Diseases of potassium regulation Flashcards
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
K+ low due to ischemic myocardium
Treatment =
1) defibrillate
2) GIve IV K and defibrillate
3) call intern
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
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
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
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
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
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
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
hyperkalemic arrhythmia and die.
not usu die immediately from eating such significant dietary K+
Internal K balance controlled by 3 hormones
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
what is the diff between nonselective bb vs. selective bb
nonselective bb (propranolol) prevents K movment
selective bb (metoprolol) does not prevent K movement
1) insulin binds receptor
2) activ Na/H antiporter bringing Na in
3) activ Na/K transporter to bring K from ECF to ICF
what is importance of external K balance
what you eat you gotta poop or pee or
you would blow up (salt) or die (K)
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
1) minor until GFR very low
2) important
3) reabsorbs and secretes
so urinary K+ depends on K+
secretion in CCT
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
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
Channels in ascending limb of Henle
1) Na/K/2Cl for reabsorption of K+
2) ROMK provides constant secretion of K+ in for Na/K/2Cl
Channels in CCT
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)
CCT is sensitive to which hormone
Diseases which cause hypomagesiumemia also imply…
Aldosterone via MR receptor
low K+ bc remove block on ROMK channel
Approach to determine cause of hypokalemia
3 causes of low serum K
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)
2 causes of low serum K by decr to body K
1) decr intake
2) incr loss = GI or renal loss
___
if you have low TB K and low urine K < 20 meq/L what could you have
chronic
___
method to approach
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
if you have low TB K and high urine K > 40 mEq what could you have
CHRONIC
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
what could you have if you have low total body K, metabolic alkalosis (urine K > 40 meQ/L) and urine chloride high >20mEq/l)
1) if low BP = Bartter’s or Gittelman’s S
2) if high BP = primary aldosterone deficiency or cushing’s syndrome
what could you have if you have low total body K, metabolic alkalosis (urine K > 40 meQ/L) and urine chloride < 20 mEq/L)
diuretics
ECG changes with hypokalemia
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
causes of transcellular shift (decreasing serum K+)
acute
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)
Hypokalemia –> decr total body K+ –> extrarenal loss (urinary K+ < 20)
causes of metabolic acidosis
1) GI loss
2) diarrhea
3) laxative abuse
4) GI fistulas
