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Internal Medicine > Renal > Flashcards

Renal Flashcards

1
Q

What is the cause of mucosal bleeding in CKD?

A

Increased urea –> inhibits arginine conversion to urea and shunts it towards GSA –> nitric oxide –> decreased vWF secretion, decreased ADP and thromboxane A2, and decreased GP IIb/IIIA receptor activation –> decreased platelet adhesion, activation and aggregation

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2
Q

Membranous nephropathy - what kind? Associated secondary causes?

A

Nephrotic syndrome, subepithelial deposits, gradual podocyte damage, subacute presentation (vs acute for minimal change disease)

Malignancy
Infection (Hep B/C, syphilis)
Autoimmune (eg lupus, thyroiditis)
Drugs (NSAIDs)

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3
Q

Amyloidosis - what kind? Risks?

A

Nephrotic syndrome - glomerular amyloid deposition

Risk of restrictive cardiomyopathy

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4
Q

What does low urine chloride in metabolic alkalosis suggest?

A

Body depletion of chloride (e.g. vomiting, diuretic overuse) –> should replete with normal saline

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5
Q

Acute papillary necrosis - most causes, signs

A
  1. Analgesic overuse
  2. Sickle cell anemia

Signs:
AKI, hematuria, flank pain, fever

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6
Q

Desmopressin indications and adverse effects

A
  1. Diabetes insipidus
  2. Mild-moderate heavy menstrual bleeding associated with vWD

Adverse: Induces effects of ADH –> hypotonic hyponatremia with euvolemia (due to increased natriuretic peptide secretion)

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7
Q

Hypercalcemia symptoms

A
  1. Nausea
  2. Polyuria
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8
Q

When does hypercalcemia of immobilization occur?

A

After 4 weeks

May be as soon as 3 days in those with chronic renal insufficiency

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9
Q

How does acute rhabdomyolysis affect calcium?

A

Precipitation of calcium and phosphorus in damaged muscles –> hypocalcemia

During diuretic/recovery phase, hypercalcemia and hyperphosphatemia

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10
Q

What are paraneoplastic syndromes of renal cell carcinoma?

A
  1. EPO production
  2. Hypercalcemia
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11
Q

What should be used to relieve urine in acute bacterial prostatitis?

A

Suprapubic catheter - don’t want to spread bacteria from prostate upward or rupture prostate

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12
Q

Ureteral stone - medication?

A

Alpha blocker (e.g. tamsulosin) for stones >5 and <=10 mm to facilitate passage

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13
Q

How do kidneys respond to metabolic acidosis from non-renal etiology?

A
  1. Increased bicarbonate reabsorption (Cl excretion increases via beta-intercalated cells in collecting duct)
  2. Increased excretion of ammonium and dihydrogen phosphate
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14
Q

Oliguria definition

A

<500 mL of urine/24 hours

Often present in prerenal AKI

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15
Q

Hypocalcemia signs

A
  1. Paresthesia
  2. Hyperreflexia
  3. Trousseau sign (BP cuff inflated >SBP 3 min causes carpopedal spasm)
  4. Chvostek sign (tapping facial nerve causes ipsilateral facial muscle contraction)

Tetany, seizure, others

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16
Q

When is bicarb indicated in metabolic acidosis?

A

When pH<7.2

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17
Q

Why does DKA have hyperkalemia but total potassium deficit?

A

Osmotic diuresis, elimination of ketoacid anions as potassium salts, and secondary hyperaldosteronism from volume contraction lead to potassium deficit

Hyperkalemia due to hyperosmolarity and diminished insulin

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18
Q

Fibroblast growth factor 23

A

Lowers phosphate by decreasing intestinal absorption and increasing renal excretion

Increased in phosphate retention and secondary hyperPTH due to CKD

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19
Q

What is suggested by hypercalcemia with renal injury?

A

Malignancy (eg multiple myeloma)

Normally kidney injury results in hypocalcemia due to decreased phosphate excretion

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20
Q

How do loop and thiazides affect calcium and sodium in kidney

A

Loop: promote Ca wasting
Thiazide: decreases urinary excretion

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21
Q

Adrenal vein sampling - purpose

A

Differentiate between adrenal hyperplasia and adenoma

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22
Q

Tumor lysis syndrome prophylaxis for AKI

A

Normal saline
Allopurinol or rasburicase

Hyperuricemia and hyperphosphatemia lead to uric acid and calcium phosphate stones, respectively

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23
Q

How to avoid contrast-induced AKI?

A

0.9% saline increases intravascular volume first

Do not give if already volume overloaded

Would expect to see creatinine rise 24-48h after administration

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24
Q

What electrolyte disturbance in alcohol use causes refractory hypokalemia?

A

Hypomagnesemia - intracellular magnesium normally inhibits renal outer medullary potassium (ROMK) pump, preventing excessive K+ loss

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25
Q

Diabetic nephropathy - injury to what part?

A

Basement membrane and adjacent structures
-Albuminuria (albumin-creatinine ratio 30-300 mg/g

Random urine test should be done at diagnosis (type 2) or 5 years after type 1

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26
Q

Diabetic nephropathy - treatment

A

BP control: ACEi/ARB
Glycemic control: SGLT2 inhibitor or GLP-1 agonist

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27
Q

Opioid meds to avoid in kidney disease

A

Morphine
Tramadol
Codeine
Meperidine

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28
Q

How to alkalinize urine for uric acid stones?

A

Potassium citrate

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29
Q

Diabetes predisposes to which stones?

A

Uric acid stones

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30
Q

How does CKD affect phosphate and calcium?

A

Hyperphosphatemia
Hypocalcemia
Secondary hyperPTH

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31
Q

Calcium in which direction causes seizures?

A

Severe hypocalcemia -> neuronal hyperexcitability

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32
Q

When is serum osmolality possible helpful in evaluating hyponatremia?

A

When suspected hypertonicity (e.g. hyperglycemia causing translocational hyponatremia) or isotonicity (e.g. hyperlipidemia causing lab artifact pseudohyponatremia)

Otherwise, most likely hypotonic

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33
Q

How does PTH affect alk phos?

A

Increased

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34
Q

Nephrotic syndrome infection risk

A

Loss of IgG -> decreased humoral immunity, particularly to encapsulated organisms

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35
Q

Nephrotic syndrome effect on anemia

A

Via loss of transferrin, erythropoietin

36
Q

Nephrotic syndrome effect on vitamin D

A

Deficiency due to loss of vit D-binding protein

37
Q

ADPKD effects from cyst development

A

Hypertension - cysts cause ischemia, resulting in RAAS
Polyuria/nocturia - mild, neprhogenic diabetes insipidus from cyst damage to distal tubules and receipt of vasopressin signals

38
Q

Milk-alkali pathogenesis

A

Calcium carbonate antacids:
Hypercalcemia causes renal vasoconstriction, decreased GFR

Calcium inhibits NaK2Cl cotransporter due to activation of calcium-sensing receptors in thick ascending tubule
Ca impairs ADH activity
These cause hypovolemia and increased bicarb reabsorption, compounding alkali intake

39
Q

Milk-alkali risk factors

A

CKD
Thiazide use (increased Ca retention)
ACEi, NSAIDs (decreased GFR)

40
Q

How do loop diuretics affect calcium and magnesium levels?

A

Hypocalcemia and hypomagnesemia - blocking NaK2Cl prevents K reabsorption, leading to Ca and Mg loss

41
Q

Why does metabolic alkalosis (hypochloremic hypokalemic from vomiting, NG, diuretics) benefit from normal saline?

A

Replenishes Cl to help bicarb excretion by kidneys
Restored volume to decrease RAAS signaling, reducing loss of K and H from kidneys

42
Q

What protein is proteinuria?

A

> 3.5 g/day

43
Q

“Spike-and-dome”: Diffuse BM thickening with subepithelial granular deposits (light) and IgG/C3 (IF)

A

Membranous nephropathy

Primary: anti-PLA2R Ab serology or antigen on tissue stain
Secondary: Solid tumors, infections, SLE, NSAIDs

44
Q

Describe typical urinalysis for myeloma at diagnosis

A

Bland with granular casts and protein detecting albumin moreso than Ig; elevated creatinine

45
Q

Severe hypercalcemia treatment

A

Aggressive hydration
Calcitonin

Bisphosphanates are more for long-term management

46
Q

Why do patients with hypercalcemia have polyuria?

A

Calcium-induced nephrogenic diabetes insipidus
Poor oral intake (hypercalcemia causes confusion, stupor)

47
Q

What is one of the most common causes of humoral hypercalcemia of malignancy?

A

Renal cell carcinoma

48
Q

Euvolemic hyponatremia occurs with…

A

SIADH

Treat with salt tablets and oral fluid restriction

49
Q

Loop diuretic-induced metabolic alkalosis - treatment

A

Acetazolamide

Do not use if volume-depleted

50
Q

What is the Cl/HCO3 exchanger?

A

Pendrin

Cl depletion (from vomiting) impairs renal HCO3 excretion

51
Q

When is ammonium chloride used?

A

Metabolic alkalosis when volume overloaded and cannot receive normal saline

52
Q

Most common causes of death in ESRD

A
  1. Cardiovascular - Metabolic (hyperphosphatemia) + increased calcium load (vitamin D supplementation) lead to arterial calcification, uremia and renal replacement therapy cause oxidative stress, anemia
  2. Infection
53
Q

Muscle cramps and weakness after thiazide for high blood pressure

A

Consider hyperaldosteronism, with hypokalemia causing symptoms

54
Q

What causes the acidosis in DKA?

A

Lipolysis and fatty acid breakdown to ketones in the liver; vomiting, abdominal pain, and Kussmaul respirations result to get rid of acidity

55
Q

Membranoproliferative GN vs membranous nephropathy vs diffuse proliferative

A

Membranoproliferative: Hep C/cryoglobulinemia, monoclonal gammopathy; nephritic

Membranous: primary PLA2R Ab or secondary solid tumors, NSAIDs, Hep B, lupus nephritis

Diffuse proliferative: lupus nephritis only

56
Q

IgA vasculitis requires what follow-up?

A

Serial urinalyses

57
Q

Nonblanching, palpable purpura of buttocks and lower extremities and arthralgia of lower extremities

A

IgA vasculitis

58
Q

Low Mg can lead to low what electrolytes?

A

K and Ca - due to impaired mobility out of cells

59
Q

Mg toxicity due to renal impairment - treatment

A

Ca gluconate IV - stabilizes myocardium similar to why it’s used with hyperkalemia

Dialysis for severe

60
Q

Mg toxicity - signs

A

Nausea, flishing, headache, hyporeflexia
Somnolence, areflexia, hypocalcemia
Cardiac or respiratory paralysis

61
Q

When to give sodium bicarb for acidosis?

A

Only when pH <7.1

Sodium bicarb can cause myocardial depression and increase lactic acid production

62
Q

What is normal osmolality, and what is formula?

A

2xNa + glu + BUN/2.8

Normal range 275-295

63
Q

How do urine findings help differentiate in setting of hypotonic, hypovolemic hyponatremia?

A

Urine Na <40: nonrenal salt loss (e.g. vomiting, diarrhea)
Urine Na >40: renal salt loss (e.g. diuretics, primary adrenal insufficiency)

64
Q

How do urine findings help differentiate in setting of hypotonic, euvolemic hyponatremia?

A

Urine osmol <100: Primary polydipsia; malnutrition (e.g. beer potomania)
Urine osmol >100 and urine Na >40: SIADH (after ruling out hypothyroidism and secondary adrenal insufficiency)

65
Q

Difference between emphysema and chronic bronchitis DLCO

A

Emphysema: decreased DLCO
Chronic bronchitis: normal DLCO

66
Q

Why is glomerular hematuria darker?

A

More time in nephrons results in hemoglobin oxidization to methemoglobin

67
Q

High osmolal gap in metabolic acidosis

A

Measured osmolality - calculated osmolality

High osmolal gap suggests active metabolites in serum, such as toxic alcohols

Normal osmolal gap indicates other causes, including lactic acidosis or salicylates

68
Q
A
69
Q

Hypernatremia algorithm: urine osmolality <300 vs >600, urine Na <1% vs >2%

A

<300: Diabetes insipidus
>600: <1% Na: extrarenal fluid loss
>2% Na: sodium gain

70
Q

Isotonic (serum osmolality 275-295) hyponatremia vs hypertonic (>295) hyponatremia

A

Isotonic: Lipids, proteins
Hypertonic: Glucose, contrast agents

Mannitol can contribute to both

71
Q

How do urine findings help differentiate in setting of hypervolemic hyponatremia?

A

Urine Na <40: CHF, cirrhosis, nephrotic syndrome
Urine Na >40: AKI, chronic kidney failure

72
Q

Envelope-shaped crystals in urine - cause

A

Urine calcium oxalate = ethylene glycol

73
Q

Saline-resistant metabolic alkalosis

A

Urine Cl >20, Cl wasting - caused by hyperaldosteronism, Bartter or Gitelman syndrome

74
Q

Negative vs positive urine anion gap

A

UAG = Na + K - Cl; increased Cl in urine means increased ammonium NH4 excretion

Negative suggests proximal/type 2 RTA or GI bicarb loss
Positive suggests distal/type 1 RTA (impaired NH4 excretion)

75
Q

Fatty casts are seen in…

A

Nephrotic syndrome

76
Q

“Tram track” double-layered basement membrane; subendothelial and mesangial deposits

A

Membranoproliferative GN - can be immune complex-mediated (primary in children, secondary to HBV/HCV/SLE/cryoglobulinemia) or complement-mediated (low C3)

77
Q

Which nephritic syndrome may require plasma exchange therapy?

A

Goodpasture syndrome
Also pulsed steroids and cyclophosphamide

78
Q

Minimal change disease - treatment

A

Steroids

79
Q

Nodular glomerulosclerosis (Kimmelstein-Wilson nodules)

A

Diabetic nephropathy or renal amyloidosis

80
Q

Low pH stones

A

Uric acid
Calcium oxalate
Cystine

Note: calcium phosphate and struvite stones are high pH

81
Q

Stone shapes

A

Envelope/dumbbell: calcium oxalate
Wedge-shaped prism: calcium phosphate
Staghorn: struvite
Rhomboid: uric acid
Hexagonal: Cystine

82
Q

Thiazides may be used to treat what stones?

A

Calcium oxalate, NOT calcium phosphate that is 2/2 hyperPTH

83
Q

Positive urinary cyanide nitroprusside test for stone

A

Cystine stone

84
Q

Chronic pyelonephritis due to infected kidney stone obstruction can cause…

A

Xanthogranulomatous pyelonephritis - observe multiple, dark round areas on CT (Bear Paw sign)

85
Q

Nephrogenic DI - treatment

A

Salt restriction, HCTZ, amiloride, low-protein diet

86
Q

SIADH - treatment

A

Fluid restriction, IV hypertonic saline if necessary
Severe: ADH antagonists (e.g. tolvaptan)
Chronic: Demeclocycline

Internal Medicine (23 decks)

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