Blood Vessel Pathology Flashcards
vessels most affected by atherosclerosis
- abdominal aorta
- coronary arteries
- popliteal arteries
- carotid arteries
- vessels of the circle of Willis
contents of a plaque
fibrous cap
necrotic center
media
step 1
chronic endothelial injury
high blood pressure damages the endothelium and activates:
inflammation
high blood pressure promotes:
turbulent flow in a blood vessel
this turbulent flow is particularly evident in areas of:
branching or constriction of the blood vessel
what effect does endothelial damage have on cholesterol invasion and clot formation
increases the likelihood
step 2
endothelial dysfunction
monocyte adhesion and emigration
step 3
macrophage activation
smooth muscle recruitment
step 4
leukocytes and smooth muscle cells engulf lipid
hyperlipidemia is a primary player in the etiology
step 5
smooth muscle proliferation
collagen and extracellular lipid deposition
(complicated plaque)
major non-modifiable risk factors
age
gender
genetics
major modifiable risk factors
lifestyle
cigarette smoking
diabetes
inflammation
complications of atherosclerosis
stenosis
thrombosis/embolus
aneurysm
calcification
what must occur for cholesterol to be a problem
oxidation
major steps of atherosclerosis
- LDL enters the intima through the inner endothelium
- Intimal LDL is oxidized into pro-inflammatory lipids
- Oxidized LDL causes adhesion and entry of monocytes and T lymphocytes across the endothelium
- monocytes differentiate into macrophages which then consume large amounts of LDL: forming foam cells
- foam cells release cytokines: that encourage atherosclerosis
How many patterns or types of LDL cholesterol are there
2
Type A cholesterol
Large, less dense
Type B cholesterol
small, more dense
Which one more easily penetrates the endothelium
Type B
Risk factors for pattern B
genetics
oral contraceptives
diet
what effect does increased glutathione activity have on atherosclerotic development?HMG
slows the atherosclerotic development
Statins
HMG-CoA Reductase inhibitors
most circulating cholesterol is synthesized de novo
80% in the liver
10% in the intestine
5% in the skin
HMG-CoA reductase inhibitors
May prolong life in those with previous cardiovascular event history
provide very little primary protection
increases risk of diabetes
other side effect
side effects of statins
increases the risk of diabetes kidney failure liver failure muscle pain rhabdomyolysis: muscle break down --perhaps a function of reduced ubiquinone(Coenzyme Q10)
What does reduced ubiquinone (Coenzyme Q10) cause
Myopathy: muscle weakness and pain reduced mitochondrial function oxidative stress intima media thickness increase cataracts
What does cholesterol do that is so important
cell membranes steroid synthesis bile salts vitamin D ubiquinone
hypertension
affects 25% of the population
asymptomatic until later
what are the different types of hypertension
benign and malignant
benign hypertension
essential: 95% of cases
secondary
essential benign hypertension
- primary hypertension
- idiopathic
- appears to be a mix of genetic and environmental factors
- erroneously assumed to result from weight gain
secondary benign hypertension
-resulting from structural, renal, or endocrine defects
structural defect causing secondary benign hypertension
aortic coarctation
renal defect causing secondary benign hypertension
renal artery stenosis
endocrine defect causing secondary benign hypertension
adrenocortical hyperfunction
benign hypertension increases risk of:
- atherogenesis
- aortic dissection
- stroke
hypertension causes what types of small blood vessel disease
hyperplastic arteriosclerosis
hyaline arteriosclerosis
malignant hypertension
lethal in 1-2 years if left untreated
malignant hypertension usually accompanies:
- renal failure
- retinal hemorrhages
- papilledema (blurred disk margins)
RAAS Dysfunction
- insulin increases kidney sodium reabsorption
- insulin increases aldosterone secretion
- a very slight increase in plasma insulin is capable of eliciting an antidiuretic effect
Enhanced growth factor activity
receptors in capillary endothelial cells
- vascular cells are esponsive to insulin
- hypertrophy of the vascular wall leads to narrowing of vascular lumen
SNS
insulin causes a dose-related increas in norepinephrine release
subsequent increase in pulse and blood pressure
dyslipidemia
reduced HDL increased VLDL increased LDL -pattern B Increased triglycerides
nitric oxide
NO reduces blood pressure: made from L-arginine
insulin increases NO production
NO is a potent vasodilator
aneurysm
localized abnormal vessel dilation
true aneurysm
involves all three layers
false aneurysm
hole covered with a hematomq (extravascular connective tissue)
causes of an aneurysm
- caused by atherosclerosis
- wall degeneration
- trauma
- congenital defects (Marfan Syndrome)
- infection
aortic dissection
aortic wall tears and blood pours into wall
Type A1 of aortic dissection
originates in ascending aorta, propagates to the ascending aorta and often beyond it distally
Type A2 of aortic dissection
Originates in ascending aorta and is confined to the ascending aorta
Type B3 of aortic dissection
originates in the descending aorta, rarely extends proximally but will extend distally
aortic dissection can be caused by
hypertension
trauma
Vasculitis
inflammation of blood vessels
Giant-cell artheritis
most common vasculitis
chronic granulomatous inflammation of the large to small arteries
accompanied by fever, headache, vision loss
treatment: corticosteroids
takayasu arteritis
granulomatous vasculitis of the aortic arch
severe narrowing in upper extremities
ocular disturbances
polyarteritis nodosa
different stages coexist in the same artery
varied symptoms
fatal if untreated, but steroids are curative
wegener granulomatosis
lung granulomas, renal disease, vasculitis
T-cell mediated hypersensitivity
fatal if untreated within a year
c-ANCA positive
churg-strauss syndrome
similar to wegener but more related to alergies and asthma, without the renal disease
microscopic poly angitis
widespread necrotizing vasculitis of smaller vessels
antibody response to the drug or bug
neutrophils heavily present in vessels
possibly type 3 hypersensitivity
removing offending agent usually resolves the problem
tumors
hemangioma
glomus tumor
kaposi sarcoma
angiosarcoma
capillary hemangioma
skin, oral mucosa, sometimes organs
strawberry type present at birth, regresses
cavernous hemangioma
organs, sometimes skin cosmetic problem (unless brain)
pyogenic granuloma
rapidly growing red nodule on skin, in mouth
microscopically resembles granulation tissue
glomus tumor
benign but painful
arise from glomus body cells
distal digits, especially under fingernails
excise
kaposi sarcoma
low-grade malignancy of endothelial cells 4 forms -chronic -african -transplant-associated -AIDS associated
clinical course varies: chronic is the best prognosis
excise
angiosarcoma
high-grade malignancy of endothelial cells
often in skin, soft tissue, breast, liver
arsenic and PVC increase risk
covers a spectrum from well-differentiated to anaplastic
metastasize rapidly
