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MBBS - Year 2 > Haematology - Anaemia, red cell metabolism and transfusion > Flashcards

Haematology - Anaemia, red cell metabolism and transfusion Flashcards

1
Q

Amount of iron in avg man

A

4g total

30-45% less in avg woman

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2
Q

What % of iron is stored as Hb

A

65%

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3
Q

What % of iron is stored as ferritin

A

20-30%

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4
Q

What is iron stored as excluding Hb and ferritin

A

Myoglobin
Catalase
Various enzymes

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5
Q

What is iron status regulated by

A

Absorption

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6
Q

Iron requirements for men and women

A

Male: 0.5 - 1.0 mg/d
Menstruating female: +0.5 - 1.0mg/d
Pregannacy: +1 - 2mg/d
Growing children: +0.6 - 1.0mg/d

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7
Q

Key players in iron metabolism

A 
DMT 1 
Ferritin 
Transferrrin and transferrin receptors
Haemosiderin 
Ferroportin 
Hepcidin 
HFE
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8
Q

Function of DMT 1

A

Take up Fe2+ from gut into gut wall

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9
Q

When is DMT1 upregulated

A

Fe deficiency

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10
Q

What is ferritin

A

Intracellular storage form of iron in the liver

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11
Q

What is ferritin upregulated by

A

Fe excess

Infl

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12
Q

Role of transferrin

A

Carries iron around body to transferrin receptors allowing uptake into cells

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13
Q

When is transferrin upregulated

A

Fe deficiency

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14
Q

Role of ferroportin

A

Transfer iron for enterocyte into plasma

Opposite to DMT - 1

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15
Q

Haemosiderin

A

Partial degradation of haemoferritin

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16
Q

Role of hepicidin

A

Acute phase protein - feedback signal
Controls absorption by binding to ferroportin
Affected in anaemia of c/c disease

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17
Q

Can we actively excrete iron

A

No

Only passive loss through gut, skin, faeces

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18
Q

Haematinics

A

What is needed for blood cell formation

Iron - incorporated into haem
AA - make globin chain
Bone marrow blasts - DNA synthesis forms dividing cells to package the O2

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19
Q

Anaemia of c/c disease and hepcidin

A

C/c disease causes release of IL6 which upregulates hepcidin
Hepcidin is a competitive inhibitor of iron on ferroportin —> decreased uptake of Fe

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20
Q

Factors increasing the absorption of iron

A 
Increased Fe2+ and haem iron 
Acids and ascorbate in diet 
Pregnancy 
Solubilising agents - sugars, AA
Increased erythropoiesis 
Haemochromatosis 
Increased DMT-1 and ferroportin
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21
Q

Hameochromatosis

A

Genetic disorder causing body to absorb excessive amount of iron from diet
Iron accumulates over time and causes damage to several organs incl liver

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22
Q

Factors decreasing the absorption of Fe

A 
Increased Fe3+ and non-organic iron 
Alkali
Phytate (tea) and phosphates 
Tetracycline 
High iron diet 
Infections - hepcidin 
High body iron stores
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23
Q

Ix and mx of IDA algorithm

A

Confirm IDA
Determine cause
Treat anaemia
Treat underlying cause

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24
Q

IDA

A

Iron deficiency Anaemia

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25
Q

Microytic anaemias

A 
Thalassaemia trait 
Anaemia of c/c disease 
IDA 
Lead poisoning 
Sideroblastic anaemia
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26
Q

Labs for IDA

A

Low MCV
Low serum Fe
Low ferritin
Increased transferrin

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27
Q

Labs of ACD

A

Low MCV
Low serum Fe
Low transferrin

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28
Q

Labs for thalassaemia

A

Low MCV

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29
Q

Sideroblastic anaemia

A

Problem of haem ring

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30
Q

Labs for sideroblastic anaemia

A

Low MCV

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31
Q

Newer metrics for measuring anaemia

A

Ret-Hb
% of hypochromic red cells
Measuring functional iron delivery to the bone marrow

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32
Q

Using Ret-Hb to measure anaemia

A

Reticulocyte-Hb

Low is abnormal

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33
Q

Using % of hypochromic red cells to measure anaemia

A

Low is abnormal

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34
Q

Measuring functional iron delivery to the bone marrow to measure anaemia

A

Shorter term changes than Hb or MCV

Abnormal in IDA, ACD and thalassaemia

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35
Q

Causes of iron deficiency

A

Inadequate diet
Increased requirements
Malabsorption
Blood loss

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36
Q

Examples of increased requirements causing iron deficiency

A

Pregnancy

Growth

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37
Q

Examples of blood loss causing iron deficiency

A

Menstrual
GI
Urinary
Lung

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38
Q

Determining cause of IDA

A

Hx and examination
In UK, dietary deficiency alone is unusual - take diet hx
Menstrual hx - duration, clots, tampons, flooding
GI ix
Othe rcxauses usually obvious - pulm haemorrhage, PMH, urinary hameosiderin

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39
Q

Who gets GI ix for IDA

A

All men and all post-menopausal women
Symptomatic women
Women 45+ (or 50) check Fhx of colon cancer

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40
Q

GI ix for IDA

A 
Hx 
Faecal Hb - FIT
Tissue transglutaminase antibody (tTG)
Image upper and lower GI tracts 
The above are usually sufficient, if not test stool for parasites
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41
Q

What is important in GI hx for IDA

A

Drugs - NSAIDs, aspirin, bisphophonates

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42
Q

Imaging upper and lower GI tract for IDA ix

A

Gastroscopy (duodenal bx) and colonoscopy

Gastroscopy plus CT colonography

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43
Q

GI causes of IDA

A 
Hookworm infections
Coeliac disease 
Crohn's disease 
Gatritis/ oesphagitis
Peptic ulceration 
Gastrectomy 
Colon cancer - esp R sided 
Large polyps 
Haemorrhoids 
Diverticular bleeding
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44
Q

Iron replacement drug therapy

A

Oral ferrous sulphate for 3/12 post Hb-normalisation - 60mg Fe/ 200mg
Ferrous gluconate - 37mg/ 300mg
Sodium ironedetate - 27.5mg/ 5ml
Feric maltose - probably better tolerated (20mg)

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45
Q

What should be avoided in iron replacement therapy

A

Slow-release preparations

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46
Q

Parenteral iron for IDA

A

Rarely required

Modern total dose replenishment in 1-2 doses of ferric caboxymaltose/ derisomaltose

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47
Q

Benefits of parenteral iron

A

Hb responds equivalent
Replensishes stores faster
May be able to overcome some ACD
Low risk of allergic reactions, hypophosphataemia

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48
Q

When should parenteral iron for IDA be considered

A

If absorption is impaired

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49
Q

When do you switch to parental iron if oral fails

A

Relatively early (2/52 to 4/52)

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50
Q

What is folic acid synthesised by

A

Bacteria

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51
Q

Where is folic acid found

A

Green vegetable, offal

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52
Q

What is folic acid biologically active as

A

Polyglutamates

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53
Q

What is required for biological activity of folic acid

A

B12

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54
Q

Store of folic acid vs vit B12

A

Relatively small store vs large store

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55
Q

What is vit B12 synthesised by

A

Microorganisms, not by humans

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56
Q

Kay players in B12 metabolism

A 
R binders 
Gasttric parietal cell 
Gastric acid 
Intrinsic factor *
Pancreatic secretion 
Ileal receptor 
Transcobalamin- I/ II/ III
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57
Q

Which cells are affected by B12 and folate deficiency

A

All cells

Rapidly dividing cells most vulnerable e.g. bone marrow precursors, gut epithelium

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58
Q

Spp symptoms of B12 deficiency

A

Neuropathy and optic atrophy

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59
Q

Ix and mx of megaloblastic anaemia algorithm

A

Confirm haematological dx
Provide replacement therapy
Determine underlying cause
Clinically significant B12 deficiency can occur w/ out haematological effects

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60
Q

Confirming haematological dx of megaloblastic anaemia

A

Blod film
B12 and red cell folate levels
Condiser other causes of macrocytosis
Bone marrow

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61
Q

Can clinically significant B12 deficiency occur w/ out haematological effects

A

Yes

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62
Q

What can microcytic anaemia be divided into

A

Megaloblastic and non-megaloblastic

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63
Q

Causes of megaloblastic microcytic anaemia

A

B12/ folate deficiency or combined
Abnormal folate metabolism - MTX
Abnormal DNA synthesis
Myelodysplasia

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64
Q

Abnormal DNA synthesis causing megaloblastic macrocytic anaemia

A

Orotic acuduria
Azathioprine
Zidovudine

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65
Q

Orotic aciduria

A

Disease caused by enzyme deficiency resulting in decreased ability to synthesise pyrimidines

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66
Q

Causes of non-megaloblastic macrocytic anaemia

A 
Pregnancy 
Liver disease 
Alcoholism 
Retiuclocytosis 
Hypothyroidism 
Drugs 
Marrow infiltration 
Sideroblastic anaemia 
Cold agglutinins
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67
Q

B12 replacement therapy

A

Parenteral hydroxycobalamin
3 monthly replacements

Oral replacement if absorption intact

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68
Q

When is B12 given as prophylaxis

A

After total gastrectomy or ileal resection

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69
Q

Folate replacement therapy

A

Oral folic acid 4/12 or continuously

Folicinic acid for DHF-reductase inhibition - MTX

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70
Q

Why is folate given after B12 in combined deficiency

A

Initial folate may exacerbate neuropathy

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71
Q

When is folate given as prophylaxis

A

Pregnancy and preconception - neural tube defects normal risk vs high risk
Haemolysis
MTX therapy

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72
Q

Causes of folate deficiency

A 
Diet 
Increased utilisation 
Malabsorption 
Urinary loss 
Drugs
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73
Q

Diet causing folate deficiency

A

Anorexia
Children
Elderly
Alcoholics

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74
Q

Increased utilisation causing folate deficiency

A

Physiological - pregnancy, growth

Pathological - haemolytic, cancers, infl

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75
Q

Malabsorption causing folate deficiency

A

Diffuse small bowel diseases

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76
Q

Urinary loss causing folate deficiency

A

Haemodialysis

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77
Q

Drugs causing folate deficiency

A

Phenytoin - anti-seizure
Primidone - anti-epileptic
SSZ & related drugs
MTX

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78
Q

Causes of B12 deficiency

A 
Diet 
Gastric disease 
Ileal disease 
Infections
Pancreatic disease 
Transcobalamin-II deficiency
B12 destruction
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79
Q

Diet causing B12 deficiency

A

Vegan

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80
Q

Gastric disease casing B12 deficiency

A

Autoimmune gastritis

Major gastrectomy

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81
Q

Ileal disease causing B12 deficiency

A

Resection

Infl

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82
Q

Infections causing B12 deficiency

A 
Small bowel bacterial overgrowth 
Fish tapeworm (D latum)
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83
Q

B12 destruction causing B12 deficiency

A

Nitrous oxide

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84
Q

B12 absorption tests

A

57/58Co labelled B12
+/- intrinsic factor
Urinary excretion or whole body counting

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85
Q

Ix for causes of B12 deficiency

A 
Dietary hx 
Autoantibodies - anti-parietal cells, anti-intrinsic factor (pernicious anaemia)
B12 absorption tests 
Small bowel FT and bx 
Gastric bx 
Gastric and pancreatic function tests
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86
Q

Ix for causes of folate deficiency

A

Dietary hx
Autoantibodies - anti-gliadin, anti-0endomysela
Duodenal bx
Consider systemic diseases

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87
Q

Nutrients essential for normal RBC formation

A 
Iron 
Folate 
Vit B12 
Vit B6 
Vit C 
Vit E 
Copper 
Protein
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88
Q

Out of the nutrients essential for normal RBC function, which are we most likely to have deficiencies in

A

Iron
Folate
Vit B12

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89
Q

Symptoms seen in anaemia

A

V non-spp

Tiredness 
Weakness 
Pale skin 
Tachycardia 
SOB 
Chest pain 
Dizziness 
Numbness or coldness in extremities 
FTT and growth retardation in children
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90
Q

Epidemiology of IDA

A

Most widespread nutritional problem WW
Caused debilitated health of 500 million women, >60,000 deaths during childbirth
Increased morbidity and mortality, decreased productivity

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91
Q

Most vulnerable groups of IDA

A

Women of child-bearing age - menstrual blood loss and pregnancies
Children - increased requirements for Fe to meet growth (muscles, tissues, menarche)

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92
Q

What does iron bioavilabity reopen on

A

Physiological factors

Dietary factors

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93
Q

Risk factors that can lead to IDA

A

Long-term use of PPIs
Blood loss
Pregnancy
H. pylori infection

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94
Q

Dietary factors that explain ID in industrialised countries

A

Low bioavailability
Sedentary lifestyle
Lower micronutrient density - processed foods

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95
Q

Dietary sources of B12

A

Products of animal origin e.g. meat (esp liver), poultry, fish, milk, eggs
Fortified breakfast cereals
Fermented foods e.g. sauerkraut

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96
Q

Is folic acid naturally present in food

A

No - it is used to fortify foods

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97
Q

Folate vs folic acid absorption

A

Folic acid is highly bioavailable (85%) and folate are less absorbed (50%) and partially destroyed on cooking
Alcohol consumption in creases requirements

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98
Q

Dietary sources of folate

A 
Liver 
Yeast extract 
Green, leafy vegetables 
Legumes (beans, lentils)
Orange juice 
Fortified cereals
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99
Q

Vulnerable group for nutritional anaemias

A 
Infants and children (Fe)
Vegans (Fe and B12)
Pregnant women (Fe and folate)
Elderly (all 3)
Low income 
Ethnic minorities
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100
Q

Why is iron deficiency v rare in infants <4-6/12

A

Foetal Hb has sufficient stores
Late (i.e 2. mins delay) cord clamping is important
High efficiency of absorption from breast milk; cows filk formulas are fortified

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101
Q

Why is iron deficiency in infants more common after 6/12

A

Inappropriate weaning

Poor wt gain
Frequent infections
Developmental delay
Behavioural disorders

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102
Q

Iron and B12 deficiency in children

A

Prolonged bottle/ breast feeding may lead to ID
If weaning foods have a low Fe content –> ID
Vein children may require Vit B12 supplements

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103
Q

How do physiological adaptations in pregnancy affect

iron absorption

A

Fe absorption increases by ~50% in 2nd trimester and 4x in 3rd trimester
Despite this, the iron deficit is 400-500mg

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104
Q

Why are pregnant women at a higher risk of folate deficiency

A

Higher physiological requirements (DNA synthesis and other 1-C transfer reactions)

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105
Q

What is the significance of women w/ MTHFR mutation and pregnancy

A

They require addn folate to reduce their increased risk of NTDs

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106
Q

Anaemia in the elderly

A 
Higher risk of nutritional deficiencies 
Impaired absorption 
Poor quality meals in institutions 
Lower socio-economic status 
Mental problems
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107
Q

Preventive action of anaemia in the elderly

A

Increase the micronutrient density of the diet

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108
Q

Dietary assessment for anaemia

A

Growth in children (percentile charts)
Detailed diet hx - meal patterns and food group
Changes in appetite and food intake
Medical hx

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109
Q

Nice pre-conception advice and nutritional deficiencies

A

Assess couple’s risk of NTD

Thos at high risk should take folic acid 5mg daily until 12th week and those at normal risk 400micrograms

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110
Q

Lymph nodes in the head & neck

A 
Submental 
Sublingual 
Submandibular 
Parotid
Anterior cervical chain 
Posterior superficial cervical chain 
Supraclavicular 
Occiptal 
Postauricular
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111
Q

Border of axillary lymph nodes

A

Medial wall (chest wall)
Lateral (humerus)
Anterior (pectoralis major)
Posterior (lat dorsi)

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112
Q

Groups in inguinal lymph nodes/ groin nodes

A

Horizontal

Vertical

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113
Q

Infectious causes of lymphadenopathy

A

Viral/ bacteria/ parasitic (generalised)

In areas drained by lymph nodes or involving lymph nodes

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114
Q

Malignant causes of lymphadenopathy

A

Haematological - lymphoma, CLL, ALL

Non-haematological - metastatic

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115
Q

Miscellaneous causes of lymphadenopathy

A

SLE
Sarcoidosis
Drugs

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116
Q

How many segments is the abdomen divided into

A

9

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117
Q

Segments of the abdomen

A 
RH/ LH - Right/ left hypochondriac 
E - epigastrium 
RF/ LF - right/ left flank 
U - umbilical region 
RIF/ LIF - right/ left iliac fossa
SP - suprapubic
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118
Q

How does the liver expand in hepatomegaly

A

Downwards

Towards RIF

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119
Q

How does the spleen expand in splenomegaly

A

Diagonally

Towards RIF

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120
Q

Types of causes of splenomegaly

A

Infection
Infl
Congestion
Infiltration

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121
Q

Infective causes of splenomegaly

A

EBV
Malaria
Leishmaniasis
TB

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122
Q

Infl causes of splenomegaly

A

RhA

SLE

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123
Q

Congestive causes of splenomegaly

A

Cirrhosis (portal HTN)

Haemolysis

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124
Q

Infiltrative causes of splenomegaly

A 
Gaucher's 
Metastatic cancers 
Lymphoma
CLL 
Myeloproliferative neoplasms (PV/ MF/ CML)
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125
Q

PV

A

Polycythemia vera

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126
Q

MF

A

Myelofibrosis

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127
Q

What do RBCs need to function

A 
Efficient production (synthesis)
To be pliable (get through small vessels)
Hb on which to carry O2
Ensymes for metabolism 
Removal of defective cells
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128
Q

Erthryopoiesis

A

Synthesis of RBC in bone marrow

Erythroblast –> nucleated RBC –> reticulocyte –> mature red cells

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129
Q

Requirements for erythropoiesis

A 
Normal stem cell 
Normal maturation 
Healthy bone marrow microenvironment 
Growth factors 
Essential components
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130
Q

Growth factors needed ion erythropoiesis

A

Erythropoietin

GM-CSF

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131
Q

Addn essential components for erythropoiesis

A

Fe
Vit B12
Folate
AA

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132
Q

What are RBC membrane’s held together by

A

Proteins - some intrinsic (Band 3 which forms vertical scaffold) and horizontal scaffold formed by spectrin

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133
Q

Hb structure

A

Tetramer - 2 pairs of globin chains
Haem molecules bound to each globin
Iron within centre of haem

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134
Q

Phases of Hb production

A

Embryonic
Foetal
Adult

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135
Q

Does embryonic Hb have clinical implications

A

No

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136
Q

When does disease caused by defect in beta chain manifest

A

3/12 - 6/12 after birth

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137
Q

What chromosome codes for alpha chain

A

16

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138
Q

Where are alpha chains in Hb found

A

In all Hb from foetal to adult

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139
Q

What chromosome codes for beta-like chains in Hb

A

11

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140
Q

How many more alpha chains do we have compared to beta chains in Hb

A

2x as many alpha

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141
Q

Beta-like chains in different Hb

A

Beta in HbA (adult) (2:2 ratio for alpha)
Gamma in HbF (foetal)
Delta in HbA2 - v low levels from week 30 gestation

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142
Q

Why do RBC need enzymes for metabolism

A

Mature RBC has no nucleus or mitochondria so require enzymes for response to oxidative stress e.g. G6PD and ATP production

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143
Q

What happens if there are defects in the enzymes RBCs use for metabolism

A

Portion of RBCs that are susceptible to oxidative stress and die early due to ATP depletion

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144
Q

Normal RBC lifespan

A

120 days

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145
Q

How are old RBC removed

A

Macrophages - phagocytosis

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146
Q

Where are macrophages that remove old RBCs found

A

Spleen
Liver
Marrow - prevent damaged cells from entering circulation (protective mechanism)

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147
Q

What is anaemia

A

Reduced g of Hb/L blood below the age/ sex adjusted normal range q

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148
Q

What may anaemia occur as a result of

A

Too few RBCs
Too little Hb
An abnormally low haematocrit

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149
Q

Haematocrit

A

Ratio of RBC:plasma - aka packed cell volume

Reduced if increased plasma or decreased RBC

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150
Q

A/c vs c/c symptoms of anaemia

A

A/c - symtoms more marked

C/c - symptoms less severe; time for body to compensate

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151
Q

Less common symptoms of anaemia

A

Muscle cramps

Angina/ heart failure - anaemia exacerbates these condns

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152
Q

Signs of anaemia

A

Pallor - look in conjuctiva in darker skinned individuals
Tachypnoea
Tachycardia
Hypotension

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153
Q

Causes of normocytic anaemia

A 
ACD
A/c blood loss 
A/c renal failure 
Bone marrow disorders 
Mixed B12/ folate and iron deficiency
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154
Q

How can we classify causes of anaemia aside from MCV

A

Reduced RBC production

Increased RBC destruction (haemolysis) or loss

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155
Q

Causes of reduced RBC production leading to anaemia

A 
Defective stem cells 
Defective maturation 
Unhealthy microenvironment 
Absence of stimulation by growth factors 
Lack of components for RBC formation
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156
Q

Reduced RBC production as a result of defective stem cells

A

Inherited e.g. Diamond-Blackfan anaemia (rare)

Acquired - drugs, infections, immune (aplastic anaemia)

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157
Q

Aplastic anaemia

A

Bone marrow does not produce new blood cells

Empty bone marrow on bx

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158
Q

Defective maturation leading to reduced RBC production

A

Lack of nutrients e.g B12 deficiency

Myelodysplasia

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159
Q

Unhealthy microenvironment leading to RBC production

A

Damaged e.g. radiation, infections

Lack fo space due to fibrosis, haematological malignancy, non-haematological malignancy

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160
Q

Reduced RBC product as a result of absence of stimulation by growth factors

A

Decreased erythropoietin - renal failure

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161
Q

Lab findings for reduced RBC production leading to anaemia

A

Usually normocytic and normochromic - unless deficiency Fe, B12 or folate
Reticulocytes not raised

162
Q

Myelodysplasia

A

Failure to produce normal RBC

163
Q

What causes ACD

A

Ineffective iron utilisation due to raised hepcidin

164
Q

What is ACD seen in

A

C/c infl e.g. RhA, IBD
C/c infection e..g pneumonia, TB
Malignant disease

165
Q

Haemolysis

A

Immature breakdown of RBCs

166
Q

What does hameolysis lead to

A

Erythropoietic hyperplasia

Reticulocytosis

167
Q

Erythropoietic hyperplasia

A

Marrow produces 6-8x normal rate

168
Q

Signs of haemolysis

A

Due to formation of bilirubin

Jaundice
Dark urine
Gallstones - (RBC pigment) +/- anaemia

169
Q

Blood results in haemolysis

A 
Anaemia - normocytic or microcytic (reticulocytosis)
Raised reticulocyte count 
Raised bilirubin 
Raised LDH 
Low haptoglobin - binds to free Hb
170
Q

How can the causes of haemolysis be divided

A

Abnormality within cell - intrinsic

Abnormality outside cell - extrinsic

171
Q

Types of cell abnormalities causing haemolysis

A

Membrane - membranopathies
Metabolism (enzymes) - enzymopathies
Hb - haemoglobinopathies

172
Q

Examples of inherited RBC membranopathies

A

RBC can’t maintain biconcave shape

Hereditary spherocytosis (HS)
Hereditary elliptocytosis (HE)
Hereditary stomatocytosis
173
Q

Consequences of RBC membranopathies

A

RBC more easily damaged

Macrophage removal - shortened RBC life

174
Q

Inheritance pattern of inherited RBC membranopathies

A

Usually autosomal dominant (occasionally recessive or sporadic)

175
Q

What may inherited RBC membranopathies cause in neonates

A

Prolonged neonatal jaundice and mild anaemia presenting at any age

176
Q

Are RBC membranopathies jaundice fluctuant

A

Yes - worse in infections

177
Q

What may aplastic crises be precipitated by

A

Parvo virus (B19)

178
Q

Lab findings for inherited RBC membranopathies

A 
Anemia - usually mild 
Reticulocytosis 
Raised bilirubin 
Raised LDH 
Blood film shows abnormally shaped RBC**
Direct antibody test -ve (not autoimmune)
179
Q

Ic for inherited RBC membranopathies

A

Fhx
Blood film
Haemolysis screen
Special tests

180
Q

Mx for inherited RBC membranopathies

A

Folic acid supplementation

Splenectomy (HS)

181
Q

Most common RBC enzymopathy

A

Deficiency in G6PD - susceptible to oxidative stress

182
Q

Inheritance pattern of G6PD deficiency

A

X linked recessive

M > F

183
Q

Where is inherited G6PD deficiency most common

A

Africa and Mediterranean

184
Q

What can oxidant stress cause in a pt w/ G6PD deficiency

A

A/c episodes of haemolysis

Oxidants may be drugs, infections, moth balls, fava beans

185
Q

Hb production

A

Alpha globin chain made from foetus onwards (4 genes, 2 each chromosome) pair w/ beta-like globin chains (2 genes, 1 each chromosome)
Adult ratio alpha: beta ~ 1:1 (2:2 of each chain)

186
Q

Thalassemia

A

Reduced alpha/ beta globin chain synthesis

187
Q

Where is thalassaemia most common WW

A

Asia
Africa
South Mediterranean

188
Q

Consequences of thalassaemia

A

Chain imbalance
Excess alphas or beta chains ppt
Precipitated chains damage RBC membrane
Damaged cells destroy prematurely by macrophages

189
Q

Thalassaemia classification

A 
Alpha thalassaemia 
Beta thalassaemia 
Thalassaemia major 
Thalassaemia trait 
Thalassaemia intermediate
190
Q

Chains in alpha thalassaemia

A

Too few alpha chains

191
Q

Chains in beta thalassaemia

A

Too few beta chains

192
Q

Number of chains in thalassaemia major

A

No alpha/ beta chains

193
Q

Chains in thalassaemia trait

A

Reduced alpha/ beta chains so no transfusions required

194
Q

Thalassaemia intermediate

A

Mixed clinical picture

Not as affected

195
Q

Clinical features of beta thalassaemia major

A

Severe anaemia from 3/12 to 6/12 - beta gene mutations as opposed to deletions
Enlargement of liver and spleen
Expansion of bone marrow

196
Q

How is beta thalassaemia detected

A

New-form screening - treat w/ transfusions

197
Q

Clinical features of alpha thalassaemia

A

Usually caused by alpha deletions, not mutations
Fatal in utero (hydrops fetalis)
People born w/ 1/4 alpha genes have HBH disease

198
Q

HBH disease

A

Tetramer of 4 beta chains

Variable phenotype - intermediate

199
Q

Clinical features of thalassaemia trait

A

Mild microcytic anaemia
Asymptomatic
‘Carrier’ - can pass gene onto child

B thalassaemia trait (1 of 2 genes affected)
Alphas thalassaemia trait (1-2 pf the 4 genes affected)

200
Q

Alpha thalassaemia - genetic counselling

A

Important to know whether 2 genes deleted from same chromosome
Antenatal screening to identify the type of alpha thalassaemia

201
Q

Alpha-0 vs alpha-plus thalassaemia

A

Alpha-0 is when 2 genes are deleted from same chromosome

Alpha-plus is when 2 genes are deleted from different chromosomes

202
Q

Thalassaemia dx

A

Hypochromic microcytic anamia (excl Fe deficiency)
Hb electrophoresis or HPLC
Genetic analysis

203
Q

Hb electrophoresis in thalassaemia

A

Beta thalassaemia trait - increased HbA2
Beta thalassameia major - absence HbA
Cannot pick up alpha trait

204
Q

Thalassaemia major mx

A

Lifelong transfusions every 3/52 - 4/52 to keep Hb > 100g/L
Splenectomy - reduce blood requirements
Allogeneic bone marrow transplantation

205
Q

Success rate of allogeneic bone marrow transplantation in thalassaemia major

A

> 80% - curative

206
Q

Allogeneic transplantation vs autologous

A

Allogeneic stem cels come from a donor

Autologous stem cell come from pt

207
Q

Mx of thalassaemia trait

A

Avoid Fe unless Fe deficient

Genetic counselling

208
Q

SCD

A

Sickle cell disease

209
Q

Genetics in SCD

A

Point mutation leads to single AA substitution valine —> glutamate at position 6 beta chain - forms HbS
Homozygous HbS = disease but heterozygous = trait

210
Q

What does HbS form

A

Crystals when exposed to low oxygen levels - causes ‘sickling’ of RBC

211
Q

Sickle cell trait

A

Benign condn - no/mild anaemia, normal appearance of RBC

212
Q

What % of total Hb is HbS in sickle cell trait

213
Q

When should sickle cell trait patients take care

A

During anaesthesia (and high altitude)

214
Q

Is genetic counselling required for sickle cell trait

215
Q

Clinical features for sickle cell disease

A

C/c haemolytic anaemia from 3/12 - 6/12 old (when HbF —> HbA)

216
Q

When is the rate of haemolysis in SCD increased

A

During crisis

217
Q

Usual Hb amount in SCD

A

60-90g/ L

Symptoms of anaemia often mild - HbS oxygen dissociation curve shifted to R

218
Q

Sickle cell complications

A

Occlude vessel

Damage to skin on legs may cause c/c ulceration and sickly in lungs may ppt chest pain

219
Q

Vessel occlusion in SCD

A

Can cause symptoms e.g.
Pain (esp bones)
Organ damage
Splenic infarction from age 2 - auto splenectomy
Organ engorgement with blood can occur (sequestration - spleen, liver)

220
Q

Blood film in SCD

A

Sickle cells
Target cells
Nucleated red cells
Howell-Jolly bodies (splenic atrophy)

221
Q

SCD lab findings

A

Spp cells on blood film
Sickle solubility screen +ve - HbS less soluble when reduced O2
Hb electrophoresis/ HPLC shows HbS, no HbA, variable amounts HbF

222
Q

What does mx of SCD focus on

A

Preventing crises and infections associated w/ hyposplenism

May requires stem cell transplantation

223
Q

Prophylactic mx of SCD

A

Avoid opting factors
Folic acid supplementation
Pneumococcal vaccine; regular oral penicillin
Hydroxycarbamide

224
Q

Hydroxycarbamide for SCD

A

For recurrent crises

Increases amount of HbF, reducing sickling

225
Q

Mx for SCD crises

A

Analgesia (opiates), rest, rehydration, oxygen +/- abx

Blood transfusion/ exchange transfusion - if severe

226
Q

Can SCD and beta thalassaemia co-exist

227
Q

Abnormalities outside the cell (extrinsic) that can cause haemolysis

A

Antibody attack
Mechanical trauma
Infection
Chemical and physical agents

228
Q

Antibody attack causing haemolysis

A

Antibodies primed to only attack foreign cells
Occasional antibodies attack own cells = autoimmune
Autoimmune atacking RBC = AIHA

229
Q

AIHA

A

Autoimmune haemolytic anaemia

230
Q

How can AIHA be detected

A

Using Direct Antiglobulin Test (Coombs)
Warm: antibody reacts w/ RBC at 37 degrees (IgG)
Cold: antibody reacts w/ RBC below 37 degrees (IgM)

231
Q

AIHA causes - warm IgG

A

Idiopathic

Secondary - autoimmune condn, disordered immune system, drugs

232
Q

Disordered immune system causing AIHA (warm IgG)

A

CLL

Low grade lymphoma

233
Q

Drugs causing AIHA (warm - IgG coated)

A

Drug: RBC membrane complex - penicillin

Ig against RBC membrane - methyldopa

234
Q

AIHA causes - cold (IgM - coated)

A

Idiopathic

Secondary - lymphoma , infections, paroxysmal cold haemoglobinuria - RARE - syphilia

235
Q

Infections causing AIHA - cold IgM

A

Mycoplasma pneumonia

EBV

236
Q

AIHA lab findings

A

Haemolysis

Anaemia 
Reticulocytosis 
Raised LDH 
Raised unconjugated bilirubin 
\+ve DAT (Coombs)
Blood film - spherocyte IgG; agglutination IgM
237
Q

AIHA mx

A 
Remove or treat underlying cause e.g. drugs/lymphoma 
Keep pt warm if IgM (cold-reacting)
Folic acid supplementation 
Transfusion 
Immune suppression 
Splenectomy
238
Q

Immune suppression as mx of AIHA

A

Corticosteroids (warm)

Rituximab (cold and relapsed warm)

239
Q

When will a splenectomy be performed for AIHA

A

Resistant cases - less helpful if IgM

240
Q

Mechanical trauma as an extrinsic cause of haemolysis

A

Microangiopathic haemolytic anaemia
Faulty mechanical heart valve
March haemoglobinuria

241
Q

Microangiopathic haemolytic anaemia

A

TTP
DIC
HUS

242
Q

TTP

A

Thrombotic thrombocytopenic purpura

243
Q

HUS

A

Haemolytic uraemic syndrome

244
Q

March haemoglobinuria

A

Repeat capillary faults in the feet

245
Q

DAT (Coombs) when mechanical trauma is causing haemolysis

A

-ve (not immune)

246
Q

Why would urine be +ve for Hb when mechanical trauma is causing hameolysis

A

Hameolysis is hapenning in blood vessels not spleen/ liver

247
Q

Infections causing haemolysis

248
Q

Chemicals and physical agents causing haemolysis

A

Drugs - dapsone (oxidative haemolysis)
Copper - Wilsons disease
Lead burns
Snake and spider bites

249
Q

PNH

A

Paroxysmal nocturnal haemoglobinuria

Small print cause of intravascular haemolysis

250
Q

Key blood tests before a blood transfusion

A 
FBC 
U&Es
LFTs 
Coag screen 
Group and antibody screen - identifies blood group
251
Q

How long is a serum sample saved for in case of transfusion

A

7/7 to be used for cross-matching

252
Q

How does antigen and antibody expression on RBCs vary with age

A

Foetus and newborns have relatively low levels of Ag on surface which protects them from incompatibility with mother’s blood group

253
Q

Antigens and antibodies in blood group A

A

“A’ antigen of red cell surface

Anti-B antibodies in plasma

254
Q

Antigens and antibodies in blood group B

A

“B’ antigens on red cell surface

Anti-A antibodies in plasma

255
Q

Antigens and antibodies in blood group AB

A

“A” + “B’ antigens on red dell surface

No antibodies in plasma

256
Q

Antigens and antibodies in blood group O

A

Small ‘H’ antigens on red cell surface

Anti-A and Anti-B antibodies in plasma

257
Q

Determining the pts ABO and Rh D status

A

Use the pt’s red cells and monoclonal IgM anti-A, anti-B, anti-D - and once agglutinated cannot fall into gel
Use pt’s serum and donor A and B to ensure correct antibodies are present

258
Q

Improving transfusion safety

A

Second sample required if no previous blood group
Compare results w/ previous blood bank results
Only accepts correctly labelled samples
Use barcodes - a ‘closed system’ in lab
Use electronic pt identification

259
Q

For avg wt pts, how much will 1 unit RBC rise Hb

260
Q

How should red cell support be given if bleeding rapidly

A

20 - 30 minutes

261
Q

How should red cell support be given if stable

A

Given over 2-4hrs

262
Q

Does ABO and RhD need to be identical for platelet transfusion

A

No just compatible

263
Q

How long should platelet support be given over

264
Q

Which pts might need platelets

A

Thrombocytopneia due to failure of marrow production e.g. after chemo
Functional platelet disorder w/ bleeding e..g inherited platt disorder
‘Dilutional’ thrombocytopenia e.g massive bleeding
Thrombocytopenia which is multifactorial and associated w/ bleeding e.g. liver

265
Q

Which clotting factors does FFP contain

A

All of them

266
Q

What can FFP be refined to

A

Cryroprecipitate - high in factor VIII and fibrinogen

267
Q

When is FFP used

A 
DIC w/ bleeding 
Massive transfusion (check clotting)
Plasma exchange in TTP
Liver disease w/ abnormal clotting 
Some factor deficiencies where factor concentrate bis not available
268
Q

Problems w/ future transfusions

A

Possible antibody formation to other red cell antigens
Pt can no longer be blood donor
Increased risk of transfusion reactions

269
Q

How can antibodies other than anti-A or anti-B be acquired

A

During pregnancy or transfusion

270
Q

When is an alloantibody likely to be formed to a red cell antigen

A

The more blood a pt receives

271
Q

What is the timing of G&S sample the basis of

A

the 72-hr rule - a new antibody may be forming

272
Q

What are pts w/ red cell antigen allaoantibodies at risk of

A

Delayed haemolytic transfusion reactions - need blood cross-matched to ensure compatibility
May form other antibodies

273
Q

What grade are most transfusion reaction

274
Q

Examples of severe transfusion reactions

A

Anaphylaxis
Bacterial contamination
A/c and delayed haemolysis

275
Q

Greatest risk to pts getting a blood transfusion

A

Getting the incorrect blood component as ABO incompatibility can be rapidly fatal

276
Q

Alternatives to blood products when treating anaemia

A

Treatment of underlying cause

Iron tablets, IV iron, Vit B12 and folic acid, erythropoietin

277
Q

Alternatives to blood products to treat thrombocytopenia

A

Platelets only if unavoidable, corticosteroids, TXA, maximise clotting - avoid aspirin, NSAIDs

278
Q

Porphyria

A

Group of disorders caused by build up of natural chemical that produce porphyrins
Porphyrins are essential for Hb function

279
Q

Symptoms in a/c attacks of porphyria

A 
Unexplained abdominal pain 
Nausea and vomiting
Constipation 
Neuropsychiatric symptoms 
\+/- hyponatraemia
280
Q

Haematinic

A

Nutrient needed for formation of blood cells

281
Q

Unconjugated vs conjugated bilirubin

A

Unconjugated bilirubin is fat soluble

Conjugated bilirubin is water soluble

282
Q

Where does conjugated bilirubin appear

A

Urine

Faeces

283
Q

Bilirubin metabolism

A

Unconjugated bilirubin is found in blood stream

Taken into canaliculus and conjugated

284
Q

How does haemolytic jaundice affect the production of bilirubin

A

Increases it
More bilirubin is conjugated and excreted than normal, but the conjugation mechanism is overwhelmed –> large amount of unconjugated bilirubin in blood

285
Q

What might cause decreased bilirubin uptake by liver cells

A

Inability of the hepatocytes to take up bilirubin from blood —> unconjugated bilirubin accumulates

286
Q

How does impaired bilirubin conjugation affect unconjugated bilirubin

A

Causes it to be retained by the body

287
Q

What is defective secretion of conjugated bilirubin from liver cells associated w/

A

The inability of the hepatocytes to secrete conjugated bilirubin after it has been formed
Conjugated bilirubin returns to the blood

288
Q

How do the blood levels of conjugated bilirubin change in an obstruction of biliary network (intrahepatic or extrahepatic)

A

Increase

Biliary calculi causes backup and reabsorption of conjugated bilirubin

289
Q

Beware painless jaundice

A

Slowly evolving
Continuous increase in bilirubin
No colic type systems
Pancreatic cancer

290
Q

Urine colour in obstructive liver disease

291
Q

Faeces colour in obstructive liver disease

292
Q

Bilirubin levels in obstructive liver disease

A

Elevated (conjugated)

293
Q

Bilirubin levels in haemolytic liver disease

A

Elevated (unconjugated)

294
Q

Urobilinogen in obstructive liver disease

295
Q

Urobilinogen in haemolytic liver disease

296
Q

Causes of neutropenia

A 
Congenital (Fanconi's anaemia)
Immune mediated (SLE, Feltys)
Infection (sepsis, HIV, influenza)
Bone marrow failure 
Chemo, drugs 
Radiation
297
Q

Bacterial causes of neutropenic sepsis

A 
Staph A 
Coagulase -ve staph 
Viridian strep 
Enterococcus
E. coli, enterobacter
Psedomonas 
Klebsiella 
Listeria
298
Q

Fungal causes of neutropenic fever

A 
Aspergillus 
Pneumocystitis jiroveci (PCP)
Fusraium 
Zygomycosis 
Candidasis
299
Q

Viral causes of neutropenic fever

A 
Herpes simples 
CMV 
VZV
RSV
Parainfluenza viruses 1-4
Influenza viruses A & B
Adenoviruses
300
Q

Primary prevention of infection

A

Prevent or reduce exposure

Immunisation

301
Q

Secondary prevention of infection

A

Chemoprophylaxis (abx, antivirals)

302
Q

Tertiary prevention of infection

A

Effective treatment

Phsyio

303
Q

Possible causes of splenectomy

A

Surgery (trauma, RTA)
Immunologic - ITP
Hypersplenism (function asplenia) - thalassaemia, portal HTN
Malignancy - Hodgkin lymphoma, ovarian cancer

304
Q

Functional asplenia

A

Splenic tissue is present but does not function well vs anatomical asplenia, where the spleen is not present

305
Q

Causes of functional hyposplenism

A 
Autoimmune disorders - SLE
Haematological diseases - SCD, haemophilia
Lymphoproliferative disease (NHL, CLL)
Infiltrative disease  
Intestinal disorders
306
Q

Functional hyposplenism

A

Splenic activity is diminished or absent in an anatomically present spleen

307
Q

Infiltrative diseases causing functional hyposplenism

A

Sarcoidosis

Amyloidosis

308
Q

Intestinal disorders causing functional hyposplenism

A

Crohns and Whipple’s disease

309
Q

Most common pathogen causing post-splenectomy sepsis

A

Strep. pneumonia followed by H. influenza

310
Q

Preventing infections in absent/ dysfunctional spleen

A 
Pneumococcal vaccine 
H. influenza vaccine 
Meningoccoal vaccine (B,. C, ACWY)
Infelunze vaccine 
Pt education, info and documentation 
Abx prophylaxis
311
Q

When should the pneumococcal vaccine be administered to prevent infections in absent spleen

A

2/52 prior to splenectomy

Re-immunisation necessary

312
Q

Abx prophylaxis to prevent infections in absnet/ dysfunctional spleen

A

Penicillin V/ amoxicillin (first 2 years)

313
Q

What does the monospot test look for

314
Q

Crossmatching blood

A

Test donor blood against pt for transfusion

315
Q

Standard admin time for red cell transfusion

316
Q

Standard admin time for platelet transfusion

317
Q

Standard admin time for FFP transfusion

318
Q

Standard admin time for cryoprecipitate transfusion

319
Q

Key things before transfusion of blood components

A

Check - you have right pt
Check - you have right blood component
Monitor - the pt before, during and after for adverse events incl reactions
Seek - clinical or transfusion lab advice if concerned/ in doubt

320
Q

Complications w/ haematinic replacement

A

Transfusion: allergic reactions, fever, a/c immune haemolytic anaemia
Fe replacement: headaches, vomiting

321
Q

When do we see anisocytosis on a blood film

A

Myelodysplasia

322
Q

When do we see target cells on a blood film

A

IDA

Post splenectomy

323
Q

When do we see Howell-Jolly bodies on a blood film

A

Severe anaemia

Post splenectomy

324
Q

When do we see Heinz bodies on a blood film

A

G6PD deficiencies

Alpha Thalassaemia

325
Q

When do we see reticulocytes (if raised) on a blood film

A

Haemolytic anaemia

326
Q

When do we see spherocytes on a blood film

327
Q

When do we see schistiocytes on a blood film

A

Haemolytic anaemia

328
Q

When do we see smudge cells on a blood film

329
Q

When do we see sideroblasts on a blood film

A

Myelodysplastic syndrome

330
Q

Reticulocytes vs RBC

A

Reticulocytes are immature so still have RNA and are larger than RBCs

331
Q

What does it mean if reticulocytes are raised by pt is NOT anaemic

A

Impaired bone marrow function

Lack of epo stimulus

332
Q

MAHA

A

Micronagiopathic Haemolytic Anaemia

333
Q

What is Micronagiopathic Haemolytic Anaemia

A

Intravascular destruction of red cells in presence of abnormal microcirculation/ structural abnormalities in small blood vessels

334
Q

What is haemolytic uraemic syndrome

A

Condn characterised by triad of MAHA, AKI and thrombocytopenia
Most cases occur in children and are diarrhoea related (E. coli)

335
Q

What is disseminated intravasc coagulation

A

Acquired syndrome characterised by activation of coagulation pathways –> intravasc thrombi and depletion of platelets and clotting factors

336
Q

What is paroxysmal nocturnal haemoglobinuria

A

Acquired disorder characterised by intravasc haemolysis and thrombophilia
Small print cause of MAHA

337
Q

What type of bilirubin is found in blood in a jaundiced pt

A

Uncojugated

338
Q

Why is there dark urine in jaundiced pts

A

Urobiliogen - haemoglobinuria

339
Q

What should LNs be assessed for

A 
Size
Position 
Shape 
Consistency 
Mobility 
Tenderness 
Isolated LN or several coalesce?
340
Q

Glossitis

A

Enlarged tongue due to infl

Seen in IDA

341
Q

Examination findings of splenomegaly

A

Spleen palpated >2cm below costal margin

342
Q

Ferritin in ACD

A

Normal or raised

343
Q

LDH in CLL

344
Q

When would you see pencil cells on a blood film

345
Q

How might platelets change in IDA

A

Can increase

346
Q

Polychromosia

A

Stained reticulocytes - RNA is bluish

347
Q

What is every blood donation tested for

A 
ABO 
Rh 
Hep B, C, E
Syphilis 
HTLA
348
Q

Risk of anaphylaxis w/ blood transfusions

A

Low in general but generally high risk in plasma based components

349
Q

Can granulocytes be given as a transfusion

A

Yes but is very rare - must be discussed w/ haem consultant

Indications incl sepsis w/ reversible BM failure

350
Q

What extra blood producst can be transfused

A

PCC
Anti D - prevents haemolytic disease of newborn, given to any pregnant women in hosp (sensitising event)
Fibrinogen concentrate

351
Q

Transfusion in Rhesus D pts

A

D -ve can receive +ve blood, but may develop anti-D antibodies
D-ve pts of child-bearing age should never receive +ve blood - risk of haemolytic disease of newborn

352
Q

Alloantibodies

A

Antibody produced in pregnancy, transfusion or transplantation against an antigen not presents on person’s RBC

353
Q

What are blood group O universal donors for

A

RBC only

Never FFP

354
Q

Why is iron given through IV infusion in an active infection

A

Oral iron is contraindicated

Part of immune response

355
Q

GVHD

A

Graft vs host disease

Graft cells recognises recipients cells as foreign and attacks them

356
Q

What type of blood component must HL pts receive

A

Irradiated

Pts are given a card to show hospitals

357
Q

Possible reactions to transfusions

A 
Febrile 
A/c haemolytic reaction 
Anaphylaxis 
TACO 
TRALI 
Delayed haemolytic reaction
358
Q

How do you respond to a febrile reaction during a blood transfusion

A

Discontinue transfusion or continue at a reduced rate

359
Q

What would cause an a/c haemolytic reaction after a transfusion

A

Incompatible blood reaction

360
Q

What is seen in an a/c haemolytic reaction to transfusion

A

Pt goes into shock, a/c renal failure or DIC

361
Q

Symptoms of an a/c haemolytic reaction to a transfusion

A 
Pyrexia 
Chills 
Rigours 
Hyper/ hypotension
Flushing 
Rashes 
Pain 
SOB 
Generally feeling unwell
Reduced urine output (late sign)
362
Q

TACO

A

Transfusion Associated Circulatory Overload

363
Q

What is seen in a TACO

A

A/c or worsening pulmonary oedema within 6 hrs of a blood transfusion

364
Q

Symptoms of a TACO

A

A/c resp distress
Tachycardia
HTN
+ve fluid balance

365
Q

How is a TACO treated

A

Stopping transfusion

Giving diuretics

366
Q

TRALI

A

Transfusion-related a/c lung injury

367
Q

What is a TRALI

A

An infl reaction caused by antibodies of donor cells in blood transfusion
Infl cells cause leakage in lungs
Occurs within 2-6 hrs

368
Q

Symptoms seen in TRALI

A 
Pink stained, frothy sputum 
Bilateral pulmonary oedema - CXR
Hypotension 
Fever 
Rigors
369
Q

Treatment of a TRALI

A

Oxygen and ventilation

Recovery in 1-3 days

370
Q

Delayed haemolytic reactions to blood transfusions

A

Secondary immune response (24hrs to 14 days)

Pt is already alloimmunised to red cell antigens

371
Q

Whats sites should be avoided for venepuncture

A 
Infection/ infl 
Brusing 
AV fistula 
Side of mastectomy/ node dissection 
Side of hemiparesis - stroke
372
Q

Order of draw of blood bottles

A 
Blue 
(Red)
Yellow 
Green
Lavender 
Pink
Grey
373
Q

What is sampled for in blue blood bottles

A

Coagulation studies

374
Q

What is sampled for in yellow blood bottles

375
Q

What is sampled for in green blood bottles

A

Cardiac enzymes

376
Q

What is sampled for in lavender blood bottles

377
Q

What is sampled for in pink blood bottles

A

G&S

Crossmatch

378
Q

What is sampled for in grey blood bottles

A

Glucose
Lactate
Ethanol

379
Q

Indications for blood cultures

A 
Pyrexia 
Focal signs of infection 
Low BP 
Raised RR 
Abnormal WCC 
New or worsening confusional state - sepsis
380
Q

What are taken first, blood culture samples or other bloods

A

Blood culture samples

381
Q

Order of draw for blood culture samples

A

Blue bottle for aerobic organisms

Red for anaerobic

382
Q

At which platelet count is it safe to anticoagulate

383
Q

Types of bleeding in low platelets vs low clotting factors

A

Low platelet is mucosal bleeds

Clotting factors is bleeding into joints

384
Q

Post-transplant lymphoproliferative disorder

A

Occurs of solid organ transplants

Immune suppression can cause lymphocytosis (may be 2’ to EBV) –> lymphoma

385
Q

Features of neutropenic sepsis

A

Can be seen in a/c leukaemia - after treatment w/ chemo

Fever >37.5 and neutropenia <1

386
Q

Treatment of neutropenic sepsis

A

Tazobactam (tazocin) and gentamicin

May give G-CSF

387
Q

Why might haemolysis cause MCV to increase

A

Presence of reticulocytosis

388
Q

Blood film for B12/ folate deficicny

A

Hypersegmented neutrophils

Poikilocytes

389
Q

Blood film for alcoholic liver disease

A

Target cells

Acanthocytes

390
Q

Why might platelets decrease in alcoholic liver disease

A

Liver produces tpo

Alcohol is toxic to BM

391
Q

Why is LDH raised in haemolysis

A

Due to increased cell turnover

392
Q

Lab features of DIC

A

Low platelets
Prolonged clotting time
Low fibrinogen

393
Q

Causes of AKI

A

Hypoperfusion
Sepsis
Dehydration
Medication

394
Q

What does it mean if blood culture results show a growth from Hickman line but not peripheral blood

A

Bacteria introduced into lumen of line, not widespread

395
Q

Drugs causing secondary erythrocytosis

A

Anabolic steroids

epo

396
Q

What kind of tumours can cause 2’ erythrocytosis

A

Tumours secreting epo (liver, kidney, thyroid, fibroid)

397
Q

What does a pt ned to know before giving consent for a transfusion

A 
Indication 
Risks vs benefits 
What the process entails 
Any spp needs for the pts
Any alternatives 
They can no longer be blood donors
398
Q

Risk factors in TACO

A 
Age > 70 
Cardiac failure 
Renal failure 
Low albumin 
Existing fluid overload
399
Q

Post transfusion care

A

Check Hb to make sure it was successful

If discharged, make sure pt is aware of who to contact if any issues arise

400
Q

What needs to be included in a discharge summary post transfusion

A

Indication fro transfusion
Any adverse events
Pt no longer eligible to be blood donor

MBBS - Year 2 (20 decks)

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