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Pharmacology > Block 2: Diuretics and Anticoagulants > Flashcards

Block 2: Diuretics and Anticoagulants Flashcards

0
Q

where in the kidney is the 2nd most sodium reabsorbed?

A

ascending limb of the loop of henle

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1
Q

where in the kidney is the most sodium reabsorbed?

A

proximal tubule

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2
Q

where in the kidney is the potassium secreted?

A

distal tubule and collecting duct

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3
Q

fenoldopam and aldosteron: therapeutic use

A

only in hypertensive crisis and shock

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4
Q

dopamine/dopamine agonists: mechanism, therapeutic use

A

increase renal blood flow and produces peripheral vasoconstriction
use: increase renal blood flow in shock

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5
Q

what is fenoldopam?

A

a DA1 agonist (dopamine receptor agonist)

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6
Q

name 3 loop diuretics

A

furosemide, bumetanide, ethacrynic acid

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7
Q

loop diuretics: high, intermediate, or low efficacy?

A

high

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8
Q

loop diuretics: ______ onset, ______ duration of action

A

rapid, short

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9
Q

loop diuretics: mechanism, site of action

A

inhibits Na-K-Cl symporter, increases excretion of sodium, potassium, chloride, and water, acts on cortical AND medllary segments of the ascending loop of Henle

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10
Q

loop diuretics: effects on kidney

A

increase renal blood flow and GFR

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11
Q

loop diuretics: side effects (6)

A

hypokalemia, alkalosis, hypovolemia, hyperuricemia, hyperglycemia (furosemide only), ototoxicity

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12
Q

loop diuretics: therapeutic uses

A
  1. edema of cardiac, hepatic, or renal origin

2. acute pulmonary edema

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13
Q

why are loop diuretics good for treating edema associated with renal disease?

A

because they increase renal blood flow and GFR

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14
Q

name 3 thiazide and thiazide-like diuretics

A

chlorothiazide, hydrochlorothiazide, metolazone

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15
Q

thiazide and thiaizide-like diuretics: high, intermediate, or low efficacy?

A

intermediate

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16
Q

thiazide and thiazide-like diuretics: ______ onset, ______ duration of action

A

moderate, long

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17
Q

thiazide and thiazide-like diuretics: mechanism, site of action

A

inhibits Na-Cl symporter, increases excretion of sodium, potassium, chloride, and water, acts on cortical segment of ascending loop of Henle

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18
Q

what happens to urine when patient is on thiazide or thiazide-like diuretics and why?

A

it is hypertonic because these drugs impair the kidney’s ability to produce a dilute urine

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19
Q

thiazide or thiazide-like diuretics: effects on kidney

A

reduce GFR

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20
Q

thiazide or thiazide-like diuretics: side effects (5)

A

hypokalemia, alkalosis, hyperuricemia, hyperglycemia, reduces GFR

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21
Q

thiazide or thiazide-like diuretics: therapeutic uses (2)

A
  1. edema due to CHF

2. hypertension

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22
Q

name 4 potassium sparing diuretics

A

spironolactone, eplerenone, triamterene, amiloride

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23
Q

name 2 sodium channel inhibitors

A

triamterene and amiloride

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24
Q

potassium-sparing diuretics: high, intermediate, or low efficacy?

A

low

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25
Q

potassium-sparing diuretics: two categories

A

aldosterone antagonists and sodium channel inhibitors

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26
Q

aldosterone antagonists: site of action

A

block the action of aldosterone on the collecting duct

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27
Q

sodium channel inhibitors: mechanism, site of action

A

inhibit the entry of sodium into the principal cells of the collecting duct, increases sodium excretion and reduces potassium excretion. inhibits sodium-potassium exchange

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28
Q

potassium-sparing diuretics: end result on excretion

A

increase the urinary excretion of sodium, chloride, and water

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29
Q

potassium-sparing diuretics: side effects (3)

A

hyperkalemia (use with care in patients with renal insufficiency), gynecomastia (spironolactone is a progesterone agonist), triamterene decreases renal blood flow and GFR

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30
Q

triamerene: effects on kidneys

A

decrease renal blood flow and GFR

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31
Q

potassium-sparing diuretics: therapeutic uses (4)

A

hypertension, edema, used in combination with thiazide or loop diuretic to enhace diuretic effect without potassium loss, aldosterone antagonists are used to improve survival in CHF

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32
Q

_____kalemia can be fatal, ______kalemia is rarely life-threatening

A

hyper, hypo

33
Q

why are diuretics good for using in combination with other antihypertensive drugs like vasodilators?

A

they prevent salt and water retention and edema caused by other drugs

34
Q

why are diuretics good for using in combination with other antihypertensive drugs like ACE inhibitors, ARBs, and renin inhibitors?

A

they enhance the antihypertensive activity of these drugs

36
Q

why should diuretics be used in combination with other drugs when treating CHF?

A

they do not improve survival in CHF, only reduce symptoms. they should be used in combination with other drugs that do improve survival (like ACE inhibitors, ARBs, or aldosterone antagonists)

37
Q

what 2 cell types are important in venous thrombosis?

A

RBCs and fibrin

38
Q

why are deep vein thromboses dangerous?

A

thrombi can embolize to the lungs and cause pulmonary infarction

39
Q

what cell type is important in arterial thrombosis?

A

platelets

40
Q

anticoagulants: 3 types

A

anticoagulants, “clot-busters” (fibrinolytic agents), antiplatelet drugs

41
Q

coagulation cascade: 3 steps

A
  1. activation of factor 10 to 10a
  2. activated 10a converts prothrombin into thrombin
  3. thrombin converts fibrinogen to fibrin which involves the conversion of factor 8 to 8a (causes cross-linking of fibrin)
42
Q

how does thrombin promote platelet aggregation? (2)

A
  1. by binding to receptors on platelets and causing a conformational change that activates a G protein
  2. activates factors 5 and 8, both needed to convert prothrombin to thrombin
43
Q

why can’t heparin be orally administered?

A

it’s too large and too negatively-charged

44
Q

heparin: mechanism of action

A

binds to antithrombin, causing a conformational change, which allows 10a and thrombin to bind better and become inactivated

45
Q

what is antithrombin?

A

a suicide substrate for a number of different activated coagulation factors, especially factor 10a and thrombin

46
Q

what is the difference between heparin and low molecular weight heparin?

A

heparin helps antithrombin inactivate both thrombin and factor 10a. LMWHs can only inactivate factor 10a

47
Q

can heparin be used in pregnancy?

A

yes, it does not cross the placental barrier

48
Q

what is the antagonist for heparin?

A

protamine sulfate

49
Q

anticoagulants: contraindications (3)

A

active bleeding, severe uncontrolled hypertension, recent surgery of eye, brain, spinal cord

50
Q

what is the drug of choice for anticoagulation during pregnancy?

A

heparin

51
Q

heparin: therapeutic uses (4)

A

DVT, pulmonary embolism, unstable angina, acute MI

52
Q

direct thrombin inhibitor

A

lepirudin

53
Q

lepirudin: mechanism, therapeutic use

A

inactivates thrombin by blocking the substrate binding site, alternative to heparin in patients who have had heparin-induced thrombocytopenia

54
Q

protamine sulfate

A

heparin antagonist

55
Q

warfarin: analog of what?

A

vitamin K

56
Q

role of vitamin K in clotting process

A

clotting factors must be carboxylated to become functional. for this to happen, vitamin K needs to be oxidixed. once vitamin K is oxidized, it needs to be recycled back to the reduced form so you can continue to synthesize more clotting factors

57
Q

what enzyme is responsible for vitamin K recycling?

A

VKORC1

58
Q

warfarin: mechanism

A

blocks VKORC1, prevents vitamin K recycling

59
Q

what enzyme metabolizes warfarin?

A

CYP2C9

60
Q

what can weaken the effects of warfarin?

A

administration of vitamin K (due to competitive inhibition)

61
Q

how long does it take to start seeing therapeutic effects of warfarin? why does it take so long?

A

48 hours, because when you give warfarin you still have active clotting factors present, and warfarin does not affect the clotting factors that have already been formed

62
Q

can warfarin be used during pregnancy?

A

no, it can cross the placenta and is teratogenic

63
Q

what will happen when patients with CYP2C9 polymorphisms take warfarin?

A

they will have increased chance of bleeding

64
Q

why is it important to monitor patients taking warfarin?

A

warfarin has a very narrow therapeutic window, too little there is risk for a clot and too much there is increased risk of bleeding

65
Q

warfarin: therapeutic uses

A

long-term treatment, prevent thromboembolism, more prophylactic and not used for immediate treatment

66
Q

dabigatran: what does it inhibit?

A

thrombin, both fibrin-bound and free

67
Q

dabigatran: advantages over warfarin

A

predictable pharmacokinetics, rapid onset via oral administration, short half-life, not a substrate for P450, less risk of bleeding

68
Q

dabigatran: disadvantages

A

no antidote, causes GI upset, can’t be used in patients with prosthetic heart valves

69
Q

dabigatran: therapeutic uses (2)

A

patients with nonvalvular atrial fibrillation at risk for stroke or systemic embolism, prophylaxis in patients with knee or hip replacement

70
Q

what is enoxaparin?

A

a LWMH

71
Q

enoxaparin: mechanism

A

binds to heparin-binding site of antithrombin and increases the affinity for factor 10a

72
Q

enoxaparin/LMWHs: advantages over heparin

A

less risk of bleeding, absorbed more uniformly, longer half-life

73
Q

rivaroxaban

A

direct factor 10a inhibitor

74
Q

why is it useful to inhibit factor 10a?

A

one molecule of 10a generates approximately 1000 molecules of thrombin

75
Q

rivaroxaban: mechanism

A

inhibits both free factor 10a and factor 10a in a clot

76
Q

rivaroxaban: therapeutic uses (2)

A

patients with nonvalvular atrial fibrillation at risk for stroke or systemic embolism, prophylaxis in patients with knee or hip replacement

77
Q

what is the role of t-Pa in fibrinolysis?

A

converts plasminogen to plasmin which digests fibrin

78
Q

alteplase

A

recombinant t-Pa

79
Q

how does low dose aspirin inhibit platelet aggregation and prevent MI?

A

it irreversibly binds COX-1 in platelets and inhibits formation of thromboxane

80
Q

clopidogrel: mechanism

A

block ADP inhibitor and prevent platelet aggregation

81
Q

abciximab: mechanism

A

prevents binding of fibrinogen and other adhesive molecules to the receptor

Pharmacology (6 decks)

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