Blood Flashcards

1
Q

causes of iron deficiency anaemia

A

blood loss (GI incl diverticulitis, menorrhagia) poor diet (vegetarians) malabsorption (coeliac)

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2
Q

features of IDA

A

brittle hair, atrophic glossitis, angular stomatitis, koilonychia

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3
Q

blood results in IDA

A
low Hb
low MCV
low serum ferritin
low serum iron
high TIBC
film- RBC microcytic hypochromic, anisocytosis (unequal size RBCs)  poikilocytosis (unequal shape)
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4
Q

what helps the absorption of Iron salts

A

vitamin C therefore give it with ascorbic acid + advice drink with OJ

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5
Q

how long should iron salts be continued for

A

check FBC after 4 weeks, then once anaemia resolved stop after 3 months

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6
Q

What is TRALI

A

transfusion related lung injury,

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7
Q

how soon after transfusion would TRALI present?

A

within 6 hours
SOB, hypoxia and fever
CXR-> inflitrates in lower zones/ parahilar nodes

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8
Q

what can occur if RBCs transfused too quickly

A

pulmonary oedema

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9
Q

what is the definition of non-haemolytic febrile reaction

A

rise in temp >1 above baseline

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10
Q

management of non-haemolytic febrile reaction

A

paracetamol and slow rate of transfusion

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11
Q

how would an allergic reaction to a transfusion present

A

in minutes- urticaria

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12
Q

↓serum iron levels
↓ TIBC
↑or normal serum ferritin.

A

anaemia of chronic disease

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13
Q

Causes of microcytic anaemia

A

iron deficiency anaemia
anaemia of chronic disease
thalassaemia
sideroblastic anaemia

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14
Q

name some causes of sideroblastic anaemia

A

any process interfering with heme production
congenital
acquired- alcohol, lead poisoning, TB drugs, malignancy

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15
Q

what would show in blood film of sideroblastic anaemia

A

ringed sideroblasts in BM and increased iron store

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16
Q

causes of macrocytic anaemia

A

normobastic- alcohol/ liver disease, hypothyroid, cytotoxic, myelodysplasia
megaloblastic- B12/ Folate deficiency

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17
Q

target cells on blood film, macrocytic anaemia

A

liver disease

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18
Q

macrocytic anaemia, hypersegmented neutrophil nuclei on blood film

A

b12 deficiency- also causes low WCC/ platelets

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19
Q

name one complication other than anaemia of B12 deficiency

A

dorsal column degenaration-> peripheral neuropathy

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20
Q

what protein is reduced in pernicious anaemia

A

intrinsic factor from gastric mucosa

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21
Q

causes of folate deficiency

A

reduced intake- alcoholics, pverty
malabsorption- coeliac
excess requirement- pregnancy, dialysis

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22
Q

name some causes of normocytic anaemia

A

hypoproliferative- leukaemia, aplastic anaemia

hyperproliferative- haemorrhage, haemolytic anaemia

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23
Q

name some causes of aplastic anaemia

A

congenital
idiopathic acquired
drugs- chemo, chloramphenicol
infections- HIV

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24
Q

causes of congenital haemolytic anaemia

A

membrane: hereditary spherocytosis/elliptocytosis
metabolism: G6PD deficiency
haemoglobinopathies: sickle cell, thalassaemia

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25
Q

what might indicate a haemolytic anaemia?

A
evidence of breakdown (increased bilirubin)
evidence of RBC production
-reticulocytosis,
-polychromasia,
-macrocytosis,
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26
Q

which test identifies immune causes of haemolytic anaemia

A

Coombs test (direct antiglobulin test)

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27
Q

some causes of acquired haemolytic anaemia

A

immune: transfusion reaction, penecillin

non-immune: DIC, HUS, prosthetic valves, malaria

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28
Q

how is B thalassaemia inherited

A

AR

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29
Q

how is sickle-cell anaemia inherited?

A

AR

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30
Q

What causes a sickle cell crisis

A

trigger causing increased O2 demand-> cells sickle and haemolyse, blocking small blood vessels and causing infarction

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31
Q

what cells form from a common myeloid progenitor?

A

megakaryocyte-> thronbocyte
erythrocyte
mast cell
myelobast-> basophil, eosinophil, neutrophil, monocyte-> macrophage

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32
Q

what cells form from a common lymphoid progenitor?

A

natural killer cell
t cell
B cell-> plasma cell

33
Q

function of neutrophils

A

made in BM

phagocytose bacteria

34
Q

function of eosinophils

A

made in BM

antiparasitic

35
Q

function of basophils

A

help mast cells in inflammation
contain histamine
allergic reactions

36
Q

function of mast cells

A

produced in BM surround BVs and nerves.
inflammation initiator
histamine release

37
Q

function of macrophages

A

made in BM
phagocytosis
antigen presenting cells

38
Q

B cell function

A

membrane bound antibodies,
binding of pathogen and antigen presenting + helper T cell stimulation-> activation
-> plasma cells via IL4 (make ABs) / memory cells

39
Q

CD4+ T cell function

A

helper T cells
MHC II complex
activate B cells and release cytokines

40
Q

CD8+ T cell function

A

cytotoxic cell to viral infected/ cancerous cells

MHC I complex

41
Q

IL1, TNF-a

A

fever and cachexia, vasodilation. TNF produced by mast cells/ macrophages

42
Q

IL2

A

T cell activation

43
Q

IL3

A

BM stimulant

44
Q

IL5

A

eosinophil activator

45
Q

IL8

A

neutrophil recruiter

46
Q

IFN-G

A

granuloma activator

47
Q

RFs for Hodgkin’s lymphoma

A

EBV (infectious mononucleosis)

HIV

48
Q

Reed-Sternberg cells

A

HL, these are B cells that no longer express surface antigens/ do not undergo apoptosis

49
Q

assymetrical painless lymph nodes above diaphragm, fever, weight loss,

A

HL (NHL can be tender)

50
Q

Staging system for HL

A

Ann Arbor

51
Q

peak age HL

A

30s/70s

52
Q

NHL peak age

A

55-60

53
Q

most common NHL

A

diffuse large B cell

54
Q

definitive diagnosis investigation for HL

A

lymph node biopsy

55
Q

what are B symptoms of HL

A

drenching night sweats
WL
fever

56
Q

first stage management for HL

A

radio +/- chemo

57
Q

spread of HL vs NHL

A

continguous in HL meaning spreads via lymph to adjacent nodes/ structures. NHL can arise in several unlinked structures

58
Q

which has worse prognosis HL/ NHL

A

NHL

59
Q

back pain, impaired renal function, normochromic normocytic anaemia
hypercalcaemia

A

myeloma

60
Q

most effective analgesia for bone pain

A

steroid

61
Q

peak age for myeloma

A

60-70 men

62
Q

investigations in suspected myeloma

A
monoclonal proteins (IgG/ IgA) in serum and Bence-Jones proteins in urine
increased plasma cells in BM
63
Q

what is DIC?

A

Cytokine mediated activation of extrinsic coagulation cascade. caused by sepsis/ major trauma

64
Q

how is haemophilia inherited?

A

X linked recessive

65
Q

which clotting factor is affected in haemophilia A/ B

A

VIII/ IX

66
Q

features of haemophilia

A

haemoarthroses, haematomas
prolonged bleeding after surgery or trauma
prolonged APTT, normal PT, Bleeding time

67
Q

most common cause of thrombophilia

A

Factor V leiden deficiency

68
Q

causes of thrombocytopenia

A
DIC
haem malignancies
heparin induced
drug induced (diuretics, aspirin)
alcohol
B12 deficiency
69
Q

pancytopenia

A

congenital

acquired- reduced BM production (myeloma, megaloblastic anaemia)/ increased destruction (liver disease)

70
Q

causes of neutropenia

A

infections
drugs- agranulocytosis
megaloblastic anaemia

71
Q

most common malignancy of childhood

A

acute lymphoblastic leukaemia

72
Q

presentation of acute leukaemias

A

Anaemia
Bleeding and bruising – as a result of thrombocytopaenia
Infection – as a result of leukopaenia
Bone pain – as a result of bone marrow infiltration

73
Q

difference between acute and chronic leukaemia

A

the malignant clones are themselves able to differentiate, and the accumulated cell population in the bone marrow is made up of a more mature variety of cells, and not just blast cells.

74
Q

which factor changes prothrombin to thrombin

A

X, which in turn changes fibrinogen to fibrin

75
Q

extrinsic pathway

A

Trauma-> tissue factor->

VII-> x

76
Q

Intrinsic pathway

A

trauma to blood cells directly

XII, XI, IX VIII

77
Q

vitamin K dependant factors

A

VII, IX, X prothrombin

78
Q

APTT measures what

A

intrinsic pathway

79
Q

PT/INR measures what

A

extrinsic pathway