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USMLE Step 1 Quick Notes > Renal > Flashcards

Renal Flashcards

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USMLE® Step 1 flashcards
1
Q

What do you see in the maintenance phase of acute renal failure?

A

Hyperkalemia and oliguria

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2
Q

What do you see in recovery phase of acute renal failure?

A

Hypokalemia and polyuria

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3
Q

What does exposure to rubber, plastics, textiles, leather increase risk for?

A

Transitional Cell carcinoma

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4
Q

What is the proximal ureter supplied by?

A

Renal artery

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5
Q

What is the distal ureter supplied by?

A

Superior vesicular artery

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6
Q

Where does RCC commonly metastasize?

A

Lungs

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7
Q

What has clear polygonal cells and can be paraneoplastic?

A

RCC

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8
Q

What are the symptoms of RCC?

A

Flank pain, hematuria, palpable mass, polycythemia

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9
Q

What do you treat calcium urine stones with?

A

Citrate, thiazides

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10
Q

What is the diagnosis? Oxalate crystals, coma, metabolic acidosis

A

Ethylene glycol poisoning

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11
Q

What do you treat UTI with?

A

Fluoroquinolones

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12
Q

What do you treat UTI in children with/

A

Penicilin, cephalosporins, TMP/sulfamethaxozole, nitrofurantoin

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13
Q

Where is urine most dilute?

A

Distal tubule

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14
Q

Where is urine most concentrated?

A

Collecting duct

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15
Q

What causes first dose hypotension?

A

ACE-I

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16
Q

What are the side effects of spironolactone?

A

Gynecomastia, antiandrogen effects, hyperklaemia

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17
Q

How do you reduce nephrolisthiasis?

A

Consume fluids because supersaturation is a major cause

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18
Q

Where is RCC most commonly found in the kidney?

A

Proximal tubule

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19
Q

Which one do you see antibodies to phospholipase A2?

A

Membranous glomerulonephritis

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20
Q

What is the diagnosis? Easy fatiguability, back pain, azotemia, constipation, eosinophilic casts?

A

Multiple Myeloma

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21
Q

What are the causes of renal papillary necrosis?

A

Phenacetin, Sickle Cell, Diabetes, pyelonephritis

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22
Q

What does renal papillary necrosis present with?

A

Acute colicky flank pain, hematuria, passage of tissue fragments

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23
Q

What is decreased in PSGN?

A

C3 levels

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24
Q

What are WBC casts seen with?

A

Pyelonephritis, interstitial nephritis

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25
Q

Which one will show clear and green IF?

A

Goodpasture

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26
Q

What prevents bradykinin breakdown?

A

ACE-I (ACE breaks it down)

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27
Q

Where is majority of water reabsorbed?

A

Proximal tubule (60%) regardless of hydration status

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28
Q

How can ethylene glycol affect the kidneys?

A

Causes oxalate crystals –> tubular injury –> ballooning and vacuolar degeneration of proximal tubules

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29
Q

What happens to RPF and GFR in hypovolemia?

A

Decreased RPF and slightly decreased GFR (due to ang II release from renin activation; causes constriction of efferent so GFR decreases to lesser extent than RPF)

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30
Q

What drug do you avoid in renal artery stenosis?

A

ACE-I because need efferent constriction to maintain GFR

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31
Q

What is the prognosis for acute PSGN in adults?

A

Poor

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32
Q

What happens to kidneys in BPH?

A

Renal parenchyma becomes atrophic and scarred due to reflux of urine

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33
Q

How do you tell PSGN and IgA nephropathy apart?

A

IgA nephropathy is after a few days and will show mesangial IgA deposits and normal complement levels. PSGN takes a few weeks to develop.

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34
Q

Whats the MCC of kidney stones?

A

Kidney stones usually Ca. Ca stones caused usually by idiopathic hypercalciuria with normocalcemia

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35
Q

Diagnosis: ballooning and vacuolar degeneration of proximal tubules, oxalate crystals, vomiting, oliguria?

A

Ethylene glycol ingestion: causes high anion gap metabolic acidosis and oxalate crystals

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36
Q

What diuretic stimulates PGE release and is inhibited by NSAIDs?

A

Furosemide

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37
Q

What are the causes of Potter sequence?

A

ARPKD, bilateral renal agenesis, posterior urethral valves

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38
Q

What cancer can horseshoe kidney lead to?

A

Turner syndrome

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39
Q

What is multicystic dysplastic kidney?

A

Abnormal interaction b/w ureteric bud and metanephric mesenchyme leading to cystics in kidney

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40
Q

What is the BF though kidney?

A

Renal –> segmental –> lobar –> interlobar –> arcuate –> interlobular

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41
Q

What is hypotonic fluid loss?

A

Dehydration, alcoholism, DI

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42
Q

What is isotonic fluid loss?

A

Hemorrhage, diarrhea, vomiting

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43
Q

What is the renal handling of creatinine?

A

Freely filtered and moderately secreted but still a good estimate of GFR

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44
Q

What is a normal FF?

A

20%

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45
Q

What inhibits afferent arteriolar dilation?

A

Age, chronic kidney disease, NSAIDs

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46
Q

What is the excretion rate?

A

(V)(Ux)

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47
Q

What does normal pregnancy do to glucose handling?

A

Decreases amino acid and glucose absorption proximal tubule

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48
Q

What is Hartnup disease?

A

AR disorder leading to deficiency of neutral aa transporters in gut and proximal tubule (ie tryptophan). Leads to pellagra like symptoms. Treat with high protein diet and nicotonic acid

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49
Q

What is the renal handling of NH3?

A

Secreted in proximal tubule

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50
Q

How does acetazolamide work?

A

Inhibits CA so HCO3 + H not being converted. Since H+ is hanging around now there is less of a drive to reabsorb Na since it uses Na/H antiporter (Na reabsorbed for H secretion)

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51
Q

How does Ang II affect tubules?

A

Stimulates Na/H exchange –> increased Na, water and Hc03 reabsorption

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52
Q

What is Bartter?

A

Na/2Cl/K transporter defect —> hypkalemia, metabolic alkalosis, hypercalciuria,

53
Q

What is Gitelman?

A

NaCl transporter defect –> hypokalemia, metabolic alkalosis

NO hypercalciuria

54
Q

What is Liddle?

A

Increased ENac activity –> hypertension, hypokelamia, metabolic alkalosis, decreased aldosterone

55
Q

How is Cl handled in the proximal tubule?

A

It’s reabsorbed slower than Na so its concentration increases at first along the proximal tubule but then its reabsorption matches Na so its concentration in the tubule levels.

56
Q

How do beta adrenergics do to potassium levels?

A

Shift K into cell because of increased Na/K ATPase

57
Q

What does alkalosis affect your K?

A

Shift K into cell

58
Q

What are the causes of high anion gap metabolic acidosis?

A

MUDPILES: methanol, uremia, DKA, propylene glycol, INH, iron tablets, Lactic acidosis, ethylene glycol, salicylates (mixed metabolic acidosis and resp alkalosis)

59
Q

What are the causes of normal anion gap metabolic acidosis?

A

HARDASS: hyperalimentation (artificial nutrient supply), addison, renal tubular acidosis, diarrhea, acetazolamide, spironolactone, saline infusio

60
Q

What do you see fatty casts with?

A

Advanced renal disease/chronic renal failure

61
Q

LM, IF, EM for FSGN?

A

LM: segmental sclerosis, hyalinosis
IF: -
EM: effacement of foot processes

62
Q

LM, IF, EM for Membranous?

A

LM: diffuse capillary & GBM thickening
IF: granular from immune complex deposition
EM: spike and dome with subepithelial deposits

63
Q

Which has a poor response to steroid therapy and may progress to chronic renal disease?

A

Membranous, FSGN

64
Q

Causes of FSGN?

A

African americans, Hispanics, HIV!!, sickle cell disease, interferon, heroin, obesity, chronic kidney disease

65
Q

Which glomerular disease has an excellent response to steroids?

A

Minimal Change Disease

66
Q

Which glomerular disease is associated with hodgkin’s lymphoma?

A

Minimal Change

67
Q

What triggers minimal change in kids?

A

Recent infection, immunization, immune stimulus

68
Q

Microscopy for type I MPGN?

A

IF: subendothelial IC deposits with granules
Tram track appearance from GBM splitting caused by mesangial ingrowth
Hypercellular and thickened

69
Q

Microscopy for type II MPGN

A

Intramembanous IC deposits “dense deposits”

70
Q

What are type I and II MPGN associated with?

A

I: HCV, HBV
II: C3 nephritic factor (stabilizes C3 convertase –> dec C3 levels)

71
Q

What do you see with diabetic nephropathy?

A

LM: Eosinophilic nodular glomerulosclerosis (kimmelstiel wilson), GBM thickening, mesangial expansion

72
Q

IF, LM, EM for PSGN?

A

LM: glomeruli enlarged and hypercellular
IF: starry sky, lumpy bumpy from IgG, IgM and C3 deposition
EM: subepithelial immune complex (Humps)

73
Q

LM and IF for RPGN?

A

Fibrin and plasma proteins (c3b) with glomerular parietal cells, monocytes, macrophages

74
Q

LM, EM, IF, of DPGN?

A

LM: wire looping of capillaries
EM: Subendothelial IgG based ICs with C3
IF: granular

75
Q

IgA nephropathy LM, EM

A

LM: mesangal proliferation
EM: IC deposits mesangial
IF: IgA based IC deposits

76
Q

What presents with deafness, lens and eye problems and glomerulonephritis?

A

Alport (mutation in type IV collagen –> thinning and splitting of GBM); XR

77
Q

Which kidney stones form in alkaline environment?

A

Both the phosphate stones (calcium phosphate and ammonium magnesium phosphate)

78
Q

What do cystine stones look like?

A

Hexagonal

79
Q

Which ones have staghorn caliculi?

A

Ammonium phosphate (aka struvite), and cystine stones

80
Q

What causes oxalate stones?

A

Crohn’s, Vit C abuse, ethylene glycol

81
Q

What causes struvite stones?

A

Urease positive bugs

82
Q

What is sodium nitroprusside test positive?

A

Cystinuria

83
Q

Which of the renal cancers is paraneopalstic?

A

RCC! Can make EPO, ACTH, PTHrp

84
Q

How do you treat RCC?

A

CAN’T DO RADIATION Or CHEMO. Immune or targeted therapy or resect

85
Q

What is a benign epithelial tumor with central stellate scar, large eosinophilic cells with abundant mitochondria without perinuclear clearing?

A

Oncocytoma

86
Q

What presents with neonatal hypoglycemia, muscular hemihypertrophy, organomegaly?

A

Beckwith- Wiedmann (aw/ wilms tumor)

87
Q

What is the WAGR complex?

A

Wilms tumor, aniridia, GU malformation, mental retardation

88
Q

What is a huge palpable flank mass with embryonic glomerular structures in early childhood?

A

Wilms Tumor (WT1 or 2 mutation on chromosome 11)

89
Q

What is a common tumor of renal calyces, pelvis, ureters, bladder that presents with painless hematuria without casts?

A

Transitional Cell Carcinoma

90
Q

What is transitional cell carcinoma ssociated with?

A

Phencetin, smoking, aniline dyes, cyclophosphamide

91
Q

What causes type 2 renal tubular acidosis (proximal, pH

A

Fanconi, toxins, and CA inhibitors

92
Q

What causes type 1 renal tubular acidosis (distal, pH > 5.5)

A

Amphotericin, analgesics, multiple myeloma, congenital

93
Q

What are the risk factors for SCC of the bladder?

A

Schistosoma, smoking, chronic nephrolithiasis, chronic cystiits

94
Q

What does it mean if you have sterile pyuria with negative urine cultures but symptoms of UTI?

A

Chlamydia or Neisseria

95
Q

Diagnosis: CT show sstriated parenchymal enhancement?

A

Acute pyelonephritis

96
Q

What does chronic pyelonephritis cause

A

Corticomedullary scarring, blunted calyx

97
Q

What causes tubules to have eosinophilic casts resembling thyroid tissue?

A

Chronic pyelonephritis

98
Q

What drugs cause drug induced interstitial nephritis?

A

Penicillin, sulfonamides, diuretics, rifampin

99
Q

How does drug induced interstitial nephritis present?

A

Maculopapular rash, hematuria, CVA tenderness, fever

100
Q

What are the causes of ATN?

A

Ischemic: from decreased BF (hypotension, shock, CHF etc)

Nephrotoxic: cisplatin, aminoglycosides, radiocontrast dye, crush injury (myglobinuria), hemoglobinuria

101
Q

What decreases BUN/creatinine ratio?

A

Intrinsic renal failure because can’t reabsorb BUN

102
Q

What happens with intrinsic renal failure?

A

Patchy necrosis leads to debris that obstructs tubule and causes backflow which decreases GFR!

103
Q

What happens with prerenal azotemia?

A

Decreased BF to kidney so dec GFR. Try to reabsorb and conserve water to compensate.

104
Q

What happens to with postrenal azotemia?

A

Obstruction in ureter that will back up and decrease GFR and FF. Can’t reabsorb or concentrate but will have high BUN/Creatinine ratio since GFR is decreased

105
Q

Where is the ADPKD mutation?

A

Chromosome 16 (MC) or chromosome 4

106
Q

What is ADPKD associated with?

A

Benign hepatic cysts, MVP, berry aneurysms

107
Q

What is ARPKD associated with?

A

Hepatic fibrosis, Potter sequence

108
Q

What is medullary cystic disease?

A

Tubulointerstitial fibrosis –> can’t concentrate urine. Can’t see medullary cysts. Poor prognosis

109
Q

When is a cyst bad?

A

Septated, enhanced, solid and not in the outer cortex –> increased risk for RCC

110
Q

What is mannitol?

A

Osmotic diuretic for increased intracranial/ocular pressure.. Causes pulmonary edema and dehydration. Don’t use in CHF and anuria

111
Q

What are the side effects of acetazolamide?

A

Hyperchloremic, metabolic acidosis, paresthesias, NH3 toxicity, sulfa allergy

112
Q

What diuretic can you use for nephrogenic DI?

A

Hydrochlorothiazide

113
Q

What diuretics can you not use in gout patients?

A

Loop, thiazide

114
Q

What diuretic do you not give to pregnant women?

A

ACE- I because its teratogen

115
Q

What are the two buffers in the tubules?

A

NH3 and HPO4 which combine in the lumen with H to become NH4 and H2PO4. Hence they increase during metabolic acidosis as kidneys are trying to get rid of H+

116
Q

What is the relationship between GFR and creatinine?

A

Nonlinear. As GFR goes down Creatinine increases (exponential decrease as GFR goes up)
Every time GFR halves, creatinine doubles

117
Q

What do you test to determine what is causing metabolic alkalosis?

A

Urine Cl:
Vomiting (low urine Cl), thiazide/loop diuretic use (high urine CL) that is saline responsive
Hyperaldosteronism or cortisolism: urine cl high that is saline unresponsive

118
Q

Where is the MC obstruction in fetus?

A

Ureteropelvic junction

119
Q

What do you see pyuria with no casts?

A

Acute cystitis

120
Q

What is lost i the urine that may cause a varicocele?

A

Antithrombin (that’s why proteinuria has hypercoagulable state)

121
Q

What drug do you give to CHF patients who have a sulfa allergy?

A

Ethacrynic Acid

122
Q

What diuretics are sulfa?

A

Loop and thiazides and acetazolamide

123
Q

What stains densely adjacent to glomerulus on IHC?

A

Juxtaglomerular cells containing renin

124
Q

What is ACE inhibitor fetopathy?

A

Blockade of angiotensingin II from mom being on ACE-I –> fetal renal atrophy and ishcemia. Causes fetal anuria, oligohydramnios, limb contractures, growth defect, pulmonary hypoplasia.

125
Q

Patient taking simvastatin and furosemide who has to pee a lot at night and has muscle weakness and cramps is due to which medication?

A

Furosemide (hypokalemia and contraction alkalosis)

126
Q

Diagnosis: microscopic hematuria + high HB?

A

RCC

127
Q

How does hypercalcemia affect water reabsorption?

A

Hypercalcemia causes nephrogenic DI by downregulating aquaporins –> can’t concentrate urine in collecting tubules

128
Q

A 56-year-old man comes to the emergency department because of a 4-day history of colicky right flank pain that radiates to the groin and hematuria. Ultrasound examination of the kidneys shows right-sided hydronephrosis and a dilated ureter. Which of the following is most likely to be found on urinalysis?

A

Kidney stone. In this case the answer was uric acid.

USMLE Step 1 Quick Notes (17 decks)

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