Warren- Diseases of Blood Vessels

Question 1

What is nephrosclerosis?

Answer 1

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

Question 2

What is seen microscopically with nephrosclerosis?

Answer 2

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

Question 3

What does Nephrosclerosis look like grossly?

Answer 3

surface has fine even granularity

Question 4

What is the pathogenesis of nephrosclerosis?

Answer 4

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

Question 5

Does nephrosclerosis typically cause renal insufficiency?

Answer 5

Not really

Question 6

What pts is nephrosclerosis commonly observed in?

Answer 6

DM
black
Severe HTN

Question 7

WHat is malignant nephrosclerosis?

Answer 7

Renal disease associated w/ malignant HTN

1-5% of pts w/ HTN get it

Question 8

Who do you commonly see malignant nephrosclerosis in?

Answer 8

Young black men

Question 9

What is observed grossly with malignant nephrosclerosis?

Answer 9

petechial hemorrhages (flea bitten)

Question 10

What is observed microscopically with malignant nephrosclerosis?

Answer 10

FIBRINOID NECROSIS of the arterioles

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

Question 11

Describe the clinical course of malignant nephrosclerosis.

Answer 11

HA, N/V, Visual impairement (scotomas)

High Diastolic pressure, papilledema, encephalopathy

Proteinuria/hematuria EARLY>
rapid renal failure

Question 12

What is renal artery stenosis?

Answer 12

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

Question 13

How do you diagnose renal artery stenosis?

Answer 13

bruit on kidney ausculation

high plasma/renal vein renin

Question 14

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

Answer 14

Ischemic SMALL kidney w/ some atrophy

Hyaline arteriosclerosis (subjected to systemic HTN)

Question 15

What can cause RAS?

Answer 15

70% d/t occlusion of RA by atheromatous plaque

Fibromuscular dysplasia

Question 16

What are thrombotic microangiopathies?

Answer 16

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

Question 17

What is seen clinically in pts w/ thrombotic microangiopathies?

Answer 17

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

Question 18

What are the thrombotic microangiopathies?

Answer 18

typical HUS
atypical HUS
familial HUS
Idiopathic TTP

Question 19

What causes HUS/TTP

Answer 19

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

Platelet activation and aggregation

Question 20

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

Answer 20

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

Question 21

What does verocytotoxin do?

Answer 21

causes endothelial lysis, increased endothelin, decreased NO

Question 22

What happens to most pts w/ typical HUS?

Answer 22

Recover w/in weeks w/ dialysis

Question 23

What is atypical HUS?

Answer 23

Unclear mechanism

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

Question 24

What causes familial HUS? What is the mortality rate?

Answer 24

Def of the copmlement regulatory protein Factor H

Factor H>
protects cells form uncontrolled complement activation

HIGH- 50%

Question 25

What causes Idiopathic TTP?

Answer 25

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

Question 26

What is the classic pentad of sxs for TTP?

Answer 26

``` Fever neurologic MAHA thrombocytopenia RF ```

Question 27

Who is commonly affected by TTP?

Answer 27

Women Pts < 40

Question 28

How do you differentiate TTP and HUS?

Answer 28

TTP- neurologic features (sometimes renal involvement) HUS- significant renal involvement and may not have neurologic features

Question 29

How do you treat TTP?

Answer 29

plasma exchange and corticosteroids

Question 30

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?

Answer 30

HUS/TTP

Question 31

What causes most renal infarcts?

Answer 31

Emboli 25% CO to kidneys> limited colateral circulation

Question 32

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

Answer 32

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

Question 33

What does obstructive uropathy lead to?

Answer 33

Hydronephrosis | renal atrophy

Question 34

How does hydronephrosis appear grossly?

Answer 34

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

Question 35

How does an acute obstruction present?

Answer 35

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

Question 36

How does unilateral hydronephrosis present?

Answer 36

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

Question 37

How does bilateral partial obstruction present?

Answer 37

Inability to concentrate urine> | polyuria/nocturia

Question 38

How does bilateral complete obstruction present?

Answer 38

anuria

Question 39

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

Answer 39

5-10% Men 20-30 y/0

Question 40

What primarily causes urolithiasis?

Answer 40

inborn errors of metabolism> stone formation gout cystinuria primary hyperoxaluria

Question 41

What are the 4 main types of calculi?

Answer 41

70% Ca oxalate and Ca phosphate 15% Struvite (Mg NH4 PO) 5-10% UA 1-2% cystine stones

Question 42

What stones are radiolucent on x ray?

Answer 42

UA stones

Question 43

What causes Struvite stones?

Answer 43

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

Question 44

What causes some of the largest "staghorn" stones?

Answer 44

Urea splitting bacteria (proteus/staph)