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103T2- Formation, composition, function and disorders of the blood > RBC's & Haemostasis > Flashcards

RBC's & Haemostasis Flashcards

1
Q

Describe the relative proportions of oxygen carried in the blood via Hb and dissolved in plasma.

A

70x oxygen bound to Hb than dissolved in plasma.

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2
Q

What type of respiration occurs in Hb and how does its efficiency compare to a normal somatic cell.

How much of a RBC is Hb in terms of a) dry mass b)wet mass?

A

Anaerobic as it lacks organelles including mitochondria.

Glucose is decarboxylated to product 2xlactate and 2ATP compared to 36ATP molecules generated in aerobic respiration.

a) 95%
b) 35%

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3
Q

Describe the structure of Hb and how it differs to foetal Hb.

A

Hb is a tetramer composed of 4 subunits; 2 alpha + 2 beta
Each subunit is bound to a haem group.

Foetal Hb also has 4 subunits; 2 alpha + 2 gamma
Foetal Hb has a greater affinity for oxygen

Adults have a very low percentage of foetal Hb.

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4
Q

Describe the haem group in Hb.

A

The haem group is responsible for oxygen transport, it is a porphyrin ring which makes it rigid, 2D and highly coloured due to the sharing of electrons. It is also conjugated to a ferrous group (Fe2+)

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5
Q

Describe the Bohr effect.

A

Takes place response to high carbon dioxide partial pressure.

High CO2, decreases the pH of the blood and this leads to a decreased affinity of Hb for O2 causing dissociation to respiring tissues.

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6
Q

Outline the respiratory thresholds.

What happens in order for the body to increase respiratory drive?

A

95- normal
90-poor
88- critical. INCREASE RESP DRIVE

H+ ions detected in cerebrospinal fluid.
CO2 is a gas and can travel to CSF quickly where it reacts with blood to form carbonic acid and H+ ions. In this sense an increase respiratory drive is more dependent on CO2 concentration than H+ ions in blood as it takes longer for these to be detected as they are only detected in the carotid bodies.

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7
Q

Describe the appearance, function, frequency and location of erythrocytes.

A

Appearance: Red (oxy-HB), 2umx7um, biconcave

Function: transport O2/CO2, lifespan approx. 120 days, flexible and stack themselves in vessels

Frequency: 5million/uL. PCV: 40-52% women; 36-48% men

Location: post birth- bone marrow. >20yo- membraneous bone

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8
Q

Describe the cell lineage that cells follow in haematopoeisis.

A

Multipotent haematopoietic stem cell (Haemotocytoblast)

Common myeloid progenitor

Reticulocyte

Erythrocyte

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9
Q

What is erythropoietin and how may it be used in the “real world”?

A

Cytokine which drives erythropoiesis. Made in kidney in response to kidney hypoxia.

Performance enhancer.

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10
Q

Describe what a Reticulocyte is.

How can detection of is help us find out whats going on in the blood?

A

Erythrocyte precursor cell
Still contains nucleus and organelles.
Lifespan- 2 days

Low reticulocyte count means low levels of erythropoiesis taking place

High reticulocyte count may indicate haemolytic anaemia.

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11
Q

Describe Methaemoglobinamia

A

Condition in which iron(II) in Hb is oxidised to iron(III) and thus unable to transport oxygen.

CAUSES:

  1. congenital globin mutations
  2. NADH hereditary diseases
  3. toxic agents
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12
Q

Describe Polycythaemias, both physiologically and pathologically.

A

Increases blood volume due to increased RBC’s. Also increases viscosity

Physiologically: in people that live at high altitudes.

Pathologically: clog blood vessels (risk of thrombosis), asymptomatic, no cure, all ages. JAK2 mutation.

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13
Q

Describe the bodies iron requirement.

A

65% iron in body in Hb. 30% intracellularly stored in FERRITIN(very easily accessible) in liver, bone marrow and blood and HAEMOSIDERIN (less accessible). 4% IN myoglobin

Iron stored in reticuloendothelial system in spleen, liver, RBCs, WBCs, bone marrow

Usage: 1mg/day (excpetions, menstruation, pregnancy, peptic ulcers)

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14
Q

What is the use of Vitamin B12 & Folic acid?

A

Important in fast dividing tissues (growth)

  1. DNA formation
  2. Nuclear maturation
  3. RBC’s, skin, gametogenesis,
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15
Q

Describe a type of anaemia caused by Folic acid & Vit-B12 defence?

A

Megaloblastic anaemia
Other causes - lymphoma, old age, diet, malnutrition, veganism

Treatment-
Oral folic acid
Intramuscular hydroxocobalamin

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16
Q

Name an anaemic condition caused by iron deficiency.

A

Hypochromic microcytic anaemia

17
Q

Describe 5 functions of the endothelial cells

A
  1. Inner lining surface
  2. Normally secretes inhibitory factors of haemostasis, injury results in secretion of von Willebraud factor
  3. Control blood fluidity (size and contribute to clotting)
  4. signal inflammatory cells to areas needing repair
  5. Gate keeper between blood &brain/ tissues. It controls extravasion
18
Q

Outline the three steps involved in platelet based pathway to repair blood vessels

A
  1. Vasoconstriction
    Platelets release vasoconstrictors and prothrombotic agents (serotonin, ADP thromboxane A2)
  2. Platelets form haemostatic plug
    By adhesion, activation and aggregation
  3. Coagulation makes meshwork on clot
    Activates cascade enzymes
    Part of coagulation requires nearby platelet membrane
19
Q

Outline the lineage that a thrombocyte (platelet) is derived from.

A

Multipotent haematopoietic stem cell

Common myeloid progenitor

Megakaryocyte

Thrombocyte (platelet)

20
Q

Describe the term thrombocytopenia.

Describe the normal platelet count and size.

A

Low platelet count in blood

Normal platelet count 50x less than RBCs

Size: 0.5um

21
Q

Explain the role of activation in platelet based pathway to repair blood vessels.

A

Requires exocytosis, change of shape and increased respiratory rate.

The change of shape involves expression of pseudopodia

22
Q

Explain the role of the haemostatic plug in platelet based pathway to repair blood vessels.

A

Adhesion to exposed collagen

Activation by exocytosis of dense granules
The mechanism of this involves extracellular ADP activating P2Y receptor which leads to cation flow. The platelets release TXA2 and the ADP stimulate a positive feedback response on the platelets.

Aggregation is stimulated by ADP & blocked by prasugrel

23
Q

Describe coagulation factors.

Define a tissue factor.

A

Coagulation factors circulate in the blood as inactive precursors. Most (exc. V VIII) are enzymes that cleave to other factors thus switching them on.

A tissue factor is a factor held behind the endothelial lining, thus only exposed when there is damage to the endothelium where they are able to interact with precursors.

24
Q

How does low BP and/or atrial fibrillation lead to thrombosis?

How is this combated?

A

Low bp increases chance of spontaneous thrombus formation.

Afib means increased risk for stroke because blood may not be properly pumped out of the heart, which may cause it to pool and form a clot.

Blood thinner adminstrated to patients. In lab, citrate and heparin stop blood clotting

25
Q

Whats the difference between plasma and serum?

A

Plasma is fluid portion of blood.

Serum is leftover fluid after clotting. It is lacking in fibrinogen, clotting factors II, V and VIII

26
Q

Outline the steps involved in producing cross linked fibrin

A

Fibrinogen (glycoprotein) is converted to fibrin by thrombin (enzyme). Factor XIII and calcium ions are involved in cross linking the fibres.

27
Q

Explain how thrombin is activated.

A

By Factor Xa (poorly) in the presence of its cofactor, Factor Va (efficient). Together= thrombinase

28
Q

Describe the three pathways in which Factor Xa is activated?

A
  1. Extrinsic Xase (Tissue factor + Factor VIIa)
  2. Intrinsic Xase (Factor VIII + Factor IX)
  3. Thrombin itself in positive feedback mechanism
29
Q

Coagulation factors can be subdivided into two categories. Prothrombins and Thrombins

Describe the differences and give examples.

A 
Prothrombins
Examples: factor 2,7,9,10
They are enzymes
They require Vitamin K for their synthesis. This is taken endogenously and is important for gamma-carboxylation of enzymes.
Require Ca2+ for activation
Thrombins
Examples: 1,5,8
Thrombin ACTIVATES them
5 and 8 are cofactors
Increased concentration in inflammation, pregnancy and oral contraceptives
30
Q

Describe the function of plasmin and how it is activated.

A

Lyses fibrin therefore breaks down clots
Circulates in blood from liver as Plasminogen
Tissue Plasminogen activator (TPA) found on surface of endothelium, causes plasminogen maturation

31
Q

Describe the function of Protein C

A

Inhibits coagulation by inactivating clotting factor Va and Xa. It works alongside co-factor protein S to inactivate Va.

Protein C itself is activate don endothelium and made in liver

32
Q

Describe the function of Antithrombin III

A

Works well with heparin, heparin increases response
Peptide made in liver
Blocks activity of thrombin, Factor 9 and 10

33
Q

Describe Vitamin K deficiency inc. prevalence, cause and the effect of warfarin.

A

Results in clotting deficiency as Vitamin-K essential to synthesis prothrombins such as clotting factor 2,7,9,10

Rare because vitamin k is made by bacteria in body and rich in green veg

Causes: GI disease/inability to absorb fat

Warfarin prevents Vit-k recycling so stores deplete after a few days

34
Q

Describe haemophilia A and detail how it is different to haemophilia B

A

Congenital lack of factor VIII
X linked
Affects longer blood vessels
Causes wounds to bleed for days, blood enters joints and muscles

Treatment- injected purified F-VIII(very expensive and rare)

Haemophilia B “Christmas disease”- same symptoms as H-A
Lack in factor IX

35
Q

Describe atherogenesis as a disease of inflammation, lipids and endothelium.

A

Formation of abnormal fatty or lipid masses in arterial walls

It causes inflammation as monocytes enter lesion, become foam cells, die and release contents which further attracts monocytes, cytokines and chemo-attractants

LDL deposits in lesion, cholesterol esters solidify and are oxidised forming toxic oxygen radicals which are immunogenic. These are consumed by macrophages, become foam cells, rupture and attract monocytes.

Endothelium express chemoattractants which leads to the attraction of monocytes which breakdown inner lining exposing collagen which stimulates coagulation. Lost endothelium decreases the vessels ability to dilate.

36
Q

Consider pharmacological control of blood clotting. Describe the function of anti-platelet drugs with examples.

A

Good in arterial clots
Used to treat acute coronary symptoms

Aspirin blocks formation of thromboxane A2
Increase bleeding time without increasing clotting time
Propylaxis for MI

ADP inhibitors e.g. Prasugrel, Clopidogrel

37
Q

Consider pharmacological control of blood clotting. Describe the function of anti-coagulants drugs with examples.

A

Prevent clotting in veins and low pressure pulmonary circulation
Prophylaxis in patients with risk of DVT and PE

Heparin - inhibit coagulation by working alongside antithrombin III to inhibit Factor Xa

Novel Oral anticoagulants

  1. Dabigatran (thrombin inhibitor)
  2. Rivaroxaban (Factor Xa inhibitor)

Warfarin
Vitamin K antagonist, slow onset, requires constant monitoring

38
Q

Consider pharmacological control of blood clotting. Describe the function of fibrinolytics with examples.

A

clotting in arteries and vessels with high BP. Treatment for MI, PE, DVT, Thromboembolytic stroke

Block tissue plasminogen activator
1. Streptokinase - produced by some species of strept
Effective and cheap
2. Urokinase

103T2- Formation, composition, function and disorders of the blood (6 decks)

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