physiology Flashcards
haematocrit
- relative vol of RBC out of total blood volume
- men 46, women 42
- low = anemia
platelet
- fragment of megakaryocytes (bone marrow bound WBC)
- mammal platelet lack nuclei
- component
1) contractile proteins: actin, myosin
2) organelle: mito, ER, golgi
3) enzyme for pg synthesis
4) growth factor (PDGF, VEGF)
5) factor XIII (Fibrin-stabilising factor)
conditions that trigger release of erythropoietin by kidney cells
1) hypoxia due to decreased RBC no. and function
2) decreased O2 availability
3) increased tissue demand for oxygen
4) anemia
5) reduced blood flow to kidney
6) blood donation
location of erythropoiesis
- fetus: yolk sac -> liver, spleen, lymph node
- < 5yo: bone marrow
- 5-20yo: bone marrow in rib, sternum, vertebrae, proximal end of long bones
- > 20yo: bone marrow in rib, sternum, vertebrae
phases of erythropoiesis
1) phase I
- ribosome synthesis in early erythroblast
2) phase II
- Hb accumulation in late erythroblast and normoblast
3) phase III
- ejection of nucleus from normoblast & formation of reticulocyte -> enter circulation -> mature RBC
- reticulocyte count indicative of erythropoiesis (normal 0.8 - 1%)
destruction of RBC
- phagocytosed by macrophage in liver/spleen/bone marrow
- broken down into heme and goblin
1) heme broken down into iron (stored as ferritin) or bilirubin
** bilirubin picked up by blood in liver -> secreted into intestine in bile -> metabolised -> excreted by faeces
** iron bind to transferrin -> leave liver -> recycled for erythropoiesis
2) globin broken down into AA -> recycled
types of anemia not covered in later IC
1) renal anemia
- kidney disease -> lack erythropoietin
2) hemorrhagic anemia
- loss significant amt of blood
3) malaria
- plasmodium falciparum amplify in blood -> rupture
- offspring invade new RBC
4) sick cell anemia
- mutate beta-globin gene -> Hb aggregate in low O2 condition to crescent -> rupture RBC membrane
5) erythroblastosis fetalis
- Rh+ RBC of fetus destroyed by anti-Rh Ab of Rh- mother
6) thalassemia
- low production of hemoglobin
- hereditary
polycythaemia/erythaemia
- too many RBC & high haematocrit
- primary polycythaemia: tumour/tumour-like condition in bone marrow
- consequences: very viscous blood -> potential plug arteries -> insufficient O2 delivery
haematostasis entire tldr phases
1) vasoconstriction (immediate)
2) platelet plug (within seconds)
3) fibrin clot (within minutes)
haematostasis - vasoconstriction
- initiated by sympathetic nerves
- mediated by vascular smooth muscle cells
- provide time for other phases
- endothelial cells of opp sides may stick together
- reduce blood loss
- endothelial cells contract -> expose basal lamina
haematostasis - platelet plug
- 2 processes: platelet adhesion, platelet aggregation
- main function
1) closure of leak with formation of temp patch
2) release chemical mediators to regulate blood clotting
3) contraction of blood clot - intact endothelial cells release nitric oxide & prostacyclin -> inhibit unintentional platelet activation/aggregation
haematostasis - platelet plug - platelet adhesion
- mediated by vWF (plasma protein produced by platelet)
- vWF bind to collagen fibre -> release granules containing platelet agonist (ADP, thromboxane A2)
- ADP attract & Activate more platelet
thromboxane A2 promote aggregation & further vasoconstriction - platelet bind to Gplb on vWF -> morphological change -> activation
haematostasis - platelet plug - platelet aggregation
- fibrinogen link platelet through glycoprotein receptor
- links are weak and require reinforcement so platelets release factor XIII
- thrombin actions
1) enhance own generation through +ve feedback loop
2) convert fibrinogen to fibrin monomer (more stable)
3) convert factor XIII -> factor XIIIa -> cross-linking of fibrin -> fibrin mesh - linkage release more platelet attracting substances -> platelet plug
- release platelet factor 3 (PF3)
** activate other factors in clotting cascade -> activate prothrombin -> activate thrombin
haematostasis - extrinsic pathway
thromboplastin or 3, 7, 10, fibrin, fibrin mesh
haematostasis - intrinsic pathway
exposure to collagen fibres or foreign surface, 12, 11, 9, 10, fibrin, fibrin mesh