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My Year 5 Pathology > Haematology > Flashcards

Haematology Flashcards

1
Q

probability of VTE recurrence?

A

20% in the first 2 years

4% pa thereafter

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2
Q

4 potential consequences of VTE

A

1) death
2) recurrance
3) thrombophlebitic syndrome
4) pulmonary hypertension

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3
Q

components of Virchow’s triad

A

1) Blood
2) Blood flow
3) Vessel wall

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4
Q

the coagulation system:
Triggered by ___(1)__
Generates __(2)____
Which converts _(3)____ to __(4)__ (the clot)

A

1) Tissue Factor
2) thrombin
3) fibrinogen
4) fibrin

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5
Q

give 4 examples of things which make blood vessel walls prothrombotic?

A

inflammation
malignancy
trauma
infection

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6
Q

what is the mechanism of thrombosis due to stasis? - 4 steps

A

1) accumulation of activated factors
2) promotes platelet adhesion
3) promotes leukocyte adhesion and transmigration
4) hypoxia produces inflammatory effect on endothelium

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7
Q

What confers the highest risk of thrombosis?

a) factor V leiden
b) Antithrombin deficiency
c) FH of thrombosis
d) deficiency of Factor VII
e) 3 hour plane journey

A

b)

factor V leiden does confer some thrombosis but not as much

FH is important

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8
Q

What 3 groups of people are especially at risk of VTE

A

1) pregnant
2) Surgery
3) malignancy

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9
Q

How does Heparin work?

A
  • immediate

- potentiates action of antithrombin

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10
Q

what are the long term effects of heparin?

A

injections

risk of osteoporisis

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11
Q

Name 2 types of immediate acting anticoagulants

A

Heparins

Direct acting factor Xa or IIa inhibtors (e.g. rivaroxaban & Dabigatran)

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12
Q

What is used to monitor Warfarin levels?

A

INR - international normalised ratio - which is derived from the prothrombin time

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13
Q

For therapeutic anticoagulation what should you give?

A
  • must be immediate acting, so wither LMWH such as tinzaparin, or rivaroxaban / apixaban
  • also give warfarin at the same time for long term anticoagulation
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14
Q

What agent is used in thrombolysis and give some common examples

A

TPA - tissue plasminogen activator

alteplase, reteplase, tenecteplase

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15
Q

what is D-dimer a breakdown product of and what does mesuring it tell you

A

Breakdown product of fibrin so gives you an indication of clot breakdown. A negative D-dimer suggests that a clot is highly unlikely, but a positive test requires further investigation

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16
Q

What are causes of Microcytic Anaemia? (LOW MCV)

A

FAST

Fe deficient anaemia
Anaemia of chronic disease
Sideroblastic anaemia
Thalassaemia

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17
Q

What are causes of normocytic anaemia

A 
Acute Blood Loss 
Anaemia of chronic disease
Bone marrow failure 
Renal Failure 
Hypothyroidism 
Haemolysis
Pregnancy
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18
Q

What are causes of Macrocytic anaemia?

A

FATRBC

Foetus (pregnancy)
Alcohol and antifolates (e.g. phenytoin)
Thyroid (hypothyroidism)
Reticulocytosis
B12 or folate deficiency 
Cirrhosis (alcohol or liver disease)
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19
Q

Give 5 signs of iron deficiency anaemia

A 
kolionchia (spoon nails)
atrophic glossitis
angular cheilitis
post-cricoid webs 
brittle hair & nails
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20
Q

What would you see on a blood film in iron deficiency anaemia?

A

microcytic, hypochromic, anisocytes (varying size), poikilocytosis (shape), pencil cells

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21
Q

What 2 ways might you have decreased absorption of Fe leading to IDA?

A

1) post gastric surgery

2) coeliac

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22
Q

Give 5 examples of types of GI blood loss leading to IDA

A

1) GI Ca / polyps
2) Meckel’s diverticulum
3) Peptic ulcer / gastritis
4) Hookworm
5) menorrhagia

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23
Q

What is the most common cause of Fe-deficiency anaemia in women <50?

A

menorrhagia related

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24
Q

Give some differentials if you find Acanthocytes ona blood film

A

abetalipoproteinaemia
liver disease
hyposplenism

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25
Q

What does acanthocytosis mean?

A

Spiky / thorny / spicules RBCs

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26
Q

describe basophilic stippling

A

RBCs have small dots at the periphery - which are ribosomes

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27
Q

Give 5 causes of basophilic stippling

A

1) lead poisoning
2) myelodysplasia
3) liver disease
4) thalassaemia
5) megaloblastic anaemia

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28
Q

What are Burr cells and what might they indicate?

A

Echinocytes - irregularly shaped/spikes cells which can arise from uraemia, GI bleeding, stomach carcinoma

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29
Q

What are Heinz bodies and what might they indicate?

A

inclusions within RBCs of denatures Hb. Can occur in G6PD deficiency and chronic liver disease

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30
Q

what are howell jolly bodies

A

Remnants of DNA in RBCs

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31
Q

what 3 main things might the presence of howell jolly bodies indicate?

A

1) Splenectomy/hyposplenism - e.g. due to sickle cell, coeliac, congenital, UC/Chrons
2) megaloblastic anaemia
3) hereditary spheocytosis

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32
Q

describe leucoerythroblastic anaemia

A

Due to bone marrow INFILTRATION

  • results in nucleated (immature) RBCs
  • poikilocytosis
  • teardrop cells
  • Also primitive WBCs
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33
Q

What cells does Pelger Huet anomoly affect?

A

Neutrophils

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34
Q

What is the name of the anomoly when a neutrophil is hyposegmented?

What might this indicate?

A

Pelger-Huet anomoly

CONGENITAL - lamin B receptor mutation

ACQUIRED - myelogenous leukaemia, myelodysplastic syndromes

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35
Q

What does ‘polychromasia’ mean?

A

RBCs of varying colours due to varying amount of Hb content - showing immature/inappropariate release from the BM

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36
Q

Reticulocytes increase in___ and decrease in___

A

Increase: haemolytic anaemia

Decrease: aplastic anaemia & chemotherapy

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37
Q

What does a ‘right shift’ on a blood film mean

A

Hypermature WBCs - so hypersegmented (>5 lobes to the nuclei) and polymorphic

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38
Q

What might hypermature, polymorphic WBCs be called, and what disease could itpoint towards?

A

‘right shift’

  • megaloblastic anaemia
  • uraemia
  • liver disease
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39
Q

What is the name for when RBCs are stacked on another?

A

Rouleaux formation

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40
Q

What does a Rouleaux formation on a blood film suggest?

A
  • chronic inflammaiton
  • paraproteinaemia
  • myeloma
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41
Q

Give 5 differentials if you see schistocytes on blood film

A

1) microangiopathic anaemia e.g. DIC
2) HUS
3) TTP
4) pre-eclampsia

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42
Q

What blood film finding is typical for DIC?

A

schistocytes

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43
Q

Give 2 differentials for spherocytosis

A

1) Hereditary spherocytosis

2) AI haemolytic anaemia (Coombs +)

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44
Q

Describe stomatocytes

A

The central white bit is straight or curved into a ‘smile’

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45
Q

Give 2 differentials for stomatocytosis

A

1) hereditary stomatocytosis

2) high alcohol consumption / liver disease

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46
Q

What 4 differentialswhen target cells are seen on blood film?

A

1) Iron deficiency anaemia
2) liver disease
3) hyposplenism
4) thalassaemia

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47
Q

What is the most common hypercoagualability disorder in Europeans?

A

Factor V leiden

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48
Q

What are the numbers for anaemia in Men and Women?

A

Men - <135 g/L

Women - <115 g/L

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49
Q

5 symptoms of anaemia

A 
fatigue 
dyspnoea 
headaches
palpitations
faitness 
(tinnitus, anorexia)
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50
Q

General causes of anaemia (3)

A

1) Increased LOSS of RBCs
2) Reduced PRODUCTION of RBCs
3) Increased plasma volume (pregnancy)

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51
Q

What are the side effects of oral iron for IDA?

A

nausea, abdo discomfort, diarrhoea/constipation, black stools

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52
Q

What is anaemia of chronic disease in one sentence?

A

cytokine driven inhibition of RBC production

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53
Q

Give 4 causes of anaemia of chronic disease

A

1) malignancy
2) vasculitis
3) RA
4) Chronic infection e.g. TB, parasitic

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54
Q

Why do you get anaemia in renal failure?

A

EPO deficiency

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55
Q

what is sideroblastic anaemia and how do you diagnose it?

A

Ineffective erythropoiesis leading to iron overload, resulting in haemosiderosis.

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56
Q

treatment for sideroblastic anaemia

A

treat the cause and pyridoxine (vitamin B6)

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57
Q

What clotting factors are affected in haemophilia A, B and C?

A

A- 8
B- 9 (one after 8)
C- 11 (one after 9, then the one after)

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58
Q

Draw the clotting cascade!

A

Look to khan acadamy video for good explanation again

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59
Q

What is the negative feedback mechanisms for the clotting cascade?

A

1) thrombin stimulates production of plasmin from plasminogen, which breaks down fibrin crosslinks
2) thrombin stimulates generation of antithrombin which decreases thrombin production but also impedes activated Xa

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60
Q

What does factor XIII do?

A

stimulates cross link formation between fibrin strands to make a stable clot

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61
Q

Which sides of the clotting cascade do you use PT and PTT

A 
PT = extrinsic 
PTT = intrinsic (table tennis)
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62
Q

Which sides of the clotting ascade are heparin and warfarin affected

A 
extrinsic = warfarin (W, PT) 
intrinsic = heparin (PTT, HEP)
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63
Q

What is haemophilia A a deficiency of?

A

Factor VIII

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64
Q

What is haemophilia B a deficiency of?

A

Factor IX

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65
Q

What are 5 causes of DIC?

A

1) malignancy
2) sepsis
3 trama
4) obstetric complication
5) toxins

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66
Q

What is TTP due to a LACK of?

A

ADAMTS13

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67
Q

If you are ADAMTS13 negative what would this indicate?

A

TTP

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68
Q

What toxin can induce Haemolytic uraemic syndrome?

A

E. Coli 0157

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69
Q

What is the treatment for HUS?

A

plasma exchange

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70
Q

What happens in factor V leiden?

A

factor Va is not broken down, meaning increased production of thrombin –> increased risk of VTE

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71
Q

Acute leukaemia GENERALLY is the overprodcution of

A

BLAST CELLS - immature

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72
Q

What are the symptoms of BM failure

A

ANAEMIA - faigue, SOB, chest pain
THROMBOCYTOPENIA - bleeding
NEUTROPENIA - infection

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73
Q

What are risk factors for leukaemia?

A
  • chemotherapy
  • radiotherapy
  • Downs syndrome
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74
Q

What cells are prominent in AML?

A

neutrophils
monocytes
macrophages

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75
Q

What are Auer rods found in?

A

AML

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76
Q

What cells feature heavily in ALL?

A

T and b cells

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77
Q

What is a faggot cell, and what might it indicate?

A

“bundle of twigs”

Acute promyelocytic leukaemia (M3 - subtype of AML)

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78
Q

if you see a leukaemia with gum infiltration what should you think of?

A

Subtype of AML - M4 and M5

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79
Q

what mutation causes the majority of CML?

A

philadelphia chromosome - 9:22

BCR-ABL fusion gene

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80
Q

What can you now use to treat CML and how does it work?

A

tyrosine kinase inhibitors - e.g. imatinib

targets the BCR-ABL fusion gene which inhibits the disease process

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81
Q

what are smear cells on a FBC film indicative of?

A

CLL

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82
Q

What is it called when CLL is associated with other autoimmune problems such as ITP?

A

Evans syndrome

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83
Q

what is first line treatment for symptomatic CLL?

A

chlorambucil

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84
Q

What are myelodysplastic syndromes characterised by?

A

development of a clone of bone marrow stem cells with abnormal maturation resulting in: 1) functionallydefective blood cells and 2) reduction in number

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85
Q

give 3 major morphological features you may find in the blood in MDS?

A

1) WBCs - pelger huet cells - bilobed / immature neutrophils
2) platelets - micromegakaryocytes, hypolobated nuclei
3) RBCs = ring sideroblasts

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86
Q

by definition all patients with myelodysplastic syndrome have

A

<20%

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87
Q

what does RCMD-RS mean? and what haematological illness might you find it?

A

refractory cytopenia with multilienage dysplasia - with ringed sideroblasts - MDS

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88
Q

whats the difference between RAEB-I and RAEB-II?

A

Refractory anaemia with excess blasts-I = cytopenias with <5% blasts in blood and NO auer rods, and 5-9% blasts in the BM

RAEB-II = in blood: cytopenia OR 5-19% blasts OR auer rods, in BM dysplasia with 10-19% blasts or auer rods

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89
Q

What % of people develop AML from MDS?

A

50% in

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90
Q

what supportive treatment can be offered for MDS?

A
  • blood transfusions
  • EPO
  • GCSF injections
  • Abx
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91
Q

What kind of age distrbution does Myelodysplasia have?

A

elderly population - over 60 generally

92
Q

What is the mortality of MDS?

A

rule of thirds:
1/3 die of infection
1/3 die of bleeding
1/3 die of acute leukaemia

93
Q

what are the most common causes of aplastic anaemia?

A

1) idiopathic (70%)
2) inherited (10%)
3) secondary to malignancy / radiation / drugs / chemo (10-15%)

94
Q

What is the supportive treatment for AA?

A
  • blood products (leuodepleted)
  • Abx
  • iron chelation
95
Q

what are 3 complications of immunosuppressive therapy for aplastic anaemia?

A

1) relapse of AA (35% over 15 years)
2) clonal haem disorders: MDS / leukaemia / PNH (20% risk over 20 years)
3) Solid tumours (3% risk)

96
Q

What is the risk of relapse of Aplastic anaemia if treated with immunosuppression

A

35% over 15 years

97
Q

what is the most common form of aplastic anaemia?

A

Fanconi anaemia

98
Q

Name some congenital abnormalies found in 70% children with fanconi anaemia

A
  • short
  • weird thumbs
  • cafe au lait spots
    micro / hydrocephaly
  • hypogonadism
  • developmental delay
99
Q

a patient presenting with skin pigmentation, nail dystrophy and leukoplakia is likely to have…?

A

Dyskeratosis congenita

100
Q

What is leucoplakia? and what haematological disorder does it feature in

A

Development of white lesions on gums, inside mouth and sometimes tongue - feature of Dyskeratosis congenita

101
Q

Name a drug that promotes bone marrow recovery

A

oxymetholone

102
Q

What is the main chromosomal abnormality featuring in idiopathic aplastic anaemia and dyskeratosis congenita?

A

short telomeres

103
Q

how is dyskeratosis congenta inherited?

A

X-linked

104
Q

what is the definition of lymphomas?

A

a neoplastic (malignant) tumour of lymphoid cells

105
Q

in lymphomas where are tumours usually found?

A
  • lymph nodes, bone marrow and blood
  • sometimes spleen and GALT (MALT)
  • occasionally anywhwhere - skin, breast
106
Q

give 3 reasons why the adaptive immune system results in the risk of lymphoma

A

1) Rapid cell proliferation
2) dependent on apoptosis (90% normal cells die)
3) antigen specificity in T cells and B cells is by cutting & rejoining DNA (VDJ) - increasing point mutations/ translocations

107
Q

What is the general molecular basis of lymphoma?

A
  • tanslocations involving the Ig locus –> area where promoter is highly active (making LOADS OF t AND b CELLS NORMALLY) –> if oncogene is translocated closely downstream of the promoter you get upregulation of oncogene expression
108
Q

Give 3 examples of lymphoma oncogenes

A

bcl2
bcl6
Myc

109
Q

give 3 risk factors/causes for lymphoma

A

1) constant antigenic stimulation
2) infection (direct viral infection of lymphocytes)
3) loss of T cell function (HIV - immunosuppression)

110
Q

why is chronic antigen stimulation a risk factor for lymphoma and give 3 examples of conditions which relate to this

A

antigen stimulation triggers lymphocyte proliferation so there’s more chance of mutation

1) Chronic gut infection with H. pylori - GALT lymphoma
2) Sjogrens syndrome - (saliva gland) parotid lymphoma
3) Coeliacs (with uncontrolled diet) - small bowel T cell lymphom, EATL (enteropathy associatedT cell lymphoma) - v aggressive

111
Q

What is the classic example of a virus which infects t CELLS BY DIRECT VERTICAL TRANSMISSion, and what can this lead to?

A

HTLV1

adult T cell leukaemia lymphoma

112
Q

WHy do HIV patients have a higher risk of lymphoma? what type particularly?

A

have 60 fold increase in risk of B cell Non Hodgkins lymphoma, due to the loss of T cell regulation of EBV infected B cells

113
Q

What cells does EBV infect?

A

B lymphocytes

114
Q

Why are post-transplant lymphomas a thing

A
  • give patients immunosuppressants like cyclosporin & steroids to prevent T cell mediated organ rejection
  • this also allows uncontrolled EBV infected B lymphocyte proliferation resulting in lymphoma
115
Q

what antigens do you look for in immunohistochemistry when diagnosing lymphoma, and what information can this tell you?

A

CD markers - over 100 types

can tell you what type of lymphoma and what stage of development

116
Q

What is the most common type of lymphoma? (what%?)

A

B cell type non-hodgkins lymphoma - 80-85%

117
Q

What is a t(11;14) chromosomal translocation diagnostic for?

A

Mantle cell lymphoma - the translocation causes overexpression of cyclin D1 - leading to unregulated overgrowth of B cells

118
Q

What is it called when a low grade lymphoma changes into a high grade?

A

Richter transformation

119
Q

What markers are typically present in B cell lymphomas which are detected with immunochemistry?

A

CD5 & CD23

120
Q

Which lymphoma typically has a starry sky appearance on a histological examination?

A

Burkitt’s lymphoma

121
Q

Name an intermediate grade B cell lymphoma

A

Burkitt’s lymphoma

122
Q

What are 4 common low grade B cell lymphomas?

A

1) Mantle zone
2) follicular
3) small lymphocytic lymphoma / chromic lymphocytic leukaemia
4) marginal zone

123
Q

Name a high grade (rapid growth, very ill, masses develop quickly) B cell lymphoma

A

Diffuse large B cell lymphoma

124
Q

What type of lymphoma do you see sheets of large lymphoid cells

A

Diffuse large B cell lymphoma

125
Q

anaplastic large cell lymphoma mainly affects who?

A

children / young adults

126
Q

what’s the difference between Hodgkin and non-Hodgkin terms of spread characteristics?

A

Hodgkin’s = Spreads CONTINUOUSLY to adjacent lymph nodes, whereas non-Hodgkins spreads discontinuously,

127
Q

what do Reed-Sternberg cells indicate?

A

Classical Hodgkin Lymphoma

128
Q

what is the incidence of Hogkins lymphoma?

A

Bimodal - young 20-29 and another peak >60

129
Q

describe the staging for lymphoma

A

I - one group of nodes
II - >1 group of nodes same side of diaphragm
III - nodes above and below diaphragm
IV- extranodal spread

then suffix A = no extra red flags
B - unexplained weight loss >10% in 6 months / night sweats / fever

130
Q

What is the treatment for hodgkins lymphoma?

A

ABVD chemotherapy (2 or 6 cycles)

+/- radiotherapy

PET scans to check for persistance of active disease

131
Q

What is the current chemotherapy reigeme for Hodgkins lymphoma?

A

ABVD - given at 4 weekly intervals

Adriamycin
Bleomycin
Vinblastine
DTIC

132
Q

What is the advantage of ABVD over MOPP chemotherapy?

A

preserves fertility

133
Q

What are 2 negative long term SEs of ABVD treatment for HL?

A
  • pulmonary fibrosis

- cardiomyopathy

134
Q

What is a typical presentation of Non hodgkins lymphoma?

A
  • painless lymphadenopathy
  • compression symptoms
  • B symptoms (fever, weight loss, night sweats)
135
Q

What is the main change to the FBC in pregnancy?

A

macrocytic anaemia

–> RBC mass rises (120-130%) and plasma volume rises (150%) so net dilution

136
Q

How does pregnancy affect iron requirements?

A

Demand increases due to fetus and red cell mass increase -
foestus = 300mg
RBC expansion = 500mg

so increase daily intake RDA: 30-60mg supplements + 400mcg folic acid daily

137
Q

What can maternal anaemia be a risk for in pregnancy?

A

Low birth weight
Miscarriage
Puerperal sepsis (infection of the uterus post partum)

138
Q

What can iron deficiency in pregnancy be a risk for (3 things)

A
  1. IUGR (intrauterine growth restriction)
  2. prematurity
  3. postpartum haemorrhage
139
Q

what is the WHO recommendation for iron supplementation in pregnancy?

A

30-60mg Fe

+ 400 mcg folic acid - however this isnt advised in the UK

140
Q

what is the benefit of taking folic acid supplements during pregnancy?

A

reduces the risk of neural tube defects

141
Q

WHat happens to the platelet count in pregnancy?

A

Thrombocytopenia

in 13% women falls below 150 x 10(9)/L

142
Q

Give 3 main causes of thrombocytopena in pregnancy

A

1) gestational (physiological)
2) pre-eclampsia
3) ITP

  • can also be due to microangiopathic syndromes or others like BM failure, leukaemia, hypersplenism, DIC
143
Q

what are the 5 general criteria for gestational thrombocytopenia?

A
  1. Mild and asymptomatic thrombocytopenia typically >70 x 10(9) /L
  2. no past Hx of thrombocytopenia
  3. happens during late gestation
  4. no association with foetal thrombocytopenia
  5. spontaneous resolution after delivery .
144
Q

what proportion of women with pre-eclampsia get thrombocytopenia?

A

50%

145
Q

What are the Tx options for ITP in pregnancy?

A
  1. IV Immunoglobulin
  2. Steroids
  3. Anti D if Rh D +
146
Q

What are the 3 most common causes of mortality in pregnancy?

A

VTE
preeclampsia
haemorrhage
genital tract sepsis

147
Q

Give 4 main coagulation changes in pregnancy?

A

HYPERCOAGULABLE and HYPOFIBRINOLYTIC

  • increased thrombin generation
  • increased fibrin cleavage
  • reduced fibrinolysisi
148
Q

What is a big risk factor for maternal death due to PE?

A

BMI

+ FHx

149
Q

How should you treat women at high risk of VTW in pregnancy?

A 
prophylactic heparin (LMWH) 
TED stockings
150
Q

Which anticoagulant is advised for pregnant women (and why!)

A

Heparin - as does not traverse the placenta (whereas warfarin DOES cross the placenta)

151
Q

What type of thrombophilia is associated with recurrant miscarriage. + persistant lupus anticoagulant (LA) / anticardiolipin abs (ACL)?

A

APLS - antiphospholipid syndrome

152
Q

What type of antibodies are against RBC surface antigens?

A

IgM antibodies - anti-A & anti-B

153
Q

what type of antibodies are anti-D antibodies?

A

IgG

154
Q

What are the majority of the population in terms of the RhD antigen?

A

85% RhD +

15% RhD negative

155
Q

What type of blood can RhD + patients recieve?

A

RhD + and - cells

156
Q

What type of blood can RhD negative patients get?

A

they lack the RhD antigen
Therefore can MAKE RhD antibodies if exposed to the RhD+ antigens on RBCs

  • so best to give RhD -ve patients negative blood, although more important in pregnancy
157
Q

What type of reaction occurs if you give an RhD - patient RhD + blood?

A

May induce formation of anti-D antibodies (IgG) –> this does not cause agglutinaton of RBCs so not immediate haemolysis and death but delayed haemolytic transfusion reaction

158
Q

What problems in pregnancy can an Rh - mother with anti-D antobodies result in?

A

If mother exposed to Rh+ blood, can cause haemolytic disease of the newborn (HDN)

or severe fatal anemai and heart failure (hydrops fatalis)

159
Q

What is the standard way to prevent anti-D formation in a RhD- woman

A

give IM anti-D Ig when at high risk of feto-haemorrhage

160
Q

What blood types should you worry about in pregnant women?

A

If mother RhD- and foetus RHD + then you’d consider giving woman anti-D Ig

161
Q

What are you checking in a blood antibody screen?

A

Immune antibodies (IgG) in the blood (not the naturally occurring ABO antibodies that are IgM) that are atypical and occur in 1-3% patients

162
Q

What kind of haemolysis can happen in a blood transfusion where the patient has atypical immune antibodies in their plasma

A

can form antibody:antigen complexes with transfused RBCs resulting in an extravascular haemolysis in the spleen

163
Q

What group of patients should you give K negative blood to and why?

A

Women of childbearing potential - because anti-K can cause HDN

164
Q

What are the routine times to give a woman anti-D Ig if she is Rh negative?

A

28 and 34 weeks
during pregnancy if a sensitising event occurs (abortion, miscarriage, abdo trauma, external cephalic version)
At delivery if the baby is Rhd +

165
Q

What type of plasma can be given to everyone, but it’s in short supply?

A

AB - has no anti-A or anti-B antibodies in it

166
Q

What volume of blood loss should trigger blood transfusion?

A

30% blood volume lost

167
Q

how much Hb does 1 unit of blood give in a 70-80kg person?

A

1 unit = 10g/L Hb

168
Q

When should you crossmatch blood sbefore surgery, and when do you not need to bother?

A

Group and screen firsat and then Must crossmatch if there are antibodies present, but if no antibodies then don’t have to - just save sample in the fridge

169
Q

What patients require irradiated blood, and what severe complication can happen if it isn’t?

A

Immunosuppressed patients who cannot destroy incoming donor lymphocytes - this can cause transfusion associated graft vs host disease (TA-GvHD)

170
Q

give 3 indications for giving FFP (fresh frozen plasma)

A
  1. massive transfusion (blood loss > 150ml/min)
  2. DIC (with bleeding)
  3. Liver disease
171
Q

What is the treatment for reversing warfarin?

A

PCC - prothrombin complex concentrate

172
Q

Give 3 examples of (immune) causes of acute adverse reactions to a blood transfusion

A
  1. ABO incompatibility
  2. allergic / anaphylactic
  3. febrile non haemolytic
173
Q

What is TACO?

A

transfusion associated circulatory overload

174
Q

name some general symptoms that may arise in an acute reaction to a blood transfusion

A

fever, rigors, flushing, vomiting, dyspnoea, pain, loin pain, chest pain, urticaria, headache, collapse

175
Q

What is the likely diagnosis and treatment in a patient receiving a blood transfusion suddenly becoming febrile and experiencing chills/rigors?

A

Febrile non haemolytic transfusion reaction (FNHTR)

paracetamol +/- slowing/ stopping/ restarting transfusion

176
Q

What is the likely diagnosis if a patient suddenly comes up in an urticarial rash and starts wheezing after a blood transfusion?

A

Allergy transfusion reaction

Tx = IV antihistamines

177
Q

what is the cause of an Allergy transfusion reaction

A

aLLERGY TO PLASMA PROTEIN IN THE particular DONOR - won’t necessrily happen again, depends how common the allergen is

178
Q

How might a bacterial contamination of donor blood affect a patient receiving it in a transfusion?

A
  • similar presentation to ABO incompatibility

- fever, vomiting, flushing, collapse, tachycardia and low blood pressure, (SHOCK)

179
Q

what is the basic mechanism causing TRALI

A

anti-wbc antibodies in the donor’s blood (usually anti HLA or neutrophil) react with the antigens of recepient’s WBCs - aggregations get stuck in the pulmonary capillaries and release of neutrophil proteolytic enzymes and toxic 02 metabolites = lung damage

180
Q

describe delayed haemolytic transfusion reaction?

A
  1. 1-3% patients having transfusions develop immune antibody to an antigen they dont have (allmmunisation)
  2. Then if transfused again with blood containing the same antigen then patient has Abs which cause RBC destruction - Extravascular haemolysis (IgG - 5-10 days later)
181
Q

Describe the symptoms you might see in TA-GvHD

A

severe diarrhoea, skin desquamation, bone marrow failure, death

182
Q

which antibodies are able to cross the placenta - potentially causing HDFN

A

IgG Rh+ antibodies

183
Q

What is the risk of a hyperbilirubinaemia in newborns

A

kernicterus

184
Q

What is the treatment for neonatal jaundice?

A

light therapy +/- exchange transfusion

185
Q

Describe how the prophylactic anti-D Ig injection works?

A

–> anti-D Ig coat the RhD+ RBCs, which are then removed by mother’s reticuloendothelial system BEFORE they can sensitise mother to produce anti-D antibodies –> Must give anti-D Ig injection within 72 hours of the sensitising event

186
Q

give some examples of “sensitising events” during pregnancy which are indications for anti-D Ig

A

basically where FMH is likely to occur (fetal maternal haemorrhage)

  • -> spontaneous miscarriages
  • -> amniocentesis & CVS
  • –> abdo trauma
  • -> external cephalic version
  • -> stillbirth / intrauterine death
187
Q

apart from anti-D , what 2 other antibodies can cause severe HDN

A

anti-K (Kell)

anti-c

188
Q

What levels of Hb are classed as anaemia in men and women?

A

Men; <135g/L

Women: <115 g/L

189
Q

Causes of Macrocytic anaemia

A 
FATRBC
pregnancy 
Antifolates 
HypoThyroidism 
Reticulocytosis 
B12 defciency 
Cirrhosis - alcohol/liver disease
190
Q

Causes of microcytic anameia

A 
FAST 
Fe iron deficiency 
Anaemia of chronic disease 
Sideroblastic anaemia 
Thalassaemia
191
Q

CAUSES OF NORMOCYTIC Anaemia

A 
Acute blood loss 
Anaemia of chronic disease 
Hypothyroidism 
Renal Failure 
Bone Marrow Failure
Pregnancy 
haemolysis
192
Q

Give the signs you would see on a blood film that would be consistent with iron deficiency anaemia

A

Microcytic, hypochromic, poikilocytosis, anisocytosis, pencil cells

193
Q

Causes of Iron deficiency anaemia

A

Bleeding until proven otherwise, but consider all:

  1. Blood loss - tends to be GI e.g. gastric ulcer, meckel’s diverticulum, malignancy, menorrhagia
  2. increased use - pregnancy, children growing
  3. decreased intake - e.g. elderly malabsorption, prematurity
  4. malabsorption - coeliacs, post surgery
  5. intravascular haemolysis - MAHA, NPH
194
Q

Is ferritin high or low in anaemia of chronic disease

A

High (unless co-existing Fe-deficiency) - because Fe gets sequestered in macrophages to protect it from invading bacteria

195
Q

how do you diagnose sideroblastic anaemia

A

look for ringed sideroblasts in the bone marrow

196
Q

What are ringed sideroblasts?

A

erythrocyte precursors with iron deposited in the mitochondria which makes a ring around the nucleus

197
Q

describe a megaloblastic blood film

A

macrocytic anaemia, hypersegmented polymorphs, leucopenia, thrombocytopenia,

198
Q

What causes megaloblastic anaemia

A

due to inhibition of DNA synthesis during RBC production. E.g. cytotoxic drugs, folate deficiency, B12 deficiency.

199
Q

What are 3 megaloblastic causes of macrocytic anaemia

A

B12 deficiency, folate deficiency, cytotoxic drugs

200
Q

what is pernicious anaemia?

A

autoimmune atropohic gastritis, resulting in attack of the parietal cells so absence of HCL and

201
Q

how do you diagnose pernicious anaemia?

A

Anti-parietal cell antibodies
- Anti-IF antibodies

(used to do schillings test but outdated now)

202
Q

Treatment for B12 deficiency?

A

IM hydroxocobalamin (B12)

203
Q

causes of folate deficiency

A

Diet - e.g. not eating enough fresh leafy veg
Malabsorption - Coeliacs
Drugs - alcohol, methotrexate, trimethoprim
Increased turnover e.g. pregnancy, malignancy, renal dialysis

204
Q

What signs in the blood would you see in intravascular haemolysis?

A 
Increased bilirubin 
increased urobilinogen 
increased LDH
reticulocytosis (so increased MCV and polychromasia) 
may have pigmented gallstones

increased free plasma Hb
decreased haptoglobin (as it binds free Hb)
Haemoglobulinuria
Haem + albumin in the blood

205
Q

What is the inheritance of G6PD deficiency?

A

X linked recessive

206
Q

What things precipitate a haemolytic episode in G6PD deficiency?

A

oxidants: drugs - primaquine, aspirin, fava beans, acute infection,

207
Q

What does G6PD help synthesise to protect RBCs from oxidate damage normally?

A

glutathione

208
Q

What signs might you see in G6PD deficiency?

A 
Heinz bodies on a blood film, 
(Neonatal) jaundice 
Dark urine 
splenomegaly 
gall stones common
209
Q

how is spherocytosis inherited

A

autosomal dominant

210
Q

spectrin deficiency is seen in which haemolytic disorders?

A

Hereditary spherocytosis

Hereditary elliptocytosis

211
Q

what is the mutation causing sickle cell disease

A

single base mutation on codon 6 of beta-chain - GAG–>GTG (Glu –> Val) creasing HbS

212
Q

Why does SSD only manifest at 3 months of age?

A

corresponds to decreasing levels of Fetal Hb (HbF)

213
Q

How is sickle cell diagnosed?

A 
Heel prick test 
Blood film - sickle cells and taget cells 
sickle solubility test 
elelctrphoresis 
Family history
214
Q

Which antibodies stick to RBCs in paroxysmal cold haemaglobinuria?

A

Donath-Lansteiner antibodies

215
Q

what are the RBC markers that indicate a patient has paroxysmal nocturnal haemaglobinuria

A

GPI marker on the surface membrane

216
Q

what are the most serious complications of Paroxysmal nocturnal haemaglobinuria?

A

Thrombosis - PE, DVT, thrombosis in the hepatic veins - Budd-Chiari, superior and anterior mesenteric veins: ischaemia

217
Q

Treatment for PNH?

A
  • iron and folate
  • prophylactic Abx
  • monoclonal antibody therapy (prevents complement binding the the RBCs causing lysis) -> eculizumab EXPENSIVE!! `
218
Q

What infection causes HUS?

A

E coli

219
Q

What is Osler-Weber-Rendu syndrome?

A

aka hereditary haemorrhagic telangectasia - autosomal dominant condition characterised by abnormal blood vessels in mucous membranes and organs - get lots of nosebleeds

220
Q

Give 2 examples of congenital disorders which are a vascular cause of bleeding disorders

A
  1. osler-weber-rendu syndome

2. Ehler-Danlos

221
Q

what is deficient in Haemophilia A?

A

Factor VIII

222
Q

What is deficient in Haemophilia B?

A

Factor IX

223
Q

What is the manaement of von willebrands disease?

A

Desmopressin (stimulated more VWF)

VWF + F VIII concentrates

224
Q

What is storage pool disease?

A

congenital condition causing reduced platelet function resulting in increased bleeding. aka gray platelet syndrome

225
Q

Which clotting factors are affected by vitamin K deficiency?

A

2, 7, 9 and 10 and protein C/S

226
Q

DVT prophylaxis =

A

injections of LMWH (eg enoxaparin/clexane) + TED stockings

227
Q

Treatment of a PE/DVT=

A

LMWH (175 units/kg) + Warfarin +/- NOAC - stop LMWH once INR in therapeutic range (2.5)

My Year 5 Pathology (5 decks)

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