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PATHOMA renal Flashcards

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USMLE® Step 1 flashcards
1
Q

name the congenital renal abnormalities

A
  1. Horseshoe kidney
  2. Renal agensis
  3. Dysplastic kidney
  4. PKD
  5. Medually cystic kidney disease
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2
Q

presentation of ARPKD

A

portal HTN in infants

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3
Q

presentation of ADPKD

A

hematuria and worsening renal failureprobably with headaches

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4
Q

associations of ADPKD

A

hepatic cysts, berry aneurysms and mitral valve prolapse

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5
Q

medullary cystic kidney diseease genetics and presentation

A
  1. Autosomal dominant

2. It has shrunken kidney due to parenchymal fibrosis while all other cyctic kidney diseases have an enlarged kidney

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6
Q

hallmark of ARF

A
  1. azotemia

2. oliguria

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7
Q

normal BUN:Cr ratio

A

15:1

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8
Q

reasons for ARF

A
  1. Azotemia (pre,intra,post)
  2. Acute interstitial nephritis
  3. Renal papillary necrosis
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9
Q

whivh parts of the renal tubulae are most susseptible to ischemis

A

PCT & medullary segment of thick ascending loop

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10
Q

what is associated with ethylene glycol intake

A

oxalate stones

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11
Q

why supportive dialysis is necessary during ongoing acute tubular necrosis therapy

A

bcoz PCT cells are stable (take time to regenrate)

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12
Q

acute interstitial nephritis causes

A

NSAIDS, PCN and diuretics. It is a drug indiced HSR

Chronic use may lead to papillary necrosis.

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13
Q

causes od renal papillary necorsis

A

NSAIDS, DM, sickle cell trait and severe acute pyelonephritis

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14
Q

nephrotoxic causes of acute tubular necrosis

A

HRU AME

  1. Heavy metals (lead)
  2. Radioactive dye
  3. Urate (tumor lysis syndrome)
  4. Aminoglycosides
  5. Myoglobin (crush injuries)
  6. Ethylene glycol
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15
Q

name the nephrotic syndromes

what conditions cause nephrotic syndrome

A
  1. Minimal change desease
  2. Focal segmantal glomeruloscleosis
  3. Membranous nephropathy
  4. Membranoproliferative glomerulonephrosis
  5. DM
  6. SLE
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16
Q

characters of nephrotic syndrome

A
  1. Hypoalbuminemia (edema)
  2. Hypogammaglobulinemia (infections)
  3. Hypercoaguable state (AT III loss)
  4. Hyperlipidemia & hypercholesterolemia
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17
Q

what is MCD associated with

A

Hodkins lymphome (redd sternberg cells produce and release cytokines which are the main cause of the disease and since it is due to cytoines, this is the only nephrotic syndrome that is very responsive to steroids)

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18
Q

presentation of MCD

A

selective albuminuria

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19
Q

differencebetween MCD & FSGS

A

MCD is very responsive to steroids but FSGS inst

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20
Q

associations of FSGS

A

sickle cell anemia, HIV & heroin usage

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21
Q

association od membranous nephropathy

A

Hep B & C , solid tumors, SLE, drugs (NSAIDS, PCN)

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22
Q

MPGN type I associations

A

HBV & HCV

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23
Q

what is C3 nephrtic factor

A

it is an antibody that is produced in MPGN type II and it stabilized the C3 convertase that breaks down C3 into C3a and C3b and this causes overactivity of the complement system
It results in infalmmation and low circulating levels of C3 in the blood

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24
Q

what are kimmelstein nodules

A

They are mesangeal sclerotic nodules seen in diabetic neohrpathy

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25
Q

How does DM cause nephrotic syndrome

A

by NEG (non enzymatic glycosylation). It causes the glucose to attach to the glomerular memebrane without the enzyme necessary for the process and it leads to leaky memebranes and the protein and fluid from the glomerulus leaks into it and causes hyaline atherosclerosis that leads to a decrease in lumen calibre (mostlyin the efferent vessel) and it initially causes fluid retention in the gloerulus nad it causes hyperfiltration and microalbuminuria and in chronic state causes fluid backup and mesangeal sclerosis (Kimmelstein Wilson Nodules) and ot leads to nephrotic syndorme

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26
Q

where does amyloid deposit in the kidney

A

In the mesangeum

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27
Q

tram track appearance

A

seen in MPGS type II

28
Q

spike and dome appearance

A

seen in MPGS type I

29
Q

characters of nephritic syndrome

A
  1. protein less than 3.5 g/day
  2. oliguria & azotemia
  3. salt retention & periorbital edema
  4. RBC casts & deformed RBC in urine
30
Q

biopsy of glomerulus in nephritic syndrome

A
  1. Immune complex deposition (which activates compliment nd this causes C5a increase tht attracts neutrophils)
  2. hypercellular (due to neutrophils), inflammed glomeruli
31
Q

types of nephritic syndrome

A
  1. PSGN
  2. RPGN
  3. IgA nephropathy
  4. Alport syndrome
32
Q

what are cresents

A

they are a mass of macrophages & fibrin in d glomerulus in RPGN

33
Q

How to diff the etiology og RPGN

A

IF test

34
Q

IgA nephropathy aka

A

BERGER disease

35
Q

where do IgA deposit in IgA nephropathy

A

in the mesangium. So the IF shows light in the mesangeum

36
Q

what is Alport syndrome

A

X linked type IV collagen defect

37
Q

characteristics of UTI with proteus

A

alkaline urine with ammnia smell

38
Q

what organisms cause cystitis

A
  1. E coli
  2. S saprophyticus
  3. Klebsiella
  4. Proteus
  5. Enterococcus fecalis
39
Q

causes of urethritis

A

chlamydia nisseria

40
Q

what does dip stick indiaicate in a UTI

A

positive for leukocyte esterase and positive for nitrite

41
Q

what does chronic pyelonephritis cause

A

interstitial fibrosis with tubular atrophy due to multiple bouts of pyelonephritis

42
Q

what is the most common cause of calcium stones and its Rx

A

isiopathic hypercalciuria

Rx : hydrochlorothoazide

43
Q

which nephrolith is radiolucent

A

uric acid stone

44
Q

characters of end stage kidney failure

A
  1. Uremia
  2. Hyperkalemia with metabolic acidosis
  3. Hypocalcemia
  4. Salt and water rentension with HTN
  5. Anemia
  6. Osteodystrophy
45
Q

where is EPO produced

A

in renal peritubular interstitial cells

46
Q

characteristics of uremia

A

nausea, pericarditis, urea crystals in the skin, encehalopathy with asterixis, anorexia and platelet dysfunction (ureima inhibits both platelet aggregation and platelet adhesion)

47
Q

where does 1 alpha hydroxilation take place

A

in PCT cells

48
Q

what risks are aassociated with dyalsis

A
  1. Renal cell carcinoma

2. dyalisis shrinks kidney upon which cysts may occur

49
Q

name the renal neoplasias

A
  1. RCC
  2. Angiolipomyoma
  3. Wilms tumor
50
Q

what is tuberous sclerosis and what is it associated with

A

tuberous sclerosis - development of benign tumors all over the body. It is a genetic condition
It is a risk factor for angiolipomyoma

51
Q

what is the RCC triad

A
  1. palpable mass
  2. hemturia
  3. flank pain
52
Q

associations of RCC

A

left sided varicocele

53
Q

pathophysiology of RCC

A

inhibited VHL gene causes over activity of IGF-1 & increased transcription of HIF gene (increases PDGF & VEGF)

54
Q

gross appearance of RCC

A

yellow colored

55
Q

Most common subtype of RCC

A

clear cell carcinoma

56
Q

what is blastema

A

immature kidney mesenchyme

57
Q

what is wilms tumor

A

it is a malignant tumor is usually 3yr old children which is made up of blastema, primitive glomeruli, tubules and stromal cells

58
Q

presentation of wilms tumor

A

large unilateral flank mass , hematuria nad HTN (dur o renin secretion)

59
Q

name the sporadic syndromes

A
  1. WAGR - it is due to deletion of WT1 at 11p13.
    It presents with wilms tumor, aniridia, genital
    abnormalities and mental and motor
    retardation
  2. Denys Drash - It is due to mutated WT1 gene
    It presents with wilms tumor,
    progressive renal (glomerular) disease
    and male pseudohermaphroditism
  3. Beckwith Whitemann - it is due to WT-2 gene cluster
    mutation especially IGF-2
    (imprinted 11q15.5)
    It presents with wilms tumor, organomegaly, muscular
    hemihypertropgy and neonatal hypoglycemia
60
Q

what are the lower urinary tract carcinomas

A
  1. Urothelil carcinoma
  2. Squamous cell carcinoma
  3. adenocarcinoma
61
Q

risk factors for uroepithelial (transitional cell) carcinoma

A

cigarette smoe (napthylamine), azo dyes, nephrolitilasis long term usage of cyclophoaphamine and phenacetin

62
Q

what are the pathways from which the uroepithelial tumora may develop

A
  1. Papillary pathway - it s a fibrovascular growth with blodd vessels in it and epithelium in it top. It is not associated with p53 gene mutation. It starts as low grade, progresses to high grade and then invades
  2. Flat pathway - it is associated with p53 gene mutation. It starts as a growth of cella layer by layer and it is flat. It starts as high grade ans then invades
63
Q

what is a feild defect and where is it seen

A

It is seen in uroepithelial carcinoma.

It is multifocal and recurrent tumor develoment

64
Q

risk factors for squamous cell carcinoma

A

chronic cystitis, long standing nephrolithiasis and Schistosomiasis hematobium

65
Q

causes of adenocarcinoma of the lower urinary tract

A
  1. Urachal remnant
  2. Bladder extrophy
  3. cystitis glandularis
66
Q

what is cyctitis glandularis

A

It is the dyslasia of te bladder epithelium to coloumnar cells due to chronic and recurent infections of the bladder

usmle step 1 (3 decks)

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