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Pharmacology > Pharm final > Flashcards

Pharm final Flashcards

1
Q

Stereoisomerism

A

Same chemical formula but different 3D structure and drug effects

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2
Q

differ toxins and poisons

A

Toxins are biological (snake venom) while poisons are pharmaceutical (cyanide, arsenic, alcohol)

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3
Q

Strongest combination of agonists, weakest?

A

Agonist + allosteric activator

Agonist + allosteric inhibitor

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4
Q

Pharmacokinetics vs pharmacodynamics

A

What the body does to the drug (ADME) vs what the drug does to the body (effects, binding, etc.)

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5
Q

If pH < pKa

A

favors protonated form (has Hydrogen attached)

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6
Q

if pH > pKa

A

Favors unprotonated form (no Hydrogen ion attached)

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7
Q

Weak Acid: pKa 3.5, pH 1.5

A

Protonated, non-charged

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8
Q

Weak base: pKa 7.0, pH 4.5

A

Protonated, Charged

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9
Q

Weak Acid: pKa 2.5, pH 5.0

A

Unprotonated, charged

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10
Q

Weak base: pKa 4.0, pH 6.5

A

Unprotonated, non-charged

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11
Q

What’s the therapeutic ratio?

A

TD50/ED50

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12
Q

Most potent curve on graph is

A

the one that starts showing effect the earliest

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13
Q

What’s the goal of rational dosing?

A

Achieve desired beneficial effect with minimal adverse effects

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14
Q

the bond strength is indirectly proportional to

A

specificity

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15
Q

Drug safety is directly proportional to

A

therapeutic index

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16
Q

Volume of distribution is directly proportional to

A

concentration of drug outside systemic circulation

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17
Q

First order elimination vs zero order elimination

A

first order elimination elimination rate changes with concentration, whereas zero-order has max and CONSTANT elimination rate until it reaches first order concentration levels.

In first order, the fraction elimination rate is constant. e.g. 10% of the drug is eliminated every hour, so the elimination rate changes but not the fractional change

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18
Q

How long does it take a drug to reach full effectiveness if the half-life is 4 hours?

How long does it take to be removed from the body/no effectiveness?

A

16 hours (4 half-lives), then another 16 hours. Totals 32 hours.

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19
Q

Parameters that affect passive diffusion

A

Weight of the drug, pKa, lipid solubility, and plasma protein binding

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20
Q

Four basic mechanisms of transmembrane signaling

A

-Direct crossing to intracellular receptor due to having lipid solubility (think aldosterone)

  • Enzymatic action mediated by ligand binding (TKR)

-Ligand gated ion channel (ACH in skeletal muscle)

-GPCRs

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21
Q

GPCR structure

A
  • 7 trans-membrane alpha-helices

-Pleiotropy: several downstream effects possible

-G-proteins: trimeric
-alpha subunit dissociates when active (GDP -> GTP) and binds to effector protein to produce second messenger cells)

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22
Q

Describe desensitization

A

The GPCR is phosphorylated by GRKs, enabling beta-arrestin to bind to the phosphorylated receptor, thereby inactivating it. The receptor-beta-arrestin complex is then internalized into a clathrin-coated pit, where the receptor can either be recycled to the membrane or degraded in lysosomes

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23
Q

Drug efflux transporters

A
  • ATP-binding cassete (ABC) transporters
    -major drug efflux transporters are B, C, G and found in
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24
Q

Where are B C and G ABC drug efflux transporters found?

A

Intestines, liver, kidneys, BBB, placenta

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25
Q

What’s the research target of the blood brain barrier?

A

Block efflux transporters, increase delivery to brain

tight junction!!

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26
Q

Biotransformation

A

Some drugs become active AFTER going through liver, but it could also be inactivation of metabolite

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27
Q

Examples of second messengers in a GPCR activation cascade

A

DAG
cAMP
IP3
cGMP

adenylyl cyclase is NOT a second messenger!!!

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28
Q

Neurotransmitter class: Esters

A

ACh - Cholinergic

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29
Q

Neurotransmitter class: Monoamines

A

Norepi, serotonin, dopamine - ADRENERGIC

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30
Q

Neurotransmitter class: Amino acids

A

Glutamate, GABA

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31
Q

Neurotransmitter class: Purines

A

Adenosine, ATP

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32
Q

Neurotransmitter class: Peptides

A

Substance P, endorphins

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33
Q

Neurotransmitter class: Inorganic gases

A

Nitric oxide

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34
Q

Sympathetic vs parasympathetic fibers

A

Symp: thoracolumbar region of spinal cord, consists of short pre and long post

Para: brain and sacral region, long pre and short post

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35
Q

a1 and a2 activates what?

A

Phospholipase C

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36
Q

b1 2 and 3 stimulates what?

A

Adenylate cyclase

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37
Q

M1 3 and 5 activate what?

A

Phospholipase

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38
Q

M2 and 4 inhibit what?

A

andeylate cyclase

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39
Q

MOA of phospholipase C activation (whole pathway)

A

Agonist binds to a1 receptor, GDP -> GTP, alpha subunit binds to effector protein phospholipase C, secrets DAG and IP3, releases stored calcium

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40
Q

MOA of adenylyl cyclase activation (whole pathway)

A

Agonist binds to beta receptor or a2 receptor, alpha subunit turns to GTP, stimulates effector protein adenylyl cyclase, ATP -> cAMP, activates protein kinase -> downstream effects

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41
Q

Receptors in heart for sympathetic activity are

A

B1 and B2

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42
Q

Receptors on skeletal muscle blood vessels

A

B2

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43
Q

Receptors on smooth vessels for sympathetic activity are

A

alpha

44
Q

Bronchiolar smooth muscle receptors for sympathetic activity are

A

B2

45
Q

Receptors in heart for parasympathetic activity are

A

M2

46
Q

Receptors in bronchioles smooth muscle for parasympathetic activity are

A

M3

47
Q

Receptors on smooth vessels for parasympathetic activity are

A

M3

48
Q

What are the second messengers for alpha 1 receptor binding?

A

DAG and IP3

49
Q

direct acting Adrenergic agonist

A

Albuterol, clonidine, dobutamine, dopamine, epi, norepi, isoproterenol

50
Q

Cardiac output equation

A

SV x HR

(70 x 75) = 5250ml/min

51
Q

Isoproterenol receptors

A

B1/B2

52
Q

dopamine receptors

A

D1-5, higher doses are A1/B1

53
Q

dobutamine receptors

A

B1

54
Q

Adrenoreceptor agonist drugs are used for

A

pheochromocytoma

ex: phentolamine, tolazoline, prazosin, labetalol

55
Q

Whats an irreversible adrenoceptor antagonist?

A

Phenoxybenzamine

56
Q

Non-specific beta blockers

A

propranolol

57
Q

B1 specific beta blockers

A

metoprolol and atenolol

58
Q

Ultra short acting beta blockers

A

Esmolol

59
Q

Muscarinic agonists cause what in the eyes?

A

Miosis and increase intraocular drainage

60
Q

Major uses of cholinomimetics

A

eye disease, GI/urinary tracts, NMJ issues (MG), atropine overdose

61
Q

Symptoms of organophosphate exposure

A

SLUDGE-M

tx with atropine and pralidoxime (ONLY for this exposure)

62
Q

Poisonous mushrooms are a what overdose and how to treat? S/S?

A

Cholinomimetic, atropine, SLUDE-M

63
Q

How to treat atropine overdose?

A

Physostigmine

(belladona is a thing to OD on, symptoms are BRAND)

64
Q

What kind of receptors are adrenergic receptors?

A

GPCRs

65
Q

AHA angina classifications of stable, unstable, and variant

A

Stable: angina with effort
Unstable: angina with rest, emergency.
Variant: vasospasms, rare

66
Q

Good and bad of nitrates/nitrites

A

Good: increased venous capacity, decreased ventricular preload, decrease heart size and CO

Bad: orthostatic hypotension, syncope, reflex tachycardia.

67
Q

Dihydropyridines CCB are specific to what?

A

Peripheral vasculature

68
Q

Verapamil and diltiazem are more specific to what?

A

heart

69
Q

Toxicity of CCBs

A

AV block, CHF, bradycardia, cardiac arrest

70
Q

Beta blockers, are they vasodilators?

A

no

71
Q

Beneficial effects of beta blockers

A

decreased HR, BP, contractility

72
Q

Hydraulic equation

A

BP = CO x PVR

73
Q

Adrenoceptor antagonist are what?

A

beta blockers

74
Q

2 examples of CNS sympathoplegics

A

Methyldopa, clonidine

75
Q

how do CNS sympathoplegics help blood pressure?

A

Decrease it by decreasing sympathetic stimulation in brainstem, bind more tightly to A2

76
Q

Examples of a1 blockers

A

Prazosin, terazosin, doxazosin. Block in the periphery.

77
Q

How does minoxidil vasodilate?

A

Opens K channels in smooth muscle, decreasing excitability.

78
Q

How does hydralazine work?

A

Increases NO production, dilating arterioles.

79
Q

How does sodium nitroprusside work?

A

Dilates arterial and venous vessels, used for HTN emergency, releases NO

80
Q

How does fenoldopam work?

A

Rapid peripheral arteriolar dilator, HTN emergencies and post-op HTN. Agonist of D1 receptors and increases flow to kidneys.

81
Q

ACE-I and ARB examples

A

ACE: captopril
ARB: losartan, valsartan.

82
Q

Where does digoxin work on the cell?

A

inhibits Na/K pumps, positive inotrope

83
Q

Compare systolic and diastolic failure in regards to cardiac output and ejection fraction

A

Systolic: decreased CO and ejection fraction, typical for acute HF

Diastolic: decreased CO but normal ejecetion fraction, wont respond to positive inotropic drugs, typical for hypertrophy

84
Q

4 factors of cardiac performance

A

preload, afterload, contractility, heart rate

85
Q

Toxicity of digoxin levels

A

EC50 1ng/mL, TC50 only 2ng/mL

86
Q

How do PDE inhibitors work?

A

inactivate cAMP and cGMP, causing vasodilation and positive inotropy.

milrinone

87
Q

order of nodal tissue

A

SA, AV, Bundle, purkinjie

88
Q

Cardiac action potential ion channels need to know

A

Phase 0: Na+ in
Phase 1: K, Cl out
Phase 2: Ca in, K out
Phase 3: K+ out
phase 4: K+ inward rectifier

200ms

89
Q

Causes of impulse conduction re-entry?

A

Scar tissue, unidirectional block, long conduction time

90
Q

Class II antiarrhythmics

A

Sympatholytic

91
Q

Class III antiarrhythmics

A

Prolong action potential duration (K channel blockers)

92
Q

Class IV antiarrhythmics

A

Block cardiac calcium channels

93
Q

Examples of sodium channel blockers

A

Quinidine, lidocaine, flecainide

94
Q

Drug of choice for VTach and why?

A

Amiodarone - has effects as all 4 classes by blocking sodium channels, inhibits receptors, increases action potential, and blocks calcium channels

95
Q

Treatment for bradycardia

A

Assess underlying cause, D/C drugs

If symptomatic, atropine and api/dopamine

If chronic: pacemaker

96
Q

Treatment for heart block

A

not usually treated for 1st degree.

If symptomatic, atropine and transcutaneous pacing

Chronic: pacemaker

97
Q

Treatment for SVT

A

assess cause, rule out atrial flutter

Adenosine

If chronic, CCBs, beta blockers

98
Q

Treatment for sinus tach

A

rule out wide complex

Adenosine, CCBs, cardioversion

If chronic, catheter ablation, ICD

99
Q

Treatment for Vtach

A

amiodarone, lidocaine, magnesium (torsades)

Chronic: amiodarone, satolol

100
Q

Treatment for Afib

A

diltiazem, verapamil

Chronic: Beta-blockers, amiodarone

101
Q

Treatment for Vfib

A

CPR, defibrillation, epi, vasopressin

Chronic: amiodarone, lidocaine, magnesium

102
Q

H1 receptors are stimulated and cause

A

Bronchoconstriction and vasodilation

103
Q

What receptors do antihistamines act on?

A

Selective H1 inverse agonists such as Benadryl which is most useful for type I hypersensitivity

104
Q

Histamine effects

A

Nervous system: stimulates pain and itching
Cardiac: Decreased BP, Increased HR

105
Q

1st gen H1 receptor antagonist

A

For sedation (children make have reverse effects), anti nausea, and antiparkinsonism

e.g. Benadryl

106
Q
A

Pharmacology (27 decks)

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