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MCC Part 1 > Nephrology > Flashcards

Nephrology Flashcards

1
Q

Acidemia

A

pH <7.35

- increase [H] ion in blood

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2
Q

Acidosis

A

Increasing [H] ion in arterial blood plasma (acidemia), pH <7.35

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3
Q

Alkalemia

A

pH >7.45

- reduced [H] in blood

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4
Q

Alkalosis

A

Reducing [H] ion in arterial blood plasma (aklalemia); pH >7.45

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5
Q

Henderson equation for H+

A

H (mEq/L) = 24 x PCO2/HCO3

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6
Q

Respiratory acidosis

A

pH <7.35
increased pCO2
increased HCO3

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7
Q

Metabolic acidosis

A

pH <7.35
decreased pCO2
decreased HCO3

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8
Q

Respiratory alkalosis

A

pH >7.45
decreased pCO2
decreased HCO3

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9
Q

Metabolic alkalosis

A

pH >7.45
increased pCO2
increased HCO3

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10
Q

Compensation appropriate?

A

Metabolic acidosis: HCO3 decreased by 1mmol/L, PCO2 decreased by 1.25 mmHg
Metabolic alkalosis: HCO3 increased by 1mmol/L, PCO2 increased by 0.2-0.9 mmHg
Acute respiratory acidosis: PCO2 increased by 10mmHg, HCO3 increased by 1mmol/L
Acute respiratory alkalosis: PCO2 decreased by 10mmHG, HCO3 reduced by 2.5mmol/L
Chronic respiratory acidosis: PCO2 increased by 10mmHg, HCO3 increased by 5mmol/L
Chronic respiratory alkalosis: PCO2 reduced by 10mmHG, HCO3 reduced by 5mmol/L

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11
Q

Anion Gap

A

AG = Na - Cl - HCO3
normal 8-14 mEq/L

increased in AG metabolic acidosis
**always calculate to make sure no mixed disorder

AG decreases by 4 for every drop of albumin by 10g/L

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12
Q

change gap

A

change HCO3 = 24 - HCO3
change AG = calculated - normal (12)

change HCO3 > change AG = simultaneous non-AG metabolic acidosis
change AG > change HCO3 = simultaneous metabolic alkalosis
change AG = change HCO3 = only AG metabolic acidosis

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13
Q

Ddx respiratory acidosis & tx

A

CNS
- brainstem injury (stroke, tumor)
- central sleep apnea
- obesity hypoventilation syndrome
Resp
- upper airway obstruction: laryngospasm, epiglottitis
- lower airway obstruction: COPD, asthma, sleep apnea
- dead space ventilation: infection, pleural effusion
Muscular
- myasthenia gravis, Guillain-Barre, myopathy, ALS, hypokalemia
Drugs
- opioids

Tx- intubation, mechanical ventilation, treat underlying disease, naloxone, etc.

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14
Q

Ddx AG metabolic acidosis & tx

A 
MUDPILES
Methanol
Uremia
DKA, alcoholic KA, starvation KA
Paraldehyde, phenformin, metformin
Iron, isoniazide
Lactic acidosis
Ethylene glycol
Salicylates
Cyanide
Arsenic
Toluene
Tx - correct underlying disorder; NaHCO3 if pH <7.2; 
HCO3 deficit (mmol) = (desired bicarb - measured bicarb) xweight (kg) x 0.6
replace 1/2 total deficit over 8-12h
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15
Q

Ddx Non-AG metabolic acidosis & tx

A 
USED CAR
Ureteroenteric fistula
Saline (IV NS)
Early renal failure
Diarrhea
Carbonic anhydrase inhibitors (acetazolamide)
Amphotericin
RTA I, II, IV
Tx - correct underlying disorder; NaHCO3 if pH <7.2; 
HCO3 deficit (mmol) = (desired bicarb - measured bicarb) xweight (kg) x 0.6
replace 1/2 total deficit over 8-12h
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16
Q

Ddx respiratory alkalosis & tx

A 
Cardiopulmonary
- hypoxia
- pneumonia
- early restrictive lung disease
- mild CHF
- PE
- mechanical ventilation
Non-cardiopulmonary
- fever, sepsis, anxiety, pregnancy, hyperthyroidism, liver failure
Drugs - salicylate, progesterone

Tx- underlying disorders, hyperventilation - rebreather into paperbag

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17
Q

Ddx metabolic alkalosis & tx

A 
Saline responders
- GI loss (vomiting, NG suction)
- renal loss (diuretics)
- skin loss (burns, sweat)
- reduced fluid intake
Saline non-responders
- mineralocortisolism (Conn's syndrome, Cushing syndrome)
- renin production (tumor)
- severe hypoK
- Gitelmann syndrome
- Barter syndrome
- HCO3 load (sodium bicarb infusion, citrate with transfusions, acetate with TPN)

Tx - saline responses = volume repletion
- saline non responders = tx underlying issue

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18
Q

Urinary Na vs. Cl re: volume status

A
  • metabolic acidosis = Na better surrogate for volume status (Cl excreted in excess with NH4+)
  • metabolic alkalosis = Cl better surrogate for volume status (Na excreted in excess with HCO3)
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19
Q

Hypomagnesemia

A
  • [Mg2+] <1.5 mEq/L pr 0.75mmol/L
    (normal 1.5-2 mEq/L or 0.75-1 mmol/L or 1.7-2.4 mg/dL)

often associated with hypoK and hypoCa (chronic hypoMg = reduced PTH secretion and bone response to PTH)

1% total Mg in ECF
70% Mg filterable -> calculating FEMg = x0.7
95% filtered Mg reabsorbed

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20
Q

Altered Mg excretion

A
  • hyperCa, hyperMg = reduced Mg reabsorption
  • reduced GFR = reduced Mg reabsorption
  • phosphate depletion = increase Mg excretion
  • chronic metabolic acidosis = increased Mg excretion
  • chronic metabolic alkalosis = decreased Mg excretion
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21
Q

Redistribution of Mg

A
  • hungry bones
  • referring syndrome (redistribution to bones)
  • DM
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22
Q

Hyperkalemia

A

Serum K >5 mEq/L

2% K extracellular
98% muscle, liver, RBCs

excretion mainly renal (minimal sweat)

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23
Q

K Adaptation

A
  • renal response to prolonged increase in K load
  • significant increase in efficiency of renal K excretion
  • mediated by enhanced activity of Na/K ATPase of renal principal cells
  • gradual return of K and aldosterone levels to normal
  • reabsorption of K in PCT and loop of Henle remains at constant rate
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24
Q

PsuedohyperK

A
  • hemolysis blood
  • severe leukocytosis
  • severe thrombocytosis
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25
Q

Ddx hyperK

A
  • shifting
  • increased efflux: damage to intracellular K storage, acidosis, succinylcholine, diazoxide, minoxidil, isoflurane, hyperkalemia period paralysis
  • decreased influx: lack of insulin, beta-blockers, dioxin OD
  • decreased excretion - reduced GFR, decreased aldosterone, volume depletion, decreased from stool/sweat
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26
Q

HyperK on ECG

A
  • peaked T waves (tented narrow based, >10mm in precordial, >5mm in limb leads or relatively tall vs. baseline)
  • shortened QT
  • prolonged PR interval, then QRS
  • P wave flattening then disappears
  • sine wave pattern (K>8)
  • ventricular standstill (flat line)
  • arrhythmias (bradycardia, v-tach, v-fib)
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27
Q

Tx hyperK

A 
ECG changes (K>7)
- calcium gluconate or calcium chloride (stabilize membrane)
No ECG changes (K = 6.5-7)
- insulin with glucose, B-agonist, sodium bicarb if acidotic (shifting) 
No ECG changes (K <6.5)
- diuretics, caution-exchange resins, dialysis (K removal)
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28
Q

HypoK

A

Serum K <3.5 mEq/L

  • often multifactorial, chronic and symptoms develop late
    approx. decrease by 0.27 mEq/L = 100mEq deficit
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29
Q

Diuretics and hypoK

A

Loop and thiazide diuretics = Cl depletion and hypovolemia with metabolic alkalosis
K depletion via
- increased flow and delivery of NaCl to CCD
- alkalemia (redistribution)
- hypovolemia with activation of RAAS

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30
Q

Severe/life threatening HypoK

A

K <2.5 - 3 mEq/L
sx - weakness starts in lower extremities and progresses to upper extremities, respiratory muscle paralysis, rhabdomyolysis; ileus; arrhythmias, ECG changes
TX
-replace immediately but caution re: rebound hyperK (max K IV rate 20 mEq/h, oral 60mEq)
40-60 mEq = increase K by 1-1.5 mEq/L

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31
Q

K shifting re: hypoK

A
  • increased Na/K ATPase activity –> insulin, b-adrenergic
  • increased pH (H out, K in)
  • hypoK periodic paralysis (mutation Ca channel)
  • increased uptake from plasma in acute increase hematopoietic cell production
  • hypothermia
  • barium, caesium, chloroquine intoxication (block K channels)
  • resperidone or quetiapine OD
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32
Q

Proteinuria

A

urinary total protein excretion >150 mg/d with >30mg/d albumin

  • > risk marker for cardiovascular disease
  • only albuminuria detected by urine dipstick (not reliable for microalbuminuria) -> check urine micro albumin to creatinine ratio (ACR) if risk of renal disease
  • urine protein to creatinine ratio (PCR) detects all protein in urine, not sensitive at low values

severity
>2g/d - likely glomerular disease
0.15 - 2g/d - likely tubular proteinuria, overflow proteinuria, or mild glomerular disease

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33
Q

Microalbuminuria

A

30-300 mg/d albumin

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34
Q

Nephrotic proteinuria

A

> 3.5g/d total protein

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35
Q

Ddx proteinuria

A
  • benign
  • transient intermittent (fever, dehydration, exercise)
  • orthostatic (>50mg/8h while upright)
    Persistent
  • Glomerular (glomerular permeability to protein)- nephritic syndrome, glomerularnephritis, systemic disorders; nephrotic syndrome, diabetic nephropathy, FSGS
  • Tubular (reduced reabsorption of filtered proteins)- tubule-interstitial disease, drugs, chronic pyelonephritis, Fanconi, sickle cell disease, etc.
  • Overflow (filtered load > tubular reabsorptive capacity)- multiple myeloma, MGUS, amyloid, hemoglobinuria, myoglobinuria
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36
Q

Normally excreted proteins

A

40% Tamm-Horsfall mucoproteins
40% albumin
20% Igs

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37
Q

Tx primary glomerular disease

A

corticosteroids, diuretics, cytotoxic agents, anti-HTN, plasmapheresis as indicated

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38
Q

Tx HTN related proteinuria

A

BP target <125/75

ACEI, ARBs preferred (proteinuria-reducing effect independent of anti-HTN)

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39
Q

Hyaline casts

A

No renal pathology - dehydration, diurectics

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40
Q

RBC casts

A

glomerular disease

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41
Q

Dysmorphic RBCs

A

upper urinary tract pathology

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42
Q

Intact RBCs

A

lower urinary tract pathology

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43
Q

WBCs, WBC casts, bacteria

A

UTI/inflammation

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44
Q

Fatty cast, oval fat bodies, free fat

A

Nephrotic proteinuria

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45
Q

Waxy, granular or cellular casts

A

Advanced chronic renal disease

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46
Q

Eosinophiluria

A

Acute interstitial nephritis

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47
Q

Glomerular filtration barrier

A
  • degree of proteinuria depends on integrity of barrier (charge and size) and intraglomerular (filtration) pressure
    Slit diaphragm - pores that limit passage
    Visceral glomerular epithelial cell (podocyte) foot processes
    GBM - limits size and negatively charged particles
    Cappilary endothelial cells - limit negative charged particles; fenestrations limit size
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48
Q

Nephrotic syndromes

A
  • proteinuria >3g/d
  • edema all over
  • BP, JVP normal/low
  • hyaline casts, lipid droplets on urine sediment
  • reduced albumin
  • Cr normal/increased
    Primary causes - minimal change disease, focal segmental glomerulosclerosis, membranous nephropathy, congenital nephrotic syndrome, Alport disease
    Secondary causes - diabetic nephropathy, amyloidosis, lupus nephritis, membranoproliferative glomerulonephritis, secondary membranous, secondary FSGS, preeclampsia, malaria, syphilis, HIV nephropathy
49
Q

Nephritic sydnrome

A
  • proteinuria <3g/d
  • minor edema
  • increased BP, JVP
  • +++ hematuria
  • urine sediment: RBC, WBC, RBC casts, granular casts
  • normal/mild decrease albumin
  • Cr usually increased
    Primary causes- IgA nephropathy, Wegener granulomatosis, antiglomerular basement membrane disease, lupus nephritis, postinfectious glomerulonephritis, endocarditis, membranoproliferative glomerulonephritis
50
Q

HyperNa

A

Na > 145 mEq/L

  • often when unable to experience or communicate thirst-
  • unreplaced H2O losses (skin, GI, GU, insensible from airway, hypothalamic lesion re: thirst)
  • sodium overload (salt poisoning, isotonic saline, hypertonic solutions, primary hyperaldosteronism)
51
Q

Serum osmolality re: HPA

A
  • increased plasma osmolality -> stimulate hypothalamic osmoreceptors -> ADH release -> maintain serum osmolality
52
Q

Na correction with hyperNa

A

max 8mEq/L for first 24h and 10mEq/L next 24h

  • overly rapid = cerebral edema
  • sx = impaired mental status, headache, memory loss, seizure, coma
53
Q

HypoNa

A

Na <135 mmol/L

- severe <120 or abrupt hypoNo = increased risk neurologic complications due to cerebral edema

54
Q

Hypovolemic hypoNa

A

pt lost both total body water and total body sodium but relative sodium loss, or water gain, is greater

55
Q

Normovolemia hypoNa

A

normal TBNa but excess TBW

56
Q

Hypervolemia hypoNa

A

increase in both TBNa and TBW, but relative excess of water

57
Q

How do you determine if ADH is present or suppressed with hypoNa?

A

Urine osmolality

- ADH surpassed if UOsm <100 most/kg, SG <1.003

58
Q

Calculation for plasma osmolality

A

= 2[Na] + [glucose] + [urea]

59
Q

Acute vs. chronic hypoNa sx

A

acute

  • mild: asx, nausea, malaise, anorexia, headache, lethargy, weakness, confusion
  • abrupt and severe: delirium, neuromuscular hyper excitability, seizure, coma, resp arrest, death
  • complications - brainstem herniation, hypothalamic and posterior pituitary infarction

chronic

  • cerebral adaptation - often asx
  • if sx: nausea, fatigue, gait instability, amnesia, confusion, lethargy, muscle cramps
60
Q

Management hypoNa

A
  • plasma osmolality
  • hypoosmolar - determine ECF volume
  • treat hypoNa re: pt sx
  • correct underlying abnormality

severe sx- 3% saline rapid correction at 1-2mmol/L/h for first 4h or sx improve
DO NOT correct >10-12 mmol/Lin first 24hr
raise Na by 4-6mEq/L within a few hours

  • Captains directly inhibit ADH - can be used in euvolemic or hypervolemic pt in hospital
61
Q

What do you do if serum Na rises by >10-12 in 24h?

A

Administer free water or exogenous ADH

62
Q

Risk of increasing Na by >8 mEq in first 24h?

A

Osmotic demyelination - central pontine myelinolysis: dysphagia, dysarthria, delirium, spastic paraparesis or quadriparxsis, locked-in syndrome, coma, death

63
Q

Acute renal failure

A

sudden, rapid, potential reversible fallen GFR leading to accumulation of nitrogenous waste products
sx - azotemia (reduced GFR, increased urea and Cr), abnormal urine volume (anuria = <100mL/24h or oliguria = 100-400mL/24h)

64
Q

Tubuloglomerular feedback

A

Na delivery to macula densa regulates afferent arteriolar tone
increased delivery = vasoconstriction

65
Q

Glomerulotubular balance

A

Proximal tubule tends to reabsorb constant proportion (rather than amount) of glomerular filtrate

66
Q

Renal portal circulation

A

afferent arteriole -> glomerular capillaries -> efferent arteriole -> vasa recta

67
Q

Countercurrent flow in vasa recta

A

PO2 higher in renal cortex and lower in renal medulla

68
Q

What part of the kidney is most vulnerable to ischemic injury (ischemic ATN)?

A

Medullary portions of proximal tubule and of the TAL - highest rate of energy-dependent solute transport

69
Q

Complications of ARF?

A
  • intravascular overload
  • hypoNa
  • hyperK
  • hyperphosphatemia
  • hypoCa
  • hyperMg
  • hyperuricemia
  • metabolic acidosis

Other

  • anemia
  • leukocytosis
  • bleeding diathesis (secondary to uraemia-induced lately dysfunction)
  • progress to CRF
  • uremic syndrome
70
Q

Ddx ARF

A

Prerenal

  • renal hypoperfusion
  • systemic hypo perfusion

Intrinsic

  • renovascular
  • glomerular
  • tubular and interstitial

Postrenal/ obstructive

  • renal pelvis
  • ureter
  • bladder
  • bladder neck/ urethral
71
Q

Chronic renal failure = chronic kidney disease

A
  • evidence of renal damage OR moderately to severe impaired GFR (<60mL/min) for at least 3mo

target BP <130/80

72
Q

Renal function?

A
  • maintain ECF volume and osmolality
  • produce EPO
  • Ca homeostasis (via activation vit. D and tubular handling of Ca and phosphate under PTH)
  • electrolyte balance
  • acid-base balance (excretion H, recovery HCO3)
73
Q

Stages of CKD

A

Stage 1: GFR >90 - normal to increased GFR with evidence of kidney damage
Stage 2: GFR 60-89 - mildly decreased GFR with evidence of kidney damage
Stage 3: GFR 30-58 - moderately decreased GFR
Stage 4: GFR 15-29 - severely decreased GFR
Stage 5: <15 or dialysis - ESRD or renal failure

74
Q

Ddx CKD

A

Prerenal
- renal vascular disease

Renal

  • glomerular disease (primary): focal segmental glomerulosclerosis, IgA nephropathy
  • glomerular disease (secondary): HTN nephropathy, SLE< diabetic nephropathy, vasculitides, HIV, HBV, HCV
  • tubulo-interstitial - chronic intersitial nephritis, cystic kidney disease

Postrenal
- Obstructive nephropathy

*DM (25-35%) and HTN (15-20%) most common causes of CKD

75
Q

Hematuria

A

> 2 RBCs per HPF

76
Q

Microhematuria

A

presence of RBCs in urine without visible change in urine colour

77
Q

Macrohematuria

A

red or brownish urine

78
Q

Persistent hematuria

A

hematuria on at least 2 urine samples at least 1 mo apart

79
Q

Ddx hematuria

A 
Dyes: medications, food, metabolites
Pigmenturia: hemoglobin, myoglobin
True hematuria: fever, exercise 
- Glomerular
- Renal
- Ureter
- Bladder
- Prostate/urethra
Mimics of hematuria - contamination of urine with menses, GI bleed, atrophic vaginitis
80
Q

Investigations hematuria

A
  • urine dipstick
  • microscopy
    + labs if indicated
    + imaging if indicated

All pt should have urine culture to r/o infection and recheck urine in 6wk
No dx with cultures and imaging -> cystoscopy to r/o malignancy

81
Q

Recurrent nephrolithiasis investigation and tx

A

investigations - stone analysis, 24h urine collection for urine volume, pH, calcium, phosphorus, oxalate, citrate, rate, cysteine, sodium; urine culture
tx - increase fluid intake at least 2L/d, dietary modifications, hydrochlorothiazide for hypercalciuria, citrate for hypocitraturia, allopurinol for hyperuricosuria

82
Q

Urine dipstick

A
  • gold standard to detect hematuria
  • very sensitive
  • detects dyuria
  • negative in pigmenturia
83
Q

Urine microscopy

A

differentiate hematuria vs. dyuria (RBCs)

84
Q

Glomerular hematuria

A
  • process involving glomerular structure and characterized by dysmorphic RBCs (acanthocytes), RBC casts, proteinuria, no blood clots
85
Q

Extraglomerular hematuria

A
  • proteinuria, blood clots
86
Q

Polyuria

A

> 3L urine output/24h in adults and 2L/m^2 in kids

87
Q

Polydipsia

A

increased thirst and water intake

88
Q

Ddx polyuria

A
  • water diuresis - urine osmolality <250mOsm/kg (primary polydipsia, hypoosmolar fluid load, central DI, nephrogenic DI)
  • osmotic diuresis - urine osmolality >250mOsm/kg (glucose, mannitol, urea, iso/hyperosmotic fluid loads)
89
Q

Where is ADH produced?

A

By magnocellular neutrons of supraoptic and paraventricular nuclei in hypothalamus and transported via their dendrites to posterior pituitary where it is released

90
Q

Stimulation of ADH release?

A

changes in blood osmolality sensed by hypothalamic osmoreceptors

91
Q

ADH action

A

ADH receptors -> aquaporins released from intracellular vesicles into the luminal membrane
-> water can enter cell and be reabsorbed into blood vessels

92
Q

Ca form in blood?

A

40% free ionized Ca (metabolically active)

60% protein bound Ca

93
Q

How is serum Ca regulated?

A

PTH -> increase Ca (PTH released bc low Ca = acts on bone to increase resorption and kidney to increase reabsorption and increase Vit. D)
Vit. D -> increases intestinal Ca absorption (produced because PTH and low serum Ca)

94
Q

What 2 blood properties can alter serum Ca?

A

albumin - low albumin = low Ca
pH - acidosis = reduced protein binding Ca
- often free ionized Ca same so measure ionized Ca levels

95
Q

How do you correct Ca for albumin?

A

Ca falls 0.2mmol/L for every 10g/L drop in albumin

96
Q

Ddx hyperCa

A
  • increased bone resorption (hyperparathyroidism, malignancy, hyperthyroidism, immobilization)
  • increased Ca absorption (increased intake, increased vit. D)
  • decreased excretion (thiazide diuretics, familial hypocalciuric hypercalcemia)
97
Q

HyperCa sx

A

Ca >3.5 mmol/L

- confusion, stupor, coma, ARF, profound weakness

98
Q

HyperCa tx

A

Pt sx and Ca >3.5

  • IV rehydration, calcitonin, bisphosphonate therapy (pamidronate)
  • hemodialysis if severe hyperCa and renal failure

If Vit D excess then start prednisone

99
Q

Ddx hypoCa

A

PseudohypoCa
- low serum Ca but normal ionized Ca (hypoalbuminemia)
Spuriouas hypoCa
- low serum Ca after injection of gadolinium-based contest agents
True hypoCa
- excessive loss (extravascular deposition, renal losses)
- decreased absorption (vit. D deficiency, reduced PTH, PTH resistance, drugs)

100
Q

Workup hypoCa

A
  • true? check ionized Ca
  • PTH?
    low PTH - check Mg
    high PTH - check GFR (low = renal failure, high = check vitamin D)
101
Q

Symptoms hypoCa

A

Ca <1.9 mmol/L

  • parenthesis, carpopedal spasm, tetany, seizure
  • Trousseau or Chvostek sign, bradycardia
  • Prolonged QT
102
Q

What is Trousseau sign?

A

A sign of latent TETANY = carpopedal spasm caused by inflating the blood-pressure cuff to a level above systolic pressure for 3 minutes

103
Q

What is Chvostek sign?

A

Twitching of the facial muscles in response to tapping over the area of the facial nerve

104
Q

Management hypoCa

A

Ca <1.9 and sx?
- if prolonged QT give IV calcium gluconate 1-2g IV
- i no QT prolongation give oral calcium carbonate 1500- 2000mg daily
If hypoMg
- start Mg replacement
If Vit D deficient or hypoparathyroid
- start 1000U vit D
- use calcitriol 0.25 micrograms if renal failure
- add thiazide diuretic if hypercalciuria develops

105
Q

Normal plasma phosphate?

A

1-1.5 mmol/L

- most abundant intracellular anion

106
Q

Where is most of total body phosphorus?

A

85% in bones and teeth

1% in extracellular fluid

107
Q

What anion is needed for metabolic processes such as formation of high energy ATP and components of cell membranes?

A

Phosphorus

108
Q

What organ is primary regulator of phosphate?

109
Q

How is plasma phosphate regulated?

A

Humoral factors regulating renal phosphate excretion and GI phosphate absorption
- PTH (increased PTH = increased urine phosphate excretion; decreased vit D = decreased dietary phosphate absorption)
- Phosphatonins
Local factors (e.g. insulin)

110
Q

Ddx hyperphosphatemia

A
  • Acute high phosphate load - cell lysis (e.g. rhabdomyolysis, hemolysis), translocation of intracellular phosphate (lactic acidosis, ketoacidosis), exogenous load (phosphate-containing laxatives, IV phosphate)
  • Renal failure (reduced filtration and excretion)
  • Increased GI absorption (excess vit. D)
  • Increased renal phosphate reabsorption (hypoparathyroidism, acromegaly, medications, familial tumoral calcinosis)

Pseudohyperphosphatemia
- interference of assay by immunoglobulins, bilirubin, hemolysis, hyperlipidemia, liposomes amphotericin B

111
Q

Does hyperphosphatemia commonly occur with CKD?

A

Yes re: reduced GFR

- dietary phosphate restriction and phosphate binders important

112
Q

What can occur with uncontrolled hyperphosphatemia?

A
  • secondary hyperparathyroidism
  • renal osteodystrophy
  • tissue calcium/ phosphate deposition
  • risk factor for death
113
Q

Investigation for hyperphosphatemia

A
  • exclude hemolysis - bilirubin, LDH, hepatoglobin, peripheral smeal
  • rhabdomyolysis - CK, myoglobinuria
  • tumor lysis - uric acid (esp. with hyperK)
  • lactate, ketones, PTH, Cr, BUN, Ca
114
Q

Management hyperphosphatemia

A

acute should resolve in hours

  • fluids may increase excretion (but avoid hypoCa)
  • hemodialysis if severe hypoCa and renal dysfunction
  • low phosphate diet and binding of dietary intestinal phosphate if chronic
115
Q

Ddx hypophosphatemia

A

Phosphate redistribution
- refeeding syndrome, DKA, insulin secretion, hungry bone syndrome, hyperventilation with acute respiratory alkalosis
Reduced GI absorption
- poor oral intake, phosphate binding GI tract by antacid medications (Al3+, Mg2+, Ca2+)
- chronic diarrhea with malabsorption
Increased renal excretion
- hyperparathyroidism, vit D deficiency, Fanconi syndrome, oncogenic osteomalacia, hereditary hypophosphatemic rickets, diuresis

Spurious hypophosphatemia with paraproteinemia and interference with assay

116
Q

Workup hypophosphatemia

A

24h urine phosphate excretion and fractional excretion phosphate - renal wasting?

117
Q

Management hypophosphatemia

A

Phosphate <0.64mmol/L and asx - replete with oral phosphate, high phosphate diet
Phosphate <0.32mmol/L and pt sx or can’t take PO, replete IV phosphate until >0.48mmol/L then switch to PO
- replace at half dose if pt has renal dysfunction
- potassium or sodium phosphate (no potassium phosphate in renal dysfunction)
Dipyridamole if primary urine potassium wasting

118
Q

Risks of rapid phosphate infusion?

A

Calcium-phosphate precipitation
AKI
Arrhythmias

119
Q

What causes the clinical consequences of hypophosphatemia?

A

Altered bone and mineral metabolism
Reduced production of cellular ATP
- often sx when <0.64 and severe <0.32

MCC Part 1 (22 decks)

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