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Step 1 (Steffanie) > Renal > Flashcards

Renal Flashcards

1
Q

In metabolic acidosis there is increased urinary excretion of which substances?

A

H+, NH4+, and H2PO4-

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2
Q

What happens to the concentrations of PAH, creatinine, inulin, and urea as fluid runs along the proximal tubule?

A

They increase

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3
Q

What happens to the concentrations of bicarb, glucose, and amino acids as fluid runs along the proximal tubule?

A

They decrease

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4
Q

How does CKD with mineral bone disease present?

A

Hyperphosphatemia, secondary hyperparathyroidism, and decreased calcitriol levels. Pts can be asymptomatic or develop weakness, bone pain, and fractures

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5
Q

Vasopressin and Desmopressin cause increased permeability of which substances?

A

Increase in water and urea permeability at the inner medullary collecting duct

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6
Q

Filtration fraction equation

A

FF=GFR/RPF

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7
Q

What is responsible for the thrombotic and thromboembolic complications of nephrotic syndrome?

A

Loss of anticoagulant factors, especially antithrombin III

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8
Q

Linear deposits of immunoglobulin along the glomerular basement membrane

A

anti-glomerular basement membrane disease

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9
Q

What are the immunoglobulin deposits composed of in anti-glomerular membrane disease

A

IgG and C3

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10
Q

What is seen on light microscopy in anti-GBM disease?

A

Glomerular crescents composed of proliferating parietal cells with an infiltration of monocytes and macrophages

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11
Q

Renal failure and pulmonary hemorrhage in patients with anti-GBM antibodies

A

Goodpasture syndrome

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12
Q

Immunofluorescence microscopy in poststreptococcal glomerulonephritis

A

Granular deposits of IgG, IgM and C3 in the mesangium and basement membranes

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13
Q

Membranous glomerulonephropathy

A

A cause of nephrotic syndrome. Can occur secondary to underlying malignant tumors, infections, and certain meds.

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14
Q

Findings on imaging with membranous glomerulopathy

A

Diffuse increased thickness of the glomerular basement membrane on light microscopy, spike and dome appearance on methenamine silver stain, and granular deposits on immunofluorescence

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15
Q

Presentation of minimal change disease

A

Weight gain, pitting edema, significant proteinuria, hypoalbuminemia, hyperlipidemia

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16
Q

Findings in minimal change disease

A

Biopsy specimen will show no obvious glomerular lesions on light microscopy and will be negative for immune deposits on immunofluorescence. Electron microscopy shows effacement of the foot processes supporting the epithelial podocytes with weakening of slit-pore membranes

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17
Q

What other conditions are associated with ADPKD?

A

Berry aneurysms, hepatic cysts, mitral valve prolapse

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18
Q

Urine findings in acute tubular necrosis

A

Brown, granular casts

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19
Q

Which parts of the kidney are particularly susceptible to ischemia?

A

Proximal tubule and medullary segment of thick ascending limb

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20
Q

Which part of the kidney is susceptible to nephrotoxic ATN?

A

Proximal tubule

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21
Q

What are key causes of acute interstitial nephritis?

A

NSAIDs, PCN, diuretics

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22
Q

Oliguria, fever, and rash days to weeks after starting a new drug. Eosinophils found in the urine

A

Acute interstitial nephritis

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23
Q

Presentation of renal papillary necrosis

A

Gross hematuria, flank pain

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24
Q

Causes of renal papillary necrosis

A

Chronic analgesic abuse, diabetes mellitus, sickle cell disease, severe acute pyelonephritis

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25
Q

What cancer is minimal change disease associated with?

A

Hodgkin lymphoma

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26
Q

Normal glomeruli on H&E stain, effacement of foot processes on EM, negative IF

A

Minimal change disease

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27
Q

How is minimal change disease treated?

A

Corticosteroids

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28
Q

What mediates the damage in minimal change disease

A

Cytokines

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29
Q

What is the most common cause of nephrotic syndrome in Hispanics and African Americans?

A

Focal segmental glomerulosclerosis

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30
Q

segmental sclerosis and hyalinosis on H&E, effacements of foot processes on EM, negative IF

A

Focal segmental glomerulosclerosis

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31
Q

Most common cause of nephrotic syndrome in Caucasian adults

A

Membranous nephropathy

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32
Q

Diffuse capillary and GBM thickening on H&E, granular IF due to immune complex deposition, “spike and dome” appearance on EM

A

Membranous nephropathy

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33
Q

Thick capillary membranes with “tram track appearance” on H&E, granular IF

A

Membranoproliferative glomerulonephritis

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34
Q

Type I MPGN

A

Associated with hepatitis B or C. Subendothelial IC deposits

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35
Q

Type II MPGN

A

Associated with C3 nephritic factor IgG antibody that stabilizes C3 convertase leading to persistent compliment activation and decreased C3 levels. Intramembranous deposits

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36
Q

Hematuria and RBC casts

A

Nephritic syndrome

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37
Q

~2-4 weeks after group A strep infection. Peripheral and periorbital edema, cola-colored urine, HTN.

A

Acute poststreptococcal glomerulonephritis

38
Q

Nephritogenic strains of group A strep

A

Carry M protein virulence factor

39
Q

“Starry sky” granular appearance on IF due to IgM, IgG, and C3 deposition along GMB and mesangium. Subepithelial IC humps on EM

A

Acute poststreptococcal glomerulonephritis

40
Q

What makes up the crescents in rapidly progressive glomerulonephritis?

A

Fibrin and plasma proteins with glomerular parietal cells, monocytes, macrophages

41
Q

Linear IF in RPGN

A

Antibodies against collagen in GBM and alveolar basement membrane. Seen in Goodpasture syndrome - hematuria/hemoptysis.

42
Q

Treatment for Goodpasture syndrome?

A

Plasmapheresis

43
Q

Granular IF in RPGN

A

PSGN or DPGN

44
Q

Negative IF (pauci-immune) in RPGN

A

Wegener granulomatosis - also nasal/sinus symptoms (PR3-ANCA/c-ANCA), microscopic polyangiitis (MPO-ANCA/p-ANCA), Churg-Strauss syndrome - asthma, eosinophilia, granulomas (MPO-ANCA/p-ANCA)

45
Q

Episodic hematuria that occurs concurrently with respiratory or GI infections

A

IgA nephropathy (Berger Disease)

46
Q

IgA immune complex deposition in mesangium on IF

A

IgA nephropathy (Berger Disease)

47
Q

Isolated hematuria, sensorineural deafness, ocular disturbances

A

Alport Syndrome

48
Q

Inheritance pattern of Alport Syndrome

A

X-linked dominant mutation in type IV collagen

49
Q

“wire looping” of capillaries on H&E, granular IF, subendothelial and sometimes intramembranous IgG-based ICs often with C3 deposition

A

Diffuse proliferative glomerulonephritis

50
Q

What is a common cause of diffuse proliferative glomerulonephritis?

A

SLE

51
Q

WBC casts

A

Pyelonephritis

52
Q

Most common type of kidney stone in adults?

A

Calcium oxalate or calcium phosphate, oxalate more common

53
Q

What kind of kidney stones are seen with Crohn disease?

A

Calcium oxalate

54
Q

Treatment for calcium stones

A

Thiazides - calcium sparing diuretic, decrease calcium in urine

55
Q

Kidney stone associated with infection with urease + bugs (Proteus mirabilis, Staphylococcus saprophyticus, Klebsiella)

A

Struvite/Ammonium magnesium phosphate

56
Q

Staghorn calculi

A

Adult - struvite/ammonium magnesium phosphate stone

Child - Cysteine stone

57
Q

Clinical features of uremia

A

Nausea and anorexia, pericarditis, asterixis, encephalopathy, platelet dysfunction

58
Q

Consequences of renal failure

A

Metabolic acidosis, dyslipidemia, hyperkalemia, uremia, sodium and water retention, growth retardation and developmental delay, erythropoietin failure (anemia), and renal osteodystrophy

59
Q

Angiomyolipoma

A

Hamartoma comprised of blood vessels, smooth muscle, and adipose tissue. Increased frequency in tuberous sclerosis

60
Q

Hematuria, palpable mass, flank pain = classic triad. May also present with fever, weight loss, paraneoplastic syndrome (EPO, renin, PTHrP, ACTH)

A

Renal cell carcinoma

61
Q

May present with left sided vericocele

A

Renal cell carcinoma

62
Q

Pathogenesis of renal cell carcinoma

A

Loss of VHL tumor suppressor gene - increased IGF-1 (promotes growth) and HIF transcription factor (increases VEGF and PDGF)

63
Q

Von Hippel-Lindau Disease

A

Aut. dominant disorder associated with inactivation of VHL gene. Increased risk for hemangioblastoma of the cerebellum and renal cell carcinoma

64
Q

Which lymph nodes does renal cell carcinoma classically go to?

A

Retroperitoneal lymph nodes

65
Q

Malignant kidney tumor comprised of blastema, primitive glomeruli and tubules, and stromal cells. Average age 3 years.

A

Wilms tumor

66
Q

Large unilateral flank mass with hematuria and HTN

A

Wilms tumor presentation

67
Q

WT1 mutation

A

Wilms tumor - especially syndromic cases such as WAGR syndrome or Beckwith-Wiedemann syndrome

68
Q

Most common type of lower urinary tract cancer

A

Urothelial carcinoma - malignant tumor arising from uroethelial lining of renal pelvis, ureter, bladder, or urethra. Usually from bladder

69
Q

Risk factor for urothelial carcinoma

A

Cigarette smoke, naphthylamine, azo dyes, long term cyclophaospahmide or phenacetin

70
Q

Squamous cell carcinoma of the urinary tract usually involves?

A

The bladder

71
Q

Risk factors for squamous cell carcinoma of the bladder?

A

Chronic cystitis, schistosoma hematobium, long standing nephrolithiasis

72
Q

Adenocarcinoma of the bladder arises from?

A

Urachal remnant (at dome of bladder), cystitis glandularis, exstrophy

73
Q

Waxy casts

A

End stage renal disease/chronic renal failure

74
Q

Urgency incontinence

A

Overactive bladder (detrusor instability) - leak with urge to void immediately.

75
Q

Treatment for urgency incontinence

A

Kegel exercises, bladder training, antimuscarinics (oxybutinin)

76
Q

Overflow incontinence

A

Incomplete emptying (detrusor underactivity or outlet obstruction) - leak with overfilling

77
Q

Treatment of overflow incontinence

A

Catheterization, relieve obstruction (alpha blockers for BPH)

78
Q

Mannitol

A

Acts on proximal convoluted tubule and descending limb. Osmotic diuretic. Use - drug overdose, elevated intracranial/intraocular pressure

79
Q

Acetazolamide

A

Acts on proximal convoluted tubule.Carbonic anhydrase inhibitor. Causes self limited NaHCO3 diuresis and decreased total body HCO3- stores. Use - glaucoma, metabolic alkalosis, altitude sickness, pseudotumor cerebri

80
Q

Adverse effects of acetazolamide

A

Proximal renal tubular acidosis, parasthesias, promotes calcium phosphate stone formation

81
Q

Name the loop diuretics

A

Furosemide, bumetanide, torsemide

82
Q

Mechanism of loop diuretics

A

Act on thick ascending limb of the loop of Henle. Inhibit cotransport system (Na+/K+/2Cl-).

83
Q

Adverse effects of loop diuretics

A

Ototoxicity, hypokalemia, hypomagnesemia, dehydration, sulfa allergy, metabolic alkalosis, interstitial nephritis, gout

84
Q

Name the thiazide diuretics

A

Hydrochlorothiazide, chlorthalidone, metolazone

85
Q

Mechanism of thiazide diuretics

A

Inhibit NaCl reabsorption in early DCT - causes decreased diluting capacity of nephron. Decrease calcium excretion.

86
Q

Adverse effects of thiazide diuretics

A

Hypokalemic metabolic alkalosis, hyponatremia, hyperglycemia, hyperlipidemia, hyperuricemia, hypercalcemia, sulfa allergy

87
Q

Name the potassium sparing diuretics

A

Spironolactone, eplerenone, amiloride, triamterene

88
Q

Mechanism of spironolactone and eplerenone

A

Competitive aldosterone receptor agonists in cortical collecting tubule

89
Q

Mechanism of triamterene and amiloride

A

Act on cortical collecting tubule by blocking Na+ channels

90
Q

Adverse effects of potassium sparing diuretics

A

Hyperkalemia

91
Q

Aliskiren

A

Direct renin inhibitor. Used for HTN. Contraindicated in pts already taking ACE inhibitor or ARB. Contraindicated in pregnancy

Step 1 (Steffanie) (21 decks)

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