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Electrolytes Flashcards

1
Q

Causes of proximal RTA?

A
  1. Primary
    1. Idiopathic/sporadic
    2. Familial:
      1. Recessive (proximal tubule Na/HCO3 co-transporter defect, carbonic anhydrase type 2 deficiency)
      2. Dominant, isolated HCO3 wasting
      3. Cystinosis
      4. Tyrosinemia
      5. Hereditary fructose intolerance
      6. Galactosemia
      7. Glycogen storage disease type I
      8. Wilsons
      9. Lowe syndrome
  2. Acquired
    1. Drugs: Ifosfamide, tenofovir/ARTs, carbonic anhydrase inhibitors, aminoglycosides, cisplatin/oxaliplatin
    2. Monoclonal: MM/light chain, amyloidosis
    3. Heavy metals: lead, mercury, copper, cadmium
    4. Vitamin D deficiency
    5. Renal transplant
    6. Paroxysmal nocturnal hemoglobinuria
    7. Sjogren’s (more commonly distal RTA)
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2
Q

DDx for Fanconi’s syndrome - congenital and acquired

A
  • Inherited:
    • Cystinosis
    • Wilson’s disease
  • Acquired:
    • Paraproteinemia – light chain nephropathy (proximal tubular uptake of light chains)
    • Drugs – carbonic anhydrase inhibitors (acetazolamide, topiramate), tenofovir, aminoglycosides, ifosfamide)
    • Heavy metal toxicity – lead, mercury, copper
    • Post-renal transplant
    • PNH
    • Sjogren’s (more commonly distal RTA)
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3
Q

Causes of distal RTA?

A
  1. Primary
    1. Idiopathic/sporadic
    2. Familial
      1. Autosomal dominant
      2. Autosomal recessive
  2. Secondary
    1. Autoimune: Sjogren’s, SLE, RA, AIH/PBC
    2. Drugs: Ibuprofen, lithium, amphotericin B, ifosfamide
    3. Hypercalciuric conditions: hyperPTH, VitD intoxication, sarcoidosis, idiopathic hypercalciuria
    4. Other: medullary sponge kidney, obstructive uropathy, RTx rejection, Wilson’s disease
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4
Q

Causes of type 4 RTA

A
  • Decreased aldosterone production
    • Decreased renin
      • CNI
      • NSAIDs
      • DM
      • HIV
    • Decreased aldosterone
      • ACE/ARBs
      • Heparin
      • Addison’s
      • Gordon’s syndrome (pseudohypoaldo type 2)
  • Increased aldosterone resistance
    • Aldo blockade
      • MRA
    • ENaC blockade
      • Amiloride
      • Triampterene
      • Septra
      • Pseudohypoaldosteronism type 1
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5
Q

What is the equation for total free water deficit?

A

Free water deficit = TBW x (Na-140)/140

TBW =0.6 male or 0.5 female x weight (kg)

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6
Q

DDx for nephrogenic DI?

A
  1. Congenital: Inherited mutations in genes for AVP V2-receptors or AQP2.
  2. Acquired
    1. Drugs: Lithium (most common), demeclocyline, amphotericin, foscarnet
    2. Hypokalemia, hypercalcemia
    3. Tubulointerstitial disease (problem with urine concentrating): CKD, post-ATN, post-obstruction, amyloid, Sjogren’s, medullary cystic
    4. Sickle cell disease (sickled RBCs occlude vasa recta, cause papillary damage -> medullary infarcts)
    5. Pregnancy/gestational DI (placenta producing AVPase)
    6. Protein malnutrition+excessive water intake
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7
Q

4 Non-drug reasons for increased ADH

A

1) Increase in serum osmolality
2) Volume contraction
3) Effective circulating volume depletion (despite low plasma osmolality): vomiting, cirrhosis, heart failure
4) Non-osmotic/Non-volume related: Nausea, Pain, Pregnancy

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8
Q

SIADH diagnostic criteria

A
  • Clinical euvolemic
  • Serum Osm low <275 mOsm/kg H20
  • Urine Na high (usually >40)
  • Urine Osm >300
  • Normal TSH and AM cortisol
  • Serum ADH high or in “normal” range (but inappropriately normal, given hypo-osmolar state)
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9
Q

8 drugs causing hyperkalemia and mechanism for each

A
  1. ACE/ARB - Blocks aldosterone production, decreased GFR
  2. Spironolactone – Blocks aldosterone receptor
  3. Septra – block EnAC
  4. Heparin – Impaired aldosterone metabolism
  5. NSAIDS – impaired release of renin, decreased GFR
  6. Beta-Blockers – impaired release of renin
  7. CNI – increased NCC at DCT, decreased delivery of sodium, impared na-k a principal cell, inhibit ROMK

Mechanisms of drug-induced hyperkalemia

1) Block ENac sodium channel in DCT Amiloride, triamterene, trimethoprim, pentamidine
2) Block Na-K ATPase in DCT Calcineurin inhibitors
3) Block aldosterone production ACEi, ARB, NSAIDS, Heparin
4) Block aldosterone receptors Spironolactone, eplerenone
5) Block K disposal Beta-blockers, digoxin, somatostatin

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10
Q

Function of principal cells and intercalated cells

A
  • Principal cells responsible for Na reabsorption and K excretion (ENAC channels and ROMK). Main Na+ reabsorbing cells and the site of action of aldosterone, K+-sparing diuretics, and spironolactone.
  • Type A and B intercalated cells make up the second cell type in the collecting duct epithelium.
    • Type A intercalated cells mediate ACID secretion and bicarbonate reabsorption.
    • Type B intercalated cells mediate BICARB secretion and acid reabsorption.
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11
Q

Tenofovir-induced RTA biopsy findings?

A
  • Biopsy shows proximal tubule eosinophilic inclusions with giant mitochondria, +/- HIV-findings
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12
Q

How does hypercalcemia affect the kidney?

A
  1. Vasoconstriction of afferent arteriole and decreased GFR
  2. Activation of Ca sensing receptors in loop of Henle -> inhibit NKCC channel -> volume contraction
  3. Inhibit ADH-dependent water reabsorption in collecting duct -> nephrogenic DI
  4. Distal RTA
  5. Nephrocalcinosis
  6. Nephrolithiasis
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13
Q

Pathophysiology of alkalosis in milk alkali syndrome for 1) initiation and 2) maintenance of alkalosois

A
  1. Initiation
    1. Alkali load from calcium carbonate
    2. Hypercalcemia-induced decreased GFR
  2. Maintenance
    1. Hypercalcemia-induced volume depletion/diuresis (CaSR LOH NKCC and AQP2) -> secondary hyperaldo
    2. Vomiting
      1. loss of H+
      2. volume contraction -> secondary hyperaldo
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14
Q

Factors influencing proximal bicarb reabsorption

A
  • Intracellular acidosis -> more available for luminal Na/H exchanger -> basolateral Na/HCO3 cotransporter
    • Metabolic acidosis
    • Hypokalemia
  • Decreased extracellular volume -> increased Na/HCO3 cotransporter reabsorption
  • Hormones:
    • Angiotensin II -> increase Na/HCO3 reabsorption
    • Glucocorticosteroids -> same
    • Endothelin-1 -> same
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15
Q

Calculation for FENa

A

FENa = [Urine Na x Serum Cr] / [Serum Na x Urine Cr] x 100%

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16
Q

Limitations of FENa

A
  1. High FENa:
    1. CKD - maximal tubular reabsorption of Na in response to volume depletion is impaired to begin with
    2. Diuretic use - can use FEUrea (<35%) instead (proximal absorption urea vs. loop/thiazide affect more distal), but has its own limitations too
    3. Non-reabsorbable anion - will impair proximal Na reabsorption (maintain urinary electroneutrality)
  2. Low FENa
    1. Neurohormonal activation leading to sodium retention/low FENa despite ATN eg. severe HF, liver failure, extensive burns
    2. Acute GN - low urine Na b/c tubular reabsorptive ability is intact and there is an acute decrease in glomerular surface area available for filtration ie. normal tubular function responding to acute decrease in GFR
    3. Non-oliguric interstitial nephritis - normal tubular function responding to acute decrease in GFR
  3. Also: Variability in timing of measurement
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17
Q

When is FEUrea not accurate?

A

When proximal salt and water reabsorption impaired:

  • acetazolamide
  • glycosuria eg. DM
  • osmotic diuresis eg. mannitol
  • cerebral salt wasting
  • increased urea excretion (high protein intake or catabolism)

Studies on FEUrea have not included patients with AIN, GN, obstruction, contrast

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18
Q

Causes of low FENa that is NOT pre-renal?

A
  1. Early ATN
  2. Acute GN
  3. Acute nonoliguric AIN
  4. Radiocontrast dye (ionic)
  5. Rhabdo
  6. TTP
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19
Q

Renal causes of hypomagnesemia

A
  • Think about sites of loss - prox tubule, TAL, and DCT
  • DDx:
    • Proximal tubule
      • Fanconi’s
    • TAL
      • Loop diuretic
      • (Barters - not really)
      • Hypercalcemia (stimulate basolateral CaSR in TAL)
      • Hypokalemia
    • DCT
      • Thiazide
      • Gitelmans
    • Other:
      • Gentamicin
      • Chemo (cisplatin)
      • CNIs
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20
Q

What is Gordon’s syndrome?

A

Pseudohypoaldosteronism type 2 (PHA2): Genetic mutation involving the NaCl transporter in DCT, causes hyperkalemia, hypertension, NAGMA, normal renal function, and low or low-normal plasma renin activity and aldosterone concentrations due to volume expansion.

Presents in childhood

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21
Q

Stimuli for ADH release?

A
  • Osmotic stimuli:
    • Hypertonic saline, mannitol
  • Non-osmotic stimuli:
    • Decreased effective circulating volume
    • Nausea
    • Pain
    • Pregnancy
    • Fructose
22
Q

How many ADH receptors and where are they located?

A
  • 3 receptors:
    • V1a - vascular and hepatioc
    • V1b - anterior pituiatry and pancreatic islet
    • V2 - renal
23
Q

Where are the AQP1, AQP2, AQP3, AQP4 channels located

A

AQP1- apical and basolateral proximal tubule and descending loop of Henle (not regulated by ADH)

AQP2 - apical collecting duct (regulated by ADH)

AQP3 - basolateral collecting duct(all)

AQP4 - basolateral collecting duct (in the inner medulla)

24
Q

Hormonal and physiologic factors that affect HCO3 reabsorption

A
  • Hormonal
    • Aldosterone
    • Angiotensin II
    • Cortisol
    • Endothelin-1
  • Physiologic
    • Hypovolemia
    • Hypokalemia
    • Acidosis
25
Q

Electrolyte abnormalities with aminoglycoside nephrotoxicity

A
  • Proximal dysfunction/Fanconi-like
    • Glycosuria, phosphaturia, uricosuria, aminoaciduria
  • Decreased proximal delivery
    • Hypomagnesemia
    • Hypokalemia
    • Hypocalcemia
26
Q

Pathophysiology and manifestations of aminoglycoside nephrotoxicity

A
  • Most of aminoglycoside gets renally excreted but 5-10% proximal tubular transport (it’s a cation)
  • Onset of AKI at 5-7 days
  • Distal tubular dysfunction
    • initially concentrating defect manifested as polyuria (decreased sensitivity to ADH)
  • Non-oliguric AKI with FeNa >1%
  • Reversible progressive loss of kidney function, lag until recovery after drug discontinued due to accumulation in renal cortical tissue. Complete recovery within several weeks.
  • Bland urinalysis
  • Fanconi-like syndrome: Urinary phosphate and magnesium wasting (magnesium depletion leads to hypokalemia and hypocalcemia)
27
Q

Mechanism of action and site of action of Lasix and amiloride

A
  1. Lasix – thick ascending Loop of Henle, inhibits NKCC channel
  2. Amiloride- Principal cell in collecting tubule, inhibits ENac at apical membrane (inhibit Na reabsorption)
28
Q

% filtered Na reabsorbed in the proximal tubule vs. TAL vs. DT, CT

A

% filtered NaCl reabsorbed:

  • Proximal tubule: 67% (Na-H exchange, Na cotransport with AAs/organic solutes, Na/H-Cl/anion exchange, paracellular reabsorption)
  • Thick ascending limb (Loop of Henle): 25% (Na-K-2Cl symport)
  • Distal tubule: 5% (NaCl symport)
  • Late distal tubule/cortical collecting duct: 3% (Na channels)
29
Q

Potassium handling in the nephron

A
  • Proximal tubule: 67% (passive reabsorption only)
  • Loop of henle (TAL): 20% (passive reabsorption only)
    • Reabsorb most K in proximal tubule, regulate with distal secretion
  • Distal convoluted tubule (late):
    • 3% reabsorbed if K-deplete (intercalated cells)… H/K ATPase (hydrogen out, k in)
    • 10-50% secreted if K-normal/high (principal cells) – predominant mechanism
  • Cortical collecting duct:
    • 9% reabsorbed if K-deplete
    • 5-30% secreted if K-normal/high
30
Q

Metabolic alkalosis DDx

A
  • Intracellular shift - hypokalemia
  • GI - vomiting (lose H), laxative abuse, villous adenoma, congenital chloride diarrhea
  • Renal
    • Excess mineralcorticoid (HTN)
    • Chloride-wasting diuretic, loop or thiazide (low/normal BP)
    • Barters, Gitelmans (low/normal BP)
    • Pendred syndrome (autorecess disorder/decreased pendrin activity ie. decreased HCO3/Cl exchanger in B-intercalated)
    • Posthypercapnic alkalosis
    • Hypercalcemia or milk-alkali
31
Q

Treatment for Bartter’s or Gitelman’s

A
  • Liberal sodium, potassium, magneisum intake and supplementation
  • NSAIDs to decrease GFR, and also inhibit prostaglandins, which are increased in Bartter’s
  • Decrease distal activity of Na/K exchanger (decrease K loss)
    • Amiloride
    • MRA
    • ACE/ARBs
  • Kidney transplantation (reverses without recurrence)
32
Q

Diagnosis in a 18 year old woman with HTN, hyperkalemia, low renin and low aldo?

A

Gordon’s syndrome

33
Q

3 drugs that inhibit Na channel in the CCD

A
  • Amiloride
  • Triamterene
  • Trimethoprim
34
Q

Patient with metabolic alkalosis and hypokalemia from vomiting, are each of the following high or low (acute):

pCO2

Urine Na

Urine K

Urine Cl

Urine HCO3

urine pH

A

pCO2 high (compensation)

Urine Na high (secrete bicarb)

Urine K high (proximal loss to get rid of bicarb, mild contribution from increased aldo activity to reabsorb Na at the cost of K secretion)

Urine Cl low (increased Na reabsorption)

Urine HCO3 high

Urine pH high (bicarbaturia)

35
Q

Patient with metabolic alkalosis and hypokalemia from vomiting, are each of the following high or low (CHRONIC):

pCO2

Urine Na

Urine K

Urine Cl

Urine HCO3

Urine NH4

urine pH

A

Everything same as acute except: (bicarb reabsorption does not exceed threshold anymore)

Urine Na low

Urine K low

Urine HCO3 low

Urine pH low

(not sure about NH4)

36
Q

Causes of hypophosphatemia

A
  1. Redistribution
    1. Insulin/refeeding syndrome
    2. Acute respiratory alkalosis
    3. Hungry bone syndrome
  2. Decreased GI absorption
    1. Malnutrition
    2. Chronic diarrhea
    3. Vitamin D deficiency
    4. Antacids - aluminum or magnesium-based
  3. Renal wasting
    1. Primary or secondary hyperparathyroidism
    2. Fanconi syndrome
    3. Acute volume repletion (proximal sodium wasting)
    4. Osmotic diuresis (glucosuria)
37
Q

Causes of hypophosphatemia early post-transplant?

A
  • Persistent hyperparathyroidism
  • High FGF-23
  • Massive initial diuresis
  • Osmotic diuresis from glucosuria
  • Impaired phosphate reabsorption from ischemic injury
  • Steroids (inhibit proximal reabsorption)
  • Continued phosphate binders
  • Malnutrition
38
Q

4 causes of hyperkalemia in HIV patient with PJP on multiple meds

A

Hyporeninic hypoaldosteronism /type 4 RTA due to HIV

Inhibition of ENaC/type 4 RTA due to Septra or pentamidine

Decreased GFR due to HIVICK

Adrenal insufficiency

39
Q

Pt w/ hypoK, low aldo, low renin, HTN. Dx?

A

Liddle’s

Apparent mineralocorticoid excess

Licorice ingeestion

Cushing’s syndrome exogenous steroids

CAH (11 B-hydroxylase deficiency)

40
Q

Factors that control renin release

A
  1. Decreased perfusion pressure in the afferent arteriole
  2. Activation of sympathetic nerve fibres via cardiac and arterial baroreceptors
  3. Decreased distal NaCl delivery to macula densa (eg. decreased GFR)
41
Q

Advantages and disadvantages of bicarb in treating cardiogenic shock

A
  1. Advantages (theoretical)
    1. Improve cardiac contractility
    2. Prevents tissue hypoperfusion from severe acidosis
  2. Disadvantages
    1. Post recovery metabolic alkalosis
    2. Hypernatremia/sodium load
    3. Volume overload
    4. Paradoxical decrease in intracellular pH (transiently increased bicarb, because converted to CO2, which moves into cells
42
Q

Why does post-hypercapnic metabolic alkalosis occur?

A

Chronic resp acidosis -> increased renal H+ excretion/NH4Cl loss, increased renal bicarb reabsorption -> normalize pH

Rapid lowering of pCO3 -> HCO3 remains elevated, especially if:

1) volume contracted
2) low eGFR
3) Cl- deficient

Treatment: volume replae with NaCl, replace K if low, acetazolamide

43
Q

Risk factors for osmotic demyelination syndrome

A
  1. Na <105 (or <120)
  2. Longer duration of hyponatremia (>2-3 days or chronic)
  3. Rapid rate of correction
  4. Alcoholic
  5. Malnourished
  6. Liver disease
  7. Hypokalemia
44
Q

Risk factors for cerebral edema

A
  1. Acute water intoxication in marathon runners, psychogenic polydipsia, ecstasy (ADH+intake)
  2. Postoperative fluid administration to those with elevated ADH (from pain, nausea, drugs, hypotension)
  3. Children
45
Q

How could you have a high FENa in DKA despite hypovolemia?

A

Osmotic diuresis, not correcting for glucose for serum Na

46
Q

% magnesium handling

A
  • PT: 25%, paracellular/passive
  • TAL: 65%, paracellular (claudin-16 and claudin-19)
  • DCT: 5% transcellular (TRPM6 apical, Na/Mg exchanger basolateral)
  • CT: <2%
47
Q

Difference between Bartters and Gitelmans

A

Bartters - concentrating defect present, hypercalciuria, usually normal Mg(or midlly low) and normal Ca, increased prostaglandins

Gitelman’s - hypoMg more prominent, hypercalcemia/hypocalciuria ie. impaired Ca excretion (normally thiazides increase proximal Ca reabsorption)

Similarities: both volume deplete, hypokalemic, metabolic alkalosis, normal UCl (because decreased Cl reabsorption with NKCC or NaCl inhibition)

48
Q

DDx for HTN and hypokalemia

A
  1. Renin (indirectly activates angiotensin II, which causes Na and water reabsorption) Increased PAC, Increased PRA
    1. Renal artery stenosis
    2. Renin-secreting tumor
  2. Adrenal: mineralocorticoid (releases aldosterone, which causes Na and water reabsorption) Increased PAC, Decreased PRA
    1. Primary hyperaldosteronism (Conns=adrenal adenoma, bilateral adrenal hyperplasia, adrenal carcinoma, GRA=glucocorticoid remediable aldosteronism)
  3. Adrenal: corticosteroid (stimulates mineralocorticoid activity) Decreased PAC, Decreased PRA
    1. Cushing’s syndrome
    2. Exogenous steroids
    3. Congenital adrenal hyperplasia
  4. Receptor (stimulates mineralocorticoid receptor) Decreased PAC, Decreased PRA
    1. 3) Licorice
    2. AMA=Apparent mineralocorticoid excess
  5. ENaC (upregulation of Na channel in DCT/CD) Decreased PAC, Decreased PRA
    1. Liddle’s syndrome
49
Q

3 electrolyte/metabolic changes with hyperglycemia

A
  1. Hyperosmolality
  2. Hyponatremia
  3. Hyperkalemia (in the setting of some insulin deficiency)
50
Q

% phosphate handling in nephron

A
  • Proximal:70-80% (Na/phos cotransporters)
  • Distal: 20-30% (unknown)

N (8 decks)

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