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Cardio exam 1 > Diuretics lecture > Flashcards

Diuretics lecture Flashcards

1
Q

arterial BP=

A

cardiac output and peripheral vascular resistance

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2
Q

cardiac output depends on:

A

myocardial contractility & ventricular filling pressure

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3
Q

ventricular filling pressure depends on:

A

blood volume and venous tone

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4
Q

vascular resistance depends on:

A

state of SMC (contracted/relaxed) and activity of systems that control the diameter

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5
Q

blood volume is the primary target of

A

diuretics- by decreasing blood volume

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6
Q

main function of the kidneys:

A

maintain normal body fluid volume & electrolyte balance

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7
Q

filtration rate under normal conditions

A

~120ml/min

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8
Q

how much of the filtered fluid & electrolytes are reabsorbed?

A

~99%

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9
Q

urine output rate:

A

1ml/min

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10
Q

what is the basic urine-forming unit?

A

the nephron

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11
Q

what part of the nephron deals with filtration?

A

glomerulus

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12
Q

what part of the nephron deals with reabsorption & conditioning?

A

tubule

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13
Q

what supplies blood to the nephron

A

afferent arteriol

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14
Q

what removes blood from the nephron

A

efferent arteriole

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15
Q

where is reabsorption the greatest?

A

proxima; tubule & declines distally toward collecting duct

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16
Q

how much Na is reabsorbed in the proximal tubule?

A

65%

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17
Q

how much Na is reabsorbed in the loop of Henle?

A

25%

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18
Q

how much Na is reabsorbed in the early distale tubule & distal convoluted tubule?

A

5%

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19
Q

what is a major determinant of extracellular fluid volume?

A

NaCl

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20
Q

diuretics increase the rate of urine flow and:

A

NaCl excretion (& water)

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21
Q

diuretics initial effects

A

incr. NaCl excretion-> decr. extracellular fluid volume-> decr. venous return-> decr. cardiac output-> decr. BP

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22
Q

diuretics chronic effects

A

incr. NACL excretion-> decr. extracellular volume-> stimulation of compensatory mechanisms-> decr. NaCl excretion & fluid volume returns to initial level-> dcr. peripheral resistance-> BP remains lowered due to VASODILATION

23
Q

chronic BP-lowering effect of diuretics is

A

vasodilation!

24
Q

initial BP-lowering effect of diuretics

A

due to Na excretion & decr. fluid volume

25
Q

loop diuretics act where?

A

thick ascending loop of Henle

26
Q

MOA of loop diuretics

A

inhibition of Na/K/Cl sympoter

27
Q

loop diuretic ion effects

A

inhibited reabsorption of Na, K, Cl

indirect disrupted reabsorption of Ca and Mg

28
Q

under normal conditions what is the potential on the kidney side?

A

negative potential

29
Q

what causes the reduced reabsorption of Ca and Mg with lop diuretics?

A

change in potential on the renal side- blocking transporter causes potential to become more positive & pull over less Ca and Mg

30
Q

ACUTE affect of loop diuretics on uric acid

A

increased excretion

31
Q

CHRONIC affect of loop diuretic on uric acid

A

decreased excretion

32
Q

main urinary & hemodynamic effects of loop diuretics

A
  1. great incr. in urine

2. volume depletion & decr. BP (initially) followed by stimulation of renin release & SNS due to low Na

33
Q

main therapeutic uses for loop diuretics

A

acute pulmonary edema, HTN & HF, edemas & ascites, drug over dose, hypercalcemia

34
Q

main ADE of loop diuretics

A
  1. fluid/electrolyte imbalance (hypo-Na, hypo-Cl, hypo-K, hypo-Mg, hypo-Ca)
  2. ototoxicity
  3. hyperuricemia & hyperglycemia
  4. may incr. LDL & decr. HDL
35
Q

most potent loop diuretic

A

bumetanide (Bumex)

36
Q

thiazide diuretics act where?

A

distal convoluted tubule

37
Q

MOA of thiazide diuretics

A

inhibition of Na/Cl symporter

38
Q

main urinary & hemodynamic effects of thiazide diuretics

A
  1. mod. increase in urine flow

2. lower BP due to incr. Na excretion

39
Q

How does chronic use of thiazide diuretics effect Ca and uric acid?

A

decrease excretion

40
Q

difference in loop and thiazide diuretics

A

K excretion is incre. INDIRECTLY with thiazide diuretics

41
Q

main therapeutic uses of thiazide diuretics

A

HTN, edema, nephrogenic diabetes insipidus, Ca nephrolithiasis,

42
Q

effect of thiazides is altered when

A

GFR is <35mL/min

except with memtolazone & indapamide

43
Q

main ADE of thiazides

A
  1. fluid/electrolyte disturbances (hypotension, hypo-Na, hypo-Cl, hypo-K, hyper-Ca, hypo-MG, hyperuricemia)
  2. < glucose tolerance
  3. sexual impotency
  4. incr. LDL, TC and TG
44
Q

most potent thiazide

A

indapamide (lozol)

45
Q

where do potassium-sparing diuretics act?

A

last distal tubule & collecting duct

46
Q

MOA of K-sparing diuretics

Na-channel blockers

A

inhibition of renal epithelial Na channels-> decr. Na reabsorption-> K (& H) is NOT excreted into the lumen in exchange

47
Q

what cell does K-sparing diuretics act on?

Na-channel blockers

A

principle cells

48
Q

main urinary effects of K-sparing diuretics

Na-channel blockers

A

slight incr. in urine flow (slight incr. excretion of Na, Cl, decr. excretion of K (&H))

49
Q

main ADE of K-sparing diuretics

Na-channel blockers

A

Hyper-K

triamterene can < glucose intolerance & cause photosensitization

50
Q

aldosterone normal actions

A

inc. retension of Na & increase excretion of K (&H)

51
Q

MOA of K-sparing diuretics

aldosterone antagonists

A

inhibition of aldosterone binding to its receptors-> decr. Na reabsorption-> K is not excreted

52
Q

cells that K-sparing diuretics act on

aldosterone antagonist

A

intercalated cells

53
Q

main therapeutic uses of K-sparing diuretics

- both kinds

A

used with other diuretics to spare K, HF, spironolactone in 1* & 2* hyperaldosteronism & hepatic cirrhosis

54
Q

main ADE of K-sparing diuretics

A

hyper-K (incr. risk of arrhythmias), spironolactone may cause gynecomastia, sexual impotency, decreased libido & alter clearance of digitalis glycosides

Cardio exam 1 (12 decks)

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