Haemodynamics Flashcards
What is the main site for haemopoiesis in an adults?
bone marrow
What are the two major risk factors for development of venous thrombi?
Stasis and Hypercoagulability
Superficial Thrombi
do not embolise and frequently give symptoms including pain and swelling
Deep Vein Thrombi (DVT)
frequently embolise. They may be asymptomatic or give mild symptoms (like swelling distal to the clot). They are often very large and not strongly attached to the wall of the vein so they can embolise as a very large mass causing catastrophic outcomes.
A deep vein thrombus that forms an embolus is likely to travel where?
Femoral or Iliac vein -> Inferior vena cava -> right atrium -> right ventricle -> pulmonary arteries -> LUNGS
What are some of the main fixed & modifiable risk factors for the development of atherosclerosis?
Being male, increasing age, being of Aboriginal or Torres Strait Islander descent. Smoking, diabetes, systemic hypertension, hyperlipidaemia (increased LDL & reduced HDL), visceral adiposity, etc.
Given atherosclerosis is a chronic inflammatory condition affecting the intimal lining of arteries, what 3 components of inflammation will be present?
- lymphocytes
- ongoing injury
- repeated attempts at repair through granulation tissue and proliferation of surrounding cells
what are 2 other things typically present within an atheroma?
- oxidized lipids (inc. cholesterol): which are eaten by macrophages & smooth muscle cells
- calcium: often gets deposited at sites of necrosis and chronic inflammation
Why do aneurysms form in vessels & ventricles
Aneurysms form in areas of high pressure where there is a weakened area. In arteries they form in area affected by atherosclerosis and in ventricles in areas of scarring. The normal tissue is strong enough to withstand the high pressures normally found in the arterial system and heart, but the altered tissue is weaker and bulges out in response to the high pressure.
Why do thrombi form on atherosclerotic lesions or within aneurysms?
Atherosclerosis encourages turbulent blood flow whereby platelets and cells bash against the endothelial lining causing further injury. When the endothelium is lost there is decreased nitric oxide and prostacyclin synthesised in the region and more pro-coagulative factors released which encourages more fibrin, platelets, and RBCs to adhere to the growing clot/thrombus. Aneurysms frequently form in areas of atherosclerosis and so the same reasoning applies. In addition, the aneurysm being a blind-ended sack can entrap cells and proteins
An embolus released from a thrombus within the abdominal aorta could cause infarction where?
Anywhere downstream like the lower limbs, bowels etc.
What is the difference between angina & a “heart attack”?
Both are caused by ischemia but in angina blood is restored to the tissue before necrosis occurs.
What are 4 ways in which atherosclerosis can cause death?
- bleeding and swelling within the atheroclerosis lesions can block the vessel leading to ischemia of downstream tissue
- thrombus formulation can lead to blockage of the vessel
- emboli may break off a thrombus and travel until stopped when it occludes a smaller vessel
- atherosclerosis is a risk factor for aneurysm formation which can burst or give rise to thombi & emboli
Atherosclerosis: whether we die depends on the location
- burst aneurysm in the brain (cerebral arteries) leads to haemorrhagic & increases intracranial pressure quickly strokes
- thrombi and emboli in the cartoid or cerebral arteries can lead to ischemic strokes which can also be life-threatening
- burst abdominal aortic aneurysms kill very quickly due to hypovolemic shock
- atherosclerosis and thrombi within the coronary artery can kill us through myocardial infractions and by causing chronic ischemic heart disease.
Are there any differences between myocardial infarctions and brain infarcts?
The heart undergoes coagulative necrosis during which the dead tissue is fixed in place until the inflammatory cells move into the area and break down the dead tissue. Because the brain has little connective tissue and the cells are rich in signalling molecules that are cytotoxic at high levels, when necrosis occurs it often encompasses a large area and unlike in solid meaty organs the tissue turns to mush a phenomenon known as liquefactive necrosis.
Unlike collagen scars that form in other parts of the body, the scars in the brain are made from what?
Glia, Glial Scars
In some parts of the body infarctions may go unnoticed but this is not true of myocardial or cerebral infarctions, why?
SEE NOTES
How does atherosclerosis in the abdominal aorta lead to our sudden death?
Predisposes to the formation of an aneurysm which if it ruptures kills us quickly. The abdominal aorta is carrying oxygenated blood downwards towards the lower limbs, it feeds into smaller arteries, arterioles & capillaries where gas exchange occurs.
A thrombus in the femoral vein that embolises is likely to end up where
Lungs
A thrombus in the Iliac vein that embolises is likely to end up where?
Lungs, clots released from ANY vein in the legs ends up in the lungs
Atherosclerosis is which vessels could lead to a stroke?
Cerebral or carotid arteries
Atherosclerosis is which vessels could lead to a myocardial infarction
Coronary arteries
Atherosclerosis is which vessels could lead to ischaemic heart disease?
Coronary arteries
Atherosclerosis is which vessels could lead to cerebral atrophy?
Cerebral or carotid arteries
Thombus
blood clot attached to the wall of a vessel or heart chamber (caused by: endothelial injury, abnormal blood flow, & hypercoagulability)
Embolus
anything undissolved traveling in the blood
Aneurysm
localised abnormal ballooning out or dilation of part of a vessel/ventricle wall (usually found in high pressure locations)
Atheroma
Sclerotic plaque which represents an area of chronic inflammation within the wall of an artery
Atherosclerosis
The process of atheroma
Causes of necrosis
Hemorrhage or ischemia
- Blockage in arterial system – ischemia – necrosis
- Blockage in venous system – congestion of poorly oxygenated blood – haemorrhage
Normal Haemostatic Process: the maintenance of fluid blood & the formation of a haemostatic clot in response to injury. Three components:
- Vascular wall, endothelium
- Platelets
- Coagulation cascade
How do kidneys contribute to systemic hypertension
the kidneys can activate RAAS. Activating RAAS decreases vasodilation and releases angiotensin II causing vasoconstriction. Angiotensin II increases heart rate, force of contraction, vascular resistance. Aldosterone increases sodium & water uptake which increases
What vascular pathology does atherosclerosis predispose towards?
Thrombus, embolus, aneurysm, systemic hypertension.
How atherosclerosis leads to death
- Bleeding & swelling within the lesion -> vessel occlusion -> infarct
- Thrombus formation -> occlusion -> infarct
- Thrombo-embolus -> occlusion -> infarct
- Aneurysm -> rupture -> hypovolemic shock -> death
- Aneurysm -> thrombus & embolus -> infarct
