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Renal 2 > Electrolyte Pathophysiology > Flashcards

Electrolyte Pathophysiology Flashcards

1
Q

diuretics and potassium

A

increased distal Na delivery + increased aldo secretion (vol depletion) leads to hypokalemia

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2
Q

K loss in diarrhea

A

lose a lot more than vomiting

metabolic acidosis

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3
Q

hypokalemia treatment

A
  1. acute - replace w KCl
  2. chronic - K sparing diuretic
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4
Q

K loss in vomiting

A

mostly HCl - low K loss

metabolic alkalosis

**major is urinary loss

To excrete excess HCO3, bicarbonate travels with a cation (sodium) through the tubules. This increases distal delivery of sodium which leads to more potassium excretion in the urine.

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5
Q

signs of ECFV depletion

A

hypotension

orthostatsis

decreased skin turgor

tenting of skin

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6
Q

Limit of hyperkalemia

A

5.5 mEq/L

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7
Q

leukocytosis

A

fragile leukemic lyphocytes

K elevated in both serum and plasma

draw in blood gas syringe, no shaking!

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8
Q

hyperkalemia EKG changes 7.0 and u

A

widened QRS

sine wave

bradycardia

VT

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9
Q

main regulators of K excretion

A
  1. aldo
  2. distal Na delivery
  3. K intake
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10
Q

aldosterone paradox

A

how does the same hormone cause different effects?

in hypovolemia - increase Na reabsorpotion (no change in K)

in hyperkalemia - K+ secretion - no significant salt retention

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11
Q

pseudohyperkalemia

A

RBC damage during blood draw

fist clenching during blood draw

thrombocytosis or leukocytosis

no intervention needed, not dangerous. High potassium levels seen on blood tests RBC damage can happen with poor blood drawing technique. Lysed RBCs release potassium. “Hemolysis” is often noted on blood tests and redraws are necessary. These usually happen as isolated incidents in patients who haven’t started new medications (that can cause hyperkalemia). Thrombocytosis and leukocytosis - high platelets can lead to pseudohyperkalemia because their membranes are more fragile and able to lyse and release potassium. Redraws won’t help here, you’ll have the same problem. A rare genetic condition can lead to high potassium levels called Familial Pseudohyperkalemia.

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12
Q

first step in hyperkalemia

A

repeat serum potassium!!

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13
Q

Hyperkalemic EKG changes at 5.5

A

tall peaked T waves (larger than R in more than one lead)

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14
Q

plasmin

A
  • There is evidence that plasmin in nephrotic urine activates the epithelial Na channel to lead to Na retention
  • Plasmin is a protease and there is a part of ENaC in the lumen that is a substrate of plasmin activity
  • Plasmin then breaks the molecule off of the lumen and activates ENaC
  • It is possible that protein in the lumen of the kidney activates ENaC and ENaC leads to Na reabsorption
  • This is blockable by amiloride
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15
Q

major causes of hyperkalemia

A
  1. excessive intake
  2. extracellular leak (no insulin, dig, cell lysis from trauma)
  3. decreased renal excretion (adrenal insufficiency, HF, meds)
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16
Q

hypokalemic periodic paralysis

A

intermittent attacks of muscle weakness assocoated w hypokalemia (shift into cells) during overstim of Na/K ATPase

triggered by large carb meals or strenuous exercise

autosomal dom or with thyrotoxicis s

high carb meal and leak of K

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17
Q

Liddle’s syndrome

A

GOF of ENAC

HTN

Hypokalemia

18
Q

mechanism of edema

A

increase hydrostatic P in capillary

push into interstitium (starling)

osmotic pressure limits filtration of plasma water from capillaries

lymphatics drain interstital space (edema when lymph can’t handle

19
Q

kayexalate

A

treatment for hyperkalemia

cation exchange resin

most effective in colon but can cause colonic necrosis

20
Q

WNK4

A

inhibits NCC, ENaC, ROMK in the distal nephron under basal conditions

in hypovolemia - inhibit WNK4 - increase ENac

in hyperkalemia - aldo turns on - increase ROM K

21
Q

hyperkalemia symptoms

A

arrhythmia

cardiac arrest

weakness

22
Q

Ways to regulate potassium balance

A
  1. redistribution/shift in and out of cells (min)
  2. urinary excretion to maintain low extracellular concentration (hours)
  3. GI (not really effective)
23
Q

Hyperkalemic changes 6.5-7.5

A

prolonged PR

no P waves

24
Q

cirrhosis and edema

A

scarring of hepatic parenchyma

portal vein HTN

NO causes vasodilation of vessels! low peripheral resistance and high CO

25
Q

hypokalemia cutoff

A

under 3.5

26
Q

pedal edema and CO

A

can be left ventricular also!! from sodium retention

renal sodium retention will always lead to pedal edema

hydrostatic P is always highest at the feet

starling forces determine where edema occurs

lowest P in genitals and periorbital tissues

27
Q

thrombocytosis

A

K is released from platelets during clotting, raising the serum but NOT plasma potassium

can get a heparinized sample

28
Q

hyperkalemia treatment

A
  1. IV Ca to stabilize cardiac cell membrane *ACUTE
  2. transcellular shift (insulin, glucose, albuterol) *ACUTE
  3. increase excretion (kidney, bowel)
  4. stop intake of K
  5. R/O urinary obstruction
29
Q

nephrotic syndrome WITHOUT hematuria

A

min change

fsgs (genetic, HIV)

membranous (idiopathic, SLE)

diebetic nephropathy

amyloidosis

30
Q

nephrotic syndrom with hematuria

A

proliferative GN

endocapillary prolif GN (lupus, endocarditis)

membranoproliferative GN (Hep C, cryoglobins)

post-infectious GN

31
Q

symptoms of hypokalemia

A

EKG changes/arrhythmia

cramps/weakness

rhabdo

polyuria and polydipsia

32
Q

lab findings of ECFV depletion

A

increased BUN and creat and BUN/creat

hyper OR hypo Na

increase in urine osmolality

33
Q

Effective Arterial Blood Volume

A

virtual volume - appears “underfilled” and signals the kidney to retain sodium

more of a concept than a measurable volume - intraarterial volume?

when eabv is decreased - activate signals to kidney

decreased CO or PVR

34
Q

psudohypoaldo type I

A

hypotension and hyperkalemia

LOF of ENaC failure in exchanging Na for K

35
Q

Bartter’s

A

LOF NKCC2

hypotension

hypokalemia

like effects of lasix

36
Q

Gitelman

A

LOF NCC

Hypotension

hypokalemia

like effect of thiazine

37
Q

causes of hypokalemia

A
  1. decreased intake
  2. intracellular shift
  3. renal/gi loss
38
Q

correct “overfilling hypothesis” in nephrotic syndrome

A

glomerular disease/tubular inflammation –> increase local AII/decrease NO –> ANP resistance –> primary Na retention

  • Glomerular disease and tubular inflammation leads to increases in local AII, decreases in NO, and ANP resistance à primary Na retention
  • The kidney is sick and it holds onto Na
  • The details of exactly how this works are not completely worked out

hypoalbuminemia may account for absence of HTN with Na retiontion in nephrotic

39
Q

Pseudohypoaldo Type II

A

GOF NCC

HTN

hyperkalemia (reduced distal delivery of salt)

40
Q

causes of edema

A
  1. incrased capillary permeability (sepsis, burns)
  2. increased hydrostatic P (DVT)
  3. lymph obstruction (cancer)
41
Q

EKG changes in hypokalemia

A

“U” wave - looks like double T waves

premature beats

AV block

VT/VF

42
Q

vasodilation in cirrhosis

A

splanchnic vasodilation - “underfilling” of ECFV (increase in size to be filled) - high renin and aldo - Na retention

  • Basically there is an excessive production of NO, not sure why
  • This particularly occurs in the splanchnic bed and leads to splanchnic vasodilation
  • That leads to low systemic vascular resistance, low bp, high CO, and an underfilling of the ECFV occurs
  • There is an increase in the size of the arterial blood volume to be filled
  • In other words, here is your blood vessels and let’s say you have diarrhea and your blood vessels don’t get filled
  • Instead of some decrease in the amount of Na and water, the size of the vessel increases
  • Thus, the size of the volume that needs to be filled to turn off the signals to the kidney dramatically increases
  • Vasodilation changes the space that needs to be filled to turn off the signals to the kidney
  • That underfilling is very different from the loss of Na and water from the fluid
  • It does lead to increased renin, aldosterone and SNS and leads to Na retention

Renal 2 (4 decks)

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