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Blood - molecules Flashcards

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Organic Chemistry 101 flashcards
1
Q

State 3 functions of blood

A

Transport: oxygen, carbon dioxide, digestion products, metabolites, hormones, plasma proteins

Haemostasis: maintenance of blood volume

Immune defence: innate and acquired immunity

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2
Q

How is composition of blood related to its function?

A

Plasma: fluid component of the blood, contains dissolved metabolites, proteins, hormones

RBCs transport oxygen and carbon dioxide bound to haemoglobin

Platelets responsd to vascular damage by forming clots to prevent blood loss
WBCs immunological defence

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3
Q

Normal Hb values in men and women

A

Men: 15g/dL

Women: 12g/dL

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4
Q

Normal cell count

A

RBCs: 5 x 10^6 cells/ul

Platelets: 250-300 x 10^9cells/ul

WBC: 6-10 000 cells/ul

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5
Q

Define hematocrit

A

Red cell fraction formed when blood is separated by centrifugation.

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6
Q

Describe the process of Haematopoiesis

A

In adults cellular components of blood is formed in bone marrow.

Multipotent Haematopoietic stem cell differentiates into myeloid stem cells which give rise to majority of the cells in the blood and lymphoid stem cells which differentiate into T-cells and b-cells

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7
Q

How is the structure of bone marrow related to its function?

A

Bone marrow composed of:

BM stromal cells
Endothelial cells:provide blood supply
Adipocytes: provide energy for haematopoiesis
Osteocytes: turnover of bone matrix
Haematopoietic islands: site of blood cell production

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8
Q

Describe how oxygen is transported by red blood cells

A

Oxygen transported around the blood bound to haemoglobin in RBCs.

Hb is a heterotetramer, each heme group binds one O2 molecule. At high partial pressures of oxygen (lung) Hb becomes saturated with oxygen.The binding of one molecule causes a change in the structure of the porphyryn ring and changes the protein conformation from tense to relaxed, exposing the oxygen binding sites on adjacent chains. Therefore binding of one oxygen molecule enhances binding of other oxygen molecules.

OxyHb is then transported from the lungs to the respiring tissue where a high pH and presence of CO2 lower its affinity for oxygen, converting it from the R to the T state which promotes oxygen release.

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9
Q

Describe the regulation of erythropoieses

A

.Synthesis of erythropoietin is stimulated by anaemia and hypoxia.

This acts in combination with other haematopoeitic growth factors to stimulate erythropoiesis.

EPO binds to the EPO receptor (Jak-stat) which activates gene transcription.

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10
Q

What is the role of EPO?

A

Growth factor that stimulates erythropoieses

Prevents apoptosis of rbcs

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11
Q

What are the causes of anaemia

A 
Chronic blood loss
Acute blood loss
Dietary deficiency (lack of iron, lack of folate)
Thalassemias 
Destruction of RBCs (haemolytic disease)
Low RBC production (aplastic)
Chronic disease
Failure to produce RBCs due to a lack of EPO e.g. kidney failure
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12
Q

Signs and symptoms of anaemia

A 
Pallor
Tiredness
Fainting
Light- headedness
Dyspnoea
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13
Q

Definition of anaemia

A

Hb lower than 12g/100ml or hematocrit of less that 37%

Chronic anaemia is where hematocrit is below 30%
Acute anaemia there is overall drop in blood volume

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14
Q

State the 3 types of anaemia

A

Normocytic, normochromic - caused by acute blood loss, anaemia of chronic disease, destruction of rbcs e.g. Sickle cell

Microcytic hypochromic - iron deficiency, thalassemia

Macrocytic normochromic - vitB12, folate deficiency (increased reticulocyte count)

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15
Q

Compensatory mechanisms for anaemia

A

Decrease affinity of Hb for oxygen by stimulating production of 2,3BPG

Redistribute blood flow, less to kidney and skin, increase in plasma volume

Increase cardiac output (tachycardia)

Premature release of reticulocytes into blood to boost cell numbers

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16
Q

Describe the destruction pathway of rbcs

A

Normal rbc life span is 120 days then they go to the spleen and liver to be destroyed.

Chemical components of rbcs broken down by macrophages in the liver, spleen and lymph nodes. Globin digested into amino acids. Heme broken down into bilirubin which is released into the blood where it complexes with albumin. In the liver it is conjugated to glucaronic acid and stored in the gall bladder, where it is secreted into the small intestine with bile. In the bowel bacteria convert bilirubin into urobilinogen. This is then mostly broken down to stercobilin and excreted in faeces. Some urobilinigen is removed in the urine.

17
Q

What are the four phases of hemostasis in response to injury

A

Vascular constriction
Platelet plugging/ activation
Clot formation
Clot lysis/ scar formation

18
Q

Describe the key events in haemostasis following injury

A
  1. Vascular spasm- following trauma the vessel may contract or close the lumen temporarily
  2. Platelet plug - injury to vessel wall exposes collagen & vWF, platelets adhere to collagen when it binds to receptors on their cell surface, this causes activation and the release of TXA2, PDGF, fibrinogen and other activators
  3. Clotting cascade initiated, factor X cleaves prothrombin to thrombin, which then cleaves fibrinogen to fibrin which polymerises, chains are stabilised by cross linking factor FSF which turns soft clot to hard clot
  4. Clot lysis- plasminogen in plasma binds to fibrin molecules, nearby cells release tPA which binds fibrin and converts plasminogen to plasmin. This degrades fibrin, dissolving the clot
19
Q

What is the role of COX enzymes platelet activation

A

Converts arachadonic acid to PGH2 which is the precursor to TXA2

20
Q

What effect does aspirin have on haematostasis?

A

Aspirin irreversibly inhibits the COX enzyme, resulting in reduced production of TXA2. This reduces the activation of platelets, and thus reduces the risk of arterial thrombosis in patients.

21
Q

Classification of erythropoietin receptor

A

Jak-stat receptor

22
Q

Explain the molecular basis of the ABO blood antigen system

A

The ABO system is under the control of two sets of genes:
A pair of allelic genes H and h, and three allelic genes which are expressed co-dominantly A, B, O.

Terminal sugars on the blood group antigens determine their specificity.

The H gene codes for an enzyme H which attaches fructose to the basic glycoprotein backbone to form H substance. This is the precursor for A and B antigens.

A and B antigens control specific enzymes responsible for the addition of different sugars to H substance (A:NAG, B:gal). The O gene is amorphic and does not transform substance H and is therefore not antigenic.

23
Q

Explain the molecular basis of the Rh system

A

The Rh system is coded by allelic genes located on chromosome 1: C and c, E and e, D and no D (d). They are inherited together as a triplet with one from each parent e.g. DCe/dCe or dCe/dcE

Individuals are classified as Rh+ or Rh- depending on the presence of the RhD antigen which is highly immunogenic.

24
Q

What are the two main blood group systems in humans?

A

The ABO antigen system and the Rh antigen system.

25
Q

Why is it important to determine a patient’s blood group prior to transfusion?

A

Blood groups are determined by surface antigens on the RBCs. As an individual ages they produce antibodies against the other antigens e.g. A blood type has anti-B antibodies.

Incompatibility can lead to haemolytic transfusion reactions because the patient recognises the donor blood as foreign and therefore mounts an immune response against it. Causes haemolysis, shock, bleeding due to coagulation of blood and renal failure.

26
Q

What is a universal donor?

A

Individuals with blood type O RhD-
Because their red blood cells lack the two major immunogenic surface antigens their red blood cells can be donated to all blood types

27
Q

Universal recipient

A

Individuals with blood type AB+ because their plasma does not contain any antibodies for the major immunogenic blood groups antigens

AB-

28
Q

Describe the process of platelet activation

A

Platelet activators (thrombin, TXA2, ADP, PAF, epinephrine) bind to a GPCR on the platelet surface which is coupled to PLC (Gq subtype). This starts a signalling cascade which activates PKC and MLCK, resulting in the platelet changing shape

29
Q

What is the function of TXA2?

A

Potent platelet activator and powerful vasoconstrictor. Also lowers cAMP levels which promotes secretion of other activators from platelets.

30
Q

Describe the basic features of the clotting cascade

A

Coagulation is initiated by tissue damage. This can be via an extrinsic pathway which is rapidly activated (10-15s) in response to vessel damage and an intrinsic pathway which is activated in response to collagen. Both cause the activation of factor X which cleaves prothrombin into thrombin which then hydrolyses fibrinogen into fibrin.

Thrombin encourages the fusion of platelets and fibrin reinforces the stability of the platelet plug, forming a clot.

31
Q

What are the cellular components of blood?

A

RBCs
WBCs
Platelets

32
Q

What are the major sites where haematopoeisis takes place?

A

Bone marrow (main site)
Lymph nodes
Spleen
Thymus (T-cell maturation)

33
Q

How does the structure of RBCs enable them to transport oxygen?

A

E-nucleated biconcave discs, increases the surface area for O2 uptake

RBCs are flexible and able to pass through vessels which are smaller than its diameter

34
Q

Describe the mode of action of warfarin and heparin

A

Warfarin: inhibits vitamin-K dependent synthesis of clotting factors e.g. Prothrombin

Heparin: binds to and activates antithrombin III which is an enzyme that inactivates thrombin and other proteases involved in clotting e.g. factor Xa.

35
Q

How is clotting regulated?

A

Serine protease inhibitors in the plasma e.g. anti-thrombin

Smooth vessels (clotting activated by vascular damage)

Normal blood flow

Calcium chelation

36
Q

How is platelet activation prevented?

A

Intact endothelium physically separates platelets from collagen.

Undamaged endothelial cells produce prostacyclin and NO. Prostacyclin binds to a platelet receptor to increase cAMP which limits activation. NO slows platelet activation via cGMP pathway.

Corticosteroids inhibit PLA2

37
Q

Describe the mode of action of clot-busters

A

During clot formation fibrin polymerises into mesh which aggregates with platelets to form a clot over the wounded site.

Clots are temporary structures and are eventually degraded by plasmin which is cleaved from plasminogen by tPA released from neighbouring cells. This digests fibrin and dissolves the clot.

Clot busters activate plasminogen and promote the activity of plasmin.

Molecules (14 decks)

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