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

1
Q

what are the components of blood

A

formed elements 45%
plasma 55%
buffy coat - less than 1%

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2
Q

what are the components of the formed elements

A

WBC- leukocytes
RBC-erythrocytes
platelets-thrombocytes

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3
Q

what is the density separation of the components of blood when doing a blood test

A

erythrocytes is the heaviest
buffy coat
plasma lightest

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4
Q

what is the function of blood

A

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

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5
Q

what is the components of plasma

A
90% water 
8% solutes such as proteins-albumin(60%, alpha beta globulins, gamma globulins and fibrinogens 
gas 
electrolytes 
organic nutrients 
hormones 
and metabolic waste
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6
Q

what is haematopoiesis

A

the process where hemocytoblasts give rise to all formed elements

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7
Q

what is another name for hemacytoblasts

A

pluripotent hemopoietic stem cells

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8
Q

what controls which cell is formed via differentiation

A

hormones and growth factors push the cell towards a certain pathway

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9
Q

why are hemacytoblasts rarely seen in blood films and cytology

A

as they are easily broken

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10
Q

what are the two pathways from the hemacytoblast cells

A

lymphoid pathway and the myeloid pathway

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11
Q

what cells form from the myeloid pathway

A

erythrocyte
mast cell
myeloblast
megakaryoyte

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12
Q

what cells form from megakaryocytic

A

thrombocytes/platelets

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13
Q

what cells form from myeloblast

A

basophil
neutrophil
eosinophil
monocyte- precursor of the macrophage

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14
Q

what is a monocyte

A

the precursor of the macrophage

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15
Q

which cells from from the lymphoid cells

A

NK cells

and small lymphocyte

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16
Q

what forms from lymphocytes

A

b lymphocytes-plasma cell

t lymphocytes

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17
Q

describe erythrocytes

A

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

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18
Q

where are RBC reproduced

A

hematopoiesis in bone- pelvis, cranium vertebrae and the sternum

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19
Q

why are the cells bioconcave

A

for increased SA and flexibility

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20
Q

what is the lifespan of RBC

A

100-120 days destroyed by macrophages in the spleen liver and bone marrow

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21
Q

how do red blood cells from

A

need vitamins b12, b9

  1. hemocytoblast–> 2.common myeloid proginator
  2. unipotent stem cells
  3. pronomoblast
  4. early normoblast
  5. intermediate normoblast
  6. late normoblast
  7. bone marrow
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22
Q

what happens as a RBC matures

A

the cell size decreases- with RNA and DNA decreasing and the colour changes from blue to red

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23
Q

what vitamins are needed in erythropoiesis

A

vitamins b9(biotin) and b12( cobalamin)

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24
Q

what happens to the RBC as it leaves the bone marrow

A

the nuclei are lost and destroyed by macrophages

it then forms a reticulocyte

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25
what is a reticulocyte
it is the immature RBC which is 1% of circulating cells
26
how long does it take for a reticulocyte to mature into a erythrocyte
1-2 days
27
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
28
What is erythropoietin
it is a hormone secreted by the kidney due to the degradation of erythrocytes
29
why is erythropoietin released
due to hypoxia- can be secondary to haemorrhage, loss of RBC, insufficient haemoglobin and increased demands of 02
30
what does testosterone do to erythropoietin levels
enhances production and therefore males have more RBC
31
describe red cell death
1. the macrophage engulfs the RBC and breaks it down into globin and haem 2. the globin is broken down into AA which can be reused 3. haem is broken down into Biliveridin and Fe3+( which is bound to transferrin) 4. the transferrin travels to the liver where it is converted into ferritin and then reconverted into transferrin for erythropoiesis
32
what happens to the biliveridin during red cell death
1. converted into bilirubin in macrophage 2. transported to liver and then LI 3. in LI, bilirubin is changed by bacteria to urobilinogen 4. this becomes urobilin in kidney and stercobilin in intestines 5. urobilin excreted through urine and stercobilin through faecal matter
33
what is anaemia
the decrease in the number of RBC- or less than the normal quantity of haemoglobin in the blood
34
why might people be anaemic
XS blood loss XS red cell destruction deficient red cell production
35
what are common causes of iron deficient anaemia
``` blood loss malabsorption pregnancy dietary deficiency parasites ```
36
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 ```
37
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
38
what are the causes of pernicious anaemia
autoimmune tapeworm poor diet celiac
39
what are the symptoms of pernicious anaemia
``` tiredness parasthesia dyspepsia glossitis angular cheilitis ```
40
what is dyspepsia
indigestion
41
what is parasthesia
abnormal sensation of the skin with no apparent physical cause.
42
how is pernicious anaemia treated
oral supplements and intramuscular B12 injections
43
what re the two type of haemoglobinopathies we will discuss
``` sickle cell ( qualitative) thalassaemia( quantitative) ```
44
what is the life span of sickle cells or RBC with thalassaemia
10-20 days
45
what happens if there is greater RBC DESTRUCTION than RBC production for a long time
haemolytic anaemia
46
what is normal haemoglobin(A) made from
2 alpha chain and 2 beta chains
47
what are the two alpha chains in normal haemoglobin coded by
chromosome 16
48
what are the two beta chains in normal haemoglobin coded by
chromosome 11
49
describe haemoglobin A2
where the haemoglobin has two ALPHA chains and 2 delta chains
50
what is haemoglobin F
where the haemoglobin has two ALPHA chains and 2 FOETAL chains
51
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
52
what mutation occurs in sickle cell anaemia
substitution from glutamine to valine at position 6 of chromosome 11
53
what do heterozygote people with sickle cell anaemia have
protection against malaria
54
what can you be treated with for sickle cell anaemia
hydroxyurea which produces HbF and forms foetal haemoglobin instead of the sickle shape
55
what can you be treated with for sickle cell anaemia
hydroxyurea which produces HbF and forms foetal haemoglobin instead of the sickle shape
56
what are the two types of thalasseaemia
alpha thalassaemia | beta thalassaemia
57
describe alpha thalassaemia
XS beta units- excess of the normally
58
describe beta thalassaemia
XS alpha units | due to reduction in the production of B unit
59
what happens in both types of thalassaemia
produced units clump together and prevent oxygen being taken up and removed effectively
60
how many genes is the alpha unit made up from
2 genes therefore 4 alleles-
61
what happens if 1 allele is lost in alpha thalassaemia
no issue
62
what happens if 2 allele is lost in alpha thalassaemia
mild anaemia/microcytosis
63
what happens if 3 allele is lost in alpha thalassaemia
severe anaemia
64
what happens if 4 allele is lost in alpha thalassaemia
incompatible with life
65
how many genes is beta thalassaemia coded by
1 gene- therefore two alleles | variable severity
66
how many white blood cells
400-11000 cells per mm3
67
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 ```
68
what is increased WBC count called
leukocytosis
69
what is decreased WBC count called
leukopenia
70
when is leukocytosis seen
``` infections autoimmune disease exercise stress allergies neoplasia- tumours ```
71
when is leukopenia seen
chemotx radiotx HIV/AIDS
72
what is the nucleus shape in neutrophils
multi lobed
73
what is the nucleus shape in lymphocytes
deeply stained | eccentric
74
what is the nucleus shape in monocytes
kidney shaped
75
what is the nucleus shaped in eosinophils
bi lobed
76
what is the nucleus shape of basophils
BI-TRI LOBED
77
what is the main target of neutrophils
fungi | bacteria
78
what is the main target of monocytes
migrate to tissue to become macrophages
79
what is the main target for eosinophils
allergic inflammatory response and parasites
80
what is the main target for basophils
release histamine for inflammatory response
81
what is the lifetime of neutrophils
6 days- few hours
82
what is the lifetime of lymphocytes
years for memory cells- weeks for other
83
what is the lifespan for monocytes
hours days
84
what is the lifespan for eosinophils
8-12 days
85
what is the lifespan for basophils
a few hours/days
86
what is diapedesis
how WBC leave the blood stream to fight infection
87
what is the steps of diapedesis
1. chemoattraction 2. rolling adhesion 3, tight adhesion 4. transmigration
88
what are platelets
small fragments of megakaryocytes blue staining outer region with purple granules biconcave shapes 2-3 micro metres
89
what is the formation of platelets regulated by
thromopoietin
90
what is contained in platelet granules
``` serotonin calcium ions enzymes ADP and platelet derived growth factor ```
91
what is the normal ration of platelets to RBC
1.1-1.2:1 RBC
92
what happens during haemostasis
1. vessel injury 2. vascular spasm- reducing blood flow 3. platelet plug formation 4. coagulation
93
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.
94
what is platelet plug formation regulated by
Von willebrand factor found in plasma
95
how is the blood clot reinforced
transformation og soluble fibrinogen to insoluble fibrin
96
how is clotting activated
by 2 different pathways
97
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
98
what factors foes the intrinsic factor include
ix xi VIII VII
99
what is the extrinsic pathway
activated by external trauma | quicker pathway and involves factor VII
100
what factor is involved in extrinsic pathway
VII
101
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
102
what is ITP
idiopathic form of thrombocytopenia- idiopathic thrombocytopenia purpura
103
describe liver function impairment
impairs ability to produce procoagulants eg vitamin K causes vitamin K deficiency, hepatitis, cirrhosis injury
104
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
105
what is the types of vitamin K
K1 | K2
106
WHICH form of vitamin K is better absorbed
K2
107
where is vitamin K1 found
kale spinach | cabbage
108
where is k2 found
synthesised by bacteria in the animal gut
109
what do we use to reverse a warfarin overdose
vitamin K
110
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 ```
111
what is type 1 von willebrand disease
autosomal dominant least severe
112
what is type 2 von willebrand disease
autosomal dominant
113
what is type 3 von willebrand disease
autosomal recessive most severe
114
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
115
how are haemophiliacs treated
with plasma transfusions and injection of missing factors
116
describe haemophilia A
factor VIII deficiency degrees of severity X linked recessive 1/5000 males
117
describe haemophilia B/ christmas disease
factor IX deficiency degrees of severity 1/30000 males
118
how do we categories blood types
presence of two major antigens A+B
119
if you have blood type A what antigen and antibody would you have
antigen A and anti B
120
if you have blood type B what antigen and antibody would you have
antigen B and anti A
121
if you have blood type AB what antigen and antibody would you have
no antibody and antigen A+B
122
if you have blood type O what antigen and antibody would you have
antibody A+B but no antigen
123
what is the genotype for blood type A
IA IA OR IA and IO
124
what is the genotype for blood type b
IB IB or IB and IO
125
what is the genotype for blood type Ab
IA IB
126
what is the genotype for blood type O
IO IO
127
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
128
when do we test for the rhoGAM
28 weeks