Renal II Flashcards

1
Q

fanconi syndrome

A

defect PCT

increased excretion AAs, glucose, HCO3, P

hereditary defect, ischemia, multi myeloma, nephrotoxin, lead poisoning

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2
Q

bartter syndrome

A

reabsorption defect in thick ascending loop henle

auto recessive
-affect Na/K.2Cl cotranspoter

get hypoK, alkalosis and hyperCa

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3
Q

gitelman syndrome

A

defect NaCl reabsorption in DCT

auto rec

hypoK, hypoMg, metabolic alkalosis, hypoCa

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4
Q

liddle syndrome

A

GOF mutation

  • increased Na reabsorption in collecting tubule
  • ENaC upregulation

auto dom

get HTN, hypoK, metabolic alkalosis, decreased aldosterone

tx - amiloride

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5
Q

syndrome apparent mineralocorticoid excess

A

hereditary deficiency - 11B hydroxysteroid DH

no cortisol > cortisone in mineralocorticosteroid receptor cells

cortisol - act on mineralocorticoid receptor

  • HTN, hypoK, metabolic alkalosis
  • low serum aldosterone

can get from licorice - block 11B hydroxysteroid DH

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6
Q

11B hydroxysteroid DH

A

conversion of cortisol > cortisone

stop cortisol from acting on mineralocorticoid receptor

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7
Q

TF/P

A

tubular fluid / plasma

greater than 1 - solute reabsorbed less quickly than water
equal to 1 - solute and water same rate
less than 1 - solute reabsorbed faster than water

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8
Q

net secretion

A

PAH

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9
Q

stimulus renin release

A

hypotension - to JG cell
low Na - to macula densa
increased sympathetic - B1

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10
Q

ANG II activity

A

AT1 receptor - vasc smooth m - vasoconstriction

constrict efferent arteriole glomeruli - preserve GFR low volume

aldosterone increase

ADH increase

increased PCT Na/H activity - contraction alkalosis

stimulate hypothalamus - thirst

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11
Q

aldosterone K and H effect

A

principal cells - K channels

a-intercalated cells - H+ ATPase

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12
Q

ANP/BNP

A

response to high volume - HTN

check on RAAS

relax vasc smooth m - cGMP - increased GFR

decreased renin

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13
Q

JG apparatus

A

mesangial cells
JG cells - smooth m of afferent arteriole
macula densa - NaCl sensor - DCT

JG cell - secrete renin

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14
Q

stimulus of JG cells

A

low blood pressure

Beta 1 sympathetic

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15
Q

macula densa cells

A

sense low NaCl to DCT

release adenosine

vasoconstriction

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16
Q

EPO

A

released from kidney

interstitial cells in peritubular cap bed - response to hypoxia

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17
Q

1-a hydroxylase

A

from PCT of kidney

convert 25 vit D to 1,25 vit D

18
Q

NSAID and renal failure

A

block renal protective PG synthesis

constriction of afferent arteriole and decreased GFR

19
Q

mechanism of ANP

A

increased GFR
increased Na filtration - no net absorption

result in Na loss and volume loss

20
Q

mechanism of PTH

A

secreted with low Ca, high P, or low 1,25 vit D

cause increases Ca reabsorption DCT
decreased P reabsorption PCT
increased vit D 1,25 production

and increased Ca and P reabsorption from gut (via vit D)

21
Q

potassium with acidosis

A

shift K out of cell and H into cell

22
Q

potassium with alkalosis

A

shift K into cell and H out of cell

23
Q

Na/K ATPase

A

shift Na out of cell and K out cell

increased with B-agonist and insulin
-get hypoK

decreased with digitalis
-get hyperK

24
Q

hypoK

A

U wave
flat T waves

arrhythmia
muscle spasm

25
Q

hypoCa

A

tetany
seizure
QT prolongation

26
Q

hypoMg

A

tetany
torsades
hypoK

27
Q

hypoP

A

bone loss, osteomalacia, rickets

28
Q

hyperK

A

wide QRS
peaked T wave

arrhythmia
muscle weakness

29
Q

hyperCa

A

stone, bones, groans, thrones, psych overtones

renal stones
bone pain
abdominal pain
urinary frequency
depression, anxiety
30
Q

hyperMg

A
low DTR
lethargy
bradycardia
hypotension
hypoCa
31
Q

hyperP

A

renal stone
metastatic calcifications
hypoCa

32
Q

acid base physiology

A

low pH and low PCO2 - metabolic acidosis

low pH and high PCO2 - respiratory acidosis

33
Q

winters formula

A

determine predicted PCO2
-suggest mixed acid base disorder

PCO2 = 1.5 [HCO3] + 8 (+/-2)

34
Q

anion gap

A

anion gap = Na - (Cl + HCO3)

high - MUDPILES
normal - HARDASS

35
Q

MUDPILES

A

high anion gap metabolic acidosis

methanol
uremia
DKA
propylene glycol
iron tabs or isoniazid
lactic acidosis
ethylene glycol
salicylates
36
Q

HARDASS

A

nomal anion gap metabolic acidosis

hyperalimentation
addison disease
renal tubular acidosis
diarrhea
acetazolamide
spironolactone
saline infusion
37
Q

metabolic alkalosis with compensation

A

compensation - hypoventilation

loop/thiazide use
vomiting
antacid use
hyperaldosterone

38
Q

type 1 renal tubular acidosis

A

urine pH >5.5

defect a-intercalated cells secrete H (collecting duct)
-no HCO3 generated

with hypokalemia

risk of Ca-P kidney stone - bc alkaline urine

cause - amphotericin B, analgesis nephropathy, urinary tract obstruction

39
Q

type 2 renal tubular acidosis

A

urine pH

40
Q

type 4 renal tubular acidosis

A

hypoaldosteronism

  • hyperK
  • decreased NH3 synthesis PCT - more NH4 excretion

low aldosterone - diabetic hyporeninism, ACE I, ARB, NSAID, heparin, cyclosporine, adrenal insufficient

or aldosterone resistance