Disorders of K balance Flashcards
1
Q
Factors affecting K distribution
A
- Insulin and B2 adrenergic receptors induce K uptake by stimulating Na/K ATPase
- Exercise can result in hyperkalemia by A1 adrenergic receptor activation leading to increased K efflux (this is offset by the B2 activation)
- Aldo: lowers serum K by stimulating K uptake into cells and by stimulating kidneys to excrete K
- Increases plasma osmolality causes water to move to ECF, resulting in increase in ICF [K]
- The resultant feedback response is an inhibition of Na/K ATPase and this shifts net K movement to efflux, leading to hyperkalemia and normalizing the ICF [K]
2
Q
Shifting K out of cells
A
- Can be due to acidosis (H+ displaces K in cells)
- Diabetic ketoacidosis and BBs lead to inhibition of Na/K ATPase and increases net K efflux
- Hemolysis, rhabdomyolysis, tumor lysis all can lead to hyperkalemia
3
Q
Shifting K into cells
A
- Alkalosis (H+ leaves the cell, K moves in to take its place)
- Insulin and B2 increase Na/K ATPase
- Aldosterone also increases Na/K ATPase
4
Q
Renal K handling
A
- Regulated at the collecting duct (principal cells secrete, intercalated cells reabsorb)
- Secretion accounts for most of the K excretion (80% of what is filtered is reabsorbed)
- K secretion based on the activity of CCD ENaC (K secretion directly proportional to ENaC reabsorption)
- Intercalated cells actively reabsorb K thru apical H/K ATPase (antiporter)
5
Q
Regulation of K secretion
A
- In order of importance:
- Luminal flow rate
- Distal Na delivery
- Aldo
- Extracellular K
- Extracellular pH
6
Q
Luminal flow rate on K secretion
A
- Increasing luminal flow rate increases K secretion b/c it decreases the extracellular K and leads to a larger gradient for secretion
- Osmotic diuresis, increased GFR, decreased Na reabsorption before CCD, diuretics, bartter/gitelmans syndrome all will increase flow rate and can cause hypokalemia
- Decreasing flow rate (low GFR, increased PT Na/H2O reabsorption, obstruction) can decrease K secretion and lead to hyperkalemia
7
Q
K sparing diuretics
A
- Block ENaC activity and thus reduce K secretion (and H+ secretion)
- Can cause hyperkalemia, possibly acidosis
- Amiloride is ex
8
Q
Other diuretics
A
- Loop and thiazide diuretics cause K wasting and alkalosis
- Decreasing Na reabsorption before CCD leads to both increased Na delivery to CCD and increased flow
- The increased flow washes out K leading to increased secretion
- The increased Na increases ENaC activity and thus more K secretion and H+ secretion
9
Q
Aldosterone on K secretion
A
- Aldo increases Na/K ATPase activity and ENaC expression
- Both of these together lead to increase in K secretion
10
Q
Pseudohyperkalemia
A
- Hemolyzed blood, leukocytosis and thrombocyosis
- Due to ischemia from prolonged tourniquet time or exercise of the limb w/ tourniquet
- Leads to abnormally increased K
11
Q
Types of hyperkalemia (serum K > 5mEq/L)
A
- Increased K intake
- Decreased urinary K excretion
- K shift from ICF to ECF
- Excessive K ingestion will not lead to hyperkalemia unless other contributing factors are present
- Chronic hyperkalemia cannot occur unless there is decreased K excretion
12
Q
Cell shift hyperkalemia
A
- Things that move K from inside the cell to outside
- Metabolic acidosis
- Hyperglycemia (osmolarity effect)
- BBs
- Digitalis
- Hyperkalemic periodic paralysis (recurrent attacks of muscle weakness lasting over 1 hr)
13
Q
K intake
A
- Blood transfusions
- Overdose of IV KCl
- Dietary supplements plus renal failure
14
Q
Decreased K excretion
A
- Decreased tubular flow either due to renal failure or low ECFV
- Decrease in CCD K secretion rate either due to ENaC block or hypoaldosteronism
- ENaC block causes: amiloride, other K sprain diuretics
- Hypoaldosteronism: type 4 RTA, NSAIDs, ACEI/ARB, heparin, spironolactone
- Type 4 RTA: hyperkalemia that is disproportionate to level of GFR, there is mild CKD, acidosis (but normal urine acidifying ability) and hyporeninemic, hypoaldosteronism
- Underlying diseases: DM, SLE, obstruction, etc
15
Q
Sx of hyperkalemia
A
- Usually ASx
- Muscle weakness
- Cardiac arrhythmias
- ECG changes: wide QRS, peaked T waves, loss of P waves, short ST int, “sine wave” idioventricular rhythm
16
Q
Rx of hyperkalemia
A
- Stabilize membrane excitability: CaCl
- Increase K entry to cells (rapid and transient): glc + insulin, B2 agonist (albuterol), NaHCO3
- Removal of excess K (slow but definitive): cation exchange resin (kayexylate), diuretics, dialysis
- Dietary K restriction
17
Q
Risks of Ca
A
- Do not give in bicarb-containing solutions, chance of precipitation
- Administer only when ECG changes (loss of P waves or widening of QRS) in pts taking digitalis (can induce digitalis toxicity)
- Can cause tissue necrosis if injected SQ
- Can precipitate CaPi in tissue in pts w/ renal failure and hyperphsophatemia
18
Q
Risks of kayexylate
A
- Can cause intestinal necrosis and severe pain
- Most likely when given w/ sorbitol
19
Q
Pseudohypokalemia
A
- Serum K artificially decreases after phlebotomy
- Usually due to acute myeloblastic leukemia (blast cells take up the K in the tube)
20
Q
Hypokalemia (serum K < 3.5 mEq/L)
A
- Can 3 possible causes
- Cellular shift
- GI loss
- Urinary K wasting
21
Q
Cellular shift hypokalemia
A
- Alkalosis
- Insulin
- B2 agonist
- Hypokalemic periodic paralysis:
- Familial: precipitated by meal or exercise, repetitive episodes of acute profound hypokalemia and paralysis lasting hrs-days
- Thyrotoxic: predominantly asians, 20-40yo, mostly male, only w/ thyrotoxicosis which may be ASx
22
Q
Urinary K wasting
A
- Due to increased K secretion
- 2 possibilities: increased tubular flow or increased CCD K secretion
- Osmotic diuresis increases tubular flow and thus increases K secretion
- Decreased PT, TAL, DT Na reabsorption leads to increased K secretion
- Increased delivery of Na w/ nonreabsorbable anion to CCD increases K secretion
- Hyperaldosteronism leads to increased K secretion
- Increased membrane permeability
- All of these can cause metabolic alkalosis
23
Q
Bartter’s syndrome
A
- Due to inactivating mutations in transporters of the TAL
- Mostly NKCC, but also K channels and Cl channels
- Leads to increased Na delivery/flow to CCD and thus hypokalemia/alkalosis
24
Q
Gitelman’s syndrome
A
- Due to inactivating mutation in the NaCl cotransporter (NCC) in DT
- Leads to increased Na delivery/flow to CCD and thus hypokalemia/alkalosis
25
Increased delivery of nonreabsorbable anions
- HCO3-, ketoanions delivery to CCD will increase K secretion (associated w/ decreased Cl delivery to CCD)
- May be due to vomiting, loss of H+
- Amphotericin can increase membrane permeability to K
26
Hyperaldosteronism
- Can be due to activating mutations of ENaC (liddle's)
- Can be due to high levels of transcribed/translated Aldo (GRA: glucocorticoid remediable aldosteronism)
- Can be due to LOF mutation of B-hydroxysteroid dehydrogenase, leading to excessive stimulation of Aldo receptor by cortisol, cushings
- Can also be due to high renin: renal artery stenosis, reninoma
27
Sx of hypokalemia
- Usually ASx, muscle weakness, polyuria/polydipsia
- Rhabdomyolysis
- ECG changes: depressed ST segment, flat T wave, prolonged QT, apparent U wave
- Arrhythmias
28
Rx of hypokalemia
- Oral KCl supplements
- IV KCl
- concaminant hypomagnesemia must be corrected
- Amiloride or spironolactone useful in pts w/ hyperaldosteronism