Haemodynamic Practical

Question 1

Infarction means?

Answer 1

Area of necrosis

Question 2

thrombus means?

Answer 2

blood clot attached to the wall of a vessel or heart chamber

Question 3

embolus means?

Answer 3

Anything undissolved travelling in the blood

Question 4

aneurysm means?

Answer 4

localised abnormal ballooning out or dilation of part of a vessel/ventricle wall

Question 5

atheroma means?

Answer 5

sclerotic plaque which represents an area of chronic inflammation within the wall of an artery

Question 6

atherosclerosis means?

Answer 6

process of atheroma formation. Chronic inflammatory process within wall of artery. Typically affects intima of artery.

Question 7

congestion means?

Answer 7

passive build-up of blood within a vessel, increasing hydrostatic pressure

Question 8

oedema means?

Answer 8

increased fluid in interstitial tissue

Question 9

effusion means?

Answer 9

increased fluid in body cavity

Question 10

exudate means?

Answer 10

High protein oedematous fluid caused by increased hydrostatic pressure from hyperaemia & increased vascular permeability

Question 11

Transudate means?

Answer 11

Low protein oedematous fluid caused by increased hydrostatic pressure &/or reduced colloidal osmotic/oncotic pressure

Question 12

Haemorrhage means?

Answer 12

Loss of blood (all of the constituents) from a damaged vessel, the blood may be lost outside of the body, into surrounding tissue or into a body cavity

Question 13

Haematoma means?

Answer 13

Bruise or accumulation of blood constituents in a tissue, organ or body cavity (typically used to describe a large accumulation).

Question 14

a. What is the main site for haemopoiesis in the adult?

Answer 14

The red marrow in the axial skeleton produces red blood cells in response to erythropoietin (EPO) which is constantly released by the kidney. In response to hypoxia or low levels of RBCs, the kidneys increase the synthesis and release of EPO.
In conditions where blood is being chronically lost or RBCs are being destroyed in excessive numbers, the red marrow can expand and the spleen, liver and other organs can produce RBCs in a process known as extramedullary haematopoiesis.

Question 15

b. Can you live without a spleen?

Answer 15

Yes and the spleen is removed in cases where there is trauma resulting in internal haemorrhage from the spleen which is a medical emergency. In addition, 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 are 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.

Question 16

lymphoma cell of origin malignant/benign

Answer 16

lymphoid cells, malignant

Question 17

leukaemia cell of origin malignant/benign

Answer 17

haemopoietic stem cells, malignant

Question 18

haemangioma cell of origin malignant/benign

Answer 18

endothelial cell, benign

Question 19

haemangiosarcoma cell of origin malignant/benign

Answer 19

endothelial cell, malignant

Question 20

d. How do the normal functions of the kidneys impact upon blood pressure and composition?

Answer 20

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.

Question 21

e. How do the normal functions of the liver impact upon blood composition?

Answer 21

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.

Question 22

a. What are the 2 major risk factors for the development of venous thrombi?

Answer 22

stasis, hypercoagulability

Question 23

b. In what ways do superficial versus deep venous thrombi differ?

Answer 23

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.

Question 24

c. A deep vein thrombi that forms an embolus is likely to travel where?

Answer 24

Femoral or Iliac vein
–> Inferior vena cava
–> Right atria
–> Right ventricle
–> Pulmonary arteries
–> LUNGS

Question 25

What are some of the main fixed & modifiable risk factors for the development of atherosclerosis?

Answer 25

Being male, increasing age, being of Aboriginal or Torres Strait Islander descent. Smoking, diabetes, systemic hypertension, hyperlipidaemia (increased LDL & reduced HDL), visceral adiposity, etc.

Question 26

Given atherosclerosis is a chronic inflammatory condition affecting the intimal lining of arteries, what 3 components of inflammation will be present?

Answer 26

1. Lymphocytes 2. Ongoing injury 3. Repeated attempts at repair through granulation tissue and proliferation of surrounding cells, in this case smooth muscle cells from the media.

Question 27

c. In addition to the above, what are 2 other things typically present within an atheroma?

Answer 27

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)

Question 28

a. Why do aneurysms form in vessels & ventricles?

Answer 28

Aneurysms for in areas of high pressure where there is a weakened area so in arteries they can form in areas affected by atherosclerosis and in the heart 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.

Question 29

b. Why do thrombi form on atherosclerotic lesions or within aneurysms?

Answer 29

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.

Question 30

c. An embolus released from a thrombus within the abdominal aorta could cause infarction where?

Answer 30

Anywhere downstream like the lower limbs, bowels etc.

Question 31

b. What is the difference between angina & a “heart attack”?

Answer 31

Both are caused by ischaemia but in angina blood is restored to the tissue before necrosis occurs.

Question 32

c. What are 4 ways in which atherosclerosis can cause death?

Answer 32

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.

Question 33

a. Are there any differences between myocardial infarctions and brain infarcts?

Answer 33

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.

Question 34

Unlike collagen scars that form in other parts of the body, the scars in the brain are made from what?

Answer 34

Glia, Glial scars.

Question 35

In some parts of the body infarctions may go unnoticed but this is not true of myocardial or cerebral infarctions, why?

Answer 35

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.

Question 36

sterile body site means?

Answer 36

no microbes present. blood, brain & CSF, bone and marrow, lower respiratory, upper urogenital, stomach?

Question 37

non-sterile body site means?

Answer 37

microbes present, sometimes as protection and function. skin, GIT, upper respiratory, lower urogenital