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CRRAB II- Week 2 > Warren- Diseases of Blood Vessels > Flashcards

Warren- Diseases of Blood Vessels Flashcards

1
Q

What is nephrosclerosis?

A

Renal pathology associated w/ sclerosis of RENAL ARTERIOLES AND SMALL ARTERIES

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2
Q

What is seen microscopically with nephrosclerosis?

A

HYALINE ARTERIOSCLEROSIS>
narrows lumen>
ischemic atrophy w/ tubular atrophy

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3
Q

What does Nephrosclerosis look like grossly?

A

surface has fine even granularity

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4
Q

What is the pathogenesis of nephrosclerosis?

A

Aging, genetics, hemocynamic changes>
medial/intimal thickening>
hyaline deposition in arterioles d/t endothelial cell injury

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5
Q

Does nephrosclerosis typically cause renal insufficiency?

A

Not really

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6
Q

What pts is nephrosclerosis commonly observed in?

A

DM
black
Severe HTN

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7
Q

WHat is malignant nephrosclerosis?

A

Renal disease associated w/ malignant HTN

1-5% of pts w/ HTN get it

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8
Q

Who do you commonly see malignant nephrosclerosis in?

A

Young black men

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9
Q

What is observed grossly with malignant nephrosclerosis?

A

petechial hemorrhages (flea bitten)

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10
Q

What is observed microscopically with malignant nephrosclerosis?

A

FIBRINOID NECROSIS of the arterioles

ONION SKINNING OF VESSELS (cocentric proliferation of smth muscle cells and collagen; correlates w/ renal failure)

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11
Q

Describe the clinical course of malignant nephrosclerosis.

A

HA, N/V, Visual impairement (scotomas)

High Diastolic pressure, papilledema, encephalopathy

Proteinuria/hematuria EARLY>
rapid renal failure

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12
Q

What is renal artery stenosis?

A

2-5% of HTN>
unilateral renal artery stenosis>
renin secretion

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13
Q

How do you diagnose renal artery stenosis?

A

bruit on kidney ausculation

high plasma/renal vein renin

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14
Q

What does a kidney w/ renal artery stenosis look like? How does the non-ischemic kidney appear?

A

Ischemic SMALL kidney w/ some atrophy

Hyaline arteriosclerosis (subjected to systemic HTN)

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15
Q

What can cause RAS?

A

70% d/t occlusion of RA by atheromatous plaque

Fibromuscular dysplasia

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16
Q

What are thrombotic microangiopathies?

A

Group of disorders characterized by THROMBOSIS in capillaries and arterioles in the body

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17
Q

What is seen clinically in pts w/ thrombotic microangiopathies?

A
  1. MAHA (shistocytes- RBC fight way through small vessels)
  2. Thrombocytopenia)- low platelets b/c they’re utilized in multiple clots)
  3. RF
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18
Q

What are the thrombotic microangiopathies?

A

typical HUS
atypical HUS
familial HUS
Idiopathic TTP

19
Q

What causes HUS/TTP

A

Endothelial cell injury>
reveals thrombogenic tissue>
clotting cascase>
decrease PG I2 and NO

Platelet activation and aggregation

20
Q

What causes Typical HUS and why does this make you NOT want to drink non-pasteurized milk?

A

75% d/t intestinal infection by verocytotoxin producing E. Coli>
sudden onset bleeding, oliguria, hematuria

21
Q

What does verocytotoxin do?

A

causes endothelial lysis, increased endothelin, decreased NO

22
Q

What happens to most pts w/ typical HUS?

A

Recover w/in weeks w/ dialysis

23
Q

What is atypical HUS?

A

Unclear mechanism

  1. Pregnancy- post partum renal failure
  2. vascular renal disease
  3. CYCLOSPORINE
24
Q

What causes familial HUS? What is the mortality rate?

A

Def of the copmlement regulatory protein Factor H

Factor H>
protects cells form uncontrolled complement activation

HIGH- 50%

25
Q

What causes Idiopathic TTP?

A

Acquired/genetic defect in protease that cleaves large von Willebrand multimers

26
Q

What is the classic pentad of sxs for TTP?

A 
Fever
neurologic
MAHA
thrombocytopenia
RF
27
Q

Who is commonly affected by TTP?

A

Women

Pts < 40

28
Q

How do you differentiate TTP and HUS?

A

TTP- neurologic features (sometimes renal involvement)

HUS- significant renal involvement and may not have neurologic features

29
Q

How do you treat TTP?

A

plasma exchange and corticosteroids

30
Q

Microscopically, a pt has deposits of FIBRIN in the capillary lumen, subendothelially and in the mesangium. They also have fibrinoid necrosis of the arterioles. What do they have?

31
Q

What causes most renal infarcts?

A

Emboli

25% CO to kidneys>
limited colateral circulation

32
Q

What is the difference between acute and chronic renal infarcts grossly? What is seen micro?

A

acute: solitary WHITE infarcts
chronic: depressed, gray-white scars w/ a V shape

coagulative necrosis

33
Q

What does obstructive uropathy lead to?

A

Hydronephrosis

renal atrophy

34
Q

How does hydronephrosis appear grossly?

A 
obstruction of urine flow>
DILATION of the renal pelivs and calyces>
atrophy of the kidney>
massive enlargement>
thin walles cyst
35
Q

How does an acute obstruction present?

A

Pain and sxs related to underlying cause (renal colic form calculus)

36
Q

How does unilateral hydronephrosis present?

A

Can be silent for a long time b/c other kidney compensates

37
Q

How does bilateral partial obstruction present?

A

Inability to concentrate urine>

polyuria/nocturia

38
Q

How does bilateral complete obstruction present?

39
Q

What percent of americans have stones? M vs. F? Peak age?

A

5-10%
Men
20-30 y/0

40
Q

What primarily causes urolithiasis?

A

inborn errors of metabolism> stone formation

gout
cystinuria
primary hyperoxaluria

41
Q

What are the 4 main types of calculi?

A

70% Ca oxalate and Ca phosphate

15% Struvite (Mg NH4 PO)

5-10% UA

1-2% cystine stones

42
Q

What stones are radiolucent on x ray?

43
Q

What causes Struvite stones?

A

Magnesium Ammonium Phospahte Stones

Formed after infection by UREA SPLITTING BACTERIA (proteus and staph)>
convert urea to ammonia>
alkaline urine

44
Q

What causes some of the largest “staghorn” stones?

A

Urea splitting bacteria (proteus/staph)

CRRAB II- Week 2 (9 decks)

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