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 
80% 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

pluripotential hemopoietic stem calls

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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

how many RBC are in males

A

4.7-6.1 million per microlitre of blood

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19
Q

how many RBC are in females

A

4.2-5.4 million per microlitre of blood

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20
Q

where are RBC reproduced

A

hematopoiesis in bone- pelvis, cranium vertebrae and the sternum

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21
Q

why are the cells bioconcave

A

for increased SA and flexibility

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22
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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23
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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24
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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25
Q

what vitamins are needed in erythropoiesis

A

vitamins b9(biotin) and b12( cobalamin)

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26
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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27
Q

what is a reticulocyte

A

it is the immature RBC which is 1% of circulating cells

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28
Q

how long does it take for a reticulocyte to mature into a erythrocyte

A

1-2 days

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29
Q

what do erythrocytes release when destroyed by macrophages

A

erythropoietin- is a hormone released by the kidney

starts the feedback loop to differentiate more into RBC

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30
Q

What is erythropoietin

A

it is a hormone secreted by the kidney due to the degradation of erythrocytes

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31
Q

why is erythropoietin released

A

due to hypoxia- can be secondary to haemorrhage, loss of RBC, insufficient haemoglobin and increased demands of 02

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32
Q

what does testosterone do to erythropoietin levels

A

enhances production and therefore males have more RBC

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33
Q

describe red cell death

A
  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
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34
Q

what happens to the biliveridin during red cell death

A
  1. converted into bilirubin which passes into the liver
  2. passed to the kidney
  3. with the help of bacteria is converted into Urobilnogen in the
    LI
  4. then urobilinogen is converted into urobilin in the kidney
  5. uroblinogen is converted into stercobilin in the LI
  6. UROBILIN leaves the kidney as urea
  7. and stercobilin leaves as faeces
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35
Q

what is anaemia

A

the decrease in the number of RBC- or less than the normal quantity of haemoglobin in the blood

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36
Q

why might people be anaemic

A

XS blood loss
XS red cell destruction
deficient red cell production

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37
Q

what are common causes of iron deficient anaemia

A
blood loss 
malabsorption
pregnancy 
dietary deficiency 
parasites
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38
Q

what are the symptoms of iron deficient anaemia

A
tired 
pale 
shake 
irritable 
lightheaded 
poor wound healing 
candida infections
burning mouth syndrome 
glossitis- can be seen with angular chelitis  
RAS- recurrent aphthous stomatitis
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39
Q

what is pernicious anaemia

A

vit B12 deficiency
due to low RBC count
may be due to lack of IF- which leads to less B12 and therefore less RBC

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40
Q

what are the causes of pernicious anaemia

A

autoimmune
tapeworm
poor diet
celiac

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41
Q

what are the symptoms of pernicious anaemia

A
tiredness 
parasthesia 
dyspepsia 
glossitis 
angular cheilitis
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42
Q

what is dyspepsia

A

indigestion

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43
Q

what is parasthesia

A

abnormal sensation of the skin with no apparent physical cause.

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44
Q

how is pernicious anaemia treated

A

oral supplements and intramuscular B12 injections

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45
Q

what re the two type of haemoglobinopathies we will discuss

A
sickle cell ( qualitative) 
thalassaemia( quantitative)
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46
Q

what is the life span of sickle cells or RBC with thalassaemia

A

10-20 days

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47
Q

what happens if there is greater RBC DESTRUCTION than RBC production for a long time

A

haemolytic anaemia

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48
Q

what is normal haemoglobin(A) made from

A

2 alpha chain and 2 beta chains

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49
Q

what are the two alpha chains in normal haemoglobin coded by

A

chromosome 16

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50
Q

what are the two beta chains in normal haemoglobin coded by

A

chromosome 11

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51
Q

describe haemoglobin A2

A

where the haemoglobin has two ALPHA chains and 2 delta chains

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52
Q

what is haemoglobin F

A

where the haemoglobin has two ALPHA chains and 2 FOETAL chains

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53
Q

what happens to the haemoglobin in sickle cell anaemia

A

the beta stands have a genetic mutation and there is a substitution at position 6 from glutamine to valine which forms a sickle component rather than the beta chain- leading to polymerisation and shrinkage

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54
Q

what mutation occurs in sickle cell anaemia

A

substitution from glutamine to valine at position 6 of chromosome 11

55
Q

what do heterozygote people with sickle cell anaemia have

A

protection against malaria

56
Q

what can you be treated with for sickle cell anaemia

A

hydroxyurea which produces HbF and forms foetal haemoglobin instead of the sickle shape

57
Q

what can you be treated with for sickle cell anaemia

A

hydroxyurea which produces HbF and forms foetal haemoglobin instead of the sickle shape

58
Q

what are the two types of thalasseaemia

A

alpha thalassaemia

beta thalassaemia

59
Q

describe alpha thalassaemia

A

XS beta units- excess of the normally

60
Q

describe beta thalassaemia

A

XS alpha units

due to reduction in the production of B unit

61
Q

what happens in both types of thalassaemia

A

produced units clump together and prevent oxygen being taken up and removed effectively

62
Q

how many genes is the alpha unit made up from

A

2 genes therefore 4 alleles-

63
Q

what happens if 1 allele is lost in alpha thalassaemia

A

no issue

64
Q

what happens if 2 allele is lost in alpha thalassaemia

A

mild anaemia/microcytosis

65
Q

what happens if 3 allele is lost in alpha thalassaemia

A

severe anaemia

66
Q

what happens if 4 allele is lost in alpha thalassaemia

A

incompatible with life

67
Q

how many genes is beta thalassaemia coded by

A

1 gene- therefore two alleles

variable severity

68
Q

describe white blood cells

A

400-11000 cells per mm3

69
Q

what is the order from greatest to least of leukocytes

A
neutrophils 65%
lymphocytes 25%
monocytes 6%
eosinophils 3%
basophils 1%
Never let monkeys eat bananas
70
Q

what is increased WBC count called

A

leukocytosis

71
Q

what is decreased WBC count called

A

leukopenia

72
Q

when is leukocytosis seen

A
infections 
autoimmune disease 
exercise 
stress
allergies 
neoplasia- tumours
73
Q

when is leukopenia seen

A

chemotx
radiotx
HIV/AIDS

74
Q

what is the nucleus shape in neutrophils

A

multi lobed

75
Q

what is the nucleus shape in lymphocytes

A

deeply stained

eccentric

76
Q

what is the nucleus shape in monocytes

A

kidney shaped

77
Q

what is the nucleus shaped in eosinophils

A

bi lobed

78
Q

what is the nucleus shape of basophils

A

BI-TRI LOBED

79
Q

what is the main target of neutrophils

A

fungi

bacteria

80
Q

what is the main target of monocytes

A

migrate to tissue to become macrophages

81
Q

what is the main target for eosinophils

A

allergic inflammatory response and parasites

82
Q

what is the main target for basophils

A

release histamine for inflammatory response

83
Q

what is the lifetime of neutrophils

A

6 days- few hours

84
Q

what is the lifetime of lymphocytes

A

years for memory cells- weeks for other

85
Q

what is the lifespan for monocytes

A

hours days

86
Q

what is the lifespan for eosinophils

A

8-12 days

87
Q

what is the lifespan for basophils

A

a few hours/days

88
Q

what is diapedesis

A

how WBC leave the blood stream to fight infection

89
Q

what is the steps of diapedesis

A
  1. chemoattraction
  2. rolling adhesion
    3, tight adhesion
  3. transmigration
90
Q

what are platelets

A

small fragments of megakaryocytes
blue staining outer region with purple granules
biconcave shapes
2-3 micro metres

91
Q

what is the formation of platelets regulated by

A

thromopoietin

92
Q

what is contained in platelet granules

A
serotonin 
calcium ions 
enzymes 
ADP 
and platelet derived growth factor
93
Q

what is the normal ration of platelets to RBC

A

1.1-1.2:1 RBC

94
Q

what happens during haemostasis

A
  1. vessel injury
  2. vascular spasm- reducing blood flow
  3. platelet plug formation
  4. coagulation
95
Q

describe what happens in platelet plug formation

A

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.

96
Q

what is platelet plug formation regulated by

A

Von willebrand factor found in plasma

97
Q

how is the blood clot reinforced

A

transformation og soluble fibrinogen to insoluble fibrin

98
Q

how is clotting activated

A

by 2 different pathways

99
Q

what is the intrinsic pathway

A

activated by trauma inside the vascular system- exposed endothelium,chemicals collagen etc
it is slower and involves factors VII,XI,IX, VIII

100
Q

what factors foes the intrinsic factor include

A

ix
xi
VIII
VII

101
Q

what is the extrinsic pathway

A

activated by external trauma

quicker pathway and involves factor VII

102
Q

what factor is involved in extrinsic pathway

A

VII

103
Q

what bleeding disorders will we discuss

A

thrombocytopenia
clotting factor deficiency
impaired liver function
von villebrand disease

104
Q

describe thrombocytopenia

A

too few platelets
causes spontaneous bleeding
due to suppression or destruction fo bone marrow
with a platelet count of less than 50000 mm3
treated by transfusion of platelets
can be idiopathic (ITP)

105
Q

what is ITP

A

idiopathic form of thrombocytopenia- idiopathic thrombocytopenia purpura

106
Q

describe liver function impairment

A

impairs ability to produce procoagulants eg vitamin K
causes vitamin K deficiency, hepatitis, cirrhosis
injury

107
Q

what is vitamin K necessary for

A

PROTHROMBIN
factor VII,IX,X
synthesis of coagulation factors
Allows binding of ca to some coagulaton factors
Caroboxylises glutamate residues in protein

108
Q

what is the types of vitamin K

A

K1

K2

109
Q

WHICH form of vitamin K is better absorbed

A

K2

110
Q

where is vitamin K1 found

A

kale spinach

cabbage

111
Q

where is k2 found

A

synthesised by bacteria in the animal gut

112
Q

what do we use to reverse a warfarin overdose

A

vitamin K

113
Q

describe von willebrand disease

A
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
114
Q

what is type 1 von willebrand disease

A

autosomal dominant least severe

115
Q

what is type 2 von willebrand disease

A

autosomal dominant

116
Q

what is type 3 von willebrand disease

A

autosomal recessive most severe

117
Q

what does von willebrand do

A

binds to factor VIII in circulation and circulates in the blood for a much longer time
forms links between platelets and vessel wall collagen

118
Q

how are haemophiliacs treated

A

with plasma transfusions and injection of missing factors

119
Q

describe haemophilia A

A

factor VIII deficiency
degrees of severity
X linked recessive
1/5000 males

120
Q

describe haemophilia B/ christmas disease

A

factor IX deficiency
degrees of severity
1/30000 males

121
Q

how many males have type 1 haemophilia

A

1/5000

122
Q

how do we categories blood types

A

presence of two major antigens A+B

123
Q

if you have blood type A what antigen and antibody would you have

A

antigen A and anti B

124
Q

if you have blood type B what antigen and antibody would you have

A

antigen B and anti A

125
Q

if you have blood type AB what antigen and antibody would you have

A

no antibody and antigen A+B

126
Q

if you have blood type O what antigen and antibody would you have

A

antibody A+B but no antigen

127
Q

what is the genotype for blood type A

A

IA IA OR IA and IO

128
Q

what is the genotype for blood type b

A

IB IB or IB and IO

129
Q

what is the genotype for blood type Ab

A

IA IB

130
Q

what is the genotype for blood type O

A

IO IO

131
Q

what percentage of the population is rhesus +ve

A

85%

132
Q

what is haemolytic disease of newborns

A

if the mother is rhesus negative and the baby is rhesus positive the mother can attack foetal blood cells causing haemolytic anaemia

133
Q

when do we test for the rhoGAM

A

28 weeks