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pom last minute stuff > haematology > Flashcards

haematology Flashcards

1
Q

functions of HSC

A

self renew or differentiate to mature progency

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2
Q

arrangement of myeloid/lymphoid progenitors

A

orderly fashion in bone marrow among mesenchymal, endothelial and vasculature

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3
Q

growth factors

A

glycoprotein hormones that bind cell surface receptors - regulate proliferation + differentiation of BCs

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4
Q

rbc growth factor

A

erythropoietin - made in kidney in response to hypoxia

also regulated by genes TF + microenvironment

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5
Q

stages of rbc maturation

A

proerythroblast
early, intermediate + late erythroblast
reticulocyte
RBC

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6
Q

iron absorption

A

in duodenum

ferrous (Fe2+) = better absorbed than ferric (Fe3+) which needs ascorbic acid

some veg (Fe3+) => phytates = hard to absorb iron

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7
Q

hepcidin

A

blocks iron storage in liver + absorption in gut when levels too high

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8
Q

proinflammatory cytokines that increase hepcidin

A

IL1
TNFa
IL 6

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9
Q

proinflammatory cytokines that inhibit erythropoiesis

A

IL1 + TNFa - inhibits EPO production

ILNy

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10
Q

FA + B12 absorption

A

both: small intestine

B12 + IF in stomach => bind receptors in ileum

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11
Q

RBC life cycle

A

destroyed by spleen phagocytic cells

bilirubin => excreted as bile
iron => returns to BM - recycled

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12
Q

membrane integrity maintenance in rbc

A

biconcave = manoeverability

bilayer w/protein cytoskeleton + transmembrane proteinsto maintain integrity, shape + elasticity

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13
Q

sperocytes

A

disruption of vertical linkages in membrane
round + irregular + no central pallor

loss of membrane without equal loss of cytoplasm
predisposed to premature haemolysis

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14
Q

elliptocytes

A

disruption of horizontal linkages in membrane
maybe due to iron deficiency

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15
Q

G6PD function

A

enz in hexose monophosphase shunt which is couples with glutathianone metabolism which prevents cell from oxidant damage

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16
Q

G6PDD

A

G6PD deficiency

RBCs more prone to oxidant damage = severe intravascular haemolysis => bite cells

X-linked
oxidants: food, chemicals, drugs

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17
Q

polycythaemia

A

too many blood cells in circulation (increased Hb, RBC, Hct)

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18
Q

pseudo vs true polycythaemia

A

pseudo = decreased plasma volume

true = increased RBC

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19
Q

4 main causes of true polycythaemia

A

blood doping/overtransfusion

appropriate increase in erythropoiesis (hypoxia)

inappropriate increase in erythropoiesis (doping/renal tumours)

polycythemia vera (myeloproliferative disorder)

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20
Q

symptoms of polycythaemia vera

A

increased blood viscosity, vascular obstruction/thrombosis

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21
Q

treatment options for PV

A

blood removed - venesection

drugs to decrease bone marrow production of RBCs

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22
Q

3 main things RBC function depends on

A

membrane integrity
Hb structure + function
cellular metabolism

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23
Q

myeloid growth factors

A

G-CSF
M-CSF
GM-CSF

m = macrophage
g = granulocyte

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24
Q

neutrophil excavasation

A

chemotaxis
adhesion + margination to lumen
rolling + diapedesis into tissue
migration + phagocytosis

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25
Q

what do granules of basophils contain

A

histamine, heparin + proteolytic enzymes

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26
Q

granulocytes involved in type 1 hypersensitivity

A

eosinophils + basophils

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27
Q

mast cell vs basophil

A

same but B = blood, M = tissue

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28
Q

monocyte function

A

phagocytosis of antibogy + comlement covered microorganisms (bac/fungi)

APC to other cells

in tissues => develop into macrophages = phag + scavenge

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29
Q

b lymphocyte development

A

in bone marrow

involves Ig heavy and light chain gene rearrangement, leading to production of different surface Igs for ags (humoral immunity)

further maturation when exposed to self antigens

mature B-cell recognises non-self in lymphoid tissue => plasma

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30
Q

B vs T function

A

B: make abs against bacteria/virus/toxins
T: destroy virus infected cells

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31
Q

transient vs persistent leukocytosis

A

transient: secondary cause => normal/healthy response to stimulus

persistent: primary blood cell disorder

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32
Q

secondary causes of neutrophilia [6]

A

infection, inflammation, tissue damage, pregnancy, exercise, corticosteroids

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33
Q

primary causes of neutrophilia

A

chronic myeloid leukaemia

leads to: left shift (non-segmented precursors - metamyelocytes in circulation)

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34
Q

causes of neutropenia

A

chemotherapy, radiotherapy
AI disorders
severe bacterial/vial infections (overload)
drugs - anticonvulsant, antipsychotic, antimalarial

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35
Q

what can neutropenia cause

A

right shift
hypersegmentation (more than 3-5)

also due to megaloblastic anaemia

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36
Q

secondary causes of eosinophilia

A

asthma, eczema, allergy, parasitic infection

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37
Q

primary cause of eosinophilia

A

CML

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38
Q

causes of basophilia

A

secondary causes = uncommon
usually due to CML

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39
Q

secondary causes of monocytosis

A

chronic infection, chronic inflammation

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40
Q

secondary causes of lymphocytosis

A

viral infection

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41
Q

primary causes of lymphocytosis

A

chronic lymphocytic leuckaemia

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42
Q

causes of lymphopenia

A

HIV, chemotherapy, radiotherapy, corticosteroids
may be caused by severe infection

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43
Q

acute vs chronic + why are blood cancers described this way

A

acute = recent/sudden onset, aggressive + severe

chronic = disease + deterioration over long time

classified like this rather than malignant/benign as not a solid tumour

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44
Q

leukaemia properties

A

due to mutations in progenitors (somatic in primitive cell => survival advantage over normal)

leukaemic cells replace normal BM cells + overspill into blood

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45
Q

mutations causing leukaemia

A

may be due to mutagen exposure or spontaneous/random

in oncogenes/TSGs

mutation leads to cell not requiring same growth factors, too much/too little maturation, no apoptosis

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46
Q

2 types of acute leukaemia

A

acute lymphoblastic
acute myeloid

mutations in progenitor transcription factors = cells cant mature but still proliferate

=> immature blast cells

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47
Q

2 types of chronic leukaemia

A

chronic lymphocytic
chronic myeloid

steady expansion of fully mature but useless clones that replace normal cells

=> mature (maybe too mature - hypersegmented) cells

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48
Q

plasma vs serum

A

plasma = liquid component of blood
serum = plasma minus clotting factors

49
Q

how serum collected

A

blood in serum separator tube (silica coating to induce clotting + gel as barrier)

no anticoagulant

centrifuged

50
Q

bodily fluids in order of amount

A

intracellular

extracellular:
interstitial
plasma
transcellular

51
Q

plasma functions

A

clotting
immune defence
osmotic pressure maintenance
metabolism
endocrine
excretion

52
Q

neg to pos plasma proteins

A

albumin
alpha 1 globulin
alpha 2 globulin
beta globulin
gamma globulin

53
Q

albumin functions

A

made in liver

lipid (from lipolysis to tissues for b-ox) , hormone + ion transport

54
Q

alpha 1 antitrypsin functions

A

liver => circ

inhibits proteases + protects tissue from enz damage (e.g neutrophil elastase)

low a1at = lug tissue degraded, decreased elasticity + resp issues

55
Q

alpha 2 globulin: haptoglobin

A

binds Hb => Hapto:Hb complex => removed by spleen

diagnose haemolytic anaemia

56
Q

alpha 2 globulin: macroglobulin

A

protease inhibitor => inactivate fibrinolysis

57
Q

beta globulins

A

c3 + c4 complement proteins

transferrin: iron transport (made in liver)

58
Q

gamma globulins

A

immunoglobulins + c-reactive proteins

59
Q

electrolytes in plasma with higher extracellular content

A

Ca2+
Mg2+
Na2+
Cl-

60
Q

electrolytes in plasma with higher intracellular content

A

K+ => high in RBC

61
Q

2 uses of plasma

A

biomarkers => diagnosis + study of how plasma proteome links to disease

passive immunotherapy => IV IgG or hyperimmune globulin to treat against specific antigen (e.g venom)

62
Q

convalescent plasma procedure

A

patient infected
develops antibodies
blood donated after recovery (convalesced)
AB rich plasma => affinity + no:abs tested
donated

63
Q

what does the beer lambert law say and what is the equation

A

shows linear relationship between conc + absorbance of solution

absorbance = extinction coefficient x conc x path length

64
Q

why might substance at high conc not follow beer lambert law

A

dimer formation => diff E value

65
Q

what happens on oxygen dissociation curve when increased affinity for oxygen

A

left shift

66
Q

myogloin

A

in muscle
1 haem group
increased affinity for O2

67
Q

carboxyhaemaglobin

A

Hb = high affinity for CO
toxic

68
Q

methaemaglobin

A

Fe2+ oxidised to 3+ => impaired O2 binding
blue or chocolate coloured blood
left shift + anoxia as O2 not released

back to Hb by methaemoglobin reductase

69
Q

3DPG

A

binds Hb = lower affinity for O2 => right shift

70
Q

HbS

A

negative glutamine => positive valine => less movement towards positive electrode

philic => phobic

71
Q

MCV

A

Hct/RBC (L)

72
Q

MCH

A

Hb/RBC (g)

73
Q

MCHC

A

Hb/Hct (g/L)

74
Q

haematoxylin + eosin

A

h = blue/purple - stains acidic components e.g nucleus

e = pink - cytosol (eosinophil = more visible due to specific granules)

75
Q

leishmans stain

A

combo of blue (nucleus) + red (cyto) dyes

76
Q

polychromasia

A

blue tinge in rbc cytoplasm
along with macrocytosis

young cells => haemolysis = increased erythropoiesis

77
Q

ansinocytosis

A

inc variation in rbc size

78
Q

poikilocytosis

A

inc variation in rbc shape

79
Q

target cell

A

hb accumulated in central pallor

80
Q

schistocytes

A

rbc fragment due to certain clotting factors

81
Q

bite cells

A

no central pallor - due to haemolysis

82
Q

group A antigen

A

N acetyl galactosamine + glycoprotein stem of H protein

83
Q

group B antigen

A

galactose + glycoprotein stem of H protein

84
Q

group O antigen

A

glycoprotein stem of H protein

85
Q

blood group inheritance

A

A&B = codominant
O = recessive

86
Q

universal RBC donor

A

O negative - no antigens to react with possible antibodies in patient blood

87
Q

universal serum donor

A

AB positive - no antibodies in blood to bind possible antigens

88
Q

what happens when wrong plasma is given

A

agglutination

89
Q

forward group testing

A

patient cells tested against ABO antibodies - no agglutination = right one

90
Q

reverse group

A

patient serum with A+B cells - no agglutination = right group

91
Q

rhesus D properties

A

dominant
anti D antibodies = not in blood already for D-ive => develop on first exposure (sensitisation)

92
Q

HTR

A

haemolytic transfusion reaction - incompatible RBCs

93
Q

HDFN

A

haemolytic disease of foetus and newborn

when foetus + mother = diff RBC + antibodies of mother cross placenta

94
Q

how do people develop antibodies against ABO

A

at early age
same/similar proteins found in lots of foods

95
Q

types of Ig

A

ABO = IgM (cause HTR but not HDFN as they cant cross placenta)

RhD => acquired allo-antibodies = IgG (delayed HTR once sensitised but DO cause HDFN)

96
Q

pre-transfusion compatibility testing

A

ABO test
RhD test
Ab screen for allo
compatibility test with donor jic

97
Q

apheresis

A

donor connected to apheresis machine which separates required part + returns the rest

means that more of required component can be taken

98
Q

red cells (donated)

A

given to increase Hb or O2

plasma removed + rbc suspended in additive solution

1 unit from whole or 2 from apheresis

store 35 days at 4oC

99
Q

platelets (donated)

A

given to bleeding patients

1 unit pooled from 4 whole blood donations
or 1 from a person via apheresis

store 7 days at 22oC

100
Q

fresh frozen plasma

A

given to decrease bleeding - has all clotting factors

1 unit from whole or 1 from apheresis

frozen: store 3 years at -25oC
once thawed: store 24 hours at 4oC

101
Q

cryoprecipitate

A

fibrinogen, factor 7, vwf + 12

when low fibrinogen or bleeding

FFP thawed overnight => ppt made => resuspended in plasma

frozen: store 3 years at -25oC
once thawed: store 4 hours at rom temp

102
Q

plasma derived medicinal products

A

made from pooling thousands of plasma donations via fractionation

produces: human albumin solution, immunoglobulin solutions, clotting factor concentrates

103
Q

stages of primary haemostasis

A

endothelial injury

exposure => release of vwf - binds to exposed collagen

adhesion of platelets to vwf by GP1b or direct adhesion of platlets to collagen

platelet activation => conformational change
aggregation as GPIIb/IIIa on platelet binds fibrinogen =>

platelet plug

104
Q

extrinsic pathway of secondary haemostasis

A

SM => tissue factor on memb
factor 7 in blood => 7a

TF + 7a + Ca2+ => complex on SM

complex: 10 => 10a

105
Q

intrinsic pathway of secondary haemostasis

A

12 => 12a

12a: 11 => 11a

11a + Ca2+ : 9 => 9a

9a + 8a + Ca2+ => complex

complex: 10 => 10a

106
Q

common pathway of secondary haemostasis

A

10a: 5 => 5a

5a + 10a + Ca2+ => prothrombinase complex

pt-complex: prothrombin (2) => thrombin (2a)

2a + Ca2+ => complex

107
Q

thrombin + Ca2+ complex function

A

platelet activation

5, 8, 9 activation

fibrinogen (1) => fibrin (1a)
(fibrin soluble - ppts out of cells + forms protein chains holding platelets together)

13 => 13a : 13a + Ca2+ => complex (forms crosslinks between fibrin chains)

108
Q

prothrombin time

A

tests extrinsic pathway - playing tennis

blood + sodium citrate => chelates Ca2+ so clots cant form

spun for platelet poor plasma

TF + phospholipid + Ca2+ added + time to clot recorded

tests: 7, 10, 5 + 2

109
Q

activated partial thromboplastin time

A

tests intrinsic pathway - playing table tennis

add sodium citrate to blood => chelate Ca2+

activate 12 by surface/contact activation

Ca2+ added => time to clot measured

110
Q

natural anticoagulant pathway

A

thrombin (2a) binds thrombomodulin on endothelial cell => activates protein C (Activated PC)

APC inactivates 5a + 8a in presence of co-factor S

thrombin + 10a inactivated by antithrombin

111
Q

3 anticoagulant drugs + how they work

A

heparin (IV) => glycosaminylglycan chain potentiates antithrombin => 10a + 2a inactivation

warfarin (oral) => interferes with protein carboxylation - less synthesis of 2, 7, 9, 10 - must be monitored

direct oral anticoagulant drugs => directly inhibit 10a + 2a

112
Q

how are clots broken naturally

A

tissue plasminogen activator: plasminogen => plasmin

plasmin => fibrin breakdown
also breaks fibrinogen, 8a, 5a

(only when plasminogen + TPA bound to lysine residues on fibrin)

inhibited by antiplasmin / alpha 2 macroglobin

113
Q

who is thrombolytic therapy given to

A

patients with pulmonary embolism

114
Q

tranexamic acid

A

antifibrinolytic drugs

binds plasminogen by competitive inhibition => stopis it binding lysine residues on fibrin

plasminogen =x=> plasmin = X fibrinolysis

115
Q

thrombosis

A

inappropriate formation of blood clot in vessel = obstruction of blood flow

116
Q

Virchow’s triad

A

contributory factors to pathological clotting (thrombosis)

blood => dominant in venous thrombosis
vessel wall => dominant in arterial
blood flow => complex, contributes to both arterial + venous

117
Q

increased risk of thrombosis

A

decreased anticoagulant proteins
decreased fibrinolytic activity
increased levels of platelets/clotting factors
hyper-viscosity

118
Q

causes of bleeding

A

reduced platelets => primary

reduced coag factors => secondary

increased fibrinolysis

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