blood lectures Flashcards
polycythaemia vera?
bone marrow tumours, cause of polycythaemia (high haematocrit)
iron absorption?
riboflavin
Hb synthesis?
vitamin B12, Folic acid
absolute erythrocytosis? (polycythaemia)
raised red cell mass, normal plasma volume
apparent erythrocytosis? (polycythaemia)
normal red cell mass, reduced plasma volume
plasma proteins? where synthesised?
about 8% of plasma volume. most synthesised by liver
albumin?
60% of plasma protein, largely responsible for plasma osmotic pressure
carbon dioxide in plasma?
significant fraction found there in form of bicarbonate
erythrocyte amound, diameter and size?
5billion/ml of blood
8micrometres
2micrometres
capillaries?
99% of bodies total blood vessels. only hold 5% of blood
RBC count in normal adult?
25-30 trillion
first, second and final site of haematopoiesis?
1 - yolk sac
2- liver/spleen
3- bone marrow
control of erythropoiesis?
kidneys detect reduced o2 carrying capacity, they secrete erythropoietin into the blood.
co2 and erythrocytes?
carbonic anhydrase catalyses co2 + h20 to carbonic acid
Hb affinity for CO compared to o2?
240x greater
Hb and NO?
binds to Hb in lungs and is released into tissues, it is a vasodilator - relaxes and dilates the arterioles.
making RBC’s?
iron comes in diet
Fe absobed by active transport
transferrin protein transports it in plasma to bone marrow
made into heme/ hb then RBC’s
Hb breakdown releases?
bilirubin - contributes to bile
what responsible for monitoring o2 levels?
kidneys
haemostasis?
mechanism to stop bleeding
3 stages of haemostasis?
vascular spasm
formation of platelet plug (thrombus)
formation of blood clot
embolus?
blood clot that has broken loose into circulation
organelles that platelets have?
mitochondria
SER
cytoplasmic granules
von willibrand factor secreted by?
megakaryocytes
von willibrand factor upon damage?
binds to exposed collagen, platelets then bind to vWf
what do platelets do after binding to vWf?
they secrete serotonin, ADP and epinephrine
the ADP causes production of thromboxane A2 which further promotes platelet aggregation
what stops platelets blocking healthy vessels?
healthy endothelium releases prostacyclin and nitric acid which prevent platelet plug formation.
fibrin clot formation?
secondary to platelet plug
requires activated platelets and their secretory procucts
removing a clot?
factor XII simultaneously activates a cascade that triggers clotting and a cascade that triggers plasmin activation.
plasmin trapped in the clot slowly dissolves it.
endothelial cells release what anticoagulants?
heparin and antithrombin III
haemophilia A?
factor VIII deficiency
haemophilia B?
factor IX deficiency
lymphatic primary tissues?
bone marrow and thymus
NK cells?
eliminate virus infected and tumour cells
role interferon alpha and beta (secreted by NK cells)?
prevent viral replication
role interferon gamma (NK cells)?
activates macrophages
inflammatory response, histamines?
from mast cells
swelling, edema and vasodilation
inflammatory response, interleukins?
make blood vessels more permeable to WBCs and proteins
inflammatory response, bradykinin?
pain and swelling
membrane attack complex?
complement proteins insert themselves into the membrane of pathogens creating a pore
water and solutes enter through pore
cell swells and lyses
IgM?
primary immune response and blood group antigens.
IgE?
allergic response
IgA?
disable pathogens before they reach internal environmet
found in tears, saliva etc
IgG?
produced in second immune response
MHC class 1?
all nucleated cells
cytotoxic T
MHC clas 2?
macrophages, B lympocytes and dendritic cells
helper T
T cells released from?
thymus gland
rhesus issue?
rhesus negative mother with rhesus positive child may develop antibodies against rh+ blood, this is fine.
if second pregnancy occurs, the memory of rh+ antibodies will generate them and they can cross the placenta causing anaemia to child.
coagulation disorders causes?
vitamin K deficiency low platelets liver disease (hepatitis, cirrhosis)
sickle cell amino acid change?
glutamate to valine
sickle cell problem?
RBCs crystallize when releasing o2 and form sickle shape, the cells then tangle together and cause tissue damage and pain from hypoxia
leukaemia?
cancers of the blood forming tissues
acute v chronic leukaemia?
acute - rapid growth/ progression
chronic - slower progression
majority of acute leukaemias involve?
chromosomal translocations
graft v host disease?
following marrow transplant
acute - T-cells present in donor marrow attack host cells
chronic - T-cells produced by donor cells after marrow has engrafted.