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CPR Exam 3 > Renal Pathology Pt. 3 > Flashcards

Renal Pathology Pt. 3 Flashcards

1
Q

what are the hereditary nephritises?

A

Alport syndrome

Thin basement membrane lesion/benign familial hematuria

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2
Q

what is alport syndrome?

A

X-linked

mutated gene encoding collagen IV

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3
Q

what is the clinical presentation of alport syndrome?

A

hematuria
CKD
nerve deafness
eye disorders

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4
Q

what are the characteristics of alport syndrome under an electron microscope?

A

moth-eaten/frayed basement membrane

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5
Q

what is thin basement membrane disease?

A

AR

mutated gene encoding a3 or a4 chains of collagen IV

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6
Q

what is the clinical presentation for thin basement membrane disease?

A

asymptomatic hematuria

usually uncovered during routine UA

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7
Q

which systemic diseases cause secondary nephrotic syndrome?

A

DM
SLE
Hep C
HIV

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8
Q

which systemic diseases cause secondary nephritic syndrome?

A

SLE
bacterial endocarditis
goodpasture syndrome
Henoch Schonlein purpura

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9
Q

what is the pathogenesis underlying diabetic nephropathy?

A

metabolic defect linked to hyperglycemia produces thick GBM

hemodynamic effects associated with glomerular hypertrophy contribute to glomerulosclerosis

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10
Q

what can be seen histologically in diabetic glomerulosclerosis?

A

diffuse capillary basement membrane thickening

diffuse mesangial sclerosis

nodular glomerulosclerosis (PAS positive)

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11
Q

what can be seen histologically in advanced renal hyaline arteriolosclerosis?

A

marked thickened, tortuous afferent arteriole

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12
Q

what are the 3 prototypical renal lesions associated with diabetes?

A

nodular glomerular lesions
vascular lesions (arteriolosclerosis)
necrotizing papillitis

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13
Q

what are the 6 classifications of glomerular disease caused by SLE?

A 
I. Minimal mesangial lupus nephritis
II. Mesangial proliferative lupus nephritis
III. focal lupus nephritis
IV. diffuse lupus nephritis
V. membranous lupus nephritis
VI. advanced sclerosing lupus nephritis
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14
Q

which class of glomerular disease are most commonly seen in SLE?

A

IV. diffuse lupus nephritis

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15
Q

how does Henoch Schonlein purpura affect the kidneys?

A

IgA is deposited in the glomerular mesangium

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16
Q

what is fibrillary glomerulonephritis?

A

morphological variant of glomerulonephritis associated with fibrillar deposits in the mesangium and capillary walls

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17
Q

what is the clinical presentation of fibrillary glomerulonephritis?

A

nephrotic syndrome
hematuria
progressive renal failure

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18
Q

which three systemic disorders manifest in the kidneys with foci of glomerular necrosis and crescent formation?

A

goodpasture syndrome
microscopic polyangiitis
Wegener granulomatosis

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19
Q

what infection is associated with essential mixed cryoglobulinemia?

A

Hep C

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20
Q

what is the pathogenesis of essential mixed cryoglobulinemia?

A

IgG-IgM complexes that induce cutaneous vasculitis, synovitis, and proliferative glomerulonephritis

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21
Q

what is acute tubular injury?

A

acute renal failure and morphologic evidence of tubular necrosis

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22
Q

what are the causes of ATI?

A

ischemia

direct toxic injury by endogenous or exogenous agents

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23
Q

what is the most common cause of acute renal failure?

A

ATI

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24
Q

what are some uncommon causes of ATI?

A

hypersensitivity to drugs

urinary obstruction

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25
Q

what is the necrosis pattern associated with ischemic necrosis ATI?

A

patchy in PCT
patchy in PST
patchy in LoH

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26
Q

what is the necrosis pattern associated with toxic necrosis ATI?

A

continuous in PCT
continuous in PST
patchy in LoH

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27
Q

what is clinically evident in the initiation stage of AKI?

A

oliguria

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28
Q

what is clinically evident in the maintenance stage of AKI?

A

oliguric crisis with some uremic features

hyperkalemia

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29
Q

what is clinically evident in the recovery stage of AKI?

A

large urine volumes
large loss of water, Na, K
hypokalemia
susceptibility to infection

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30
Q

what is tubulointerstitial nephritis?

A

a group of renal diseases involving inflammatory injuries to tubules and interstitium that are insidious in onset

31
Q

what are the clinical manifestations of tubulointerstitial nephritis?

A

azotemia

inability to concentrate urine (polyuria)

32
Q

what are the primary etiologies of tubulointerstitial nephritis?

A 
infections
toxins
metabolic diseases
chronic obstruction
neoplasms
immunologic reactions
vascular diseases
33
Q

what is the pathway of infection to the kidneys?

A

UTI –> cystitis –> pyelonephritis

34
Q

what is chronic pyelonephritis?

A

recurrent or continuous infection of the kidney with resultant damage to the pelvis/calyces/parenchyma resulting in anatomic distortion

35
Q

what is the most common UTI causing bacteria?

A

E. coli

36
Q

what other bacteria are known to cause UTI?

A

Proteus
Klebsiella
Enterobacter sp.

37
Q

what anatomic defects predispose a patient to pyelonephritis?

A

vesicoureteral reflux

intrarenal reflux

38
Q

what medical conditions predispose a patient to pyelonephritis?

A

diabetes
pregnancy
BPH

being female

39
Q

what are possible complications of pyelonephritis?

A

papillary necrosis
pyonephrosis
perinephric abscess

40
Q

what is the most common cause of pyelonephritis?

A

ascending cystitis combined with a predisposing anatomical defect

41
Q

what is the most common cause of vesicoureteral reflux?

A

congenital partial or complete lack of oblique angle of the intravesical portion of the ureter

42
Q

what is the most common cause of AKI?

A

pyelonephritis

43
Q

what is the second most common cause of AKI?

A

tubulointerstitial nephritis induced by drugs or toxins

44
Q

what drugs cause tubulointerstitial nephritis?

A 
analgesics
synthetic penicillins (methicillin, ampicillin)
rifampin
diuretics
NSAIDs
allopurinol
cimetidine
45
Q

what is the clinical presentation of tubulointerstitial nephritis induced by drugs/toxins?

A

fever
eosinophilia
interstitial renal parenchymal infiltrates

46
Q

what is a potential complication of analgesic nephropathy?

A

urothelial carcinoma

47
Q

what is urate nephropathy?

A

precipitation of uric acid crystals in the renal tubules leading to obstruction of the nephrons and acute renal failure

48
Q

what is the primary cause of acute uric acid nephropathy?

A

chemotherapy causing tumor lysis syndrome

49
Q

what is the primary cause of chronic urate nephropathy?

A

hyperuremic syndrome –> gout

50
Q

what is a potential complication of hyperuricemia?

A

renal stones/nephrolithiasis

51
Q

what are potential complications of hypercalcemia?

A

formation of calcium stones

deposition of calcium in the kidney

52
Q

what is acute phosphate nephropathy?

A

accumulations of calcium phosphate crystals in the tubules that can occur in patients after consuming high doses of oral phosphate solutions in preparation for colonoscopy

53
Q

what is myeloma kidney?

A

renal insufficiency as a result of multiple myeloma

54
Q

what factors contribute to renal damage in myeloma kidney?

A 
Bence-Jones proteinuria
cast nephropathy
amyloidosis
light-chain deposition disease
hypercalcemia
hyperuricemia
55
Q

what is bile cast nephropathy?

A

hepatorenal syndrome in which renal dysfunction manifests in patients with advanced liver failure due to bile cast formation in the distal nephron

56
Q

what are the renal vascular diseases?

A 
nephrosclerosis
renal artery stenosis
thrombotic microangiopathies
atheroembolic renal disease
sickle-cell nephropathy
57
Q

what is benign nephrosclerosis?

A

morphologic changes associated with hyaline sclerosis of the renal arterioles and small arteries

58
Q

what is the effect of benign nephrosclerosis?

A

multi-focal ischemia of the renal parenchyma supplied by the sclerotic vessels

59
Q

what conditions contribute to the formation of benign nephrosclerosis?

A

age
HTN
DM

60
Q

what is malignant arteriosclerosis?

A

a medical emergency

renal vascular disorder exhibiting injury associated with accelerated HTN

61
Q

what are the pathologic effects of malignant arteriosclerosis?

A

ischemic kidney injury
elevated renin
a self-perpetuating cycle of damage and HTN

62
Q

what is the pathogenic pathway of malignant HTN?

A

renal vascular damage
increased permeability of small vessels
endothelial irreversible injury
focal vascular cell death/hemorrhage
platelet deposition/thrombosis
fibrinoid necrosis of arterioles and small vessels
hyperplastic arteriolitis (renal failure)

63
Q

what are the renal morphological changes associated with malignant htn?

A

“flea-bitten” appearance of renal hemorrhages

64
Q

what is the clinical presentation of malignant htn?

A 
BP >180/120
papilledema
retinal hemorrhages
encephalopathy
CV abnormalities
renal failure
65
Q

what is renal artery stenosis?

A

potentially curable form of HTN secondary to atherosclerosis or fibromuscular dysplasia

66
Q

what are the thrombotic microangiopathies that result in renal damage?

A

hemolytic uremic syndrome

thrombotic thrombocytopenic purpura

67
Q

what is HUS?

A

endothelial cell injury and activation due to Shiga-like toxin (E. coli O157:H7)

68
Q

what is TTP?

A

acquired deficiency of ADAMTS13 resulting in abnormal function of vWF

69
Q

what is the clinical presentation of TTP?

A 
fever
neurological symptoms
microangiopathic hemolytic anemia
thrombocytopenia
renal failure
70
Q

what is the most common cause of renal atheroembolism?

A

mural thrombosis from left side of the heart

71
Q

what are the clinical signs of renal atheroembolism?

A 
flank pain
hematuria
HTN
arrhythmia
nausea/vomiting
oliguria/anuria
72
Q

what is sickle cell nephropathy?

A

papillar necrosis due to accelerated sickling in the renal medulla

73
Q

what are the clinical features of sickle cell nephropathy?

A

hematuria
hyposthenuria (diminished concentrating ability)
proteinuria

CPR Exam 3 (15 decks)

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