Diseases of potassium regulation Flashcards

1
Q

54 y/o male with acute MI

cardiac arrest

Lab 145/2.8/120/15

ECG: Vfib

1) What was cause of arrest
2) How would you treat patient

A

K+ low due to ischemic myocardium

Treatment =

1) defibrillate
2) GIve IV K and defibrillate
3) call intern

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2
Q

24 y/o male with HIV/AIDS

Diarrhea several days

145/2.6/120/14

urine K < 10 mEq/d

workup?

what would you say if urine K was 80 mEq/d

A

Workup =

1) low serum K
2) diarrhea
3) low urine K
4) extrarenal problem (GI problem) and acidotic with diarrhea so hypokalemia due to diarrhea

Trematnet

1) treat the diarrhea
2) give him K

if patient had high urine K

1) look at his acid/base status

if acidotic = look for RTA

if normal pH = magnesium

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3
Q

16 y/o woman with DKA

136/6.5/95/6

Glucose 650

Metabolic acidosis

what is cause of hyperkalemia

how would you treat high K

A

1) cause = insulin deficiency causing hyperglycemia –> acidosis –> inability to move K+ from ECF to intracellular –> hyperkalemia
2) treatment = treat the DKA with insulin - lower serum K to reasonable leve

then become hypokalemic and treat

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4
Q

16 y/o woman with DKA

20 years later

developed CKD due to diabetes

meds = insulin, BB, ACEI, HCTZ

Labs = 139/6.2/109/19

BUN 42, creat 1.8

Glucose = 118; Hg A1C = 6.5

what is cause of hyperkalemia

how would you treat

A

1) bb depending could be problme

ACEI = problme = lowers aldosterone levels by blocking angiotensin II

HCTZ = hypokalemic

Treatment =

1) start with urine K
2) if urine K low and GFR okay –> figur eout if sufficient aldo or no aldo
3) if no aldo, she is probably due to ACEI –> hypoaldosteronism

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5
Q

Problem:

intracellular K = 3500 mEq

extracellular K = 60 mEq

Serum K = 3.5-5 mEq/L

Dietary K = 30 mEq/meal

After eating why doesn’t extracellular K go from 60 –> 90 and serum K from 4–> 6 mEq/L

A

hyperkalemic arrhythmia and die.

not usu die immediately from eating such significant dietary K+

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6
Q

Internal K balance controlled by 3 hormones

A

1) insulin = insulin moves K+ from ECF to ICF by activ Na/K transporter
2) catecholamines = B2 adrenergic receptor =moves K+ from ECF to intracellular
3) aldosterone

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7
Q

what is the diff between nonselective bb vs. selective bb

A

nonselective bb (propranolol) prevents K movment

selective bb (metoprolol) does not prevent K movement

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8
Q
A

1) insulin binds receptor
2) activ Na/H antiporter bringing Na in
3) activ Na/K transporter to bring K from ECF to ICF

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9
Q

what is importance of external K balance

A

what you eat you gotta poop or pee or

you would blow up (salt) or die (K)

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10
Q

GFR = ___ (minor/major) player

cortical collecting tubule = ___ (important or not)

Kidney __ and ___ K in contrast to Na, water, Ca, PO4 where there is just reabsorption

A

1) minor until GFR very low
2) important
3) reabsorbs and secretes

so urinary K+ depends on K+
secretion in CCT

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11
Q

Division of renal tubules

1) what % of filtered K load is excreted
2) proximal tubule affects K how
3) descending loop of Henle affects K how
4) ascending limb of henle affects K how
5) CCT affects K how
6) MCT and PCT affect K how

A

1) K excreted = 50%
2) prox tubule reabosrbs 50% of filtered load at end of PCT
3) 120% K+ added by end of descending loop
5) at ascending limb 15-20% leftover after reabs
4) K+ now at 120% due to secretion
5) after K+ reabsorption, K+ at 30% in urine

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12
Q

Channels in ascending limb of Henle

A

1) Na/K/2Cl for reabsorption of K+
2) ROMK provides constant secretion of K+ in for Na/K/2Cl

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13
Q

Channels in CCT

A

1) ENaC brings Na from lumen into cell
2) Na/K atpase pumps Na out and bring K in
3) outward rectifying K+ for leak of K+ into lumen (channel blocked by Mg)

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14
Q
A
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15
Q

CCT is sensitive to which hormone

Diseases which cause hypomagesiumemia also imply…

A

Aldosterone via MR receptor

low K+ bc remove block on ROMK channel

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16
Q

Approach to determine cause of hypokalemia

3 causes of low serum K

A

1) spurious (high WBC count) = WBC > 100,000 = NOT SIGNIFICANT
2) decr TOTAL body K = decr intake OR incr loss (GI vs renal)
3) transcellular shift (stress)

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17
Q

2 causes of low serum K by decr to body K

A

1) decr intake
2) incr loss = GI or renal loss

___

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18
Q

if you have low TB K and low urine K < 20 meq/L what could you have

chronic

___

method to approach

A

EXTRARENAL PROBLEM =

1) if in metabolic acidosis (diarrhea= causes bicarbonate loss)
2) if in normal pH (decr dietary intake)

____

1) if no acid/base disorder, decr intake
2) if metabolic acidosis = GI loss

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19
Q

if you have low TB K and high urine K > 40 mEq what could you have

CHRONIC

A

RENAL PROBLEM = look at CCT

1) metabolic alkalosis - aldosterone drives K+ and H+ secretion; moving H+ out of cell
2) normal pH ( low Mg)
3) metabolic acidosis (DKA, RTA)

____

if no acid base disorder = mg despletion

if metab acidosis = RTA type 1 or 2

if metab alkalosis = hyperaldosteronism (primary vs secondary) = K+ and H+ out of cell

20
Q

what could you have if you have low total body K, metabolic alkalosis (urine K > 40 meQ/L) and urine chloride high >20mEq/l)

A

1) if low BP = Bartter’s or Gittelman’s S
2) if high BP = primary aldosterone deficiency or cushing’s syndrome

21
Q

what could you have if you have low total body K, metabolic alkalosis (urine K > 40 meQ/L) and urine chloride < 20 mEq/L)

A

diuretics

22
Q

ECG changes with hypokalemia

A

As K+ decr, ECG becomes flatter

but no relationship btwn level of serum K+ and ECG abnormalities because normal ECG can rapidly jump to most severe ECG

23
Q

causes of transcellular shift (decreasing serum K+)

acute

A

1) catechoalmine excess = B2 AR
2) medication = b2AR agonists

3) Physiology = stress (chest pain and substernal MI, acute asthma = hypoxic and hypercarbic= sudden death
alcohol or drug withdrawal)

4) Insulin excess (rare)

24
Q

Hypokalemia –> decr total body K+ –> extrarenal loss (urinary K+ < 20)

causes of metabolic acidosis

A

1) GI loss
2) diarrhea
3) laxative abuse
4) GI fistulas

25
Q

Hypokalemia –> decr total body K+ –> extrarenal loss (urinary K+ < 20)

normal acid base

A

1) decr intake
2) cutaneous or GI loss
3) laxative abuse
4) geophagia

26
Q

Hypokalemia –> decr total body K+ –> extrarenal loss (urinary K+ < 20)

metabolic alkalosis

A

1) GI loss
2) laxative abuse
3) congenital chloride losing diarrhea

27
Q

Hypokalemia –> decr total body K+ –> renal loss (urinary K+ > 20)

variable acid base balance

A

1) recovery phase of ATN
2) postobstructive diuresis
3) Mg depletion
4) leukemia
5) drugs
6) cisplatin or penicillin large dose

28
Q

Hypokalemia –> decr total body K+ –> renal loss (urinary K+ > 20)

metabolic acidosis

A

1) RTA
2) carbonic anhydrase inhib
3) DKA

29
Q

Hypokalemia –> decr total body K+ –> renal loss (urinary K+ > 20) –> metabolic alkalosis

low urinary chloride (< 10 mEq/L)

A

1) diuretics
2) vomiting/nasogastric drainage
3) chloride losing diarrhea
4) cystic fibrosis

30
Q

Hypokalemia –> decr total body K+ –> renal loss (urinary K+ > 20) –> metabolic alkalosis

high urinary chloride (> 20 mEq/L)

normotension

A

1) diuretics
2) severe K+ depletion
3) bartters vs gittelman

31
Q
A
32
Q

major consequences of hypokalemia

A

1) neuromuscular = weakness, paralysis, resp distress from diaphragm paralysis
2) cardiac

33
Q

Approach to treating hypokalemia ALWAYS

A

1) reverse correctable causes
2) stop diuretics
3) correct magnesium

34
Q

Approach to treating hypokalemia additionally if symptomatic (arrhythmia +/- digitalis, paralysis, or weakness)

A

1) IV replacement up to 40 mEq/hr–> if give orally limited dose, if give IV limited by rate
2) continuous ECG monitoring and serum K+ monitoring

35
Q

Approach to treating hypokalemia additionally if asymptomatic with metabolic acidosis (diarrhea or RTA)

A

1) K+ citrate or K+ bicarbonate

36
Q

Approach to treating hypokalemia additionally if asymptomatic with metabolic alkalosis or normal pH

1) normotensive
2) Hypertensive

A

1) KCl or volume replacement
2) consider K+ sparing diuretic

37
Q

3 causes of high serum K+

A

1) spurious (incr platelet count) = pseudohyperkalemia
2) decr renal K+ excretion (GFR < 20 = exogenous vs. endogenous K vs meds)
3) transcellular (DKA or hyperglycemia)

38
Q

if high serum K with high GFR > 20 mL/min

with low aldosterone

causes?

A

PROBLEM WITH RAAS

1) low renin = DM
2) high renin = adrenal insufficiency

39
Q

if high serum K with high GFR > 20 mL/min

with high aldosterone

CAUSES?

A

with low urine Na = decr Na delivery

with high urine Na = drugs, PHA

40
Q

what happens if you get a spurious cause of high serum K

A

1) repeat serum K
2) plasma rather than serum K because platelets haven’t time to coagulate (thrombocytosis)

41
Q

What is the first test you would order in a patient with hyperkalemia?

A

ALWAYS REPEAT THE ECG

if ecg normal, continue workup
if ecg abnormal, treat first and workup next

42
Q

ECG consequences of hyperkalemia

A

peaking of T wave and widening of segment (PR, QRS, QT, etc.)
but not linearly related so can jump stages from normal to abnormal ECG easily

43
Q

Approach to treating hyperkalemia

if ECG changes present,

A

1) acutely give Calcium right away = stabilize the membrane = lasts for 15 min

2) sodium bicarbonate to push into ICF (lasts for 1 hr)
3) insulin and glucose
4) albuterol nebulizer
5) K exchange resins (K-xcylat) exchanges K for Na in the gut

6) DIALYSIS

44
Q

Acute causes of hyperkalemia (transcellular shift)

A

1) inadequate insulin response = diabetes (type 1 or type 2)
2) medications = nonselective BB and take large dose of K+

3) ischemic or dead body part = rhabdomyolysis or interstitial/peripheral vascular arterial insufficiency
dumping of K+ into cell from intracellular to ECF

45
Q

Chronic causes of hyperkalemia

major problem is…NOT

urine K is usu…

A

1) high K+ dietary intake RARELY SUFFICIENT
2) must be renal excretory defect as well

major problem is K secretion by the CCT NOT GFR until ESRD
Urine K is usually (but not always low < 20 mEq/L

46
Q
A
47
Q
A