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Unit 2 Pharm II > MOAs > Flashcards

MOAs Flashcards

1
Q

Mechanism for enhancing/decreasing potassium reabsorption

A

cannot be influenced by drugs

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2
Q

How do acidic drugs cause gout?

A

They compete with uric acid for excretion by OAT carrier, causing increased serum uric acid levels and gouty attacks

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3
Q

Diffusion rate depends on

A

lipid solubility, pKa, pH

→ weak acids at low pH remain mostly unionized/lipid soluble→ easily diffuse

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4
Q

Carbonic anhydrase inhibitors (Acetazolamide)

A

Proximal tubule and loop of henle
Inhibit carbonic anhydrase:

→ no H+ + HCO3 production inside of cells→ decreased H+ in cell for exchange with Na+ in lumen (by Na+/H+ antiporter) → increase Na+ and H2O loss
→ In lumen: H2CO3 can’t convert to H2O + CO2 by CA → bicarb trapped

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5
Q

Loop diuretics (furosemide) block

A

Thick ascending limb of loop of henle

Block the Na+/K+/2 Cl- cotransporter (reabsorption)
→reduced renal medulla concentration gradient→impaired concentration and dilution

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6
Q

Loop diuretics (furosemide) induce

A

Induce kidney prostaglandins
→ decreased salt transport
→ renal and systemic vasodilation

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7
Q

Loop diuretics mechanism for improving pulmonary edema

A

reduce congestion by venodilation→ increased systemic venous capacitance→ decreased cardiac return→ decreased RV volume→ decreased pulmonary BP

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8
Q

Thiazide diuretics Effects on Sodium

A

Inhibition of Na+ reabsorption by Na+ Cl+ co-transporter at early distal tubule (not a major site of Na+ reabsorption→ less potent)

Increased luminal Na+ → increased cell membrane potential→ increased Ca++ reabsorption by PTH dependent Ca++ channels (good for nephrolithiasis)

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9
Q

Loop diuretics for hypercalcemia

A

reduce K+ gradient→ decreased Mg++ and Ca++ reabsorption

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10
Q

Thiazide diuretics effects are dependent on

A

Effects are dependent on prostaglandin synthesis and GFR

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11
Q

Thiazide diuretics systemic effects

A

Increased systemic ATP-dependent K+ channel opening→ hyperpolarization of cell membranes→ relaxation of smooth muscle cells→ vasodilation
→ also causes reduced insulin secretion

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12
Q

Potassium-sparing diuretics effects

A

Interfere with Na+ reabsorption at distal exchange site→ loss of Na+ and H2O → conservation of K+. Weak. Used in combination with other K+ losing drugs.

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13
Q

Spironolactone MOA

A

Competitive inhibitor of aldosterone:

Promotes excretion of Na+ and retention of K+ at late distal tubule and collecting duct:

  1. less Na+ channels
  2. blocked Na+ conductance→ hyperpolarized cell→ decreased K+ excretion
  3. decreased Na+/K+ ATPase activity→ decreased K+ excretion
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14
Q

Eplerenone MOA

A

Selective aldosterone receptor antagonist (SARA)

Spironolactone effects at aldosterone receptor with decreased affinity for other steroid receptors

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15
Q

Spironolactone at high doses

A

inhibits glucocorticoid and sex hormone receptors

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16
Q

Amiloride/Triamterene MOA

A

Inhibit Na+/K+ ion exchange in an aldosterone independent manner:

  1. Directly inhibit aldosterone sensitive Na+ channel (ENaC)–> increased sodium loss
  2. Leads to decreased K+ excretion (sparing)
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17
Q

Desmopressin MOA

A

Synthetic ADH agonist→ activation of V2 (some V1) receptors→ decreased H2O excretion

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18
Q

Conivaptan/tolvaptan MOA

A

ADH antagonist:

Non-peptide V1a and V2 receptor antagonist→ increased Na+ concentration and increased free H2O clearance

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19
Q

Digitalis/Digoxin MOA for contractility

A

Cardiac glycoside→ inhibition of membrane Na+/K+ ATPase (digitalis receptor)
→ increased intracellular Na+
→ decreased expulsion of intracellular Ca++ → increased SR storage→ increased actin-myosin interaction by Ca++ → increased contractility

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20
Q

Digitalis/Digoxin MOA for heart rate in the normal heart

A

antiarrhythmic:

sensitization of baroreceptors→ stimulate central vagal nuclei→ vagal stimulation→ increased SA node sensitivity to ACh (PNS: slows HR)

CO doesn’t increase due to increased PVR

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21
Q

Digitalis/Digoxin MOA for heart rate in the failing heart

A

Sensitization baroreceptors→ stimulate central vagal nuclei→ vagal stimulation→ increased SA node sensitivity to ACh (PNS: slows HR)

Sympathetic tone is already high, will be reduced by increased contractility→ reduced heart rate. CO increases because peripheral vasoconstriction response does not occur

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22
Q

Milrinone MOA

A

Inhibits cAMP phosphodiesterase→ increased cAMP→ increased Ca++ (similar to dobutamine)→ vasodilation

Positive inotropic drug+vasodilation= inodilator

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23
Q

Dobutamine MOA

A

Selective B1 agonist→ Inotropic

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24
Q

Diuretics for Heart failure

A

Decrease Na+ + H2O retention

Decrease venous pressure→ less edema, decreased cardiac size

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25
Q

Spironolactone/epleronone for heart failure

A

reduce mortality

blocking aldosterone receptors is beneficial compared to other diuretics

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26
Q

Dopamine in low doses

A

D1 receptors in kidney→ renal vasodilation

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27
Q

Dopamine in moderate doses

A

B1 receptors in heart → inotropic effect

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28
Q

Dopamine in high doses

A

Alpha receptors in vessels→ vasoconstriction

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29
Q

Angiotensin II in heart failure causes

A

increased afterload, increased preload, increased remodeling
Use ACE-I/ARBs to counteract

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30
Q

ACE inhibitors (captopril) MOA

A

inhibit angiotensin converting enzyme

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31
Q

Angiotensin II antagonists (ARBs) (losartan) MOA

A

block angiotensin II from binding to AT1 receptor

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32
Q

Decreasing aldosterone in HF causes

A

decreased preload (Na+ isn’t retained)

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33
Q

Dry cough side effect of ACE-I or Sacubitril comes from

A

Reduction in bradykinin metabolism (increased levels of bradykinin)→ dry cough

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34
Q

Sacubitril/Valsartan MOA

A

2 drugs (ARNI)
Sacubitril: neprilysin inhibitor
Neprilysin degrades natruretic peptides, bradykinin
Inhibtion: decreased vasoconstriction, soidum retention, cardiac remodeling

Valsaratan: ARB

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35
Q

Beta blockers and early heart failure

A

Decrease mortality:
Decrease renin secretion, HR, remodeling
Up-regulate B receptors
Attenuate effect of high concentrations of catecholamines

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36
Q

Beta blockers and end stage heart failure

A

Dangerous due to negative inotropic effect

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37
Q

Vasodilators (Sodium nitroprusside, Isosorbide dinitrate, hydralazine) for heart failure

A 
Reduce preload (venodilation)
Reduce afterload (arteriolar dilation)
Decrease damaging remodeling
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38
Q

Ivabradine MOA

A

Blocks If current in heart→ reduced HR (when B blockers can’t)
Improvement in mortality rates, hospitalizations
No benefit in cardiovascular endpoints

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39
Q

Thiazide monotherapy for htn

A

decreases BP

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40
Q

Thiazide combination therapy for htn

A

enhances efficacy of other antihypertensive drugs, counteracts sodium and fluid retention

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41
Q

Thiazide which is a direct vasodilator and beneficial in hypertension

A

Indampamide

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42
Q

Thiazide for diuresis vs for hypertension

A

diuresis requires a much higher dose

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43
Q

Thiazide short term effects on BP

A

reduce Na+ stores which decreases blood volume and CO

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44
Q

Thiazide long term effects on BP

A

decrease Na+ in muscle cells, activate K+ channels which decreases sensitivity to vasopressors
→ decreased peripheral resistance→ BP lowered 10-15 mmHg

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45
Q

Central alpha agonists (clonidine, methyldopa) MOA

A

Stimulate medullary a2→ decreased peripheral sympathetic nerve activity
Stimulate presynaptic a2 receptors→ decreased transmitter release
→ decreased sympathetic outflow and renin secretion→ decreased BP

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46
Q

Prazosin, terazosin, doxasozin MOA

A

Block alpha-1 adrenergic receptors→ reduce NE vasoconstriction→ artery/vein dilation→ decreased peripheral resistance→ decreased BP

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47
Q

Why are sympathomimetics combined with diuretics?

A

generally, they increase Na+ and water retention (by increased renin)

48
Q

Beta blockers MOA for htn

A

Reduce CO, renin secretion and sympathetic vasomotor tone→ decreased BP

More effective in: Caucasian, young, males. High renin patients

Combined with other drugs to counteract reflex tachycardia and increased renin secretion

49
Q

Hydralazine MOA

A

Acts through nitric oxide

Dilates arterioles but not veins

50
Q

Sodium nitroprusside MOA

A

Acts through nitric oxide
Rapidly lowers blood pressure in minutes, effects disappear quickly upon discontinuation→ emergency hypertensive situations

51
Q

Minoxidil MOA

A

Opens potassium channels→ stabilizes membrane→ potent BP reduction

52
Q

Fenoldopam MOA

A

Postsynaptic D1 receptor stimulation relaxes arteriolar smooth muscle

53
Q

CCB MOA

A

Bind to L-type channels:

  1. Myocardium→ decreased contractility (inotropy), SA node impulse generation (chronotropy), AV node conduction (dromotropy)
  2. Vascular smooth muscle→ vasodilation
  3. Relax ALL smooth muscle that requires Ca++ for contraction: bronchiolar, GI, uterine muscles
54
Q

CCBs and HR

A

Due to differences in tissue selectivity:
Nifedipine→ increased HR (reflex tachycardia)
Verapamil→ decreased heart rate

55
Q

ACE-I mechanism of action for decreasing BP

A

ACE-I→ decreased ATII→ decreased BP:

  1. Reduced vasoconstriction by ATII
  2. Reduced aldosterone→ natriuresis
56
Q

ACE-I + diuretics for htn

A

Enhance antihypertensive efficacy of diuretics by increasing natriuresis
Increased K+–> balance hypokalemia of diuretic

57
Q

Nitrites and nitrates MOA

A

Endothelial cell NO→ activate guanylyl cyclase→ cGMP→ uneven vasodilation:

1. Large vein dilate more 
→ increased venous capacitance
→ decreased preload
2. Arterioles and precapillary sphincters dilate less
→ decrease afterload
58
Q

GOOD effects of nitrites

A

Decrease cardiac workload
→ Decreased preload and afterload
decreased myocardial oxygen requirement is main mechanism by which angina is relieved

59
Q

BAD effects of nitrites

A

Increased cardiac workload

→ decreased blood pressure → baroreceptor reflex → increased HR and contractility → decreased diastolic perfusion time

60
Q

Good effects of dihydropyridines for angina

A

Good:
Coronary vasodilation→ relaxes vasospasms, some increased myocardial O2
Systemic arteriodilation→ decreased afterload

61
Q

Bad effects of dihydropyridines for angina

A

enhanced development of MI

Rapid hypotension→ reflex sympathetic activation→ increased cardiac workload→ ischemic attack

62
Q

Good effects of diltiazem and verapamil for angina

A

decreased cardiac workload
Decreased myocardial contractility
Decreased SA node automaticity and AV node conduction→ bradycardia

63
Q

Bad effects of diltiazem and verapamil for angina

A

serious cardiac depression
→ Cardiac arrest
→ AV block
→ heart failure

64
Q

CCBs MOA for angina

A

Arterioles>veins, chronic tx (not rapid)
Cardiac effects:
1. Negative inotropic effect
2. Reduced impulse generation at SA node (automaticity)
3. Slowed AV node conduction

65
Q

Beta blockers for angina

A
  1. Decreased SNS→ decreased cardiac activity and vasoconstriction → hypotension and bradycardia → decreased cardiac workload→ decreased myocardial O2 demand
  2. Bradycardia→ increased myocardial perfusion time
66
Q

Ranolazone MOA

A

Anti-angina
1. Partial fatty-acid oxidation (PFox) inhibitor
2. Inhibits late inward sodium current
Effects:
1. Decreases left ventricular wall stiffness
2. Improves coronary circulation

67
Q

PDE5 is

A

the enzyme that metabolizes cGMP in the corpus cavernosum

68
Q

Sildenafil, Vardenafil, Avanafil, Tadalafil MOA

A

Inhibit PDE5

cGMP stays active longer, producing vasodilation

69
Q

1st line for hyperlipidemia

A

dietary management

recheck cholesterol 1 month after losing weight

70
Q

coronary or peripheral vascular disease
familial hypercholesterolemia
Familial hyperlipidemia
1st line

A

Medicate, dietary changes not 1st line

71
Q

Statins MOA

A

Analogs of HMG-CoA reductase intermediate in mevalonate synthesis→ inhibit reductase→ increased high affinity LDL receptors in liver→ reduced plasma LDL

72
Q

2 statins which have to be hydrolyzed to active form

A

Simvastatin

Lovastatin

73
Q

Other effects of statins

A 
CHD: decreased CRP
Increased endothelial NO production
Increased plaque stability
Reduced lipoprotein oxidation
Decreased platelet aggregation
74
Q

Resins MOA

A

Binding bile acids and preventing their intestinal resabsorption
Decreased bile acids→ increased hepatic expression of LDL receptors→ LDL used to make more bile acids→ decreased serum LDL → decreased plasma cholesterol

75
Q

Niacin MOA

A

Inhibits VLDL secretion→ Lowered plasma VLDL and LDL

Also inhibits hepatic cholesterologenesis

76
Q

Fibric acid derivatives/fibrates MOA

A

PPAR-alpha ligand (nuclear receptor) → upregulates LPL and other genes involved in fatty acid oxidation

77
Q

Ezetimibe MOA

A

Selectively blocks intestinal absorption of cholesterol and related phytosterols

78
Q

PCSK9 inhibitors MOA

A

Human monoclonal Antibodies which inhibit PCSK9 from binding to LDLR, bind, and promote LDL degradation

79
Q

Quinidine MOA

A

Binding to open and activated sodium channels:

a. Normal cells: slow maximal rate of rise of the cellular action potential (Vmax of 0 phase)

B. Damaged cells: no polarization at all

Secondary MOA:
Blocking K+channels→ prolonged action potential duration and effective refractory period

80
Q

Procainamide MOA

A

similar to quinidine

81
Q

Lidocaine MOA

A

Blocks inactivated Na+ channels, fast binding and dissociation
Preferentially affects damaged tissue→ more receptors are inactivated
Blocks the “window” current → shortens APD

82
Q

Flecainide MOA

A

Blocks all sodium channel states
Slow dissociation from bingin
No effect on ERP

83
Q

3 beta blockers used as antiarrhythmatics

A

Propranolol: non-specific

Acebutolol: B1

Esmolol: B1, short half life, IV only
→ 2nd line for acute treatment of PSVTs (paroxysmal supraventricular tachycardia)

84
Q

Amiodarone MOA

A 
Blocks K+ channels
Other effects:
BLocks Na+ channels (class I)
B-blocker (class II)
Some Ca+ channel blocking (Class IV)
Alpha blocker
85
Q

Sotalol MOA

A

K+ blocker→ prolongs duration of action potential

Non selective Beta blocker

86
Q

Verapamil and Diltiazem as antiarrhythmatics

A

Block slow L-type cardiac Ca++ channels

Ca+ ONLY depolarizes atria→ CCBs only effective in atria

87
Q

Adenosine MOA

A

Enhanced K+ conduction and inhibition of cAMP-induced Ca++ influx→ hyperpolarization→ heart “resets”

88
Q

Magnesium MOA

A

unknown

89
Q

Heparin MOA

A

Activity is dependent on antithrombin III
Mainly affects Xa and thrombin
+ IXa, XIa, XIIa
Pentasaccharide acts as a catalyst for antithrombin III

90
Q

Protamine sulfate MOA

A

reverses heparin by competing for binding

Does not completely reverse enoxaparin, has no effect on fondaparinux

91
Q

Fondaparinux is a

A

synthetic pentasaccharide

92
Q

LMWH MOA

A

Similar to high molecular weight heparins except:

Main inhibition of Factor Xa (no thrombin)

93
Q

Bivalirudin MOA

A

Highly specific direct inhibitor of thrombin (not AT III)

94
Q

Argatroban MOA

A

thrombin inhibitor

95
Q

Dabigatran MOA

A

thrombin inhibitor

96
Q

Rivaroxaban MOA

A

inhibits factor Xa

97
Q

Betrixaban MOA

A

inhibits factor Xa

98
Q

Apixaban MOA

A

inhibits factor Xa

99
Q

Edoxaban MOA

A

inhibits factor Xa

100
Q

Andexxa MOA

A

a factor Xa decoy, reversal for direct factor Xa inhibitors

101
Q

Warfarin MOA

A

Inhibit vitamin K epoxide reductase→ no reduced vitamin K for carboxylation of clotting factors→ interferes with synthesis of II, VII, IX, X, protein C and S

102
Q

Fibrinolytic agents (thrombolytic agents) MOA

A

Convert plasminogen to plasmin

Internal plasmin is protected→ lyses thrombus from within

103
Q

Alteplase (tissue plasminogen activator/t-PA)

A

Higher activity for fibrin-bound plasminogen vs plasma plasminogen: “clot-selective”

104
Q

Tenecteplase

A

Higher activity for fibrin-bound plasminogen vs plasma plasminogen: “clot-selective”

105
Q

Urokinase

A

Directly activates plasminogen, not clot-fibrin specific→ generalized systemic fibrinolysis

106
Q

Anstreplase=

A

streptokinase + plasminogen

off market

107
Q

Aminocaproic acid MOA

A

Inhibit plasminogen activity

108
Q

Tranexamic acid MOA

A

Inhibit plasminogen activity

109
Q

Aspirin MOA

A

Irreversible inhibitor of Cyclooxygenase (COX) enzyme → Decreased TXA1 → decreased platelet aggregation

110
Q

Abciximab MOA

A

Antibody

Inhibits GP IIb/IIIa receptors from binding fibrinogen→ decreased platelet aggregation

111
Q

Eptifibatide MOA

A

analog of carboxy end of fibrinogen

Inhibit GP IIb/IIIa receptors from binding fibrinogen→ decreased platelet aggregation

112
Q

Tirofiban MOA

A

analog of carboxy end of fibrinogen

Inhibit GP IIb/IIIa receptors from binding fibrinogen→ decreased platelet aggregation

113
Q

Clopidogrel MOA

A

Irreversibly blocks ADP receptor on platelets→ decreased platelet aggregation

114
Q

Ticlopidine MOA

A

Irreversibly blocks ADP receptor on platelets→ decreased platelet aggregation

115
Q

Prasugrel MOA

A

Irreversibly blocks ADP receptor on platelets→ decreased platelet aggregation

116
Q

Vorapaxar MOA

A

Antagonist of protease-activated receptor-1 (PAR-1): major thrombin receptor on human platelets

Unit 2 Pharm II (13 decks)

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