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Flashcards in Vascular Path Deck (79)
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1

causes of 2* HTN

any cardio, renal, and endocrine dx
=inc cardiac output +inc vasoconstriction= inc BP

a. Renal disease:polycystic disease, renal cell carcinoma (RCC), chronic renal failure, glomerulonephritis, renal artery
stenosis and fibromuscular dysplasia
b. Adrenocortical hyperfunction:congenital adrenal hyperplasia, adrenal tumors
c. Adrenal medullary hyperfunction: pheochromocytoma
d. Thyroid dysfunction: myxedema)
e. Pituitary dysfunction: acromegaly
f. Cardiovascular disease: coarctation of the aorta, polyarteritis nodosa
g. Pregnancy: eclampsia and pre-eclampsia
h. Neurologic disease:↑ intracranial pressure
i. Medications and drugs: glucocorticoids, cyclosporine, sympathomimetics, cocaine

2

describe hypertnsion (HTN)

sustained BP >139 systolic or > 89 diastolic
M>F, Afro-Am, smokers, obesity
90% primary (essential HTN/ unknown cause- linked to calories, salt or alcohol)
10% secondary (adrenal/renal cause)

3

HTN: increased risk for

eye (blindness), heart (LVH, IHD/MI, CHF, aortic dissection),
renal (ESRD), & brain (stroke)
INCREASE RISK OF ATHEROSCLEROSIS

4

(2) hitso pathologic features of HTN

Hyaline arteriolosclerosis- protein leaks
hyperplastic arteriolosclerosis- onion-skin
INCREASE RISK OF ATHEROSCLEROSIS

5

describe iodiopathic/primary/essential HTN

genetic + environmental causes ( linked to calories, salt or alcohol)
90% HTN cases
defects in renal homeostasis + vasoconstriction + defects in smooth muscle= inc cardiac output and inc peripheral resistance= HTN

6

(4) hormones maintaining BP homeostasis

renin- renal (increases BP)
angiotensinogen- hepatic (increases BP)
aldosterone- adrenal (increases BP)
ANP- cardiac (decreases BP)

7

Aortic Dissection: types

bad= proximal aorta=risk of rupture into the pericardial sac with cardiac tamponade and harm to coronary or cerebral vessels
Type A (DI/DII): med/surgical
emergency (poor prognosis);
Type B (DIII): distal dissections= better prognosis

8

high risk for aortic dissection

-Connective tissue diseases (Marfan, Ehlers-Danlos= cystic medial degeneration)
-hypertension (Hypertrophy of the vasa vasorum)
-complication of arterial cannulation ( loss of smooth muscle)
-pregnancy

9

Aortic Dissection

Intimal tear, dissection into media (middle/outer
third), thru adventitia HMG into chest, abdominal,
or pericardial sac (poor prognosis);
false channel (better prognosis)

10

Hyaline Arteriolosclerosis

Hyaline protein deposits, narrowed
endothelial cell damage:
DM, HTN (decades), elderly
• endothelial cell dysfunction: plasma protein leakage/inc. SM cell & ECM synthesis
• a/w Nephrosclerosis  Renal Failure

11

Hyperplastic Arteriolosclerosis

Laminated “onion-skin” lesions
smooth muscle proliferation) obliterates lumen
Causes: fibrinoid nectosis, "flea bitten" kidney
• Life-threatening organ damage: brain, kidneys, heart medical emergency

12

Atherosclerosis

Affects elastic and muscular arteries
• Progressive accumulation of
lipid/lipid debris, smooth muscle cells, extracellular matrix, T-lymphocytes, macrophages/foam
cells in the intima
• Encroaches on the media &
adventitia (Atheroma) narrowing of the lumen (e.g., IHD, thrombus)
**chronic inflammation**

13

Atherosclerosis: modifiable risk factors

-Hypercholesterolemia(HC)/ Hyperlipidemia(HL) (Most important cause)
– HTN (major risk factor)
– DM (inc. HC/HL)
– Cigarette Smoking (inc. CRP)

14

steps in Pathogenesis of Atherosclerosis

1. endothelial cell injury/dysfunction
2. increase permeablility
3. cytokine release and leukocyte/monocyte/macrophage emigration
4. smooth muscle proliferation
5. engulf lipid
6. fatty streak
7. ECM deposition
8. fibrofatty atheroma
9. plaque
10. intimal ischemia

15

Elevated serum levels of CRP

Inflammation marker
Risk Factor:
- Atherosclerosis
- Acute Myocardial Infarction
- Stroke
- Peripheral arterial disease
- Sudden cardiac death

16

Atheromas: Thick vs Thin Fibrous Cap

Thin Fibrous Cap: Increase Risk of
Acute Coronary Thrombosis (AMI)

17

saccular aneurysms

1. Saccular- spherical outpouchings

18

fusiform aneurysms

2. Fusiform- diffuse, long, circumferential dilation

19

What are the two most important causes of aortic aneurysms?

HTN+atherosclerosis

other Risk: CT dx: Marfan (fibrillin), Scurvy, Ehler-Danlos; Matrix Metalloprotease (MMP)

20

What are the two most common locations for aortic aneurysms?

Below the renal arteries and above the bifurcation of the aorta. They may be fusiform or saccular, up to 15 cm in diameter and up to 25 cm in length. They are often accompanied by smaller aneurysms of the iliac arteries.

21

describe inflammatory aneurysms

Fibrosis; lymphocytes, marcophages, giant cells

Microbes infect plaque

22

describe mycotic aneurysms

invades Vasa vasorum= ischemia
Obliterative endarteritis

23

endarteritis

inflammation of the inner lining of an artery

24

Obliterative endarteritis

Obliterative endarteritis- severe proliferating inflammation of the inner lining of an artery that results in an occlusion of the lumen of the artery

25

Dissections:

Intimal tear within the wall of a blood vessel, which allows blood to separate the wall layers
Massive hemorrhage

26

Aortic dissection: Types A/B

Type A: Debakey 1- ascending + descending aorta
Type A: Debakey 2- ascending aorta
Type B: Debakey 3- descending aorta
(*worst= closest to aortic valve)

27

Non-infectious Vasculitis:

Inflammation of vessel walls
Thick, nodular
Distrupts elastic lamina
1) Positive for immune
complex deposition,
2) Antineutrophil
cytoplasmic antibodies
(ANCA),
3) Antiendothelial cell
antibodiess

28

what Non-infectious Vasculitis
affect Large vessels: aorta, extremities, head, neck (2)

Giant cell (temporal) arteritis
Takayasu arteritis

29

what Non-infectious Vasculitis affect Medium vessels: visceral (2)

Polyarteritis nodosa
Kawasaki disease

30

what Non-infectious Vasculitis affect Small vessels: arterioles, venules capillaries (4)

Microscopic polyangiitis
Wegner granulomatosis
Churg-Strauss syndrome
Henoch-Schonlein Purpura