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PSC1002- Physiology > Blood L2-4 > Flashcards

Blood L2-4 Flashcards

1
Q

blood functions

A

gas transport/ exchange
solute distribution
immunity
body temp
blood clot regulation
acid-base homeostasis preservation
BP stability

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2
Q

blood constituents

A

erythrocytes
leukocytes
thrombocytes
soluble materials
plasma
cellular elements

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3
Q

plasma constituents and functions

A

water/ plasma proteins/ globulins/ fibrinogen
thermoregulation
transport

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4
Q

plasma proteins

A

serum albumin > large protein
liver-synthesised
osmotic pressure/ lipid and steroid hormone transport

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5
Q

globulins

A

bind/ transport ions/ hormones/ lipids
immune proteins

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6
Q

electrophoresis function

A

identifies plasma proteins for diagnostics

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7
Q

erythrocytes

A

~35% Hb
primary oxygen transport
80-96 femtolitre volume

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8
Q

microcytic

A

small RBC
found in Fe-deficiency anaemia

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9
Q

macrocytic

A

large RBC
folate-deficiency anaemia

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10
Q

erythropoiesis

A

RBC formation
26 day feedback loop
starts in bone marrow, ends in vessels

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11
Q

cirrhosis
disorder
causes?

A

progressive decrease in plasma production proteins
causes: viral hepatitis, cancer, alcoholism

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12
Q

number oxygen per Hb

A

4

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13
Q

haemoglobin components/ structure

A

4 subunits> 2 alpha, 2 beta
4 Fe-containing haem to reversibly bind O2 molecules

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14
Q

haem

A

iron-containing pigment
porphyrin ring w 1 Fe central atom

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15
Q

4 types of globin

A

alpha (2 genes on ch16)
beta (1 gene on ch11)
delta
gamma

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16
Q

HbA

A

97%
2a 2b

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17
Q

HbA2

A

~2.5%
2a 2delta

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18
Q

HbF

A

foetal
2a 2gamma

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19
Q

Hb binding factors

A

oxygen partial pressure
no. free oxygen binding sites in molecule

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20
Q

2 forms of Hb

A

taut
relaxed

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21
Q

taut Hb

A

decreasing oxygen affinity/ partial pressure
releases oxygen

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22
Q

relaxed Hb

A

increasing oxygen affin/ partial pressure
firm oxygen binding

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23
Q

what does Hb bind to?

A

O2, CO2, H+ of carbonic acid, CO, NO

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24
Q

haemoglobinopathies

A

abnormal globin chain production

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25
Q

thalassemia types

A

minor
intermediate
major

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26
Q

thalassemia

A

decreased production / absence of normal globin chains
defect at gene expression/ recessive
gross deletion of >1 globin genes

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27
Q

sickle cell anaemia

A

Glut-6-val mutation in B sub-unit
therefore polymerises at low partial pressure
causes ischaemia/ infarction
RBC life-span reduction

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28
Q

sickle cell trait

A

heterozygotes
rarely symptomatic

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29
Q

Glucose-6-phosphate

A

rate-limiting enzyme in pentose phosphate pathway required for energy and glutathione production
lacking in sickle cell RBCs

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30
Q

a-thalassemia

A

from India
a-globin deficiency
excess beta chains/ unstable b tetramers

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31
Q

B-thalassemia

A

mediterranean
b-globin deficiency
a chain excess/ no tetramers
RBC membrane damage therefore toxic aggregates at high conc
Fe overload

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32
Q

electrophoresis a-thalassemia

A

decreasing HbA
HbH presence

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33
Q

electrophoresis b-thalassemia

A

decreasing HbB

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34
Q

haemostasis

A

arrest of bleeding from a broken blood vessel

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35
Q

platelets

A

anuclear cell fragments
budded off of megakaryocytes

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36
Q

megakaryocyte

A

large bone marrow cell

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37
Q

thrombopoietin

A

hormone produced in liver/ kidney regualting megakryocyte/ platelet production
stimulates megakaryocytic extended arm via bone marrow sinusoids to vessels

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38
Q

no. platelets per megakaryocyte

A

1000-3000

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39
Q

platelet storage/ activation

A

stored in spleen
activated by sympathetic nervous system

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40
Q

platelet life span and end

A

~7-10 day life span prior to apoptosis/ phagocytosis in spleen/ liver

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41
Q

dense tubular system

A

regulates platelet activation by calcium release
thromboxane A2 synthesis site

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42
Q

platelet granule types

A

alpha > clotting mediators
delta > platelet activators/ clotting agent/ contain ADP/ Ca2+/ serotonin

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43
Q

vascular spasm

A

vessel damage releases vasoconstrictors, slowing blood flow and therefore minimising blood loss
endothelial surfaces adhere via platelets sticking to exposed collagen

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44
Q

platelet plug formation

A

von willebrand’s factor aid sticking
plug seals break in vessel lining fro compaction/ vasoconstriction/ clotting cascade stimulation

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45
Q

prostacyclin PG12

A

Normal blood vessel lining release
inhibits platelet aggregation
restricts platelet plug to damaged region

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46
Q

final step of blood clotting

A

fibrinogen conversion to fibrin (soluble> insoluble)
fibrin plug enmeshes RBC’s

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47
Q

cascade of reactions in clotting

A

fibrinogen > (thrombin)> fibrin monomers> (factor VIII)> fibrin polymer

48
Q

2 thrombin stimulating pathways

A

intrinsic > initial stimuli exposed to collagen
extrinsic > initial stimuli blood contact exposing tissue factor

49
Q

anti-clotting systems

A

anti-thrombin
thrombomodulin
tissue factor pathway inhibitor
thrombin receptor

50
Q

anti-thrombin

A

inhibits clotting factors
enhanced by heparin

51
Q

thrombomodulin

A

expressed by endothelial cells
binds thrombin
decreases coagulant effects/ inactivates factors V / VIII

52
Q

tissue factor pathway inhibitor

A

binds to factor III/VII, prevents activation
binds factor X directly

53
Q

thrombin reeptor

A

stimulates PGI/ NO/ ADP to inhibit aggregation

54
Q

fibrinolysis

A

clot breakdown

55
Q

fibrinolysis process

A

clots secrete PDGF beta, recruiting fibroblasts from surrounding tissue
forms scar tissue surrounding
plasmin fibrolytic enzyme dissolves

56
Q

plasmin

A

tissue plasminogen factor activated > needs to bind to fibrin for activity
endothelial cell activated

57
Q

clotting factors

A

proteases activating downstream factors
III, V, VIII glycoproteins
XIII transglutaminase

58
Q

quantitative platelet defects

A

thrombocytopaenia

59
Q

qualitative platelet defects

A

thrombopathy

60
Q

coagulopathy

A

dysfunction/ deficiency of coagulation factors

61
Q

acquired haemostasis disorders

A

renal disease
hepatic disease
vitamin K deficiency
drug-induced disorders

62
Q

inherited haemostasis disorders

A

structural defects of vascular system
thrombotic disorder
thrombocytopaenia
thrombopathy
coagulopathy

63
Q

thrombotic disorder

A

haemostasis alteration impairing clot formation combatting capacity

64
Q

coagulopathy

A

deficiency of coagulation factors

65
Q

haemorrhage

A

bruising/ contusion caused by Hb degradation to biliverdin/ bilizubin/ haemosiderin

66
Q

biliverdin removal

A

plasmin and phagocytosis

67
Q

thrombosis

A

excessive / unwanted clotting

68
Q

thrombus

A

clot in vessel/ heart

69
Q

embolus

A

detached mass able to travel in vessel

70
Q

embolism

A

lodging of embolus

71
Q

thrombo-embolism

A

blockage by thrombus

72
Q

stenosis

A

abnormal narrowing of body passage

73
Q

virchow’s triad

A

3 risk factors for thrombosis
1. blood stasis
2. vessel wall changes
3. thrombosis changes to blood

74
Q

anticoagulants example

A

warfarin
heparin

75
Q

warfarin

A

oral anticoagulant
inhibits vit K

76
Q

heparin

A

injection
activates antithrombin III

77
Q

when are anticoagulants used?

A

atrial fibrillation
aortic valve replacement
recent surgery
autoimmune diseases

78
Q

thrombocytopaenia

A

low platelet count

79
Q

thrombocytopaenia causes

A

autoimmune disease
drug-induced > platelet synthesis interference and immunologic destruction of platelets

80
Q

clinical characteristics of thrombocytopaenia

A

easy bruising
petechial rash
excessive bleeding
mucous membrane bleeding

81
Q

petchiae

A

pin-point haemorrhages w blood leakage from capillaries, ^vascular permeability/ platelet function failure

82
Q

inherited coagulopathies

A

von willebrand’s disease
haemofilia A
haemofilia B

83
Q

von willebrand’s disease

A

autosomal dominant
lack of VW factor
poor platelet aggregation
excessive gum bleeding

84
Q

haemofilia A

A

x-linked recessive
factor VIII deficiency

85
Q

haemofilia B

A

factor IX deficiency

86
Q

haemofilia treatment

A

replacement of missing factor

87
Q

blood groups

A

blood classification based on inherited antigenic substances on RBC surface and presence/ absence of rhesus D antigen

88
Q

blood group discovery

A

karl landsteiner in vienna 1901 as A/B/C blood groups

89
Q

RBC antigen substance

A

protein/ glycoprotein/ glycolipid mixture

90
Q

why may someone’s complete blood group change in their life time?

A

infection
malignancy
bone marrow transplant
autoimmune disease

91
Q

5 sugars in ABO system and most common 3?

A

fucose*
Galactose*
N-acetylglucosamine*
sialic acid

92
Q

3 enzymes in ABO system

A

fucosyl transferase (FUT1)
N-acetylgalactosamine transferase (A transferase)
galactose transferase (B transferase)

93
Q

2 genes in blood groups

A

ABO
H

94
Q

ABO determination

A

terminal sugar structure on galactose of H substance on RBC surface

95
Q

function of glycosyl transferases

A

transfer monosaccharides to polysaccharides

96
Q

O allele encodes

A

truncated/ non-functional proteins

97
Q

H gene

A

encodes fucosyl transferase/ FUT1
located on Ch19
dominant to h

98
Q

bombay phenotype

A

hh
v rare/ no symptoms
transfuse w other hh

99
Q

ABO gene

A

7 exon gene on Ch19

100
Q

O-allele

A

deletioin on exon 6 > frameshift> inactive protein

101
Q

A/B alleles

A

7 nuc substitutions
4 translate into amino acid differences in gene product

102
Q

hh phenotype

A

no functional FUT1
May have A/B transferases
no sub. H / ABO antigens

103
Q

blood type O

A

no A/B transferase
only H substance

104
Q

blood type AB

A

both A/B transferase
add galactose/ N-acetylglucosamine to terminal galactose on H substance

105
Q

antibodies belonging to A/B/O

A

A> beta
B> alpha
O> alpha/beta

106
Q

agglutinogens

A

blood group antigens

107
Q

agglutinins

A

antibodies against blood groups

108
Q

adverse agglutinin reaction

A

cause RBC clumping
RBC lysis> kidney failure/ uncontrolled clotting/ circulatory shock

109
Q

Rh+ genotypes

A

DD/ Dd

110
Q

Rh- genotypes

A

dd

111
Q

anti-Rh(D) antibodies

A

exposure required
destroy Rh(D)+ cells > RBC bound by IgG, engulfed by macrophages/ transported to liver/ spleen for removal

112
Q

universal donor

A

O-

113
Q

universal acceptor

A

AB+

114
Q

newborn haemolytic disease process

A

Rh- mother has Rh + baby, causing anti-Rh antibody production, damaged foetal RBC w next Rh+ baby

115
Q

newborn haemolytic disease symptoms

A

anaemia
jaundice
fatality

116
Q

newborn haemolytic disease treatment

A

mother given anti-D immunoglobulin

117
Q

class of ABO antibodies

A

IgM therefore don’t cross placenta

PSC1002- Physiology (8 decks)

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