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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
potassium-sparing diuretics: high, intermediate, or low efficacy?
low
25
potassium-sparing diuretics: two categories
aldosterone antagonists and sodium channel inhibitors
26
aldosterone antagonists: site of action
block the action of aldosterone on the collecting duct
27
sodium channel inhibitors: mechanism, site of action
inhibit the entry of sodium into the principal cells of the collecting duct, increases sodium excretion and reduces potassium excretion. inhibits sodium-potassium exchange
28
potassium-sparing diuretics: end result on excretion
increase the urinary excretion of sodium, chloride, and water
29
potassium-sparing diuretics: side effects (3)
hyperkalemia (use with care in patients with renal insufficiency), gynecomastia (spironolactone is a progesterone agonist), triamterene decreases renal blood flow and GFR
30
triamerene: effects on kidneys
decrease renal blood flow and GFR
31
potassium-sparing diuretics: therapeutic uses (4)
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
32
_____kalemia can be fatal, ______kalemia is rarely life-threatening
hyper, hypo
33
why are diuretics good for using in combination with other antihypertensive drugs like vasodilators?
they prevent salt and water retention and edema caused by other drugs
34
why are diuretics good for using in combination with other antihypertensive drugs like ACE inhibitors, ARBs, and renin inhibitors?
they enhance the antihypertensive activity of these drugs
36
why should diuretics be used in combination with other drugs when treating CHF?
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
what 2 cell types are important in venous thrombosis?
RBCs and fibrin
38
why are deep vein thromboses dangerous?
thrombi can embolize to the lungs and cause pulmonary infarction
39
what cell type is important in arterial thrombosis?
platelets
40
anticoagulants: 3 types
anticoagulants, "clot-busters" (fibrinolytic agents), antiplatelet drugs
41
coagulation cascade: 3 steps
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
how does thrombin promote platelet aggregation? (2)
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
why can't heparin be orally administered?
it's too large and too negatively-charged
44
heparin: mechanism of action
binds to antithrombin, causing a conformational change, which allows 10a and thrombin to bind better and become inactivated
45
what is antithrombin?
a suicide substrate for a number of different activated coagulation factors, especially factor 10a and thrombin
46
what is the difference between heparin and low molecular weight heparin?
heparin helps antithrombin inactivate both thrombin and factor 10a. LMWHs can only inactivate factor 10a
47
can heparin be used in pregnancy?
yes, it does not cross the placental barrier
48
what is the antagonist for heparin?
protamine sulfate
49
anticoagulants: contraindications (3)
active bleeding, severe uncontrolled hypertension, recent surgery of eye, brain, spinal cord
50
what is the drug of choice for anticoagulation during pregnancy?
heparin
51
heparin: therapeutic uses (4)
DVT, pulmonary embolism, unstable angina, acute MI
52
direct thrombin inhibitor
lepirudin
53
lepirudin: mechanism, therapeutic use
inactivates thrombin by blocking the substrate binding site, alternative to heparin in patients who have had heparin-induced thrombocytopenia
54
protamine sulfate
heparin antagonist
55
warfarin: analog of what?
vitamin K
56
role of vitamin K in clotting process
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
what enzyme is responsible for vitamin K recycling?
VKORC1
58
warfarin: mechanism
blocks VKORC1, prevents vitamin K recycling
59
what enzyme metabolizes warfarin?
CYP2C9
60
what can weaken the effects of warfarin?
administration of vitamin K (due to competitive inhibition)
61
how long does it take to start seeing therapeutic effects of warfarin? why does it take so long?
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
can warfarin be used during pregnancy?
no, it can cross the placenta and is teratogenic
63
what will happen when patients with CYP2C9 polymorphisms take warfarin?
they will have increased chance of bleeding
64
why is it important to monitor patients taking warfarin?
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
warfarin: therapeutic uses
long-term treatment, prevent thromboembolism, more prophylactic and not used for immediate treatment
66
dabigatran: what does it inhibit?
thrombin, both fibrin-bound and free
67
dabigatran: advantages over warfarin
predictable pharmacokinetics, rapid onset via oral administration, short half-life, not a substrate for P450, less risk of bleeding
68
dabigatran: disadvantages
no antidote, causes GI upset, can't be used in patients with prosthetic heart valves
69
dabigatran: therapeutic uses (2)
patients with nonvalvular atrial fibrillation at risk for stroke or systemic embolism, prophylaxis in patients with knee or hip replacement
70
what is enoxaparin?
a LWMH
71
enoxaparin: mechanism
binds to heparin-binding site of antithrombin and increases the affinity for factor 10a
72
enoxaparin/LMWHs: advantages over heparin
less risk of bleeding, absorbed more uniformly, longer half-life
73
rivaroxaban
direct factor 10a inhibitor
74
why is it useful to inhibit factor 10a?
one molecule of 10a generates approximately 1000 molecules of thrombin
75
rivaroxaban: mechanism
inhibits both free factor 10a and factor 10a in a clot
76
rivaroxaban: therapeutic uses (2)
patients with nonvalvular atrial fibrillation at risk for stroke or systemic embolism, prophylaxis in patients with knee or hip replacement
77
what is the role of t-Pa in fibrinolysis?
converts plasminogen to plasmin which digests fibrin
78
alteplase
recombinant t-Pa
79
how does low dose aspirin inhibit platelet aggregation and prevent MI?
it irreversibly binds COX-1 in platelets and inhibits formation of thromboxane
80
clopidogrel: mechanism
block ADP inhibitor and prevent platelet aggregation
81
abciximab: mechanism
prevents binding of fibrinogen and other adhesive molecules to the receptor

Pharmacology (6 decks)

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