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 (133 cards)

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
what vitamins are needed in erythropoiesis
vitamins b9(biotin) and b12( cobalamin)
26
what happens to the RBC as it leaves the bone marrow
the nuclei are lost and destroyed by macrophages | it then forms a reticulocyte
27
what is a reticulocyte
it is the immature RBC which is 1% of circulating cells
28
how long does it take for a reticulocyte to mature into a erythrocyte
1-2 days
29
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
30
What is erythropoietin
it is a hormone secreted by the kidney due to the degradation of erythrocytes
31
why is erythropoietin released
due to hypoxia- can be secondary to haemorrhage, loss of RBC, insufficient haemoglobin and increased demands of 02
32
what does testosterone do to erythropoietin levels
enhances production and therefore males have more RBC
33
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
34
what happens to the biliveridin during red cell death
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
35
what is anaemia
the decrease in the number of RBC- or less than the normal quantity of haemoglobin in the blood
36
why might people be anaemic
XS blood loss XS red cell destruction deficient red cell production
37
what are common causes of iron deficient anaemia
``` blood loss malabsorption pregnancy dietary deficiency parasites ```
38
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 ```
39
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
40
what are the causes of pernicious anaemia
autoimmune tapeworm poor diet celiac
41
what are the symptoms of pernicious anaemia
``` tiredness parasthesia dyspepsia glossitis angular cheilitis ```
42
what is dyspepsia
indigestion
43
what is parasthesia
abnormal sensation of the skin with no apparent physical cause.
44
how is pernicious anaemia treated
oral supplements and intramuscular B12 injections
45
what re the two type of haemoglobinopathies we will discuss
``` sickle cell ( qualitative) thalassaemia( quantitative) ```
46
what is the life span of sickle cells or RBC with thalassaemia
10-20 days
47
what happens if there is greater RBC DESTRUCTION than RBC production for a long time
haemolytic anaemia
48
what is normal haemoglobin(A) made from
2 alpha chain and 2 beta chains
49
what are the two alpha chains in normal haemoglobin coded by
chromosome 16
50
what are the two beta chains in normal haemoglobin coded by
chromosome 11
51
describe haemoglobin A2
where the haemoglobin has two ALPHA chains and 2 delta chains
52
what is haemoglobin F
where the haemoglobin has two ALPHA chains and 2 FOETAL chains
53
what happens to the haemoglobin in sickle cell anaemia
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
54
what mutation occurs in sickle cell anaemia
substitution from glutamine to valine at position 6 of chromosome 11
55
what do heterozygote people with sickle cell anaemia have
protection against malaria
56
what can you be treated with for sickle cell anaemia
hydroxyurea which produces HbF and forms foetal haemoglobin instead of the sickle shape
57
what can you be treated with for sickle cell anaemia
hydroxyurea which produces HbF and forms foetal haemoglobin instead of the sickle shape
58
what are the two types of thalasseaemia
alpha thalassaemia | beta thalassaemia
59
describe alpha thalassaemia
XS beta units- excess of the normally
60
describe beta thalassaemia
XS alpha units | due to reduction in the production of B unit
61
what happens in both types of thalassaemia
produced units clump together and prevent oxygen being taken up and removed effectively
62
how many genes is the alpha unit made up from
2 genes therefore 4 alleles-
63
what happens if 1 allele is lost in alpha thalassaemia
no issue
64
what happens if 2 allele is lost in alpha thalassaemia
mild anaemia/microcytosis
65
what happens if 3 allele is lost in alpha thalassaemia
severe anaemia
66
what happens if 4 allele is lost in alpha thalassaemia
incompatible with life
67
how many genes is beta thalassaemia coded by
1 gene- therefore two alleles | variable severity
68
describe white blood cells
400-11000 cells per mm3
69
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 ```
70
what is increased WBC count called
leukocytosis
71
what is decreased WBC count called
leukopenia
72
when is leukocytosis seen
``` infections autoimmune disease exercise stress allergies neoplasia- tumours ```
73
when is leukopenia seen
chemotx radiotx HIV/AIDS
74
what is the nucleus shape in neutrophils
multi lobed
75
what is the nucleus shape in lymphocytes
deeply stained | eccentric
76
what is the nucleus shape in monocytes
kidney shaped
77
what is the nucleus shaped in eosinophils
bi lobed
78
what is the nucleus shape of basophils
BI-TRI LOBED
79
what is the main target of neutrophils
fungi | bacteria
80
what is the main target of monocytes
migrate to tissue to become macrophages
81
what is the main target for eosinophils
allergic inflammatory response and parasites
82
what is the main target for basophils
release histamine for inflammatory response
83
what is the lifetime of neutrophils
6 days- few hours
84
what is the lifetime of lymphocytes
years for memory cells- weeks for other
85
what is the lifespan for monocytes
hours days
86
what is the lifespan for eosinophils
8-12 days
87
what is the lifespan for basophils
a few hours/days
88
what is diapedesis
how WBC leave the blood stream to fight infection
89
what is the steps of diapedesis
1. chemoattraction 2. rolling adhesion 3, tight adhesion 4. transmigration
90
what are platelets
small fragments of megakaryocytes blue staining outer region with purple granules biconcave shapes 2-3 micro metres
91
what is the formation of platelets regulated by
thromopoietin
92
what is contained in platelet granules
``` serotonin calcium ions enzymes ADP and platelet derived growth factor ```
93
what is the normal ration of platelets to RBC
1.1-1.2:1 RBC
94
what happens during haemostasis
1. vessel injury 2. vascular spasm- reducing blood flow 3. platelet plug formation 4. coagulation
95
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.
96
what is platelet plug formation regulated by
Von willebrand factor found in plasma
97
how is the blood clot reinforced
transformation og soluble fibrinogen to insoluble fibrin
98
how is clotting activated
by 2 different pathways
99
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
100
what factors foes the intrinsic factor include
ix xi VIII VII
101
what is the extrinsic pathway
activated by external trauma | quicker pathway and involves factor VII
102
what factor is involved in extrinsic pathway
VII
103
what bleeding disorders will we discuss
thrombocytopenia clotting factor deficiency impaired liver function von villebrand disease
104
describe thrombocytopenia
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
what is ITP
idiopathic form of thrombocytopenia- idiopathic thrombocytopenia purpura
106
describe liver function impairment
impairs ability to produce procoagulants eg vitamin K causes vitamin K deficiency, hepatitis, cirrhosis injury
107
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
108
what is the types of vitamin K
K1 | K2
109
WHICH form of vitamin K is better absorbed
K2
110
where is vitamin K1 found
kale spinach | cabbage
111
where is k2 found
synthesised by bacteria in the animal gut
112
what do we use to reverse a warfarin overdose
vitamin K
113
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 ```
114
what is type 1 von willebrand disease
autosomal dominant least severe
115
what is type 2 von willebrand disease
autosomal dominant
116
what is type 3 von willebrand disease
autosomal recessive most severe
117
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
118
how are haemophiliacs treated
with plasma transfusions and injection of missing factors
119
describe haemophilia A
factor VIII deficiency degrees of severity X linked recessive 1/5000 males
120
describe haemophilia B/ christmas disease
factor IX deficiency degrees of severity 1/30000 males
121
how many males have type 1 haemophilia
1/5000
122
how do we categories blood types
presence of two major antigens A+B
123
if you have blood type A what antigen and antibody would you have
antigen A and anti B
124
if you have blood type B what antigen and antibody would you have
antigen B and anti A
125
if you have blood type AB what antigen and antibody would you have
no antibody and antigen A+B
126
if you have blood type O what antigen and antibody would you have
antibody A+B but no antigen
127
what is the genotype for blood type A
IA IA OR IA and IO
128
what is the genotype for blood type b
IB IB or IB and IO
129
what is the genotype for blood type Ab
IA IB
130
what is the genotype for blood type O
IO IO
131
what percentage of the population is rhesus +ve
85%
132
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
133
when do we test for the rhoGAM
28 weeks