Haematology Flashcards
(45 cards)
Granulocyte and monocytes growth factors?
G-CSF, GM-CSF, cytokines (interleukins)
Megakaryocytopoiesis and platelet production growth factors?
Thrombopoietin
Iron deficiency symptoms?
Koilonychia, glossitis, angular stomatitis
What are B12 and folate needed for?
dTTP synthesis for synthesis of thymidine for DNA synthesis
Disruption of vertical linkages of RBC?
Disruption of ankyrin/spectrin vertical linkages causes hereditary spherocytosis (spherocytes, autosomal dominant)
Disruption of horizontal linkages on RBCs?
Hereditary elliptocytosis (also in iron deficiency)
What is G6PD important for?
Hexose monophosphate (HMP) shunt, coupled to glutathionine metabolism, protects RBC from oxidative damage.
Bohr effect?
High CO2, low pH, right shift, O2 release.
cooperativity - O2 affinity of Hb increases as oxygen is added to it.
2,3-BPG
Biphosphoglycerate, competitive inhibitor of O2, right shift. Bind to beta-globin chain in central cavity.
Heinz bodies?
In G6PD deficiency, irregularly contracted cells
MCV?
Hct
—— L
RBC
MCH?
Hb
—— g
RBC
MCHC?
Hb
—— g/L
Hct
Myeloid growth factors?
G-CSF - granulocyte colony-stimulating factors
M-CSF - macrophage colony-stimulating factors
GM-CSF - granulocyte-macrophage colony-stimulating factors
Contents of basophil granules?
Histamine, heparin and proteolytic enzymes.
CML cause?
Translocation between chromosome 9 (tyrosine kinase) and 22, uncontrolled tyrosine activity.
Tyrosine kinase inhibitor treatment.
Vasoconstriction in primary Haemostasis?
Nitric oxide and prostacyclin (vasodilators) concentration lower than endothelin (vasoconstrictor)
Platelet adhesion in primary Haemostasis?
Stick to vessel wall directly to collagen through GPIa or to VWF through GPIb receptors.
Causes activation, from disc to rounded shape. Form spicules to encourage platelet interactions.
Platelets release in primary Haemostasis?
ADP (binds to P2Y12 receptor and thromboxane A2, positive feedback).
Fibrinogen, VWF.
Prostaglandin thromboxane A2 and prostacyclin (from endothelial cells) from arachidonic acid using cyclo-oxygenase.
Fibrinogen?
Activates platelets, conformational change, binds to GPIIb/IIIa, platelet plug.
Anti-platelet drugs?
Aspirin - irreversibly binds COX, platelets cannot produce more but endothelial cells can (as have nucleus).
Clopidogrel - irreversibly blocks ADP receptor P2Y12.
Secondary Haemostasis factors?
TF + VIIa = IX -> IXa + X -> Xa = II -> IIa
IIa = V -> Va, VIII -> VIIIa, XI -> XIa + platelets
XIa = IX -> IXa
IXa + VIIIa = X -> Xa + II -> IIa
IIa = fibrinogen -> fibrin.
Vitamin K?
Needed for carboxylation of glutamic acid residues in factors II, VII, IX + X
Anticoagulant drugs?
Heparin - potentiates antithrombin which inactivates Xa and IIa.
Warfarin - vitamin K antagonist, reduces synthesis of factors II, VII, IX + X by liver.
Direct oral anti coagulants - inhibit thrombin or factor Xa.