physiology of blood Flashcards
RBC- function, production,destruction,morphology and associated disease WBC- function production and morphology platelets clotting and disorders blood groups plasma function and components
what are the components of blood
formed elements 45%
plasma 55%
buffy coat - less than 1%
what are the components of the formed elements
WBC- leukocytes
RBC-erythrocytes
platelets-thrombocytes
what is the density separation of the components of blood when doing a blood test
erythrocytes is the heaviest
buffy coat
plasma lightest
what is the function of blood
carries oxygen
removes carbon dioxide
transport of hormone and nutrients
clotting factors- important so we don’t loose fluid and bleed to death
Maintain temp,ph,fluid volume- homeostasis
Protection from fluid loss
Prevent infection- leukocytes and antibodies
Transportation of waste products eg urea
what is the components of plasma
90% water 8% solutes such as proteins-albumin(60%, alpha beta globulins, gamma globulins and fibrinogens gas electrolytes organic nutrients hormones and metabolic waste
what is haematopoiesis
the process where hemocytoblasts give rise to all formed elements
what is another name for hemacytoblasts
pluripotent hemopoietic stem cells
what controls which cell is formed via differentiation
hormones and growth factors push the cell towards a certain pathway
why are hemacytoblasts rarely seen in blood films and cytology
as they are easily broken
what are the two pathways from the hemacytoblast cells
lymphoid pathway and the myeloid pathway
what cells form from the myeloid pathway
erythrocyte
mast cell
myeloblast
megakaryoyte
what cells form from megakaryocytic
thrombocytes/platelets
what cells form from myeloblast
basophil
neutrophil
eosinophil
monocyte- precursor of the macrophage
what is a monocyte
the precursor of the macrophage
which cells from from the lymphoid cells
NK cells
and small lymphocyte
what forms from lymphocytes
b lymphocytes-plasma cell
t lymphocytes
describe erythrocytes
contain haemoglobin which transport respiratory gases
males have more than female
7.5 micrometres in diameter- capillaries is 8 micrometers
lack mitochondria
lack nucleus- increased space for haemoglobin
biconcave- for increase SA and flexibility
reproduced by hematopoiesis in bone
where are RBC reproduced
hematopoiesis in bone- pelvis, cranium vertebrae and the sternum
why are the cells bioconcave
for increased SA and flexibility
what is the lifespan of RBC
100-120 days destroyed by macrophages in the spleen liver and bone marrow
how do red blood cells from
need vitamins b12, b9
- hemocytoblast–> 2.common myeloid proginator
- unipotent stem cells
- pronomoblast
- early normoblast
- intermediate normoblast
- late normoblast
- bone marrow
what happens as a RBC matures
the cell size decreases- with RNA and DNA decreasing and the colour changes from blue to red
what vitamins are needed in erythropoiesis
vitamins b9(biotin) and b12( cobalamin)
what happens to the RBC as it leaves the bone marrow
the nuclei are lost and destroyed by macrophages
it then forms a reticulocyte
what is a reticulocyte
it is the immature RBC which is 1% of circulating cells
how long does it take for a reticulocyte to mature into a erythrocyte
1-2 days
what do erythrocytes release when destroyed by macrophages
erythropoietin- is a hormone released by the kidney
starts the feedback loop to differentiate more into RBC
What is erythropoietin
it is a hormone secreted by the kidney due to the degradation of erythrocytes
why is erythropoietin released
due to hypoxia- can be secondary to haemorrhage, loss of RBC, insufficient haemoglobin and increased demands of 02
what does testosterone do to erythropoietin levels
enhances production and therefore males have more RBC
describe red cell death
- the macrophage engulfs the RBC and breaks it down into globin and haem
- the globin is broken down into AA which can be reused
- haem is broken down into Biliveridin and Fe3+( which is bound to transferrin)
- the transferrin travels to the liver where it is converted into ferritin and then reconverted into transferrin for erythropoiesis
what happens to the biliveridin during red cell death
- converted into bilirubin in macrophage
- transported to liver and then LI
- in LI, bilirubin is changed by bacteria to urobilinogen
- this becomes urobilin in kidney and stercobilin in intestines
- urobilin excreted through urine and stercobilin through faecal matter
what is anaemia
the decrease in the number of RBC- or less than the normal quantity of haemoglobin in the blood
why might people be anaemic
XS blood loss
XS red cell destruction
deficient red cell production
what are common causes of iron deficient anaemia
blood loss malabsorption pregnancy dietary deficiency parasites
what are the symptoms of iron deficient anaemia
tired pale shake irritable lightheaded poor wound healing candida infections burning mouth syndrome glossitis- can be seen with angular chelitis RAS- recurrent aphthous stomatitis
what is pernicious anaemia
vit B12 deficiency
due to low RBC count
may be due to lack of IF- which leads to less B12 and therefore less RBC
what are the causes of pernicious anaemia
autoimmune
tapeworm
poor diet
celiac
what are the symptoms of pernicious anaemia
tiredness parasthesia dyspepsia glossitis angular cheilitis
what is dyspepsia
indigestion
what is parasthesia
abnormal sensation of the skin with no apparent physical cause.
how is pernicious anaemia treated
oral supplements and intramuscular B12 injections
what re the two type of haemoglobinopathies we will discuss
sickle cell ( qualitative) thalassaemia( quantitative)
what is the life span of sickle cells or RBC with thalassaemia
10-20 days
what happens if there is greater RBC DESTRUCTION than RBC production for a long time
haemolytic anaemia
what is normal haemoglobin(A) made from
2 alpha chain and 2 beta chains
what are the two alpha chains in normal haemoglobin coded by
chromosome 16
what are the two beta chains in normal haemoglobin coded by
chromosome 11
describe haemoglobin A2
where the haemoglobin has two ALPHA chains and 2 delta chains
what is haemoglobin F
where the haemoglobin has two ALPHA chains and 2 FOETAL chains
what happens to the haemoglobin in sickle cell anaemia
the beta strands have a genetic mutation
there is a substitution at position 6 of chromosome 11 from glutamine to valine which forms a sickle component rather than the beta chain
leads to polymerisation and shrinkage
what mutation occurs in sickle cell anaemia
substitution from glutamine to valine at position 6 of chromosome 11
what do heterozygote people with sickle cell anaemia have
protection against malaria
what can you be treated with for sickle cell anaemia
hydroxyurea which produces HbF and forms foetal haemoglobin instead of the sickle shape
what can you be treated with for sickle cell anaemia
hydroxyurea which produces HbF and forms foetal haemoglobin instead of the sickle shape
what are the two types of thalasseaemia
alpha thalassaemia
beta thalassaemia
describe alpha thalassaemia
XS beta units- excess of the normally
describe beta thalassaemia
XS alpha units
due to reduction in the production of B unit
what happens in both types of thalassaemia
produced units clump together and prevent oxygen being taken up and removed effectively
how many genes is the alpha unit made up from
2 genes therefore 4 alleles-
what happens if 1 allele is lost in alpha thalassaemia
no issue
what happens if 2 allele is lost in alpha thalassaemia
mild anaemia/microcytosis
what happens if 3 allele is lost in alpha thalassaemia
severe anaemia
what happens if 4 allele is lost in alpha thalassaemia
incompatible with life
how many genes is beta thalassaemia coded by
1 gene- therefore two alleles
variable severity
how many white blood cells
400-11000 cells per mm3
what is the order from greatest to least of leukocytes
neutrophils 65% lymphocytes 25% monocytes 6% eosinophils 3% basophils 1% Never let monkeys eat bananas
what is increased WBC count called
leukocytosis
what is decreased WBC count called
leukopenia
when is leukocytosis seen
infections autoimmune disease exercise stress allergies neoplasia- tumours
when is leukopenia seen
chemotx
radiotx
HIV/AIDS
what is the nucleus shape in neutrophils
multi lobed
what is the nucleus shape in lymphocytes
deeply stained
eccentric
what is the nucleus shape in monocytes
kidney shaped
what is the nucleus shaped in eosinophils
bi lobed
what is the nucleus shape of basophils
BI-TRI LOBED
what is the main target of neutrophils
fungi
bacteria
what is the main target of monocytes
migrate to tissue to become macrophages
what is the main target for eosinophils
allergic inflammatory response and parasites
what is the main target for basophils
release histamine for inflammatory response
what is the lifetime of neutrophils
6 days- few hours
what is the lifetime of lymphocytes
years for memory cells- weeks for other
what is the lifespan for monocytes
hours days
what is the lifespan for eosinophils
8-12 days
what is the lifespan for basophils
a few hours/days
what is diapedesis
how WBC leave the blood stream to fight infection
what is the steps of diapedesis
- chemoattraction
- rolling adhesion
3, tight adhesion - transmigration
what are platelets
small fragments of megakaryocytes
blue staining outer region with purple granules
biconcave shapes
2-3 micro metres
what is the formation of platelets regulated by
thromopoietin
what is contained in platelet granules
serotonin calcium ions enzymes ADP and platelet derived growth factor
what is the normal ration of platelets to RBC
1.1-1.2:1 RBC
what happens during haemostasis
- vessel injury
- vascular spasm- reducing blood flow
- platelet plug formation
- coagulation
describe what happens in platelet plug formation
Plug activation is regulated by Von Willebrand factor, found in plasma.
Platelets adhere to the collagen fibers in the wound, becoming spiky and sticky.
They release chemicals (ADP, serotonin), causing more platelets to stick to the plug and cause further vasoconstriction creating a feedback loop
Clotting factors become activated and begin deposition of fibrin, creating a meshwork.
what is platelet plug formation regulated by
Von willebrand factor found in plasma
how is the blood clot reinforced
transformation og soluble fibrinogen to insoluble fibrin
how is clotting activated
by 2 different pathways
what is the intrinsic pathway
activated by trauma inside the vascular system- exposed endothelium,chemicals collagen etc
it is slower and involves factors VII,XI,IX, VIII
what factors foes the intrinsic factor include
ix
xi
VIII
VII
what is the extrinsic pathway
activated by external trauma
quicker pathway and involves factor VII
what factor is involved in extrinsic pathway
VII
describe thrombocytopenia
how is it treated
too few platelets due to suppression or destruction to bone marrow
causes spontaneous bleeding
platelet count of less than 50000 mm3
can be idiopathic (ITP)
treated by transfusion of platelets
what is ITP
idiopathic form of thrombocytopenia- idiopathic thrombocytopenia purpura
describe liver function impairment
impairs ability to produce procoagulants eg vitamin K
causes vitamin K deficiency, hepatitis, cirrhosis
injury
what is vitamin K necessary for
PROTHROMBIN
factor VII,IX,X
synthesis of coagulation factors
Allows binding of ca to some coagulaton factors
Caroboxylises glutamate residues in protein
what is the types of vitamin K
K1
K2
WHICH form of vitamin K is better absorbed
K2
where is vitamin K1 found
kale spinach
cabbage
where is k2 found
synthesised by bacteria in the animal gut
what do we use to reverse a warfarin overdose
vitamin K
describe von willebrand disease
1-2% in the UK type 1 type 2 type 3 platelet type deficiency of von willebrand factor found in plasma and the subendothelial connective tissue
what is type 1 von willebrand disease
autosomal dominant least severe
what is type 2 von willebrand disease
autosomal dominant
what is type 3 von willebrand disease
autosomal recessive most severe
what does von willebrand do
binds to factor VIII in circulation and circulates in the blood for a much longer time
forms links between platelets and vessel wall collagen
how are haemophiliacs treated
with plasma transfusions and injection of missing factors
describe haemophilia A
factor VIII deficiency
degrees of severity
X linked recessive
1/5000 males
describe haemophilia B/ christmas disease
factor IX deficiency
degrees of severity
1/30000 males
how do we categories blood types
presence of two major antigens A+B
if you have blood type A what antigen and antibody would you have
antigen A and anti B
if you have blood type B what antigen and antibody would you have
antigen B and anti A
if you have blood type AB what antigen and antibody would you have
no antibody and antigen A+B
if you have blood type O what antigen and antibody would you have
antibody A+B but no antigen
what is the genotype for blood type A
IA IA OR IA and IO
what is the genotype for blood type b
IB IB or IB and IO
what is the genotype for blood type Ab
IA IB
what is the genotype for blood type O
IO IO
what is haemolytic disease of newborns
if the mother is rhesus negative and the baby is rhesus positive the mother can attack foetal blood cells causing haemolytic anaemia
when do we test for the rhoGAM
28 weeks
