Physiology of Blood Flashcards

1
Q

What makes up the blood plasma?

A

It makes up about 4% (3L) body weight. 95% water & various substances in solution and suspension: ions, small organic molecules, and plasma proteins. Also sometimes enzymes, hormones, vitamins and products of digestion.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the components of blood?

A

Plasma and the formed elements: erythrocytes, leukocytes and thrombocytes.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the three categories of plasma protein?

A

Globulins, Albumins and clotting factors (fibrinogen and prothrombin)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Describe the albumins

A

smallest and most abundant (60%) plasma proteins. Import for lipid and liver-produced steroid hormone transport and oncotic pressure.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Describe the globulins

A

About 40% of total plasma protein. Alpha and Beta made in liver and transport lipids and fat-soluble vitamins. Gamma are antibodies.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is a haematocrit?

A

The haematocrit or packed cell volume is found by centrifuging a small sample of blood until the cellular contents are packed at the bottom. Ratio of red cells to total. About 0.4-0.52:1L, after correcting for plasma trapped between cells. Lower in larger blood vessels because of axial streaming.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What makes up the buffy coat of a haematocrit?

A

Leukocytes and platelets. White layer that moves around when swilled and is bigger following infection.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Describe red blood cells

A

small biconcave disks, diameter 7-8micrometers. No nucleus. Thin and flexible to squeeze through capillaries. Large SA:V ratio. Haemoglobin synthesised by red cell precursors in the bone marrow.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Describe white blood cells in general

A

larger than RBCs and have a nucleus. Involved in immunity, able to pass though capillary walls - diapedesis. Able to then move through tissues by an amoeboid motion.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Describe the granulocytes

A

AKA polymorphonuclear leukocytes with lobes nuclei. neutrophils, eosinophils and basophils. Their function is to destroy invading pathogens. They are motile and are attracted to injury sites by chemicals released from injured
tissue or foreign organisms - chemotaxis. The cells engulf these organisms and destroy them by enzymes stored within lysosomes - phagocytosis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Describe the monocytes

A

AKA Macrophages. Larger with kidney shaped nuclei. Migrate from bone marrow to spleen, liver, lungs, lymph nodes and more. Antigen presenting phagocytes. Recognised by T cells to stimulate B cell production.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Describe the lymphocytes

A

B & T lymphocytes. Producing antibodies and carrying out cell mediated immune response respectively.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Describe Thrombocytes

A

Platelets aren’t really cells but membrane bound cell fragments which bud off from megakaryocytes in the bone marrow. No nucleus, life span of ~10 days. Help control bleeding and maintain endothelium.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is the Starling equilibrium?

A

Hydrostatic pressure (about 25 mm Hg) forces water through the leaky capillary fenestrations, but this is offset by the colloid osmotic, or oncotic absorption pressure due to the plasma proteins.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the Starling equation?

A

Jᵥ = Kf [(Pc - Pi) - σ(πc - πi)]
Where:
Jᵥ = Net fluid flux
Kf = Filtration coefficient
Pc = Capillary hydrostatic pressure
Pi = Interstitial hydrostatic pressure
σ = Reflection coefficient
πc = Capillary oncotic pressure
πi = Interstitial oncotic pressure
Note:
[(Pc - Pi) - σ(πc - πi)] is the net driving pressure.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the importance of the filtration coefficient?

A

Describes the leakiness of the capillary walls - larger = more fluid can be filtered across. Can be changed for example by histamine release of mechanical damage.

17
Q

What is the reflection coefficient?

A

Reflects how some plasma proteins are able to diffuse across the capillary walls, which would bring down oncotic pressure in the capillaries. 1 in Glomerular capillaries and about 0 in hepatic sinusoids.

18
Q

What is Oedema and what are its causes?

A

When filtration forces significantly exceed absorption forces an accumulation of extravascular fluid occurs called an oedema. Can be caused by decreased oncotic pressure: e.g. loss of plasma proteins due to liver failure or starvation. OR increased hydrostatic pressure e.g. due to congestive heart failure.

19
Q

Describe the A(O) blood group

A

These individuals have agglutinogen A antigens on their RBCs, and as such don’t have anti-A antibodies in their plasma, but do have anti-B

20
Q

Describe the B(O) blood group

A

These individuals have agglutinogen B antigens on their RBCs, and as such don’t have anti-B antibodies in their plasma, but do have anti-A

21
Q

Describe the AB Blood group (least common)

A

These individuals have agglutinogen A&B antigens on their RBCs, and as such don’t have any agglutinins in their plasma

22
Q

Describe the O Blood group (most common)

A

Also known as universal donors, these individuals have no agglutinogen antigens on their RBCs, and as such their blood doesn’t clump when donated to anyone, but they can only receive transfusions from other O individuals as they have both anti-A and anti-B agglutinins.

23
Q

What is the Rhesus blood group system?

A

Rh positive individuals have the D-antigen, or Rhesus factor, on their RBCs. Heritable in the same way as ABO groups.

24
Q

What causes hemolytic disease of the newborn (HDN)?

A

HDN happens when an Rh-negative mother produces anti-Rh antibodies after exposure to Rh-positive fetal blood. This often occurs during birth or in later pregnancies, leading to immune attacks on the fetus’s red blood cells. It affects ~1 in 160 births.

25
How is hemolytic disease of the newborn prevented, and why does ABO incompatibility rarely cause issues?
HDN is prevented by giving anti-D IgG (RhoGAM) to Rh-negative mothers after delivery of the previous child. ABO issues are rare because anti-A/B antibodies are IgM, which are too large (900 kDa) to cross the placenta, unlike anti-Rh IgG (150 kDa).
26
What is Haemostasis?
The prevention of excessive blood loss following injury, involving vasoconstriction, platelet aggregation and blood coagulation.
27
What is the role of vasoconstriction in haemostasis?
Damage to the vascular endothelium causes a localized contractile response by vascular smooth muscle to narrow the vessel. This is mediated by humoral factors or by mechanical stimulation and in arterioles and small arteries closure may be virtually complete. However, this response is only short-lived to permit further mechanisms to be activated.
28
Describe platelet plug formation.
Seconds after injury, platelets adhere to site of damage and secrete ADP & 5-hydroxytryptamine (causing more to build up) and synthesise arachidonic acid and thromboxane A2 which change platelet surface characteristics so they adhere to walls and each other
29
What is thrombocytopenia?
Platelet deficiency causing increased capillary permeability and blotchy skin, as platelets have a role in normal vascular integrity.
30
What is blood coagulation?
fibrin strands create a mesh to bind blood components together and form a blood clot. Clotting factors are often synthesised in the liver and Vit. K dependent. one activated factor activates another in the intrinsic and extrinsic pathways.
31
Intrinsic vs Extrinsic pathways
Intrinsic slower, occurs when blood contacts damaged wall, all necessary elements present in normal blood. Extrinsic occurs when blood is exposed to the products of damaged tissue - thromboplastin. Extrinsic pathway activated by tissue factor from outside the blood.
32
Describe the intrinsic pathway up to the final common path
Contact with a damaged vessel activates factor XII, activated XI, with Ca2+ activates IX, then with Ca2+, VIII & phospholipids activates factor X
33
Describe the extrinsic pathway up to the final common path
Damaged tissue releases thromboplastin and phospholipids. Thromboplastin combines with Factor VII and then Factor VIIa with V (all in the presence of Ca2+) to activate factor X
34
Describe the final common path of coagulation
Factor Xa, with V, phospholipids and Ca2+ converts prothrombin to thrombin, which among other things converts fibrinogen to fibrin.
35
How is inappropriate blood clotting prevented?
Undamaged tissue prevents clotting by releasing endogenous anticoagulants, and these can be used clinically. Prostacyclin prevents platelet aggregation, as is heparin, which also inhibits the action of thrombin.