Blood💘 Flashcards
What’s is plasma and serum
Plasma is yellow coloured non clotted liquid mate up of 93% water 7% plasma proteins
Serum is plasma devoid of clotting factors
Blood cell production
Haematopoiesis
Occurs in bone marrow
Rbcs migrate into blood WBC’s migrate into peripheral tissues and lymphoid organs
Controlled by cytokines and growth factors eg EPO TPO IL SCF
Kidney cells detect change in blood oxygen and release EPO into blood which regulates erythropiesis by binding to its receptor in progenitor cells
Harmatopiesis order (common myeloid path
Haemopoietic stem cell Multi potent progenitor Common myeloid Becomes either Megakaryocyte erythrocyte Mast cell Myeloblast> blood cells BNEM M FOR MONOCYTES BECOMES EITHER MACROPHAGE OR DENDRITIC CELL
Haematopoiesis order (Common lymphoid path)
HSC MPP Common lymphoid progenitor Becomes either natural killer cell Or small lymphocyte> T cell or B cell> plasma cell B
RBC life span
120 days
Don’t repair
Aged cells removed by macrophages of spleen
Haemoglobin digestion and structure
Two alpha to beta subunits
Made from iron and poryphyrin ring
Iron transported to bone marrow via transferrin for RBC production
Poryphrin ring excreted via digestive urinary tract
Bilirubin via urine bilidervin via faeces
Blood tests
Haematocrit is when u centrifuge a blood sample
Eg full blood count
WBC subsets are determined by flow cytometry due to differential cellular properties
Haematopaoises before hearth sites
In embryo it occurs in yolk sac
In fetus it’s in liver
Innate immune cells vs adaptive immune cells
Innate:neutrophils eosinophils basophils monocytes nk cells
Lymphocytes are adaptive
Platelets
Also known as thrombocytes 30% stored in spleen Production regulated by TPO 1 megakaryocyte can make 5000 platelets Contain three types of granules dense lambda and alpha
Life span of neutrophil
18hrs
Lifespan of basophils
1-2 days
Life span of natural killer cell
14 days
Life span of platelets
5-9 days
Anemia
Reduced number of rbcs or haemoglobin causing reduced oxygen delivery to tissues
Causes weakness shortness of breath thirst etc
EPOand tissue oxygenation relationship
Inversely related
Can increase up to 1000% in anaemia
Condition affecting erythropiseis in bone marrow
Condition affecting other cell types
Pure red cell aplasia eg diamond black fan anemia (rare one per 5mil)
Pancytopneia
Haemolytic anaemia
Due to extrinsic or intrinsic factors
Extrinsic is immune mediated eg autoimmune haemolytic anaemia AIHA
There’s idiopathic AIHA or secondary (eg due to leukaemia or arthritis etc)
Haemoglobinpathy
Autosomal codominant genetic defects causing abnormal structure in global chains
Sickle cell most common beta glob in gene mutation
Abnormal shape affecting movement oxygen carrying ang increased haemolysis
Other anaemia
Iron deficiency
Vitamin b12 and b6\ folate deficiency (regulator of haem production)
Thalassemia (reduction in number of alpha or beta glob in chain)
MCV
Size of RBC
Low is microcytic (due to iron defined toe thalessemua)
Normal is normocytic (haemolytic anaemia or bone marrow disorders)
High is macrocytic (vitamin or folic acid deficiencies liver disease etc)
Blood types
A B O AB are carb structures on rbc membrane glycolipids +glycoproteins
Genes that encode these are glycosyltransferase
Type a is acetylgalactosaminyltransferase
Type b is galactosyltransferase and type o has none
Encoded by one gene on chromosome 9
AB codominant o recessive
Rhd antigens
Five antigens D C c E e D most immunogenic in
encoded by genes RHD and RHCE
Can be homozygous for RHD (2 copies) or hemizygous (1 copy) all express d antigen
Individuals are RHD+ or RHD- (both copies deleted)
Causes a+ a- etc
If RH- mother has RH+ baby she produces antibodies for RH next time she has RH+ baby these antibodies will attack babies rbcs called Rhesus disease
Genetic anaemia
Glutamic acid position 6 replaced by valine in HBB gene one copy is sickle cell trait
Similar in thalessemia but can happen in any chain
Blood haemostasis
Maintaining blood flow within the vasculature
Forming blood clot but still maintaining blood flow
Thrombosis
Restricting or blocking causing hypoxia and tissue damage
Thrombi can also dislodge causing embolisation
Three stages of haemostasis
Vascular spasm- damaged blood vessels construct reducing blood flow to damaged area
Platelet plug formation- platelets binding to damaged vessel wall
Coagulation- stable clot forms forming fibrinogen to fibrin
Platelets
Small fragments of megakaryocyte cytoplasm
Contains membrane proteins secretory granules and surface connected open cannalicular system
How are old platelets destroyed
By Kupffer cells in liver
What does an alpha granule contain
Adhesive proteins eg fibrinogen
Platelet specific proteins eg PDGF
Membrane proteins (glycoproteins)
Specific protein- p selectin
What do sense granules contain
Vasoconstrictive agents (serotonin)
Platelet agonists (ADP ATP)
Calcium
Magnesium
Platelet plug formation
Gp1b on platelet binds to von wilebrand factor
Blood flow rolls platelet along promoting more GPlb/vwf associations creating firmer adhesion
Causing platelet activation
Granule release
Conformational changes in adhesion molecules
Strong adhesion shape change
Further activation
Plug made by platelet mono layer which releases platelet agonists such as as thromboxane, fibrinogen recruiting further platelets
Recruited platelets change shape allowing mor platelet interactions and fibrinogen cross bridges
Coagulation cascade
Has two pathways extrinsic (triggered by trauma) and intrinsic (internal damage to vessels
Coagulation factors are a group of zygomens (inactive precursors of enzymes)
Bleeding disorders
Thrombocytopenia- low platelets autoimmune condition
Glanzmanns thrombasthenia- autosomal recessive bleeding syndrome affecting megakaryocyte lineage and characterized by lack of platelet aggregation
Haemophilia- recessive x linked due to changes in clotting proteins type a due to deficiency in FVIII b due to FIX
Causes bleeding and pain in joints
Antithromhotic Drugs
Aspirin- inhibits COX 1 key enzyme in thromboxane generation
ADP receptor agonists - prevents blockage of coronary artery stents eg clopidogrel
Anti coagulants - heparin (increases anti thromboxane) and warfarin (vitamin k inhibited needed for the thromboxane stuff)
Lab tests for platelet and coagulation
Platelet aggregometry platelet rich plasma and agonist in tube use light machine yo see how much light shines through (chromatography?)
Coagulation tests- no cells in plasma mixed rapidly with reagents should form gel time how long it takes for ball to stop moving
Parietal cells release
Intrinsic factor
Heridatry sphercityosis test
Coombs test
G6pdhw anaemia test
Heinz bodies
Intrinsic order
12 11 9 8 10 5 2 1
Extrinsic pathway
3 7 10 5 2 1
What factor is thrombin and pro thrombin
Factor 2 (prothrombin) factor 2a (thrombin)
Clot retraction and repair
Platelet contraction pulls ruptured edges of vessels together
Platelet derived growth factor released which repairs any damage eg smooth muscle or tissue damage
Vascular endothelial growth factor regenerates endothelial lining
