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Renal > Renal UWorld 1 > Flashcards

Renal UWorld 1 Flashcards

0
Q

What is under the 12th rib?

A

Medially: parietal pleura
Laterally: kidney (fractured rib can lacerate kidney)

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1
Q

Tx of mucormycosis and side effects

A

Amphotericin B. High renal toxicity. Renal vasoconstriction, reduced GFR. Acute tubular necrosis, renal tubular acidosis, severe hypokalemia and hypomagnesema

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2
Q

Fabry Disease

A

X-linked recessive lysosomal storage disesae: deficiency in a-galactosidase A –> buildup of ceramide trihexoside in tissues. Presents with decreased sweating, angiokeratoma, peripheral neuropathy/pain. Can cause cardio/renal disease, progress to renal failure.

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3
Q

DKA urine findings

A

Kidneys are attempting to correct: high H+, low bicarb (to try to recycle it and get it back up to normal), high H2PO4- and NH4+ to help get rid of more acid

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4
Q

Initial tx for acute decompensated CHF

A

Loop diuretics

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5
Q

Most potent class of diuretic

A

Loop

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6
Q

Side effects of loop diuretics

A

OH DANG: ototoxicity, hypokalemia, dehydration, allergy, nephritis, gout

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7
Q

Diuretic that causes gynecomastia

A

Spironolactone

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8
Q

Wegener’s granulomatosis with angiitis: 3 major symptoms, marker

A
  1. Lung - cough, hemoptysis, etc.
  2. Upper respiratory
  3. Renal disease - RPGN, aka crescentic

c-ANCA

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9
Q

PAH (para-aminohippurate) used to estimate

A

Filtered and secreted, not resorbed. Estimates renal plasma flow

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10
Q

Kidney transplant: fever, decreased urine, and interstitial infiltration by mononuclear cells one week after. What kind of rejection? Mediated by what? Prevention?

A

Acute. Mediated by host T-cell sensitization against graft MHC antigens. Prevention with calcineurin inhibitors and steroids.

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11
Q

Renal cell carcinoma: Chromosomal deletion? Involving what genes?

A

3p deletion, involving vHL gene (hereditary form of RCC).

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12
Q

Von Hippel-Lindau disease

A

Autisomal dominant deletion of VHL gene on chromosome 3p. Cerebellar hemangioblastomas, renal cell carcinomas, pheochromocytomas. VHL is a tumor suppressor.

NOTE: VHL disease is rare, but deletions/mutations are pretty common

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13
Q

What drug prevents recurrence of calcium oxalate stone formation?

A

HCTZ or citrate. Need something that decreases calcium in urine. HCTZ causes hypovolemia –> salt reabsorption, including passive Ca. Also, by inhibition of Na/Cl cotransporter –> activation of basolateral Na/Ca antiporter, enhancing Ca reabsorption

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14
Q

Proteinuria > 4.5g in 24 hours, glomerular capillary wall thickening with no increase in cellularity, stain shows irregular spikes from GBM. Hx of colon cancer. Dx?

A

Membranous glomerulopathy

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15
Q

Acute angle glaucoma treatment

A

Acetazolamide, c.a. inhibitor. Block NaHCO3 and water reabsorption. Also reduces aqueous humor production

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16
Q

Nephrotic syndrome associated with IgG antibodies to phospholipase A2 receptor

A

Membranous nephropathy

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17
Q

Nephrotic syndrome associated with SLE

A

membranous nephropathy

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18
Q

antibodies to GBM and alveolar BM

A

Goodpasture syndrome, a rapidly progressive, crescentic, glomerularnephritis

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19
Q

In Crescent glomerulonephritis (RPGN), what is the crescent made of?

A

Fibrin, plasma proteins (C3b), IgG

20
Q

Filtration fraction

A

= GFR/RPF
Normal = 20%

RPF = (1-Hct)(Renal blood flow)

21
Q

What can you use to estimate GFR?

A

Creatinine clearance

22
Q

What can you use to estimate PAH clearance

A

Renal plasma flow

Remember RPF = (1-Hct)(Renal blood flow)

23
Q

Aspirin OD: what happens?

A

1) Respiratory alkalosis via salicylate induced hyperventilation (immediate)
2) Anion gap metabolic acidosis via accumulation of organic acids (hours)

24
Q

Winter’s formula: what is it and how is it used?

A

Used for predicted respiratory compensation for a metabolic acidosis: PCO2 = 1.5 [HCO3] + 8, +/- 2

If measured PCO2 is different from predicted, there is a mixed disturbance

25
Q

Calculation of anion gap

A

AG = Na - (Cl + HCO3) in a metabolic acidosis

26
Q

Metabolic acidosis with normal anion gap

A

HARDASS

Hyperalimentation, addison disease, renal tubular acidosis, diarrhea, acetazolimide, spironolactone, saline infusion

27
Q

Metabolic acidosis with high anion gap

A

Indicates presence of some unmeasured anion (acid)
MUDPILES
Methanol, uremia, dka, propylene glycol, Iron tabs, lactic acidosis, ethylene glycol, salicylates

28
Q

Hyperacute rejection of transplant mediated by

A

Preformed antibodies against donor antigens. Type II hypersensitivity

29
Q

Immediate hypersensitivity

A

Type I hypersensitivity. Occurs after initial exposure to antigen –> IgE class switching. Anaphylaxis, urticaria, asthma, seasonal allergies.

30
Q

Calculate GFR

A

= k (Pc-Pb) - (oncotic pc - oncotic pb)

C is capillary, b is bowman

31
Q

Where is potassium resorbed/secreted?

A

Most 65% resorbed in PCT, 25% in loop, and then secretion in principal cells of DCT

32
Q

Calculation of Renal blood flow

A

RBF = RPF / (1-Hct)

RPF = PAH clearance = (urine conc x urine flow) / serum conc

33
Q

How is vitamin D modulated in kidney?

A

25-OH-D3 is converted to active form, 1,25-diOH-D3 in kidney.

Active form is also called calcitriol

34
Q

How does chronic renal disease affect bone? (2 ways)

A

Diminished urinary excretion of phosphate –> elevated serum phosphate –> calcium phosphate complexes form –> less Ca available for tissues. High phosphate and low Ca –> PTH secretion.

Decreased renal calcitriol production –> decreased Ca absorption –> increased Ca excretion –> low serum Ca and high serum phosphate.

This all results in PTH mobilizing Ca from bones to raise serum Ca, causes renal osteodystrophy, bone pain and signs of osteopenia

35
Q

Amphoterecin B premature ventricular beats are from

A

nephrotoxicity, including hypokalemia and hypomagnesemia

36
Q

Principal site for uric acid crystals

A

collecting ducts due to low pH

37
Q

Prevention of tumor lysis syndrome

A

Intracellular ions like K, uric acid, and phosphorus are released into serum. Alkalization of urine and hydration, which prevents uric acid from precipitating

38
Q

If the renal artery is clamped, what cell types would undergo hypertrophy and hyperplasia?

A

Compensation would be the renin angiotensin system, so the JG apparatus and macula densa would hypertrophy/hyperplasia. Smooth muscle cells of afferent and efferent glomerular arteries synthesize renin.

39
Q

Sudden onset flank pain, hematuria, and left sided varicocele in the setting of a nephrotic syndrome

A

Suggests renal vein thrombosis. Nephrotic syndrome is hypercoagulable state due to loss of anticoagulant factors like antithrombin III.

40
Q

Oliguria, anorexia, flank pain, calcium oxalate crystals in a homeless alcoholic. Toxic renal injury due to

A

ethylene glycol

41
Q

Side effects of osmotic diuretics. Overaggressive tx can lead to?

A

normal side effects = pulmonary htn, headache, nausea, vomiting

Overaggressive treatment leads to volume depletion, hypernatremia, death.

42
Q

Why are osmotic diuretics useful in increased intracranial pressure?

A

Water distribution from tissues to plasma

43
Q

Causes of secondary hyperaldosteronism, and findings

A

Caused by renovascular or malignant hypertension, renin-secreting tumor, or diuretic use.

Hypertension, hypokalemia, high renin, high aldo

44
Q

Findings in primary hyperaldosteronism

A

Hypertension, hypokalemia, low renin, high aldo

45
Q

Poststreptococcal glomerulonephritis: biopsy, LM, IF, EM findings

A

LM: glomeruli large and hypercellular with leukocyte infiltration and proliferation of endothelial and mesangial cells.

EM: electron-dense subepithelial IC humps

IF: Granular appearance, “starry sky” or “lumpy bumpy” due to IgM, IgG, and C3 deposition.

46
Q

Acute tubular necrosis secondary to low cardiac output: what part of the kidney is hurt most?

A

Proximal tubule and thick ascending loop of henle

47
Q

Low cardiac output, high BUN and Cr, low urine flow, muddy brown casts in urine

A

Ischemic acute tubular necrosis

Renal (3 decks)

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