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
Winter's formula: what is it and how is it used?
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
Calculation of anion gap
AG = Na - (Cl + HCO3) in a metabolic acidosis
26
Metabolic acidosis with normal anion gap
HARDASS | Hyperalimentation, addison disease, renal tubular acidosis, diarrhea, acetazolimide, spironolactone, saline infusion
27
Metabolic acidosis with high anion gap
Indicates presence of some unmeasured anion (acid) MUDPILES Methanol, uremia, dka, propylene glycol, Iron tabs, lactic acidosis, ethylene glycol, salicylates
28
Hyperacute rejection of transplant mediated by
Preformed antibodies against donor antigens. Type II hypersensitivity
29
Immediate hypersensitivity
Type I hypersensitivity. Occurs after initial exposure to antigen --> IgE class switching. Anaphylaxis, urticaria, asthma, seasonal allergies.
30
Calculate GFR
= k (Pc-Pb) - (oncotic pc - oncotic pb) C is capillary, b is bowman
31
Where is potassium resorbed/secreted?
Most 65% resorbed in PCT, 25% in loop, and then secretion in principal cells of DCT
32
Calculation of Renal blood flow
RBF = RPF / (1-Hct) RPF = PAH clearance = (urine conc x urine flow) / serum conc
33
How is vitamin D modulated in kidney?
25-OH-D3 is converted to active form, 1,25-diOH-D3 in kidney. Active form is also called calcitriol
34
How does chronic renal disease affect bone? (2 ways)
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
Amphoterecin B premature ventricular beats are from
nephrotoxicity, including hypokalemia and hypomagnesemia
36
Principal site for uric acid crystals
collecting ducts due to low pH
37
Prevention of tumor lysis syndrome
Intracellular ions like K, uric acid, and phosphorus are released into serum. Alkalization of urine and hydration, which prevents uric acid from precipitating
38
If the renal artery is clamped, what cell types would undergo hypertrophy and hyperplasia?
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
Sudden onset flank pain, hematuria, and left sided varicocele in the setting of a nephrotic syndrome
Suggests renal vein thrombosis. Nephrotic syndrome is hypercoagulable state due to loss of anticoagulant factors like antithrombin III.
40
Oliguria, anorexia, flank pain, calcium oxalate crystals in a homeless alcoholic. Toxic renal injury due to
ethylene glycol
41
Side effects of osmotic diuretics. Overaggressive tx can lead to?
normal side effects = pulmonary htn, headache, nausea, vomiting Overaggressive treatment leads to volume depletion, hypernatremia, death.
42
Why are osmotic diuretics useful in increased intracranial pressure?
Water distribution from tissues to plasma
43
Causes of secondary hyperaldosteronism, and findings
Caused by renovascular or malignant hypertension, renin-secreting tumor, or diuretic use. Hypertension, hypokalemia, high renin, high aldo
44
Findings in primary hyperaldosteronism
Hypertension, hypokalemia, low renin, high aldo
45
Poststreptococcal glomerulonephritis: biopsy, LM, IF, EM findings
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
Acute tubular necrosis secondary to low cardiac output: what part of the kidney is hurt most?
Proximal tubule and thick ascending loop of henle
47
Low cardiac output, high BUN and Cr, low urine flow, muddy brown casts in urine
Ischemic acute tubular necrosis