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Unit 2 Pharm II > MOAs > Flashcards

MOAs Flashcards

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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
Spironolactone/epleronone for heart failure
***reduce mortality*** | blocking aldosterone receptors is beneficial compared to other diuretics
26
Dopamine in low doses
D1 receptors in kidney→ renal vasodilation
27
Dopamine in moderate doses
B1 receptors in heart → inotropic effect
28
Dopamine in high doses
Alpha receptors in vessels→ vasoconstriction
29
Angiotensin II in heart failure causes
increased afterload, increased preload, increased remodeling Use ACE-I/ARBs to counteract
30
ACE inhibitors (captopril) MOA
inhibit angiotensin converting enzyme
31
Angiotensin II antagonists (ARBs) (losartan) MOA
block angiotensin II from binding to AT1 receptor
32
Decreasing aldosterone in HF causes
decreased preload (Na+ isn't retained)
33
Dry cough side effect of ACE-I or Sacubitril comes from
Reduction in bradykinin metabolism (increased levels of bradykinin)→ dry cough
34
Sacubitril/Valsartan MOA
2 drugs (ARNI) Sacubitril: neprilysin inhibitor Neprilysin degrades natruretic peptides, bradykinin Inhibtion: decreased vasoconstriction, soidum retention, cardiac remodeling Valsaratan: ARB
35
Beta blockers and early heart failure
Decrease mortality: Decrease renin secretion, HR, remodeling Up-regulate B receptors Attenuate effect of high concentrations of catecholamines
36
Beta blockers and end stage heart failure
Dangerous due to negative inotropic effect
37
Vasodilators (Sodium nitroprusside, Isosorbide dinitrate, hydralazine) for heart failure
``` Reduce preload (venodilation) Reduce afterload (arteriolar dilation) Decrease damaging remodeling ```
38
Ivabradine MOA
Blocks If current in heart→ reduced HR (when B blockers can't) Improvement in mortality rates, hospitalizations No benefit in cardiovascular endpoints
39
Thiazide monotherapy for htn
decreases BP
40
Thiazide combination therapy for htn
enhances efficacy of other antihypertensive drugs, counteracts sodium and fluid retention
41
Thiazide which is a direct vasodilator and beneficial in hypertension
Indampamide
42
Thiazide for diuresis vs for hypertension
diuresis requires a much higher dose
43
Thiazide short term effects on BP
reduce Na+ stores which decreases blood volume and CO
44
Thiazide long term effects on BP
decrease Na+ in muscle cells, activate K+ channels which decreases sensitivity to vasopressors → decreased peripheral resistance→ BP lowered 10-15 mmHg
45
Central alpha agonists (clonidine, methyldopa) MOA
Stimulate medullary a2→ decreased peripheral sympathetic nerve activity Stimulate presynaptic a2 receptors→ decreased transmitter release → decreased sympathetic outflow and renin secretion→ decreased BP
46
Prazosin, terazosin, doxasozin MOA
Block alpha-1 adrenergic receptors→ reduce NE vasoconstriction→ artery/vein dilation→ decreased peripheral resistance→ decreased BP
47
Why are sympathomimetics combined with diuretics?
generally, they increase Na+ and water retention (by increased renin)
48
Beta blockers MOA for htn
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
Hydralazine MOA
Acts through nitric oxide | Dilates arterioles but not veins
50
Sodium nitroprusside MOA
Acts through nitric oxide Rapidly lowers blood pressure in minutes, effects disappear quickly upon discontinuation→ emergency hypertensive situations
51
Minoxidil MOA
Opens potassium channels→ stabilizes membrane→ potent BP reduction
52
Fenoldopam MOA
Postsynaptic D1 receptor stimulation relaxes arteriolar smooth muscle
53
CCB MOA
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
CCBs and HR
Due to differences in tissue selectivity: Nifedipine→ increased HR (reflex tachycardia) Verapamil→ decreased heart rate
55
ACE-I mechanism of action for decreasing BP
ACE-I→ decreased ATII→ decreased BP: 1. Reduced vasoconstriction by ATII 2. Reduced aldosterone→ natriuresis
56
ACE-I + diuretics for htn
Enhance antihypertensive efficacy of diuretics by increasing natriuresis Increased K+--> balance hypokalemia of diuretic
57
Nitrites and nitrates MOA
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
GOOD effects of nitrites
Decrease cardiac workload → Decreased preload and afterload *decreased myocardial oxygen requirement* is main mechanism by which angina is relieved
59
BAD effects of nitrites
Increased cardiac workload | → decreased blood pressure → baroreceptor reflex → increased HR and contractility → decreased diastolic perfusion time
60
Good effects of dihydropyridines for angina
Good: Coronary vasodilation→ relaxes vasospasms, some increased myocardial O2 Systemic arteriodilation→ decreased afterload
61
Bad effects of dihydropyridines for angina
enhanced development of MI | Rapid hypotension→ reflex sympathetic activation→ increased cardiac workload→ ischemic attack
62
Good effects of diltiazem and verapamil for angina
decreased cardiac workload Decreased myocardial contractility Decreased SA node automaticity and AV node conduction→ bradycardia
63
Bad effects of diltiazem and verapamil for angina
serious cardiac depression → Cardiac arrest → AV block → heart failure
64
CCBs MOA for angina
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
Beta blockers for angina
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
Ranolazone MOA
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
PDE5 is
the enzyme that metabolizes cGMP in the corpus cavernosum
68
Sildenafil, Vardenafil, Avanafil, Tadalafil MOA
Inhibit PDE5 | cGMP stays active longer, producing vasodilation
69
1st line for hyperlipidemia
dietary management | recheck cholesterol 1 month after losing weight
70
coronary or peripheral vascular disease familial hypercholesterolemia Familial hyperlipidemia 1st line
Medicate, dietary changes not 1st line
71
Statins MOA
Analogs of HMG-CoA reductase intermediate in mevalonate synthesis→ inhibit reductase→ increased high affinity LDL receptors in liver→ reduced plasma LDL
72
2 statins which have to be hydrolyzed to active form
Simvastatin | Lovastatin
73
Other effects of statins
``` CHD: decreased CRP Increased endothelial NO production Increased plaque stability Reduced lipoprotein oxidation Decreased platelet aggregation ```
74
Resins MOA
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
Niacin MOA
Inhibits VLDL secretion→ Lowered plasma VLDL and LDL | Also inhibits hepatic cholesterologenesis
76
Fibric acid derivatives/fibrates MOA
PPAR-alpha ligand (nuclear receptor) → upregulates LPL and other genes involved in fatty acid oxidation
77
Ezetimibe MOA
Selectively blocks intestinal absorption of cholesterol and related phytosterols
78
PCSK9 inhibitors MOA
Human monoclonal Antibodies which inhibit PCSK9 from binding to LDLR, bind, and promote LDL degradation
79
Quinidine MOA
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
Procainamide MOA
similar to quinidine
81
Lidocaine MOA
Blocks inactivated Na+ channels, fast binding and dissociation Preferentially affects damaged tissue→ more receptors are inactivated Blocks the “window” current → shortens APD
82
Flecainide MOA
Blocks all sodium channel states Slow dissociation from bingin No effect on ERP
83
3 beta blockers used as antiarrhythmatics
Propranolol: non-specific Acebutolol: B1 Esmolol: B1, short half life, IV only → 2nd line for acute treatment of PSVTs (paroxysmal supraventricular tachycardia)
84
Amiodarone MOA
``` Blocks K+ channels Other effects: BLocks Na+ channels (class I) B-blocker (class II) Some Ca+ channel blocking (Class IV) Alpha blocker ```
85
Sotalol MOA
K+ blocker→ prolongs duration of action potential | Non selective Beta blocker
86
Verapamil and Diltiazem as antiarrhythmatics
Block slow L-type cardiac Ca++ channels | Ca+ ONLY depolarizes atria→ CCBs only effective in atria
87
Adenosine MOA
Enhanced K+ conduction and inhibition of cAMP-induced Ca++ influx→ hyperpolarization→ heart “resets”
88
Magnesium MOA
unknown
89
Heparin MOA
Activity is dependent on antithrombin III Mainly affects Xa and thrombin + IXa, XIa, XIIa Pentasaccharide acts as a catalyst for antithrombin III
90
Protamine sulfate MOA
reverses heparin by competing for binding | Does not completely reverse enoxaparin, has no effect on fondaparinux
91
Fondaparinux is a
synthetic pentasaccharide
92
LMWH MOA
Similar to high molecular weight heparins except: | Main inhibition of Factor Xa (no thrombin)
93
Bivalirudin MOA
Highly specific direct inhibitor of thrombin (not AT III)
94
Argatroban MOA
thrombin inhibitor
95
Dabigatran MOA
thrombin inhibitor
96
Rivaroxaban MOA
inhibits factor Xa
97
Betrixaban MOA
inhibits factor Xa
98
Apixaban MOA
inhibits factor Xa
99
Edoxaban MOA
inhibits factor Xa
100
Andexxa MOA
a factor Xa decoy, reversal for direct factor Xa inhibitors
101
Warfarin MOA
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
Fibrinolytic agents (thrombolytic agents) MOA
Convert plasminogen to plasmin | Internal plasmin is protected→ lyses thrombus from within
103
Alteplase (tissue plasminogen activator/t-PA)
Higher activity for fibrin-bound plasminogen vs plasma plasminogen: “clot-selective”
104
Tenecteplase
Higher activity for fibrin-bound plasminogen vs plasma plasminogen: “clot-selective”
105
Urokinase
Directly activates plasminogen, not clot-fibrin specific→ generalized systemic fibrinolysis
106
Anstreplase=
streptokinase + plasminogen | off market
107
Aminocaproic acid MOA
Inhibit plasminogen activity
108
Tranexamic acid MOA
Inhibit plasminogen activity
109
Aspirin MOA
Irreversible inhibitor of Cyclooxygenase (COX) enzyme → Decreased TXA1 → decreased platelet aggregation
110
Abciximab MOA
Antibody | Inhibits GP IIb/IIIa receptors from binding fibrinogen→ decreased platelet aggregation
111
Eptifibatide MOA
analog of carboxy end of fibrinogen | Inhibit GP IIb/IIIa receptors from binding fibrinogen→ decreased platelet aggregation
112
Tirofiban MOA
analog of carboxy end of fibrinogen | Inhibit GP IIb/IIIa receptors from binding fibrinogen→ decreased platelet aggregation
113
Clopidogrel MOA
Irreversibly blocks ADP receptor on platelets→ decreased platelet aggregation
114
Ticlopidine MOA
Irreversibly blocks ADP receptor on platelets→ decreased platelet aggregation
115
Prasugrel MOA
Irreversibly blocks ADP receptor on platelets→ decreased platelet aggregation
116
Vorapaxar MOA
Antagonist of protease-activated receptor-1 (PAR-1): major thrombin receptor on human platelets

Unit 2 Pharm II (13 decks)

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