A

Direct sympathomimetics. Receptors depend on dose. low = D1, med = D1,B2,B1, high = A1,A2,B1,B2,D1. Used in shock and heart failure (ionotropic and chronotropic). pharmacology autonomics

63
Q

dobutamine(Mechanism, receptors bound, use, toxicity)

A

Direct sympathomimetic. Mostly B1, little a1,a2,b2. Used in heart failure and cardiac stresstest (ionotrpic and chronotropic) pharmacology autonomics

64
Q

Phenylephrine(Mechanism, receptors bound, use, toxicity)

A

Direct sympathomimetic. A1, A2. Used in hypotension, to cause mydriasis, and rhinitis (decongestant). pharmacology autonomics

65
Q

Albuterol, salmetrol, terbutaline (Mechanism, receptors bound, use, toxicity)

A

Direct sympathomimetic. Mostly B2, some b1. Sal = long term ashtma or copd. Albuterol for short term asthma. Terbutaline for to reduce premture uterine contractions. pharmacology autonomics

66
Q

Ritodrine(Mechanism, receptors bound, use, toxicity)

A

Direct sympathomimetic. B2 only. Used to reduce premature uterine contractions. pharmacology autonomics

67
Q

Amphetamine (mechanism, use)

A

indirect sympathomimetic. Releases stored catecholamines. Used for narcolepsy, obesity, ADD. pharmacology autonomics

68
Q

Epinephrine(Mechanism, use, toxicity)

A

indirect sympathomimetic. Releases stored catecholamines. Used for nasal decongestion, urinary incontience, hypotension. pharmacology autonomics

69
Q

Cocaine (mechanims, use).

A

direct sympathomimetic. Reuptake inhibitor. Causes vasoconstriction and local anesthesia. pharmacology autonomics

70
Q

Why must B-Blockers be avoided in suspected cocaine intoxication?

A

mixing them can lead to unopposed A1 activation and extreme hypertenion. pharmacology autonomics

71
Q

How does norepinephrine cause reflex bradycardia?

A

stimulates A1>B2. Causes increased vasoconstrciton -> increased BP. This causes reflex bradycardia and slowing of HR. pharmacology autonomics

72
Q

How does isoproterenol cause reflex tachycardia?

A

Stimulates B2>A1. This cause vasodilation and dropping of BP. B1 is stimulated and causes tachycardia. pharmacology autonomics

73
Q

Clonidine, alpha-methyldopa(Mechanism, receptors bound, use)

A

Centrally acting alpha-2 agonists, this causes LESS peripheral sympathetic release.Used in hypertension, especially renal disease due to no increase in renal blood flow! pharmacology autonomics

74
Q

Phenoxybenzamine(Mechanism, receptors bound, use, toxicity)

A

IRREVERSIBLE nonslective alpha blocker. Used in pheochromosytoma BEFORE surgery! toxic: orhtostatic hypotension, reflec tachycardia. pharmacology autonomics

75
Q

phentolamine(Mechanism, receptors bound, use, toxicity)

A

REVERSBILE nonselective alpha blocker. give to patients on MAOI who each tyramine contraining foods. pharmacology autonomics

76
Q

Prazosin, Terazosin, Doxazosin,Tamsulosin(Mechanism, receptors bound, use, toxicity)

A

Alpha-1 blocker. Used in hypertension, urinary rentention in BPH. tox:orthostatic hypotension, dizziness, headache. pharmacology autonomics

77
Q

Mirtazapine (mechanism, use, toxicity)

A

Alpha-2 blocker. Used in depression. tox: sedation, hypercholesterolemia, increased apetite. pharmacology autonomics

78
Q

Describe what occurs when you alpha-blockade epi vs. phenylephrine.

A

Before blockade: Both epi and phen RAISES BP. After alpha blockade: only epi raises, no change in phenyl. Why: Epi has B binding, phenyl does NOT. pharmacology autonomics

79
Q

Give 6 applications of Beta-blockers in general.

A

Angina - decreases HR and contractility, decreasing oxygen use. MI - decrease mortality. SVT - decrease AV duction. Hypertension - decrease CO and renin secretion. CHF - slows progression. Glaucoma - decrease secretion of aqueous humor. pharmacology autonomics

80
Q

give general toxicites of b-blockers

A

impotence, asthma exacerbation, bradycardia, seizures, sedation, hides hypoglycemia. pharmacology autonomics

81
Q

What are the B1 selective b-blockers? When are they useful?

A

A BEAM. acebutolol, betaxolol, Esmolol, Atenolol, Metoprolol. Useful in comorbid pum. disease. pharmacology autonomics

82
Q

What are the nonselective ( b1 = b2) b-blockers?

A

Please Try Not Being Picky. Propranolol, Timolol, Nadolol, Pindolol. B = B-blocker. pharmacology autonomics

83
Q

what are the nonselective a and b-antagonists?

A

Carvedilol, labetalol. pharmacology autonomics

84
Q

What are the partial B-agonists?

A

Pindolol, Acebutolol. pharmacology autonomics

Rapid Review STEP 1 (13 decks)

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