IC2: Physiology Flashcards
What is the pH of blood?
7.35-7.45
What are the 3 main functions of blood?
Transportation, regulation, protection
What does hematocrit refer to?
Relative volume of red blood cells out of the total blood volume
What does each hemoglobin molecule contain?
Heme (pigment) containing 1 iron
Globin (4 protein chains)
What does each hemoglobin molecule contain?
Heme (pigment) containing 1 iron
Globin (4 protein chains)
Describe the different ages and the respective locations of erythropoiesis
Fetus → yolk sac then liver, spleen and lymph nodes
<5yo → all bone marrow (mostly big bones)
5-20yo → bone marrow in ribs, sternum, vertebrae and proximal ends of long bones
> 20 yo → bone marrow in ribs, sternum and vertebrae
Explain the negative feedback loop in erythropoiesis
If oxygen delivery to the kidneys is decreased, the cells in the kidneys produce more EPO, increasing the rate of erythropoiesis
In what cases will the kidneys stimulate EPO release? (6)
- hypoxia due to decreased RBC number or function
- decreased O2 availability
- increased tissue demand for O2
- anemia,
- reduced blood flow to kidneys
- blood donation
What are the 3 phases of progression of proerythroblasts into erythroblasts
Phase 1 → ribosome synthesis in early erythroblasts
Phase 2 → Hb accumulation in late erythroblasts and normoblasts
Phase 3 → ejection of the nucleus from normoblasts and formation of reticulocytes
Where are red blood cells destroyed? (2)
- Tiny vessels of the spleen
- Macrophages
How are the components of RBCs recycled? (3)
Iron - recycled in bone marrow or stored in liver
Globin - metabolised into AA and released into circulation
Heme - degraded into bilirubin, excreted via liver
What does polycythemia refer to?
Excess in circulating erythrocytes
Describe primary and secondary polycythemia
Primary polycythemia is caused by a tumour or tumour-like condition in the bone marrow
Secondary polycythemia is an EPO-induced adaptive mechanism to improve O2-carrying capacity of blood, for example for people living in high altitudes
What are the 3 phases of hemostasis?
Vasoconstriction (immediate)
Platelet plug (within seconds)
Fibrin clot (within minutes)
How is vasoconstriction initiated and mediated
initiated by the sympathetic nerves, mediated by vascular smooth muscle cells
What happens to endothelial cells during vasoconstriction? (2)
Endothelial cells of opposite sides may stick together to reduce blood loss
Endothelial cells contract and expose the basal lamina
Outline the processes that occur during the platelet phase
Endothelial wall dmg exposes collagen
Platelets stick and secrete vWF
Positive feedback causes more platelets to stick
What molecules do platelets contain and what are their functions? (3)
Enzymes (PG and TXA synthesis)
Growth factors (PDGF and VEGF)
Factor XIII (fibrin stabilising factor)
Explain how vWF leads to platelet aggregation?
- vWF binds to platelets and exposed collagen via glycoprotein receptors
- Adhesion activates morphological change in platelets
- Platelets release granules containing platelet agonists (more platelet aggregation)
Explain how the extrinsic pathway works (2)
Damaged tissues release tissue factor, that activates VII to VIIa, which activates X to Xa
(7 to 10)
Explain how the intrinsic pathway works (4)
Exposure to collagen fibres or exposure to foreign surfaces (eg. glass) causes a conformational change that actives XII to XIIa
This then activates XI to IX to X
(12 to 11 to 9 to 10)
Explain how the intrinsic and extrinsic pathways combine to induce clot formation (4)
X is activated to Xa (in the presence of Ca2+ ions and factor Va)
This activates prothrombin (II) to thrombin (IIa)
Thrombin cleaves fibrinogen (I) to fibrin (Ia) monomers that aggregate to form fibrin strands
Thrombin (IIa) also activates factor XIIIa which forms cross-links between fibrin strands to form a fibrin mesh
Explain how the intrinsic and extrinsic pathways combine to induce clot formation (4)
X is activated to Xa (in the presence of Ca2+ ions and factor Va)
This activates prothrombin (II) to thrombin (IIa)
Thrombin cleaves fibrinogen (I) to fibrin (Ia) monomers that aggregate to form fibrin strands
Thrombin (IIa) also activates factor XIIIa which forms cross-links between fibrin strands to form a fibrin mesh
List the 3 functions of thrombin
- Cleaves fibrinogen to fibrin
- Activates factor XIII for fibrin mesh stabilisation
- Causes platelets to release PF3 (activates intrinsic pathway)
How does clot repair occur? (2)
PDGF stimulates vascular SM to build new vessel walls
VEGF stimulates endothelial cell multiplication and restores the inner endothelial lining
Explain the two mechanisms of regulation of blood clotting
Prostacyclin inhibits platelet activation and limits clot spreads
Blood clots limit the spread of thrombin and other procoagulants to other locations (localises it at site of injury)
Explain the process of fibrinolysis
Surrounding tissue and vascular endothelial cells slowly release tissue plasminogen activator (tPA) which cleaves inactive plasminogen to protease plasmin
Plasmin then digests fibrin and dissolves the clot
Macrophages remove the remains of the clot
What is hemophilia
Excessive bleeding after an injury
What are the three types of hemophilia and what factor deficiencies cause them?
- Hemophilia A is caused by deficiency of factor VIII
- Hemophilia B is caused by deficiency of factor IX
- Hemophilia C is caused by deficiency of factor XI
(A8, B9, C11)
Which 4 factors require vitamin K for production?
Factors II, VII, IX and XI
Which 5 factors does Prothrombin Time (PT) assess and which pathway?
Factors I, II, V, VII and X (VII most important)
Extrinsic pathway
