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USMLE > Renal > Flashcards

Renal Flashcards

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USMLE® Step 1 flashcards
1
Q

What % of total body weight is plasma volume? Interstitial fluid?

A

Plasma volume - 5%
Interstitial volume - 15%
(Total ECF is 20%)

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2
Q

What is the maximum serum glucose concentration that can be fully reabsorbed in the tubules?

A

350 mg/dL

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3
Q

What is exchanged for secretion of organic anions in the distal proximal tubule?

A

alpha-ketoglutarate

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4
Q

Where in the nephron is Mg reabsorbed?

A

Thick ascending limb

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5
Q

Where does PTH exert its action on the nephron?

A

Na/Ca channels in the early distal tubule

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6
Q

Indications for acetazolamide

A

Metabolic alkalosis (altitude sickness), glaucoma, pseudo tumor cerebri

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7
Q

Indications for mannitol

A

Shock, acute angle-closure glaucoma, and elevated ICP

pulls water out of tissues into vasculature + free water loss in kidneys

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8
Q

Do loop diuretics concentrate or dilute urine?

A

Dilute - even though you keep more ions in the tubule, since they are not reabsorbed into the nodular interstitium there is less water absorption in the thin descending limb = dilution

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9
Q

Why should aminoglycosides not be used with loop diuretics?

A

Both cause ototoxicity and nephrotoxicity

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10
Q

When should HCTZ be used: idiopathic calciuria or hyperparathyroidism?

A

Only in idiopathic calciuria because decreased Ca in the urine will only worsen the hypercalcemia in hyperparathyroidism

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11
Q

What are 3 other side effects of HCTZ?

A

Hyperglycemia, hyperlipidemia, and hyperuricemia (increases glucose, lipids, and uric acid)

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12
Q

What 3 diuretic classes are sulfa drugs?

A

Acetazolamide (carbonic anhydrase inhibitor), loop diuretics (except ethacrynic acid), and thiazides

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13
Q

What diuretic doesn’t increase urinary NaCl?

A

Acetazolamide

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14
Q

Pregnant mother given medications to stop preterm labor. Now has reduced DTRs, why?

A

IV Mg given to stop the uterine contractions, but hyperMg can also cause hyporeflexia

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15
Q

How does hypoMg affect an EKG?

A

Lengthens QT intercal, can cause TdP

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16
Q

What causes K to shift outside the cell = hyperK?

“Do Insulin LABs”

A

Digitalis (blocks Na/K ATPase), Insulin deficiency (DKA), Lysis of cells, Acidosis (Na/H pumps), B blockers

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17
Q

3 treatments for peaked T waves on EKG

A

HyperK = B agonist (shifts K into cells), bicarbonate (metabolic alkalosis), and dextrose + insulin

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18
Q

What 3 drugs are used to treat nephrogenic DI?

A
  1. Indomethacin (decrease RBF/GFR)
  2. HCTZ (volume contraction stimulates more water retention at the proximal tubule)
  3. IF Li induced - Amiloride (blocks Na channel Li uses to enter the principal cells)
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19
Q

What causes high anion gap metabolic acidosis?

“MUDPILES”

A

Methanol, uremia, DKA, propylene glycol, iron/isoniazid, lactic acid, ethylene glycol, and salicylates

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20
Q

What causes normal anion gap metabolic acidosis?

A

HCO3 loss - diarrhea, renal tubular acidosis, acetazolamide

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21
Q

HTN + hypoK + metabolic alkalosis

A

Primary hyperaldosteronism
Na - normal due to ANP activation
K - aldosterone promotes loss
HCO3 - aldosterone promotes H loss = HCO3 retention

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22
Q

What causes metabolic alkalosis?

A

Vomiting (H loss), loops/HCTZ (HCO3 retention), and hyperaldosteronism (HCO3 retention)

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23
Q

Normal ion gap metabolic acidosis + urine pH > 5.5 + hypoK +/- nephrocalcinosis/nephrolithiasis

A 
Type 1 (distal) renal tubular acidosis - a-intercalated cells fail to secrete H 
"Type 1 = H"
Acidosis activates aldosterone to increase H+ secretion but doesn't work = hypoK
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24
Q

Normal ion gap metabolic acidosis + urine pH

A 
Type 4 (hyperkalemic) renal tubular acidosis - hypoaldosteronism
"Type 4 = NH4, aldo"
Low aldosterone = hyperK = decreased NH3 production in the proximal tubule = impaired filtrate H+ buffering = H retention
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25
Q

Normal ion gap metabolic acidosis + urine pH

A 
Type 2 (proximal) renal tubular acidosis - failure to reabsorb HCO3 in the proximal tubule (Fanconi syndrome)
"Type 2 = BIcarb"
Urine pH still acidotic because HCO3 isn't made, stays as CO2 + H20 in the urine
PO4 normally reabsorbed in the proximal tubule, but the entire PCT is nonfunctional so PO4 loss leads to rickets
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26
Q

Waxy casts in urine

A

Chronic renal failure

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27
Q

Hyaline casts in urine

A

Normal, concentrated urine

28
Q

What is the most common type of kidney stone?

A

Ca (with oxalate or phosphate)

29
Q

What are 3 causes of calcium kidney stones?

A

Ethylene glycol ingestion, vitamin C abuse, and Chron’s disease (saponification of fat within GI tract allows more oxalate to be absorbed = supersaturation in the kidneys)

30
Q

Treatment for Ca kidney stones

A

HCTZ

31
Q

What causes NH4-Mg-PO4 stones?

A

Struvite stones - urease + bacterial UTIs (Proteus mirabilis, klebsiella pneumoniae)

32
Q

Where in the nephron does uric acid precipitate to form uric acid stones? Why?

A

Collecting ducts because this is where pH is lowest

33
Q

What causes cysteine stones?

A

Cystinuria - genetic mutation that impairs intestinal and renal (proximal tubule) reabsorption of Cys, Ornithine, Lys, and Arg (COLA)

34
Q

Treatment for cysteine stones

A

Alkalinize the urine (acetazolamide)

35
Q

What 2 types of stones can form stag horn calculi (that fill the entire renal pelvis)?

A

Struvite and cysteine

36
Q

Infant with cysts in both kidneys + cartilage on histology
What is the diagnosis?
What is the inheritance pattern?

A 
Dysplastic kidney
NOT inherited (de novo mutation)
37
Q

Where are cysts found in PKD?

A

Cortex and the medulla

38
Q

Infant with HTN and renal failure

A

ARPKD

39
Q

What extra-renal findings are associated with ARPKD?

A

Hepatic cysts and congenital hepatic fibrosis

40
Q

Newborn with portal HTN

A

ARPKD

41
Q

HTN with increased plasma renin + hematuria + worsening kidney failure in young adults

A

ADPKD

42
Q

What extra-renal findings are associated with ADPKD?

A

Hepatic cysts, berry aneurysms, and mitral valve prolapse

“Liver, brain, heart, and kidney cysts”

43
Q

Bilateral shrunken kidneys with cysts

A

Medullary cystic disease (cysts are only in the medulla)

Autosomal dominant

44
Q

Why is the BUN:creatinine ratio > 15 in pre-renal and post-renal azotemia?

A 
Pre-renal = decreased RBF will activate RAAS, increased water reabsorption will pull BUN with it
Post-renal = increased hydrostatic P in the tubules will force more BUN back into the blood
45
Q

What are 5 causes of nephrotoxic acute tubular necrosis?

“Renal Endothelium Aggregates Like Mud” - muddy brown casts seen in ATN

A

Radiocontrast, ethylene glycol, aminoglycosides, lead, myoglobinuria

46
Q

How does ATN affect K and acid-base status?

A

HyperK + increased anion gap metabolic acidosis

Due to decreased renal clearance of K and organic acids (also BUN and creatinine)

47
Q

Eosinophils in the urine

A

Drug-induced interstitial nephritis

48
Q

What are 4 causes of renal papillary necrosis?

A

NSAIDs - afferent arteriole constriction = decreased RBF (medulla susceptible to ischemia)
Sickle cell anemia OR TRAIT - high osmolarity in the medulla causes even heterozygous HbS cells to sickle = ischemia
DM and acute polynephritis

49
Q

Pyuria with negative urine cultures

A

Chlamydia or gonorrhea

50
Q

Scarring of the upper and lower poles of the kidney + blunted calyx + thyroidization of renal tissue

A 
Chronic pyelonephritis (typically due to vesicourethral reflex)
Thyroidization = proteinaceous material left within atrophic tubules forms pink casts
51
Q

What type of kidney stone is NOT visible on Xray?

A

Uric acid stones

52
Q

Pericarditis + increased bleeding time + asterixis + crystal deposition in skin

A

Uremia associated with chronic renal failure

Impeded platelet adhesion and aggregation

53
Q

What cell type makes EPO?

A

Renal peritubular interstitial cells

54
Q

What 4 paraneoplastic syndromes are associated with renal cell CA?

A

EPO, renin, PTHrp, and ACTH

55
Q

What must be considered if a patient presents with a L sided varicocele?

A

RCC - propensity to invade the renal vein which could block venous drainage from the L testicular vein

56
Q

What genetic mutation is associated with RCC?

A

Loss of VHL = increases IGH and HIF (TF for VEGF and PDGF)

57
Q

What is the most important risk factor for sporadic RCC?

A

Smoking

58
Q

What syndrome is associated with RCC?

What other cancer is associated with this syndrome?

A

Von Hippel Lindau (hence VHL gene)

Cerebellar hemangioblastoma

59
Q

Wilms tumor + aniridia + genital abnormalities + mental/motor retardation

A

WARG syndrome

60
Q

What is the histology of Wilms tumor?

A

Primitive renal precursors = “blastema”

May form primitive renal tubules and stroma, but primarily the small dark blue primitive cells

61
Q

What genetic mutation is associated with flat urothelial CA?

A

Early p53 mutations

62
Q

Why is urothelial multifocal with high recurrence rate?

A

Because the entire bladder is mutated from the exposure

63
Q

What are the risk factors for urothelial CA?

“SAC”

A

Smoking, aniline dyes (hair dye), and cyclophosphamide

64
Q

Young middle eastern male with painless hematuria

A

Bladder squamous cell CA secondary to Schistosome haematobium infection

65
Q

What does a arches remnant put you at increased risk for?

A

AdenoCA at the dome of the bladder

USMLE (12 decks)

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