Jan8 M2-Edema and Diuretics Flashcards

(36 cards)

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)

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

25
K sparing diuretics 2 modes of action
block (nuclear) aldoR (a TF) so no enac channels made. (spironolactone) -block ENac channels (triamterine, amiloride)
26
how diuretics get to the tubular lumen usually
are secreted
27
why must increase diuretic dose if low GFR
to get more blood to peritubular capillaries and the vasa recta
28
why is there an upper limit to the dose of diuretic that should be given
maximum dose where transporter is completely inhibited exists. beyond that, no benefit and only side effects
29
limiting factor in loop diuretics
more Na is delivered (and therefore reabsorbed) distally
30
limiting factors in thiazides (2)
- they have unknown mechanisms to lower BP | - low Na reabso there
31
how to follow GFR in patients on diuretics
urea and Cr concentrations
32
big side effect of diuretics
renal failure
33
consequence of giving too much diuretics too fast
loss of IV volume is too big to be compensated: AKI (rise in urea and Cr), less tissue perfusion, drop in CO, etc.
34
rate of fluid removal in pulm edema, ascites and peripheral edema
all slow except pulm edema if hypoxic
35
why diuretics can cause hypokalemia
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
why diuretics can cause hyperuricemia
nephron compensates to reabso Na so more Na reabso in PCT and urea reabso linked to Na in PCT