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CRR NEW > L5- blood cells and disorders 2 > Flashcards

L5- blood cells and disorders 2 Flashcards

1
Q

what does thrombopoietin cause?

A

causes heamopoietic stem cells to differentiate into megakaryoblasts

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2
Q

what do megakaryoblasts produce?

A

megakaryocytes

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3
Q

what are megakaryocytes responsible for?

A

production of platelets

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4
Q

what are platelets

A

small nucleate cells required for haemostasis

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5
Q

volume of platelets

A

150,000-400,000/ml

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6
Q

life span of platelets

A

life span 5-9 days

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7
Q

what 3 things occur upon injury

A

platelet plug formation
blood clotting
vascular spasm

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8
Q

what happens in vascular plasm

A

arteries/arterioles constrict to reduce blood flow

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9
Q

what does platelet plug formation require?

A

exposure of extracellular matrix proteins

requires several steps

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10
Q

example of extracellular matrix proteins needed for platelet plug formation

A

vWF
fibrogen
collagen

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11
Q

5 steps of platelet plug formation

A 
adhesion
outside-in
signalling-integrin
activation
secretion
aggregation
thrombin production
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12
Q

what is the platelet disorder Bernard-soulier caused by

A

abnormality in the genes for glycoprotein lb/V/IX

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13
Q

what is the platelet disorder Glanzmann thromasthenia caused by?

A

abnormaily in the genes for glycoproteins llb/llla

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14
Q

symptoms of Glanzmann thrombasthenia and Bernard-soulier

A
  • easy bruising
  • nose bleeds
  • bleeding from gums
  • heavy or prolongued menstrual bleeding (menorrhagia) or bleeding after childbirth
  • abnormal bleeding after surgery or dental work
  • rarely, vomiting blood or passing blood in stool due to bleeding from the gut (gastrointestinal haemorrhage)
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15
Q

what are some storage pool deficiencies caused by?

A

a lack of granules

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16
Q

what are most storage pool deficiencies caused by?

A

most common ones are caused by a failure of the platelets to empty the granules

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17
Q

what causes delta storage pool deficiency

A

a lack of dense granules

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18
Q

what can delta storage pool deficiency be a feature of

A

other inherited conditions (such as hermansky-pudlak syndrome and chediak-higashi syndrome)

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19
Q

what is grey platelet syndrome, how is it caused

A

a very rare platelet disorder caused by lack of alpha granules and the chemicals normally stored inside them

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20
Q

what happens if there is a deficiency in alpha granules

A

without these proteins, platelets cannot stick to the blood vessel wall, clump together the way they should or repair the injured blood vessel

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21
Q

characteristics of extrinsic pathway of blood clotting

A

fewer steps and rapid

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22
Q

how is extrinsic pathway of blood clotting initiated

A

is initiated by TF leaking into the blood from cells outside the bloodstream

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23
Q

characteristics of intrinsic pathway of blood clotting

A

more complex and is slower

outside tissue damage is not needed e.g caused by endothelial cell damage

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24
Q

in the intrinsic pathway of blood clotting, what activates FXII

A

Surface contact

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25
Q

in the intrinsic pathway of blood clotting, what activates FXI?

A

FXlla

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26
Q

in the intrinsic pathway of blood clotting, what releases bradykinin

A

FXlla

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27
Q

what is bradykinin

A

a vasodilator from HMWK

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28
Q

in the intrinsic pathway of blood clotting, what activates FIX

A

Ca2+ and FXla

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29
Q

what is FIX

A

a serine protease

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30
Q

in the intrinsic pathway of blood clotting, what hydrolyses FX

A

FXla

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31
Q

in the intrinsic pathway of blood clotting, what hydrolyses Ca2+ and phosphatidylserine

A

FXla

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32
Q

in the intrinsic pathway of blood clotting where are Ca2+ and phosphatidylserine found

A

on activated platelets, and FVllla - the tenase complex

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33
Q

in the intrinsic pathway of blood clotting, what is FVIII

A

a cofactor

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34
Q

in the intrinsic pathway of blood clotting, what is FVIII activated by?

A

thrombin from platelets

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35
Q

in the intrinsic pathway of blood clotting, FX is activated leading to what

A

the common pathway

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36
Q

in the intrinsic pathway of blood clotting, what is FVII activated by?

A

by thrombin and FXa

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37
Q

in the intrinsic pathway of blood clotting, what is FX activated by?

A

FVIIa and its cofactor TF (FIII)

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38
Q

In the common pathway of blood clotting, what cleaves prothrombin (FII)

A

FXa

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39
Q

in the common pathway of blood clotting, where is prothrombin (FII) cleaved

A

on the surface of activated platelets

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40
Q

in the common pathway of blood clotting, what does the cleavage of prothrombin (FII) create

A

a prothrombinase complex with Ca2+, phospholipids, prothrombin, FXa and FV

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41
Q

in the common pathway of blood clotting, what is FV activated by

A

small amounts of thrombin

42
Q

in the common pathway of blood clotting, what is fibrogen converted to and by what

A

converted to fibrin by thrombin

43
Q

in the common pathway of blood clotting, what activates FXIII and what does this do

A

thrombin which cross links the fibrin clot

44
Q

what plugs the ruptured area

A

the clot

45
Q

what is clot retraction

A

the tightening of the fibrin clot

46
Q

what contracts when platelets pull on them

A

fibrin threads attached to the damaged surfaces of the blood vessel

47
Q

what does fibrin threads attached to the damaged surfaces of the blood vessel do

A

pulls the edges of the wound together

48
Q

what does fibrinolysis dissolve

A

small inappropriate clots and dissolved clots at sites of repair

49
Q

what is incorporated into the clot

A

inactive plasminogen

50
Q

what is inactive plasminogen activated to?

A

plasmin

51
Q

how is inactive plasminogen activated

A

by substances in the body tissue (thrombin and t-PA)

52
Q

what does plasmin digest

A

fibrin threads

53
Q

what does plasmin inactivate

A

fibrinogen, prothrombin, FV and FXII

54
Q

What type of genetic disease is haemophilia A

A

X linked

55
Q

what does haemophilia A lead to

A

leads to FVIII deficiency

56
Q

how is extrinsic pathway assessed by in haemophilia A

A

assessed by prothrombin time (PT) by addition of TF to plasma

57
Q

in haemophilia A which pathway works

A

extrinsic pathway

58
Q

how is the intrinsic pathway assessed by in haemophilia A

A

assessed by activated partial thrombosplastin time- APTT

59
Q

in haemophilia A why are phospholipids added in the intrinsic pathway

A

added to mimic contact factor

60
Q

how many males affected by haemophilia A

A

affects 1:5,000 males

61
Q

what is haemophilia B?

A

Christmas disease, X linked disorder leading to FIX deficiency

62
Q

what is normal in haemophilia B

A

normal PT time

63
Q

what is abnormal in haemophilia B

A

abnormal APTT time

64
Q

how many males affected by haemophilia B

A

affects 1:30,000 males

65
Q

what is warfarin

A

vitamin K antagonist to prevent clotting factor activation

66
Q

what is EDTA

A

compound used in medicine settings to chelate calcium in donated blood

67
Q

define chelate

A

a compound containing a ligand (typically organic) bonded to a central metal atom at 2 or more points

68
Q

what does aspirin inhibit

A

inhibits TxA2 synthesis

69
Q

what does streptokinase do

A

activates t-PA

70
Q

what does the surface of RBCs contain which act as antigens

A

range of glycoproteins and glycolipids

71
Q

if a RBC has antigen A what antibody does it have

A

anti-B antibody

72
Q

if a RBC has antigen B what antibody does it have

A

anti-A antibody

73
Q

if a RBC has antigen A+B what antibody does it have

A

neither

74
Q

if a RBC has neither antigen A or B what antibody does it have

A

both antibodies

75
Q

what is missing if a person is rhesus negative

A

the D antigen

don’t normally have Rh antibodies

76
Q

when can rhesus negative develop

A

after blood transfusion, causes problem for later transfusions

77
Q

what problem can rhesus negative cause in pregnancy

A

in the next Rh positive pregnancy, maternal antibodies attack fatal RBCs

78
Q

symptoms of severe anaemia

A

fainting
chest pain
angina
heart attack

79
Q

causes of anaemia

A

reduced oxygen carrying capacity

80
Q

what can reduced oxygen carrying capacity cause

A 
iron- deficiency
megaloblastic (large RBC)
pernicious
haemorrhagic
haemolytic
thalassemias
81
Q

what is thalassemias

A

haemoglobin problems

82
Q

what is pernicious

A

lack of haemopoiesis

83
Q

what can kill malaria

A

low potassium levels

84
Q

in haemophilia what happens if the father has the disease and the mother is healthy

A

1/4 chance son will have haemophilia

1/4 chance the daughter is a carrier

85
Q

what is leukaemia

A

production of malignant WBC cells, supress production of all normal cells in RBM

86
Q

what can oncogenes cause

A

cause malignancy when mutated leading to their activation (growth factors, receptors, DNA binding proteins)

87
Q

what can tumour suppressor genes cause

A

cause malignancy when mutated leading to their supressed growth)

88
Q

characteristics of acute lymphoblastic leukaemia

A

short onset, derived from lymphoid stem cells

89
Q

where is acute lymphoblastic leukaemia more common

A

most common in children

90
Q

what ages do acute myelogenous leukaemia affect

A

affects all ages

91
Q

where is chronic lymphoblastic leukaemia more common

A

most common in adults (55+)

92
Q

characteristics of chronic myelogenous leukaemia

A

prolonged onset, derived from myeloid stem cells

93
Q

where is chronic myelogenous leukaemia more common

A

mostly in adults

94
Q

causes of leukaemia

A

unknown but can be radiation or chemotherapy, genetics (down syndrome), environmental factors,viral .g Epstein-barr virus

95
Q

what does bone marrow transplant involve

A

replacement of cancerous or abnormal red bone marrow with healthy RBM

96
Q

how is patient RBM destroyed

A

by chemotherapy and whole body radiation

97
Q

where can healthy RBM be from

A

a donor or patient if in remission

98
Q

where does marrow migrate to and then what does it do

A

to red bone marrow cavities and multiplies

99
Q

what can bone marrow transplant create

A

graft vs. host disease

100
Q

what does the patient need to stay on when going through a bone marrow transplant

A

need to stay on immunosuppresants

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