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Step 1 2019 First Aid Flashcards > Renal - FA Patho p582 - 592 > Flashcards

Renal - FA Patho p582 - 592 Flashcards

1
Q

where do you see RBC casts

A

Glomerulonephritis, malignant hypertension

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2
Q

where do you see WBC casts

A

Tubulointerstitial inflammation, acute pyelonephritis, transplant rejection.

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3
Q

what kind of cast do you see in nephrotic syndrome

A

fatty cast

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4
Q

Acute tubular necrosis, what cast do you see?

A

Granular (“muddy brown”) casts

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5
Q

Waxy casts is seen in

A

End-stage renal disease/chronic renal failure.

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6
Q

Hyaline casts

A

Nonspecific, can be a normal finding, often seen in concentrated urine samples

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7
Q

> 50% of glomeruli are involved

A

Diffuse proliferative glomerulonephritis

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8
Q

Thickening of glomerular basement membrane (GBM)

A

Membranous nephropathy

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9
Q

due to IgG, IgM, and C3 deposition along GBM and mesangium.

A

Acute post streptococcal glomerulonephritis

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10
Q

EM—subepithelial immune complex (IC) humps.

A

Acute post streptococcal glomerulonephritis

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11
Q

what are the presentation of Acute post streptococcal glomerulonephritis

A

Presents with peripheral and periorbital edema, cola-colored urine, hypertension.  inc anti-DNase B titers,  dec complement (C3) levels.

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12
Q

what type of cast is associated with Maltese cross sign

A

Fatty cast/oval fat bodies

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13
Q

“lumpy-bumpy” appearance on IF with which renal disease? What causes the lumps and bumps?

A

Acute poststreptococcal glomerulonephritis - granular appearance (“lumpy-bumpy”) B due to IgG, IgM, and C3 deposition along GBM and mesangium.

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14
Q

What type of HS rxn is Post strep GN?

A

HS-III

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15
Q

What are cresents in rapidly progressive GN made of?

A

Crescents consist of fibrin and plasma proteins (eg, C3b) with glomerular parietal cells, monocytes, macrophages

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16
Q

Type of HS and HLA # of Good Pasture?

A

HS -II, and HLA DR2

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17
Q

A vasculitis associated with Rapidly progressing GN?

A

Granulomatous polyangiitis, Microscopic polyangiitis

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18
Q

What does pauci-immune mean?

A

There is no Ig/C3 deposition involved.

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19
Q

Which GN is associated with “wire looping” of capillaries?

A

Diffuse Proliferative GN

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20
Q

Difference in deposition in Diffuse and Post strep GN and IgA nephropathy?

A

Diffuse has subENDOthelial and sometimes, intramembranous deposition where as Post Strep Gn has subEPIthelial deposits. IgA has mesangial deposits

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21
Q

Which GN is assoc with hemoptysis?

A

Rapidly Progressive - fun fact - most common on exam - Pick this unless proven otherwise

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22
Q

Most common cause of death in SLE?

A

Diffuse Prolif GN

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23
Q

IgA nephropathy assoc with what other diseases?

A

Henoch Schonlein, Celiac (w/ Dermatitis Herpetiformis), seen with resp/GI infections

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24
Q

GN + deafness (+blindness)?

A

Alports

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25
Q

Difference in IF between the GNs?

A

Linear - Good Pasture

Granular - PSGN (Diffuse Prolif)

Neg - Wagener’s, - PR3 ANCA Microscopic, MPA ANCA Churg strauss - eosinophilia, asthma

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26
Q

Difference between type I and II Membrano Prolif GN?

A

Type I - subendothelial immune complex seen on IF, “train track” appearence

Type II - intramembranous immune deposition of BM, “dense deposits”

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27
Q

MPGN is associated with which infectious disease?

A

Hep B and C

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28
Q

c3 nephritic factor is associated with which Nephritic syndrome?

A

MPGN, C3 nephritic factor stabilizes C3 convertase –> dec C3 levels

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29
Q

Which Nephrotic syndrome assoc with PLA2 - R Ab?

A

Membranous nephropathy

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30
Q

Minimal change disease can be secondary to what disease?

A

Hodgkin’s Lymphoma, due to cytokine mediated damage

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31
Q

Which two Nephrotic syndromes assoc with effacement of foot processes? So how do u know which one it is?

A

Minimal change disease and Focal Segmental Former = Children; Latter = adults

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32
Q

Populations associated with different Nephrotic syndrome?

A

Focal - African Americans, Latinx

Membranous - Caucasians

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33
Q

Secondary causes of Nephrotic syndrome?

Drugs, Diseases, Infections

A

Drugs - Penacillamine, NSAIDS (membranous), heroin (focal segment)

Infections - Hep B, C, syphyllis (Membranous), HIV - FSGS

Diseases - SLE, Solid tumors (colon, lung), (membranous)

Sickle cell (Focal segmental)

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34
Q

EM signs of Nephrotic syndromes

A

EM:

Minimal Change and Focal Segmental - effacement of podocyte foot processes

Membranous - spike and dome SubEPIthelial deposits

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35
Q

LM signs of nephrotic syndrome

A

Minimal change - looks Normal

Focal segmental - segmental sclerosis and hyalinosis

Membranous - diffuse capillary and GBM thickening

Diabetic GN - mesangial expansion and GBM thickening.

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36
Q

Apple green birefrigence under polarized light?

A

Amyloidosis

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37
Q

Pathomech of DB Glomerulonephropathy

A

Hyperglycemia –> nonenzymatic glycation of tissue proteins –> mesangial expansion; GBM thickening and Inc permeability.

Hyperfiltration (glomerular HTN and Inc GFR) –> glomerular hypertrophy and glomerular scarring (glomerulosclerosis) leading to further progression of nephropathy.

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38
Q

Most common cause of end stage kidney disease in US?

A

Diabetic GN

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39
Q

Kidney stones assoc with dec/inc PH?

A

Dec pH - uric acid, cysteine Inc pH - Struvite, CaPO4

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40
Q

Most common kidney stone

A

Calcium stones - calcium oxalate > calcium phosphate stones

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41
Q

Causes of calcium oxalate stones and Tx

A

ethylene glycol (antifreeze) ingestion, vitamin C abuse, hypocitraturia (associated with dec urine pH), malabsorption (eg, Crohn disease)

Tx thiazids, citrate, low sodium diet

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42
Q

Ammonium magnesium phosphate is assoc w. which bugs

A

Urease (+) - Proteus, Cryptococcus, H pylori, Ureaplasma, Nocardia, Klebsiella, S epidermidis, S saprophyticus

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43
Q

Which stones radiolucent/opaque?

A

Radiol -U -cent - Uric acid Radioopaque - Ca ones, Struvite, cysteine

44
Q

How to treat uric acid stones?

A

alkinization of urine, allopurinol

45
Q

Defect leading to cysteine kidney stones - which amino acids affected?

A

Cystein, Ornithine, Lysine, Arginine

46
Q

Test for Cysteine stones?

A

Sodium cyanide nitroprusside test ⊕.

47
Q

Name…that… stoneeee!

A
48
Q

When does Creatinine rise with hydronephrosis?

A

If both kidneys affected, or obstruction bilat

49
Q

polygonal clear cells, golden-yellow (poss) - what disease? Why the color?

A

RCC, yellow color due to inc lipid content (clear if more carbs)

50
Q

Tell me how RCC spreads (v –> blood spread to where?)

A

From PCT –> Invades renal v –> IVC –> hematogenous spread –> metastasis lung, bone

51
Q

RCC assoc with which chromosomal mutation?

A

VHL on Chr 3

52
Q

Most common presentation of RCC? why?

A

As a lung or bone metastasis, bc invades renal v, then IVC, spread thru blood to lung or bone but can present with painless hematuria, palpable mass

53
Q

RCC assoc with which paraneoplastic syndrome?

A

PTHrP, Ectopic EPO, ACTH, Renin

PEAR-aneoplastic

54
Q

8 year old child develops respiratory infection, which resolves without antiobiotics. However, shortly thereafter, child’s mother notices his face is swelling. Takes child to Dr after his limbs started swelling and he is also gaining weight. 24hr urine - total protein of 4.2 g. Which of the following is likely elevated in patient’s serum? Albumin Cholesterol Antithrombin Creatinine Sodium

A

Cholesterol - Pt has minimal change disease. Often in children follows viral infection or bee sting. Nephrotic syndrome assoc with hyperlipidemia/hypercholesterolemia and is hypercoag state.

55
Q

7 year old presents with nausea, fever, anorexia. He appears ill and has prominent swelling around the eyes. BP elevated, Lab show inc creatinine and BUN. Fresh urine sediment show RBC casts. Most likely outcome? Complete recovery Development of Cresenteric GN Development of Focal and segmental Glomerulosclerosis Persistent nonprogressive proteinuria steroid dependency

A

Choice A is correct. Pt has PSGN. Other tests shown could be inc ASO titers and dec C3, with normal C4 - bacteria activate the alternative, not classical complement pathway. Acute PGSN is benign and self limiting. Major sx resolve in 1-3 mo, and protein/hematuria resolve in 6mo. Complete resolution less likely with inc age.

56
Q

65 yr old African Am male has 3-4 day history of burning sensation upon mictruition and inc urgency. Urinalysis shows white blood cells, LAP, nitrites. CBC - mild anemia. Pt reports that his father and two brothers also have anemia. To treat his UTI while considering his family Hx, which antibiotic is best choice? (Bonus - mech of action of Tx) Ciprofloxacin Erythromycin Nitrofurantoin Penicillin TMP-SMX

A

A is correct. Ciprofloxacin is used to treat UTI and is safe with family Hx of hemoyltic anemia due to G6PD( Is common in both Af Am and Mediterranean populations) Flouroquionolones (-) DNA replication by blocking topoisomerases Erythromycin and Penicillin are not recommended choices for UTI, as normally caused by G- bact Nitrofurantoin and TMP-SMX are oxidants and can trigger a hemolytic attack.

57
Q

Diseases with low c3

A

SLE, Type II Membranoprolif GN, PSGN

58
Q

CH50 tests for what?

A

screening test for total complement activity

59
Q

2’ sx of RCC?

A

polycythemia, flank pain, fever, weight loss

60
Q

large eosinophillic cells with lots of mitochondira w/o perinuclear clearing

A

renal oncocytoma

61
Q

most common renal malignancy of childhood

A

Wilms tumor (age 2-4) - Nephroblastoma

62
Q

malignancy that contains embryonic glomerular structures

A

Wilms - made of blastema, 1’ glom tubules, stromal cells

63
Q

Genetic cause of WIlms?

A

loos of function mutation of tumor suppressor gene WT1/WT2 on Chr 11, next to PAX

64
Q

Wilms assoc w. which other paths

A

ƒ WAGR complex—Wilms tumor, Aniridia (absence of iris), Genitourinary malformations, mental Retardation/intellectual disability (WT1 deletion)

Denys Drash

Beckwith Widermann

65
Q

painless hematuria with no casts in elderly casts

A

bladder cancer

66
Q

Which risk factors assoc with transitional cell bladder cancer?

A

Phenacetin, Smoking, Aniline dyes, Cyclophosphamide

67
Q

Denys Drash

A

-Denys Drash

Wilms, early onset nephrotic syndrome (Diffuse mesangial sclerosis) , male pseudohermaphroditism (Dysgenesis of gonad)

68
Q

Beckwith Wiedemann -

A

Wilms, macroglossia, organomegaly, hemihyperplasia, neonatal hypoglycemia

Everything is WIDEman, big tongue, big organs, hemihyperplasia (one part or half of the body is better)

69
Q

Risk factors for Sq cell carcinoma of the bladder

A

Schistosoma heamatobium (Middle East), smoking, cystitis, chronic nephrolithiasis

=SCC

70
Q

Most common causes of bact cystitis?

A

E. coli (MOST COMMON) Staph saprophyticus Klebsiella Proteus mirabilis

71
Q

Lab findings for UTI

A

(+) leukocyte esterase (+) for nitrates - G- organisms

72
Q

Pyelonephritis presents with which urine finding?

A

wbc casts in urine

73
Q

sterile pyuria and neg urine cultures in UTI indicate which cause?

A

Nesseria or Chlamydia

74
Q

which part of the kidney does acute pyelonephritis affect?

A

affects cortex, with relative sparing of glomeruli/vessels

75
Q

why does pregnancy cause higher risk of pyelonephritis?

A

dec basal tone of uterus –> urine pooling –> inc risk of infection

76
Q

Difference in G- org v Saprophyticus pyelonephritis?

A

G- org = Esterase and nitrate +

S.saprophyticus = esterase + and nitrate -

77
Q

Microscopic findings in chronic pyelonephritis?

A

Coarse, asymmetric corticomedullary scarring, blunted calyx. Tubules can contain eosinophilic casts resembling thyroid tissue C (thyroidization of kidney)

78
Q

rare grossly orange nodules that can look like tumors, damage due to granulomatous tissue w/ foamy macrophages

A

Xanthogranulomatous pyelonephritis

79
Q

Xanthogranulomatous pyelonephritis is assoc with which organism?

A

Proteus

80
Q

what kidney issue is assoc with obstetric issues?

A

diffuse cortical necross - acute gen cortical infarction of both kidneys - due to a combo of vasospasm and DIC

Associated with obstetric catastrophes (eg, abruptio placentae), septic shock.

81
Q

Prerenal azotemia

A

Due to dec RBF (eg, hypotension) –> dec GFR. Na+/H2O and BUN retained by kidney in an attempt to conserve volume –> INC BUN/creatinine ratio (BUN is reabsorbed, creatinine is not) and DEC FENa.

82
Q

Intrinsic renal failure - causes?

A

Generally due to acute tubular necrosis or ischemia/toxins; less commonly due to acute glomerulonephritis (eg, RPGN, hemolytic uremic syndrome) or acute interstitial nephritis.

83
Q

Pathomech of renal failure in ATN, why the change in BUN/Cr ratio?

A

In ATN, patchy necrosis –> debris obstructing tubule and uid backflow across necrotic tubule –> DEC GFR. Urine has epithelial/granular casts. BUN reabsorption is impaired = DEC BUN/creatinine ratio and INC FENa

84
Q

Postrenal azotemia

A

Due to out ow obstruction (stones, BPH, neoplasia, congenital anomalies). Develops only with bilateral obstruction.

85
Q

Consequences of Renal Failure

A

Consequences (MAD HUNGER):

  • Metabolic Acidosis
  • Dyslipidemia (especially triglycerides)
  • Hyperkalemia
  • Uremia
  • Na+/H2O retention (HF, pulmonary edema, hypertension)
  • Growth retardation and developmental delay
  • Erythropoietin failure (anemia)
  • Renal osteodystrophy
86
Q

Sx of Uremia

A

Nausea and anorexia
Pericarditis
Asterixis
Encephalopathy
Platelet dysfunction

87
Q

Explain Renal osteodystrophy

A

Hypocalcemia, hyperphosphatemia, and failure of vitamin D hydroxylation associated with chronic kidney disease

88
Q

Renal osteodystrophy lead to which endocrine issues?

A

2° hyperparathyroidism –> 3° hyperparathyroidism (if 2° poorly managed).

High serum phosphate can bind with Ca2+ Ž–> tissue deposits –> DEC serum Ca2+.

Dec 1,25-(OH)2D3 –> intestinal Ca2+ absorption

89
Q

Pyuria w. eosinophils and azotemia after drug admin?

A

Acute interstitial nephritis

90
Q

Causes of Acute interstitial nephritis

A
  • Pee (diuretics)
  • Pain-free (NSAIDs)
  • Penicillins and cephalosporins
  • Proton pump inhibitors
  • RifamPin
91
Q

Most common cause of acute kidney injury in hospitalized patients.

A

Acute Tubular necrosis

92
Q

Part of nephron most susceptible to injury with Ischemic Acute Tubular necrosis

A

PCT and thick ascending limb are highly susceptible to injury

93
Q

Drugs and other causes that can lead to nephrotoxic acute tubular necrosis

A
  • aminoglycosides,
  • radiocontrast agents,
  • lead,
  • cisplatin,
  • ethylene glycol
  • crush injury (myoglobinuria),
  • hemoglobinuria
94
Q

Part of nephron most susceptible to injury with nephrotoxic acute tubular necrosis?

A

PCT

95
Q

Types of casts seen in acute tubular necrosis, and what happens to FENa

A

granular casts, and Inc FENa

96
Q

Sloughing of necrotic renal papillae gross hematuria and proteinuria.

A

Renal Papillary necrosis

97
Q

Causes assoc with renal papillary necrosis

A

SAAD papa with papillary necrosis:

  • Sickle cell disease or trait
  • Acute pyelonephritis
  • Analgesics (NSAIDs)
  • Diabetes mellitus
98
Q

Causes of renal artery stenosis - prox vs distal?

A

Atherosclerotic plaques—proximal 1/3rd of renal artery, usually in older males, smokers.

Fibromuscular dysplasia—distal 2/3rd of renal artery or segmental branches, usually young or middle-aged females

99
Q

Complications of ADPKD?

A

death from complications of chronic kidney dz or HTN caused by inc renin

100
Q

3 pathologic conditions associated with ADPKD?

A

berry aneurysms, mitral valve prolapse, benign hepatic cysts, diverticulosis

101
Q

5 clinical symptoms of ADPKD?

A

flank pain, hematuria, HTN, urinary infection, progressive renal failure

102
Q

what are 2 genes associated with ADPKD?

A

85%, ch 16, PKD1 15%, ch 4, PKD2

103
Q

Rx for ADPKD?

A

ACEI/ARBs

104
Q

cystic dilations of collecting ducts that often presents in infancy?

A

ARPKD

105
Q

Cause of portal HTN in ARPKD?

A

is assoc w/ congenital hepatic fibrosis & hepatic cysts -> portal HTN

106
Q

tubulo interstitial fibrosis and progressive renal insuff?

A

Autosomal dominant tubulointerstitial kidney disease - has flat true cysts - segments of collecting ducts abnormally dilated in medulla @ tips of papillae, shrunken kidneys

Step 1 2019 First Aid Flashcards (63 decks)

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