4/4 Flashcards
4 types of arteries
- elastic: aorta & beginnings of branches
- muscular: thick smooth muscle t. media
- small: autonomic blood flow regulation
- arterioles: fewer that 5 layers of muscle
Lipoproteins are…
formed in…
- any complex of lipids with proteins
2. usually formed in liver or intestine
Atherosclerosis
definition
pathology process
nomenclature
Atheroschlerosis is the #1 killer in US.
1. It is a response to injury featuring the accumulation of cholesterol-rich fat in the intima of the large and medium-sized arteries (these are macrophages that have appetite for LDL cholesterol forming plaques or atheromas).
- Plaques occlude arteries (slowly over time or suddenly by rupture of plaques) causing ischemic heart disease, myocardial infarction, stroke and gangrene of the extremities.
- This term derives from Greek word meaning “hardening” or “induration”.
Pathologists recognise four kinds of arteriosclerotic lesion:
- atherosclerosis
- arteriolosclerosis
- hypertensive arteriosclerosis
- medial calcific sclerosis (produces calcification in the media of large arteries in elderly people)
6 risk factors for atherosclerosis are:
a) high LDL level - heredity, diet, exercise
b) cigarette smoking - smoke oxidizes LDL
c) high blood pressure - intima damage
d) lack of exercise - change in lipoprotein receptor count
e) heredity - familial hypercholesterolemia
f) low HDL levels - HDL keep LDL from binding to plaques
The risk factors for atherosclerosis can be divided into three groups:
- factors that we cannot do anything about: heredity, male sex, and advancing age
- “deadly quartet”: hypertension, hyperlipidemia (cholesterol and LDL), cigarette smoking, and diabetes mellitus
- “soft” factors of uncertain importance: obesity, inactivity and personality characteristics
Examination of the ocular fundus is an important test for :
monitoring of any patient who is liable to develop any form of arteriosclerosis.
Vascular smooth muscle is important factor in atherosclerosis because (2)
- it has receptors for LDL
2. it can get into intima through holes in the internal elastic membrane.
Atherosclerosis development has different stages, it starts with:
an early lesion of the endothelial surface of large arteries.
Pathogenesis of atherosclerosis is today explained as
response-to-injury hypothesis (3)
- the development of focal areas of chronic endothelial injury: fatty streaks, intimal masse
proliferation of smooth muscle cells in the intima with the formation of connective tissue - insudation of lipoproteins (oxidized LDL and VLDL) producing cell injury
- accumulation of macrophages & platelets and formation of fibrous cap & atheroma
fibrolipid plaque phase:
At this point intimal changes are not reversible.
In general the intimal surface shows a layer of fibrosis - “fibrous cap” which encloses a zone of fatty, necrotic, and partly calcified debris full of elongated smooth muscle cells, fibroblasts and macrophages.
Two kinds of this early lesion are described:
- fatty streaks: are lesions which begin in children in all populations and show collections of foamy lipid-laden macrophages and smooth muscle cells just beneath the intimal surface of the arteries.
- diffuse intimal fibrosis: is also a change that develops over the first few decades of life, and may be related to the development of atheroma.
When plaques are formed they may become confluent and (3)
- calcified: producing the “eggshell aorta”
- ulcerate: this is more important complication that may lead to
embolization of plaque debris - atheroembolism, and also provides a naked non-endothelialized surface which is a site for thrombosis and possible thromboembolism - bleed: haemorrhage into plaques can also occur
Hypertension : pressures
systolic blood pressure over 160 mmHg and /or diastolic pressure over 90 mmHg
With expansion of plaques, what would happen to the the internal layer of the intima?
What do Media damages lead to?
If it is not surgically repaired what is the most important complication of aneurysm?
With expansion of plaques, the internal layer of the intima may become broken up and the lesion may induce pressure changes on the tunica media.
Media damage leads to the formation of atherosclerotic aneurysm that can be fusiform or saccular, depending of the shape. Most common location of this aneurysm is in the aorta below the a. renalis, and often going down into the iliac arteries.
If it is not surgically repaired the most important complication of aneurysm is rupture followed by severe haemorrhage into the peritoneal cavity.
Hypertension is result from an imbalance in the interactions between: (4)
- cardiac output: systemic pressure, venous return
- renal function: renin-angiotensin-aldosteron
- peripheral resistance: arteriosclerosis
- sodium homeostasis: diet, pheochromocytoma
Aneurysms
Abnormal dilatations of arteries or veins are called aneurysms. They develop as a result of marked weakening of the wall of a vessel (t. media). Any vessel may be affected, but they are much more frequent in aorta.
Vasculitis (3)
Vasculitis is defined as inflammation and necrosis of blood vessels (aortitis).
a) Raynaud phenomenon (vasculitis) b) polyarteritis nodosa c) thromboangiitis obliterans - Buerger disease
Aneurism caused by wide variety of disorders: (3)
- congenital (atherosclerosis)
- infections (syphilis),
- trauma.