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11 Potassium Homeostasis & Disorders Flashcards

1
Q

Physiologic role of potassium

  • Intracellular K
  • Extracellular K
  • Conc gradient b/n intracellular & extracellular compartments
A
  • K: primary intracellular cation
    • Conc = 120-150 mEq/L
    • Regulates cell membrane potential, transporter protein & enzyme function, & cell volume
  • Extracellular K
    • Conc = 50-100 mEq
    • Tightly requlated –> 3.5-5 mEq/L
    • Low conc (< 3.4 mEq/L) –> hypokalemia
    • High conc (> 5 mEq/L) –> hyperkalemia
  • Conc gradient b/n intracellular & extracellular compartments
    • Maintained by the Na/K ATPase
    • Transport 2 K in for 3 Na out of the cell
    • Na & K flow back down their conc gradients through specific Na & K channels
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2
Q

Transcellular K conc

  • Critical to certain cellular functions
  • Alterations in the transcellular K gradient may…
  • Hypokalemia
  • Hyperkalemia
A
  • Critical to certain cellular functions
    • Provides K ions as substrates for membrane transport processes
    • Major determinant of the cell resting membrane potential
      • Plays roles in cardiac & neuromuscular functions
  • Alterations in the transcellular K gradient may…
    • Alter the cell membrane resting potential
    • Impair neuromuscular excitability (ex. cardiac pacemaker rhythmicity & cardiac conduction)
    • Impair cell membrane transport processes
  • Hypokalemia: low K in blood
    • Resting membrane potential hyperpolarizes (–> more negative)
    • Takes a longer time for cells to repolarize
  • Hyperkalemia: high K in blood
    • Resting membrane potential depolarizes (–> less negative)
    • Cells repolarize faster
    • Fewer Na channels are open –> conduction through the heart becomes sluggish
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3
Q

Regulation of K homeostasis

  • External balance
    • Definition
    • K intake
    • K excretion
  • Internal balancve
    • Definition
    • Ex. ingest 50 mmeq of K
    • Net result of 2 processes
A
  • External balance
    • Definition
      • Regulation of total body K content by altering K intake & excretion
    • K intake
      • Normal dietary K intake = 50-150 meq K / day
      • Foods high in K: potatoes, tomatoes, melons, bananas, citrus fruits, dried fruits, nuts, coffee, chocolate, & salt substitutes
      • Other sources of K: IV fluids, IV hyperalimentation, K-containing drugs, blood transfusions, & herbal medications (alfalfa, dandelion, noni juice)
    • K excretion
      • 90% of K: excreted by kidneys
      • 10% of K: excreted in stool & sweat
        • Fecal K losses = 50-10 meq/day
        • Sweat K losses = 0-10 meq/day
      • Only renal K excretion is under strict & complex regulation
        • Basis for K homeostasis
        • Regulation of final urinary K content occurs in the collecting duct
  • Internal balance
    • Definition
      • Regulation of the distribution of K b/n ICF & ECF compartments
      • Responsible for moment-to-moment control of EC K conc
    • Ex. ingest 50 mmeq of K
      • –> 40% excreted over 4 hours
      • –> 60% remains in ECF –> increase K conc
      • Hyperkalemia doesn’t develop due to internal balance regulation
    • Net result of 2 processes
      • K uptake via Na/K ATPase
      • K secretion via K permeability of the cell membrane
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4
Q

Renal K handling

  • K reabsorption
    • PT + LOH
    • CD
  • Final urinary K content & excretion is determined primarily by…
A
  • K filtration
    • K is freely filtered by the glomerulus
  • K reabsorption
    • PT + LOH: 90% reabsorbed
      • PT: 65% (passive, not tightly regulated)
      • TkAL: 25% (passive & active via Na/K/2Cl)
    • CD: K is both reabsorbed & secreted
      • CCD & MCD: type A & B intercalated cells (active via H/K ATPase)
  • Final urinary K content & excretion is determined primarily by…
    • Relative rates of K secretion & reabsorption in teh distal nephron
    • Secretion of K in teh CD is highly regulated & responsive to physiological needs
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5
Q

Cellular mechs for CD K secretion

  • Principal cells
    • K secretion vs. urinary flow
    • Key features
  • Intercalated cells
    • K secretion vs. urinary flow
    • Key featuress
A
  • Principal cells
    • K secretion vs. urinary flow
      • Main K secretory cells
      • Actively secrete K regardless of rate of urinary flow
    • Key features
      • Na/K ATPase
        • Basolateral channel that pushes 3 Na into the interstitium for 2 K into the cell
      • ROMK & BK K channels
        • Mediate voltage dependent K secretion across the apical membrane into the tubule lumen
      • ENAC channel
        • Apical epithelial Na channel
      • High resistance tight junctions b/n cells
  • Intercalated cells
    • K secretion vs. urinary flow
      • Secrete K only during states of high urinary flow
    • Key features
      • Na/K ATPase
        • Basolateral channel that pushes 3 Na into the interstitium for 2 K into the cell
      • BK
        • Mediate voltage dependent K secretion across the apical membrane into the tubule lumen
      • High-resistance tight junctions b/n cells
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6
Q

At the cellular level…

  • K secretion depends on…
    • K conc gradient across the cell membrane
    • K permeability across the apical membrane
    • Voltage across the apical membrane
    • Urinary flow
  • K reabsorption depends on…
A
  • K secretion depends on…
    • K conc gradient across the cell membrane
      • Established by the Na/K ATPase
      • Transports K from the interstitium into the principal & intercalated cells
        • Maintains a high intracellular conc of K
      • BK & ROMK channels require a high conc of intracellular K
        • Allows K to be secreted into the lumen across the apical side
    • K permeability across the apical membrane
      • Determined by the number of open K channels at the apical membrane
    • Voltage across the apical membrane
      • Transporting charged ions across teh luminal membrane into cells –> electrical voltage
      • Primarily generated by ENAC (Na transport)
        • Na uptake through the apical Na channel down the Na gradient created by the Na/K ATPase –> negative charges in the lumen
        • Creates a lumen-negative electrical potential difference across the apical membrane
        • Excess negative charges in the tubule lumen favors K secretion into the urinary space
      • Voltage-dependent K secretion in principal cells is mediated by the apical ROMK
      • K & Na transport are stimulated by aldo
    • Urinary flow
      • High urinary flow –> increase K secretion
      • BK channel-mediated K secretion is flow-dependent
        • Principal & intercalated cells sense high urinary flow –> open BK K channels
  • K reabsorption depends on…
    • Intercalated cells
      • K-absorbing cells in teh CD
      • Also responsible for H secretion
    • H/K ATPase
      • Apical membrane pump that mediates K reabsorption by the intercalated cell (active process)
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7
Q

Regulation of renal K excretion

  • Location
  • Factors that directly affect distal tubular K handling
A
  • Location
    • Occurs in the distal nephron
    • Alterations in glomerular filtration rates & PT function have little direct effect on net K handling
  • Factors that directly affect distal tubular K handling
    • Peritubular factors
      • Serum K conc
      • Serum aldo
      • Extracellular pH
    • Luminal factors
      • Distal tubular flow rate
      • Distal tubular Na delivery
      • Luminal anion composition
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8
Q

Regulation of renal K excretion:
Peritubular factors:
Serum K concentration / dietary K intake

  • Dietary K intake & extracellular K
  • K adaptation
  • Adaptive K changes during K excess
  • Required for a max response
  • Adaptive K changes during K deprivation
A
  • Dietary K intake & extracellular K
    • Significantly influence tubular K secretion
    • Increase dietary K intake –> increase serum K –> increase apical Na & K transport –> increase Na/K ATPase –> increase K secretion
    • Via both aldo-dependent & aldo-independent mechanisms
  • K adaptation
    • Gradual process i.r.t. changes in dietary K intake
    • At any given level of serum K, K secretion will be higher w/ a high K diet compared to a normal or low K diet
    • Increase in urinary K excretion is mediated by increased K secretion in the distal nephron
  • Adaptive K changes during K excess
    • Increase Na/K ATPase activity –> increase apical membrane Na & K transport
      • –> morphologic changes in principal cells (increase basolateral membrane area)
    • Decrease K reabsorption by intercalated cells
  • Required for a max response
    • Increased plasma K & aldo
  • Adaptive K changes during K deprivation
    • Morphologic changes in intercalated cells (increase apical cell membrane area + increase apical K transporters)
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9
Q

Regulation of renal K excretion:
​Peritubular factors:
Aldosterone

  • Effect on K
  • Effect on Na
  • Na vs. K
A
  • Stimulates K secretion by the CD
    • Binds to an intracellular receptor –> synths aldo-induced proteins
    • Increases basolateral Na/K ATPase –> increases K entry –> generates Na gradient for apical Na reabsorption
    • Increases the number of apical Na & K channels –> increases Na reabsoprtion –> generates an apical lumen-negative electrical potential difference –> favors K secretion into the lumen
  • Stimulates Na reabsorption
  • K vs. Na
    • Na excretion comes back into balance after several days (“aldo escape”)
    • K excretion remains elevated –> progressive renal K loss
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10
Q

Regulation of renal K excretion:
​Peritubular factors:
Extracellular pH

  • Changes in EC pH
  • Acidemia
  • Alkalemia
  • pH-induced effects
A
  • Changes in EC pH
    • Associated w/ limited reciprocal shifts in H & K b/n the ECF & ICF
  • Acidemia
    • Decreases intracellular K in CD cells
    • Decreases K secretion
  • Alkalemia
    • Increases intracellular K in CD cells
    • Increases K secretion
  • pH-induced effects
    • Limited & transient
    • Frequently masked by other factors
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11
Q

Regulation of renal K excretion:
Luminal factors:
Distal tubular flow rate

  • Tubular flow rate vs. K secretion
  • BK K channels
  • Tubular flow vs. K gradient
A
  • Tubular flow rate vs. K secretion
    • Increase tubular flow rate in the distal nephron –> increase K secretion
    • Decrease tubular flow rate in the distal nephron –> decrease K secretion
  • BK K channels
    • Expressed in principal & intercalated CCD cells
    • Facilitate flow-dependent K secretion
  • Tubular flow vs. K gradient
    • Increase tubular flow –> clears secreted K from distal nephron lumen –> introduces fresh low K-containing fluid from the more proximal nephron
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12
Q

Regulation of renal K excretion:
Luminal factors:
Distal tubular Na delivery

  • Distal tubular Na delivery vs. Na reabsorption
  • Distal tubular Na delivery vs. flow rate
A
  • Distal tubular Na delivery vs. Na reabsorption
    • Increase Na delivery –> increase Na reabsorption –> lumen-negative potential difference –> increase K secretion
  • Distal tubular Na delivery vs. flow rate
    • Difficult to dissociate
    • Increased distal flow is usually associated w/ increased distal Na delivery
      • Ex. intravascular volume expansion, diuretics
    • Decreased distal flow is usually associated w/ decreased distal Na delivery
      • Ex. intravascular volume depletion
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13
Q

Regulation of renal K excretion:
Luminal factors:
Distal tubular fluid anion composition & summary

  • Substition of another anion for Cl
  • Other anions besides Cl
  • Greatest factors in K secretion
A
  • Substition of another anion for Cl
    • Decreases distal tubular Cl delivery –> increases K secretion
  • Other anions besides Cl
    • Ex. bicarb, penicillin salts (e.g. carbenicillin), acetoacetate, beta-hydroxybutyrate, hippurate
    • Less well reabsorbed in the CD
    • Increase conc of these poorly reabsorbable anions –> increase lumen-negative potential –> increase Na reabsorption –> increase K secretion
  • Greatest factors in K secretion
    • Distal tubular flow rate & aldo
    • Variations in these factors have opposing effects that maintain a constant rate of K secretion despite variations in Na balance
    • Ex. intravascular volume depletion
      • –> increases PT Na reabsorption –> decreases tubular flow –> decreases K secretion
      • –> increases aldo secretion –> increases K secretion
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14
Q

Transtubular K gradient (TTKG)

A
  • Clinical index to assess renal K secretion
  • Ratio of the estimated K conc in the CCD (CCDK) to the plasma K conc (PK)
  • CCDK​ can’t be measured directly
    • Estimated by correcting the urinary K conc for water reabsorption in the medullary CD
  • During K depletion
    • TTKG < 2.5 (usually close to 1)
  • During K loading
    • TTKG > 10
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15
Q

Regulation of internal balance:
Physiologic factors

  • Insulin
  • Catecholamines
  • Aldo
A
  • Insulin
    • Stimulates cellular uptake of K
      • Mediated by increased Na/K ATPase activity
      • Independent of glucose transport
    • Insulin + K: components of a regulatory loop
      • Increase splanchnic K –> increase pancreatic insulin secretion
      • Insulin –> K uptake by the liver 7 muscle –> returns serum K conc to normal
  • Catecholamines
    • Stimulate cellular uptake of K
    • Mediated by beta2-adrenergic receptors
    • Results from increased Na/K ATPase activity
  • Aldo
    • Stimulates cellular uptake of K
    • Effect is less than its effect on external K balance
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16
Q

Regulation of internal balance:
Pathophysiologic factors

  • Acid-base disturbances
    • H vs. K shifts
    • Effects of changes in blood pH on EC K conc
    • Effects of changes in serum bicarb conc
  • Plasma tonicity
  • Cell lysis & cell proliferation
  • Cell membrane disorders
    • Hyperkalemic & hypokalemic periodic paralysis
    • Primary hyperkalemic defect
    • Primary hypokalemic defect
A
  • Acid-base disturbances
    • H vs. K shifts
      • H shifts into or out of the IC compartment
        • Buffers changes in the EC H ion conc
      • K shifts in the opp direction of H to maintain electroneutrality
    • Effects of changes in blood pH on EC K conc
      • Metabolic distrubances have a greater effect than respiratory disturbances
      • Metabolic acidoses due to organic acids (ketoacidosis, lactic acidosis) have smaller effects than due to mineral acids
        • Effect is dependent on the duration of disturbance & degree of IC buffering
    • Effects of changes in serum bicarb conc
      • Increase bicarb under isohydric conditions –> K shifts into cells
      • Decrease bicarb under isohydric conditions –> K shifts out of cells
  • Plasma tonicity
    • Increase plasma tonicity –> fluid shifts from IC to EC compartments
    • K exits the IC compartment w/ water via solvent drag
  • Cell lysis & cell proliferation
    • Cell lysis –> IC contents release into EC space
      • Since IC K > EC K, EC K can rise abruptly
    • Cell proliferation –> K is taken up into proliferating cells –> decrease EC K
  • Cell membrane disorders
    • Hyperkalemic & hypokalemic periodic paralysis
      • Disorders of skeletal muscle cel lmembrane ion channels
      • –> flaccid paralysis & transmembrane K shifts
    • Primary hyperkalemic defect
      • Skeletal muscle voltage-gated Na channel mutaiton
    • Primary hypokalemic defect
      • Skeletal muscle dihydropyridine-type Ca channel mutation
17
Q

Clinical disorders of K homeostasis

  • Hyperkalemia may result from disturbances in…
  • Hypokalemia may result from disturbances in…
A
  • Hyperkalemia may result from disturbances in…
    • External balance –> total body K excess –> chronic hyperkalemia
    • Internal balance –> shift of K from the IC to EC compartment –> acute hyperkalemia
  • Hypokalemia may result from disturbances in…
    • External balance –> total body K deficiency
      • Inadequate K intake
      • Increased extrarenal K losses
      • Increased renal K losses (renal K wasting)
    • Internal balance –> transcellular K shifts
18
Q

Disorders of hyperkalemia (plasma K > 5):
Factors affecting external balance:
Excessive K intake

  • When K excretion is not impaired
  • When K excretion is impaired
A
  • When K excretion is not impaired
    • Won’t produce significant hyperkalemia
  • When K excretion is impaired
    • Tolerance of…
      • Acute potassium loads (dietary potassium (fruits, vegetables, nuts, chocolate, coffee, salt substitutes)
      • Potassium supplements
      • IV fluids
      • Intravenous hyperalimentation
      • Potassium-containing medications (potassium salts of penicillin)
      • Blood transfusions
    • …can be severely limited
19
Q

Disorders of hyperkalemia (plasma K > 5):
Factors affecting external balance:
Decreaed renal excretion & renal insufficiency

  • Decreased renal excretion
  • Renal insufficiency
    • Acute renal failure
    • Chronic renal failure
A
  • Decreased renal excretion
    • From impaired GFR or defects in tubular K handling
    • Common for multiple defects to be present simultaneously
  • Renal insufficiency
    • Acute renal failure
      • Esp oliguric renal failure (<400 ml urine / 24 hr)
      • K excrection is impaired
      • Hyperkalemia is common
    • Chronic renal failure
      • Significant impairment of K exrection doesn’t occur until the GFR decreases < 15-20 ml/min
        • Above this level, distal tubular delivery is sufficient ot maintain K balance (at the expense of increased single nephron secretory rates)
      • Adaptation occurs similar to chronic K loading in a normal kidney
        • Due to elevated aldo
        • Ability to compensate for sudden increase in K intake is impared in renal disease
20
Q

Disorders of hyperkalemia (plasma K > 5):
Factors affecting external balance:
Decreased distal tubular flow

  • Decrease distal tubular Na delivery & flow –>
  • Volume depletion
  • Decrease EABV
  • Medications
A
  • Decrease distal tubular Na delivery & flow –> decrease renal capacity for K excretion
  • Volume depletion
    • Ex. dehydration, blood loss
  • Decrease EABV
    • Ex. CHF, cirrhosis, nephrotic syndrome
  • Medications
    • Prostaglandins preserve AffA flow –> antagonize AII vasoconstriction in states of volume depletion or decreased EABV
      • NSAIDS inhibit prostaglandin synth –> decrease GFR in these states
    • ACE-Is & ARBs block AII on EffAs –> decrease glomerular capillary pressure
21
Q

Disorders of hyperkalemia (plasma K > 5):
Factors affecting external balance:
Mineralocorticoid deficiency

A
  • Mineralocorticoids maintain K homeostasis in states where distal tubular flow is impaired & in renal insufficiency
  • Combined glucocorticoid & mineralocorticoid dificiency
    • Primary adrenal insufficiency / Addison’s disease
  • Hyporeninemic hypoaldosteronism
    • Diabetes mellitus
  • Drug-induced hypoaldosteronism
    • ACE-Is
    • Heparin
    • NSAIDs
22
Q

Disorders of hyperkalemia (plasma K > 5):
Factors affecting external balance:
Distal tubular dysfunction

  • Impaired tubular function + hyporesponsiveness to aldo & decreased K secretion –>
  • K sparing diuretics
A
  • Impaired tubular function + hyporesponsiveness to aldo & decreased K secretion
    • –> interstitial nephritis
    • –> sickle cell disease
    • –> lupus nephritis
  • K sparing diuretics
    • Ex. amiloride, triamterene, spironolactone
    • Decrease Na reabsoprtion by ENACs in CCD principal cells –> decrease K secretion
23
Q

Disorders of hyperkalemia (plasma K > 5):
Factors affecting internal balance

A
  • General
    • Disturbances of internal K balance frequently contribute to acute hyperkalemia
  • Insulin deficiency
    • Diabetes mellitus
  • Beta-adrenergic blockade
    • Beta-blocker therapy
  • Hypertonicity
    • Hyperglycemia
  • Acidemia
    • Metabolic acidosis > respiratory acidosis
    • Hyperchloremic acidosis > high-anion gap metabolic acidosis
  • Cell lysis (release of IC K)
    • Burns
    • Tissue necrosis
    • Rhabdomyolysis
    • Hemolysis
    • Tumor lysis syndrome
24
Q

Disorders of hyperkalemia (plasma K > 5):
Pseudohyperkalemia

  • Definition
  • May result from…
  • Suggested by…
A
  • Significant hyperkalemia is reported by labs despite a normal plasma K conc
  • May result from…
    • Incorrect phlebotomy technique
      • Prolonged tourniquet applicatoin
      • Muscle exercise –> local muscle K release
    • In vitro K release from cells
      • Hemolyzed specimens
      • Thrombocytosis (platelet count > 1,000,000/mm3)
      • Leukocytosis (WBC > 100,000/mm3)
  • Suggested by the absence of hyperkalemic ECG changes
25
Q

Clinical manifestations of hyperkalemia

  • Result from…
  • Resting cell membrane potential in hyperkalemia
  • Cardiac toxicity
    • Hyperkalemia –>
    • Associated ECG changes
  • Neuromuscular symptoms
A
  • Result from…
    • Changes in transmembrane K gradients
    • Resulting change in resting membrane potential in excitable tissues
  • Resting cell membrane potential in hyperkalemia
    • Depolarized in myocytes & neurons
    • –> decreased membrane na permeability via inactivated Na channels
    • –> net reduction in membrane excitability
  • Cardiac toxicity
    • Hyperkalemia –> sudden, lethal ventricular arrhythmias (VTach, VFib)
      • Medical emergency that requires urgent therapy
    • Associated ECG changes
      • Peaked T waves
      • Wideneed QRS
      • PR prolongatoin
      • QT shortening
      • Decreaed P wave amplitdue
      • QRS & T waves fuse –> sine-wave pattern
  • Neuromuscular symptoms
    • May develop w/ ascending muscular weakness –> quadriplegia & respiratory arrest
26
Q

Medical treatment of hyperkalemia

  • Severe hyperkalemia
  • Pts w/ serum K > 6-6.5 meq/L or ECG manifestations of hyperkalemia
  • Acute therapy
    • Membrane stabilization
    • Redistribution of K into cells
    • Enhanced elimination of K
  • Chronic therapy
A
  • Severe hyperkalemia
    • Medical emergency requiring urgent therapy
  • Pts w/ serum K > 6-6.5 meq/L or ECG manifestations of hyperkalemia
    • –> continuous ECG monitoring
  • Acute therapy
    • Membrane stabilization: IV Ca
      • –> raise threshold potential –> decrease cardiotoxic effects
      • Rapid onset, shorr duraiton
      • No effect on plasma K
    • Redistribution of K into cells
      • IV insulin
        • Longer onset, longer duration
        • Accompanied by glucose infusion to prevent insulin-induced hypoglycemia (but avoid glucose bolus)
      • Beta-adrenergic agonists: albuterol
        • Longer onset, longer duration
      • IV Na bicarb
        • Medium onset, longer duration
    • Enhanced elimination of K
      • Increase urine flow & distal nephron Na delivery (diuretics, IV saline)
      • GI ion exchange resins (Na polystyrene sulfonate)
        • Long onset, variable duration
        • Given orally or as retention enema
      • Acute hemodialysis
  • Chronic therapy
    • Treat underlying process
    • Restrict K intake
    • Stop offending drugs
      • NSAIDs, ACE-Is, beta-adrenergic blockers, heparin
    • Enhance distal tubular Na delivery & flow
      • Liberalize na intake, diuretics
    • Mineralocorticoid replacement (rare)
      • Fludrocortisone
27
Q

Disorders of hypokalemia (plasma K < 3.5):
Factors affecting external balance:
Inadequate intake

A
  • K conservation is never complete (unlike Na)
  • Even w/ K depletion, obligate renal & extrarenal K losses can only be reduced to 10 meq/day
  • Intake < 10 meq/day –> progressive K depletion & hypokalemia
  • Ex. alcoholism, malnutrition
28
Q

Disorders of hypokalemia (plasma K < 3.5):
Factors affecting external balance:
Increased extrarenal K losses

  • If extrarenal K losses > dietary intake
  • If hypokalemia is due to extrarenal K losses
  • Losses may occur from…
    • GI tract
    • Skin (cutaneous)
A
  • If extrarenal K losses > dietary intake
    • –> max renal K conservation will be inadequate to prevent progressive K depletion
  • If hypokalemia is due to extrarenal K losses
    • Transtubular K gradient (TTKG) will be appropriately low (<2.5)
  • Losses may occur from…
    • GI tract
      • Diarrhea
      • Laxative abuse
      • Vomiting
      • Nasogastric suction/drainage
        • majority of K losses result form renal K wasting due to metabolic alkalosis & secondary hyperaldosteronism
    • Skin (cutaneous)
      • Profuse sweating
      • Severe burns
29
Q

Disorders of hypokalemia (plasma K < 3.5):
Factors affecting external balance:
Increased renal K losses (renal K wasting)

  • Hypertensive disorders (HTN) are due to…
  • Normotensive disorders (no HTN) are due to…
A
  • Hypertensive disorders (HTN) are due to…
    • (Apparent) mineralocorticoid excess
  • Normotensive disorders (no HTN) are due to…
    • Increased distal tubular flow rates
    • Presence of poorly reabsorbable anions
    • Primary tubular dysfunction
    • Secondary hyperaldosteronism
30
Q

Disorders of hypokalemia (plasma K < 3.5):
Hypertensive hypokalemic disorders (effective mineralocorticoid excess)

A
  • Hyperreninemia
    • Renal artery stenosis
    • Renin-secreting tumor
  • Primary hyperaldosteronism (Conn’s syndrome)
    • Mineralocorticoid excess secretion (adrenal hyperplasia, adenoma, carcinoma)
  • Cushing’s syndrome
    • Exogenous steroid therapy
    • Cortisol hypersecretion (adrenal or pituitary adenoma, ACTH-secreting tumor)
  • Congenital adrenal hyperplasia
    • Increased ACTH levels resulting from enzymatic defects in cortisol biosynthesis
31
Q

Disorders of hypokalemia (plasma K < 3.5):
Normotensive hypokalemic disorders

A
  • Diuretic therapy
  • Osmotic diuresis
    • Glucosuria with diabetes mellitus
    • Urea from acute renal failure
  • Renal tubular acidosis
    • Proximal (Type II) RTA
    • Classical distal (Type I) RTA
  • Prolonged vomiting or nasogastric drainage
    • Prolonged loss of gastric secretions –> severe metabolic alkalosis
    • Increased delivery of bicarb (poorly reabsorbable anion) to the distal nephron and secondary hyperaldosteronism –> renal K wasting
  • Ureteral diversion
    • Ureteroileostomy or ureterosigmoidostomy
      • Diversion of urine into a loop of ileum or sigmoid colon for the treatment of ureteral or bladder disease
    • Exchange of K & bicarb by the intestinal epithelium for Na & Cl int eh urine –> hypokalemia & metabolic acidosis
32
Q

Disorders of hypokalemia (plasma K < 3.5):
Factors affecting internal balance

A
  • General
    • Associated w/ increased translocatioon of K from the EC into the IC compartment –> hypokalemia or exacerbate pre-existing electrolyte disturbances
  • Insnsulin excess
    • Insulin therapy
  • Catecholamine excess
    • Associated with medical disorders
    • E.g. myocardial ischemia/infarction or delirium tremens, and medications
  • Alkalemia
  • Cell proliferation
    • Rapidly proliferating leukemia or lymphoma
    • Treatment of megaloblastic anemia
33
Q

Manifestations of hypokalemia

  • Primary manifestations of hypokalemia result from…
  • Initial hypokalemia
  • Severe hypokalemia
  • Effects beyond excitable tissues
  • Renal manifestations
A
  • Primary manifestations of hypokalemia result from…
    • Alterations int he resting potential of excitable tissues
  • Initial hypokalemia
    • –> decreased EC : IC K conc ratio
    • –> membrane hyperpolarization
  • Severe hypokalemia
    • –> secondary increase in Na conductance
    • –> membrane depoalrizaiton
  • Effects beyond excitable tissues
    • ECG abnormalities
    • Cardiac arrhythmias
      • Flat T wave –> prominent U wave –> depressed ST
    • HTN
    • Decreased neuromuscular excitability
    • Rhabdomyolysis
  • Renal manifestations
    • Increased renal generatoin of ammonia
      • IC K –> EC fluid compartment
      • H move IC to maintain electroneutrality
      • Increased IC H conc –> renal ammoniagenesis
    • Decreased responsiveness of the CCD to ADH –> nephrogenic diabetes insipidus
34
Q

Treatment of hypokalemia

A
  • Correct the underlying disorder
  • K replacement/repletion
    • Oral route prefered
    • IV route cautioned
      • Max rate of replacement = 10 meq/hr
      • K requires a finite time to enter cells
      • Too rapid administratoin –> transient hyperkalemia –> neuromuscular & cardiac toxicity
  • K sparing diuretics
    • Amiloride & triamtereine in pts w/ primary renal K wasting
    • Spironolactone (MR antagonist) in pts w/ hyperaldosteronism

Renal (24 decks)

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