patho sheet #6 of Dr Faisal - Ruaa Rawa

بسم الله الرحمن الرحيم

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http://www.mediafire.com/?gw238s8rcea5g6v
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Shock: clinical rather than pathology “the Doc. Will give us handout about this item “.

Cardiovascular system
We will introduce diseases of the blood vessels and heart diseases,

Blood vessels diseases are too many to discuss in details or even to mention, so we are going to select the most important and the most common.

Atherosclerosis : hardening of the blood vessels ,in general when they say arteriosclerosis they mean atherosclerosis, actually atherosclerosis is one member among other members of arteriosclerosis

Atherosclerosis includes:

1- atherosclerosis
2- medial sclerosis or medial calcification “ it also called Monck burg medial sclerosis or calcification, Monck burg Is discoverer of this disease”
3- arteriolosclerosis: thickening of the arterioles

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Medial sclerosis: from the name it is sclerosis or calcification of the media of medium size muscular arteries “a little smaller or little larger possible to be infected”, this disease infect adults age both male and female more than 50 years

Remember: Monck burg medial calcification it is media
Doesn’t effect intima nor adventitia

The x-ray shows the smooth muscles are replaced by collagen fiber (the media consist of large amount of smooth muscles)


The fig. shows the three layers of the blood vessels wall

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Arteriolosclerosis: effect the arterioles (stamp of the systemic hypertension)

Note the systemic hypertension associated with other changes not only the arteriolar change but it is the essential change.

Atherosclerosis; essentially it is disease of the intima but might effect other layers .effects medium size arteries, muscular or elastic arteries (like aorta, subclevian, carotid) (not arterioles, not veins and not lymphatic).

Atherosclerosis occur by deposition of materials (mainly fatty materials) in the intima these materials come from the plasma and followed by the migration of the smooth muscle from the media into the intima

When the smooth muscles deposited in the intima the characteristics and features of smooth muscles changed, it will have secretion and proliferation functions instead of contraction and relaxation functions in normal cases.

The first material deposited and appears called fatty streaks; it begins from the first decade (If we give the child a lot of chocolate these fatty streaks increase) these fatty streaks doesn’t elevated upon the surface, with time (through decades) enlargement of fatty streaks in all direction and called fibro-fatty plaques



0 The lesion in the atherosclerosis called atheroma






The most sever and most common atherosclerosis as follow: (distributions)

1-abdominal aorta (especially lower abdominal aorta)
2-coronary arteries
3-popliteal artery and thoracic aorta
4-carotid arteries (especially internal carotid artery)

Important note: arteries of the lower limbs are saved from hardening of blood vessels, why?
Answer: there are many theories but none of them explains what really happens.

There is association of two things with the deposition of fatty materials: 1-proliferation of the cells (these cells include smooth muscle cells and other cells)
2-inflammation

0We can detect the disease (atherosclerosis) by the indicators of inflammation these indicators are
1- C-Reactive Protein
2- ECR (ErythroCyte Rate)
3- Homocystiene (the higher level in the blood the higher risk to have atherosclerosis).

The continuous deposition of fat materials and smooth muscles will cause narrowing of the lumen and can effect the underlying media make it thinner.

Thickening of the intima make it weaker, since the materials which are deposited inferior in qualities and strength compare with the original one.

Complications: caused by atherosclerosis are infarction (and / or) ischemia, both happen due to the narrowing of blood vessels lumen.

0When media become thinner this can lead to arterial anuerysmal and rupture (arterial aneurysm: permanent arterial dilatation usually caused by weakening of blood vessels wall)

Risk Factors
There is group of risk factors part of these factor are constitution (can’t be controlled)
1- Aging: the older the human get the more liable to atherosclerosis “major risk factor”
2- Gender: male more liable than female till the middle of age (at 50) WHY?
Answer: because before that the lady being protected by endogenous estrogen (we said endogenous because exogenous estrogen might not be protective as the endogenous), after age of 50 there are no more estrogen the gap in the incidence and severity between male and female decrease to become equal at age of (70-80)

Q/Why we don’t use exogenous estrogen?
Answer: in some diseases like osteoporosis we give the females (older than 50 of age) an exogenous estrogen we called this treatment hormone therapy replacement (HTR)
Essentially estrogen and sometimes progesterone. The HTR
Isn’t treatment for atherosclerosis since it doesn’t effect the arteries, the exogenous not like the endogenous one (general role).

Q/How the endogenous estrogen protect the arteries ?
Answer: it decrease the deposition of LDL (low density lipoprotein) on the intima of the arteries at least this one but not there are other factors.

3-Heredofamilial and genetics

Major factors we can control:
1- Hypercholestremia, hyperlipimia, hypertriglyceremia, hyper LDL and etc…..
When the lipid level increased in the blood might be followed or associated by atherosclerosis except for HDL “high density lipoprotein” makes reverse effect.


(When the HDL increase in the blood the incidence and severity of the atherosclerosis decrease)
(if the cholesterol increase in the blood the incidence and severity of the atherosclerosis increase)
(drug that act by decreasing the lipid level in the blood decrease the incidence and severity of the atherosclerosis)



0saturated fatty acid differs from unsaturated fatty acid
0we can decrease the incidence and frequency of atherosclerosis by:
1- consumption of low dietary product
2- consumption of products that lead to increase HDL (like omega 3)
3- usage of unsaturated fatty acid (vegetable oils) are much more healthy and protective than the saturated fatty acid)

Back to the factors (that we can control )
3-systemic hypertension: any elevation of the blood pressure (systolic or diastolic) might be associated or followed by atherosclerosis (high blood pressure accelerates atherosclerosis).

People with high blood pressure have more tendency to accumulate lipid from those doesn’t have high blood pressure, also have risk to develop Diabetes Miletus
More)

3-Diabetes Miletus: the diabetes effect the endothelium cells function “endothelial cells have a lot of functions it secret substance that act as anti-atherogenecity and other act as atherogenic substances “so injury to these cells “chemical, physical, or infection” cause it is dysfunction

4-Smoking: any type of smoking, have a lot of toxic substances these can reach the blood stream that might cause atherosclerosis, smoking also have direct effect on the endothelial cells.

Minor Factors

1-life style: the more stress the incidence for atherosclerosis increase.

“The people that are in stress most of the time called personality type one in other hand people that are relaxed called personality type two”

0The stress increase the incidence of the atherosclerosis by sympathetic stimulation

2- Obesity
3- Oral contraceptive
Morphology
Two main types:
1-Fatty streaks: doesn’t elevate upon the surface
2-Fibro-fatty plaques.

The first change in atherosclerosis (the fatty streaks deposition) begins from the first decade of the life, yellowish discoloration in the form of spots on the abdominal aorta (the most common artery for atherosclerosis), through second and third decades some of these fatty streaks might undergo changes forming fibro-fatty plaques

0 Not all the fibro-fatty plaques originate from fatty streaks (that formed in the first decade).

0 Fatty streaks morphologically it is macrophage filled with fat with time accumulate and become fibrous tissue (fibro-fatty plaques)

0Fibrouse tissue very irregular changing the arteries from
Smooth and regular to irregular forms



Notes: regarding the previous fig.
A-Normal artery
B-fatty streaks appears
e- Rupture, hemorrhage and thrombosis (again the ruptures occur because the media effect and begin to thinner and thinner)

0There are complications followed the atherosclerosis the most important are thrombosis and ulceration (ulceration occur because of the inflammation and some substances at the site of atherosclerosis act as chemotaxis).

0Atherosclerosis can lead to stroke of the brain, infarction of the heart, gangrene (due to ischemia) and can make on it self aneurysms of the artery.

0There are a lot of theories that describe what happens in the atherosclerosis (the Doc. Introduce this theory to collect all the previous):
There are a lot of changes one of them endothelial injury or dysfunction due to a lot of things the most important thing is the toxic effect of the hypercholestremia (when the fat level elevate) this will intoxicate the underlying endothelium rendering it dysfunctional, the epithelium will be leaky (important).
After the endothelium being leaky the lipid will settle into the Intima there the lipid will act as chemotaxis brings the smooth muscle from the media toward the intima, making the media thin.



Note: hypertension and smoking can also rendering the endothelium dysfunctional.
Hypertension
In the past, was thought when the age increases normally the blood pressure increases, these days this is not acceptable, at any age the pressure must be normal around 120/80 mercury any thing above 140/90 mercury means hypertension
Note: (20-25) % is the incidence of hypertension in both male and female.
Two major types:
1-Idiopathic, primary or essential (90-95) % from the hypertension types, the underlying cause not known
2-Secondary (5-10) %, it is secondary to known disease,
The known disease mostly chronic renal diseases.


THE END
Done by: Ruaa Rawa
Lec: 6 of Doc.faisal