Jan8 M2-Edema and Diuretics Flashcards

1
Q

2 components to edema pathophysiology

A
  1. alteration in capillary hemodynamics favoring Na and water mvmt to interstitium
  2. renal retention of dietary Na and water with ECF expansion
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2
Q

2 components to edema pathophysiology

A
  1. alteration in capillary hemodynamics favoring Na and water mvmt to interstitium
  2. renal retention of dietary Na and water with ECF expansion
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3
Q

example of cause of edema

A

low oncotic pressure (ex. loss of albumin in nephrotic syndrome)

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4
Q

example of cause of edema related to lymphatics drainage

A

lymph node infection, blockage, breast cancer surgery

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5
Q

example of cause of edema related to high capillary hydrostatic pressure

A

rise in venous pressure

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6
Q

urine protein and urine Na in nephrotic syndrome and why

A

above 3g protein/day

less than 15 meq/L U Na (holding on to Na)

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7
Q

hormones activated in nephrotic syndrome and why

A
  • RAAS because low IV volume so low renal perfusion (renin activated)
  • ADH (low IV volume)
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8
Q

condition where Na retention, edema and RAAS and ADH always active and why

A

CHF. low CO = sensed hypovolemia, state of volume contraction

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9
Q

what hormones act on the kidney in CHF

A
  • NE and AT2 for proximal Na reabso
  • ADH distally
  • aldo distally
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10
Q

example of cause of edema

A

low oncotic pressure (ex. loss of albumin in nephrotic syndrome)

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11
Q

example of cause of edema related to lymphatics drainage

A

lymph node infection, blockage, breast cancer surgery

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12
Q

example of cause of edema related to high capillary hydrostatic pressure

A

rise in venous pressure

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13
Q

urine protein and urine Na in nephrotic syndrome and why

A

above 3g protein/day

less than 15 meq/L U Na (holding on to Na)

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14
Q

hormones activated in nephrotic syndrome and why

A
  • RAAS because low IV volume so low renal perfusion (renin activated)
  • ADH (low IV volume)
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15
Q

condition where Na retention, edema and RAAS and ADH always active and why

A

CHF. low CO = sensed hypovolemia, state of volume contraction

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16
Q

what hormones act on the kidney in CHF

A
  • NE and AT2 for proximal Na reabso
  • ADH distally
  • aldo distally
17
Q

SV as fct ov LVEDP curves: how does it change in heart failure and how kidney can change it

A

curve drops. lower SV for a same LVEDP. kidney retains water and sodium so increases it and moves the curve up

18
Q

why K sparing diuretics called like that

A

because don’t cause hypoK

19
Q

ascites in what disease and why

A

fibrotic liver so blood coming from splanchnic circulation is turned away and liver loses serous fluid in peritoneal cavity

20
Q

where to look for edema

A

feet, hands, face, around the eyes, pulmonary, abdomen

21
Q

normal urine output (per 8 hour shift)

A

300-400 cc

22
Q

if notice edema, next step in physical exam

A

weigh the patient

23
Q

limiting factors in thiazides (2)

A
  • they have unknown mechanisms to lower BP

- low Na reabso there

24
Q

thiazide used for what condition

A

BP control

25
Q

K sparing diuretics 2 modes of action

A

block (nuclear) aldoR (a TF) so no enac channels made. (spironolactone)
-block ENac channels (triamterine, amiloride)

26
Q

how diuretics get to the tubular lumen usually

A

are secreted

27
Q

why must increase diuretic dose if low GFR

A

to get more blood to peritubular capillaries and the vasa recta

28
Q

why is there an upper limit to the dose of diuretic that should be given

A

maximum dose where transporter is completely inhibited exists. beyond that, no benefit and only side effects

29
Q

limiting factor in loop diuretics

A

more Na is delivered (and therefore reabsorbed) distally

30
Q

limiting factors in thiazides (2)

A
  • they have unknown mechanisms to lower BP

- low Na reabso there

31
Q

how to follow GFR in patients on diuretics

A

urea and Cr concentrations

32
Q

big side effect of diuretics

A

renal failure

33
Q

consequence of giving too much diuretics too fast

A

loss of IV volume is too big to be compensated: AKI (rise in urea and Cr), less tissue perfusion, drop in CO, etc.

34
Q

rate of fluid removal in pulm edema, ascites and peripheral edema

A

all slow except pulm edema if hypoxic

35
Q

why diuretics can cause hypokalemia

A

more Na flow to the distal nephron (CT and CD) so more entry in ENac channels and consequent secretion of K from K channels

36
Q

why diuretics can cause hyperuricemia

A

nephron compensates to reabso Na so more Na reabso in PCT and urea reabso linked to Na in PCT