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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
loop diuretics act where?
thick ascending loop of Henle
26
MOA of loop diuretics
inhibition of Na/K/Cl sympoter
27
loop diuretic ion effects
inhibited reabsorption of Na, K, Cl | indirect disrupted reabsorption of Ca and Mg
28
under normal conditions what is the potential on the kidney side?
negative potential
29
what causes the reduced reabsorption of Ca and Mg with lop diuretics?
change in potential on the renal side- blocking transporter causes potential to become more positive & pull over less Ca and Mg
30
ACUTE affect of loop diuretics on uric acid
increased excretion
31
CHRONIC affect of loop diuretic on uric acid
decreased excretion
32
main urinary & hemodynamic effects of loop diuretics
1. great incr. in urine | 2. volume depletion & decr. BP (initially) followed by stimulation of renin release & SNS due to low Na
33
main therapeutic uses for loop diuretics
acute pulmonary edema, HTN & HF, edemas & ascites, drug over dose, hypercalcemia
34
main ADE of loop diuretics
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
most potent loop diuretic
bumetanide (Bumex)
36
thiazide diuretics act where?
distal convoluted tubule
37
MOA of thiazide diuretics
inhibition of Na/Cl symporter
38
main urinary & hemodynamic effects of thiazide diuretics
1. mod. increase in urine flow | 2. lower BP due to incr. Na excretion
39
How does chronic use of thiazide diuretics effect Ca and uric acid?
decrease excretion
40
difference in loop and thiazide diuretics
K excretion is incre. INDIRECTLY with thiazide diuretics
41
main therapeutic uses of thiazide diuretics
HTN, edema, nephrogenic diabetes insipidus, Ca nephrolithiasis,
42
effect of thiazides is altered when
GFR is <35mL/min | except with memtolazone & indapamide
43
main ADE of thiazides
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
most potent thiazide
indapamide (lozol)
45
where do potassium-sparing diuretics act?
last distal tubule & collecting duct
46
MOA of K-sparing diuretics | Na-channel blockers
inhibition of renal epithelial Na channels-> decr. Na reabsorption-> K (& H) is NOT excreted into the lumen in exchange
47
what cell does K-sparing diuretics act on? | Na-channel blockers
principle cells
48
main urinary effects of K-sparing diuretics | Na-channel blockers
slight incr. in urine flow (slight incr. excretion of Na, Cl, decr. excretion of K (&H))
49
main ADE of K-sparing diuretics | Na-channel blockers
Hyper-K | triamterene can < glucose intolerance & cause photosensitization
50
aldosterone normal actions
inc. retension of Na & increase excretion of K (&H)
51
MOA of K-sparing diuretics | aldosterone antagonists
inhibition of aldosterone binding to its receptors-> decr. Na reabsorption-> K is not excreted
52
cells that K-sparing diuretics act on | aldosterone antagonist
intercalated cells
53
main therapeutic uses of K-sparing diuretics | - both kinds
used with other diuretics to spare K, HF, spironolactone in 1* & 2* hyperaldosteronism & hepatic cirrhosis
54
main ADE of K-sparing diuretics
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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