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Prac 4. Haemodynamics
Terms in this set (19)
1) a. What is the main site for haemopoiesis in the adult?
The red bone marrow in the axial skeleton produces red blood cells in response to erythropoietin (EPO) which is constantly released by the kidney. ↑EPO release by kidney when hypoxia/↓ RBCs.
"extramedullary haematopoiesis" - When blood is chronically lost/ RBCs are excessively destroyed, the red marrow expands and the spleen, liver and other organs produces RBCs
1) b. Can you live without a spleen?
Yes and the spleen is removed in cases where there is trauma resulting in internal haemorrhage from the spleen which is a medical emergency.
+ some autoimmune conditions involve inappropriate and excessive destruction of RBCs by the spleen which will be removed as a consequence.
The spleen filters the blood looking for antigens, recycles RBC constituents and serves as a store for platelets and monocytes. People who have a splenectomy have more RBCs with intracellular inclusions and are more vulnerable to infections. For planned splenectomies (when it is not a medical emergency) vaccinations against common bacterial infections are given a few weeks before the operation.
1) c. Fill in the table as revision of week 2 Neoplasia
Cell of origin & nature of: Lymphoma & leukaemia
Tumour of: endothelial cell & benign
Tumour of: endothelial cell & malignant
1) d. How do the normal functions of the kidneys impact upon blood pressure and composition?
The kidneys produce EPO which acts on the red bone marrow to stimulate the synthesis of RBCs. Blood is mainly water and the levels of water are regulated by the kidney through the renin - angiotensin - aldosterone system (RAAS).
- Aldosterone acts at the distal convoluted tubules to increase the amount of water and salt reabsorbed from the filtrate so instead of being lost in urine it is retained in the blood thus increasing blood volume.
The kidneys also regulate the levels of various ions and blood pH by reabsorption from the filtrate (future urine) and secretion into it.
In addition to controlling blood volume, the kidneys are able to control vascular resistance through the release of renin and the activation of angiotensin 2, which as the name suggests causes vascular constriction thus increasing blood pressure. There is cross stimulation between the sympathetic nervous system and RAAS so that stimulation of RAAS will also result in an increase in SNS stimulation.
1) e. How do the normal functions of the liver impact upon blood composition?
The liver is responsible for the synthesis of most plasma proteins, which are the determinants of colloidal osmotic pressure which counters the hydrostatic pressure and discourages oedema formation. Therefore if the liver fails, there will be reduced plasma proteins leading to reduced colloidal pressure and the formation of oedema (transudate) throughout the body including effusion into the abdominal cavity, which is referred to as ascites.
The liver is our major metabolic organ and stores large amounts of glycogen which can be released when blood glucose levels fall. The liver also stores iron, B12 and folic acid which along with amino acids are required for the synthesis of RBCs. On average our bodies make 100 billion new RBCs every day, 2 million per second.
2) a. What are the 2 major risk factors for the development of venous thrombi?
2) b. In what ways do superficial versus deep venous thrombi differ?
Superficial venous thrombi do not usually embolise.
Superficial thrombi frequently give symptoms including pain and swelling.
Deep vein thrombi (DVT) frequently embolise.
DVTs may be asymptomatic or give mild symptoms like swelling distal to the clot. DVTs are often very large and not strongly attached to the wall of the vein and so they can embolise as a very large mass causing catastrophic outcomes.
2) c. A deep vein thrombi that forms an embolus is likely to travel where?
Femoral or Iliac vein --> Inferior vena cava --> Right atria --> right ventricle -> Pulmonary arteries --> LUNGS
3) a. What are some of the main fixed & modifiable risk factors for the development of atherosclerosis?
Being male, increasing age, genetics.
Smoking, diabetes, systemic hypertension, hyperlipidaemia (increased LDL & reduced HDL), visceral adiposity, etc.
3) b. Given atherosclerosis is a chronic inflammatory condition affecting the intimal lining of arteries, what 3 components of inflammation will be present?
2. Ongoing injury
Repeated attempts at repair through granulation tissue and proliferation of surrounding cells, in this case smooth muscle cells from the media.
3) c. In addition to the above, what are 2 other things typically present within an atheroma?
Oxidised lipids (which are eaten by macrophages and smooth muscle cells turning them into foam cells) including cholesterol.
Calcium (calcium often gets deposited at sites of necrosis and chronic inflammation)
4) a. Why do aneurysms form in vessels & ventricles?
Aneurysms happen in areas of high pressure where there is a weakened area. So they can be formed in areas of arteries affected by atherosclerosis and in areas of scarring in heart ventricles.
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.
4) b. 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.
4) c. An embolus released from a thrombus within the abdominal aorta could cause infarction where?
Anywhere downstream like the lower limbs, bowels etc
5) b. What is the difference between angina & a "heart attack"?
Both are caused by ischaemia but in angina blood is restored to the tissue before necrosis occurs.
5) c. What are 4 ways in which atherosclerosis can cause death?
A. Bleeding and swelling within the atherosclerotic lesion can block/occlude the vessel leading to ischemia of downstream tissue.
B. Thrombus formation can lead to occlusion of the vessel.
C. Emboli may break off a thrombus and travel until stopped when it occludes a smaller vessel.
D. Atherosclerosis is a risk factor for aneurysm formation which can burst or give rise to thrombi and emboli.
The above can happen in any artery or even the heart, whether we die depends upon the location:
1. Burst aneurysms in the brain (cerebral arteries) lead to haemorrhagic strokes which are particularly devastating as an arterial bleed quickly raises intracranial pressure.
2. Thrombi and emboli in the carotid or cerebral arteries can lead to ischaemic strokes which can also be life-threatening.
3. Burst abdominal aortic aneurysms kill very quickly due to hypovolemic shock.
4. Atherosclerosis and thrombi within the coronary arteries can kill us through myocardial infarctions and by causing chronic ischaemic heart disease.
In addition, atherosclerosis can lead to slow chronic reductions in blood supply causing tissue atrophy, which while not life-threatening reduce the functional reserve of organs and in the brain predispose us towards further pathologies.
6) a. 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.
6) b. Unlike collagen scars that form in other parts of the body, the scars in the brain are made from what?
Glia, Glial scars.
6) c. In some parts of the body infarctions may go unnoticed but this is not true of myocardial or cerebral infarctions, why?
The heart is permanent so must heal by scarring, which will inevitably be weaker than the heart tissue that has been lost. The cardiac myocytes must work together contracting and relaxing in a coordinated fashion.
The brain has regionalized functions so damage to one part results in noticeable functional decline/loss. The brain is also a permanent tissue, however, we can 'relearn' lost functions and form new synaptic connections between surviving neurons, which is known as brain plasticity. Brain plasticity generally declines with age so a stroke, while rare in young people, is associated with a better recovery when it occurs in young versus older individuals.
An additional problem with glial scars in the brain and collagen scars in the heart is the scar does not conduct electrical impulses in the same way that the normal tissue does and so predisposes the individual towards epilepsy and arrhythmias respectively.
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