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Haematology > Anaemia - normocytic + macrocytic > Flashcards

Anaemia - normocytic + macrocytic Flashcards

1
Q

What is aplastic anaemia?

A

BM stops making cells leading to pancytopenia

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2
Q

What are the causes of aplastic anaemia?

A
  1. autoimmune - paroxysmal nocturnal haemoglobinuria
  2. drugs - chloramphenicol + NSAIDS + TOXINS
  3. viruses - HEPATITIS
  4. irradiation
  5. congenital - fanconi anaemia
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3
Q

What tests would u do for aplastic anaemia? what may u find

A
  1. FBC

2. hypo cellular marrow w no abnormal cell

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4
Q

How may someone present w aplastic anaemia?

A

Hx of recurrent infection
Fatigue
Pallor
Hx of bleeding or easy bruising

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5
Q

What is involved in treatment of aplastic anaemia?

A

Supportive if asymptomatic
Immunosuppression - lymphocyte Ig, antithymocyte globulin, methylpred, ciclosporin
Severe - allogeneic marrow transplant HLA matched

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6
Q

How would u differentiate between IDA and AOCD?

A

TIBC is high in IDA

Ferritin is low in IDA and high in AOCD

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7
Q

What is the most common cause of anaemia in renal failure?

A

reduced erythropoietin levels

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8
Q

at what GFR does anaemia become apparent in CKD?

A

<35

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9
Q

What are complications of anaemia of chronic disease?

A

worsening of pre-existing heart failure due to increased CO necessitated by anaemia

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10
Q

What causes hypochromic cells?

A

reduced Hb in the cell leading to reduced mean corpuscular Hb conc (MCHC)

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11
Q

when should you suspect marrow failure in normocytic anaemia?

A

if WCC or platelets decreased

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12
Q

What can the causes of macrocytic anaemia be divided into?

A
  1. Megaloblastic - vit B12 deficiency + folate deficiency
  2. Normoblastic:
    - alcohol
    - liver disease
    - hypothyroidism
    - reticulocytosis e.g. haemolysis
    - myelodysplasia
    - cytotoxics
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13
Q

What are megaloblasts?

A

cell in which nuclear maturation is delayed compared with the cytoplasm

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14
Q

What is the function of vitamin B12

A

synthesises thymidine so DNA - maturation of rbc in BM

synthesis of myelin

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15
Q

What are the causes of vitamin B12 deficiency?

A
  1. Diet
  2. Malabsorption - lack of IF (pernicious anaemia) or terminal ileal resection, Crohns, post gastrectomy
  3. Congenital metabolic errors
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16
Q

What foods is vitamin B12 found in?

A

meat fish dairy

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17
Q

How and where is vitamin B12 absorbed?

A

binds to intrinsic factor (parietal cells in stomach produce) and absorbed in terminal ileum

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18
Q

What are the general features of vitamin B12 deficiency?

A
  1. Sx of anaemia
  2. Lemon tinge to skin due to combination of pallor and mild jaundice (haemolysis)
  3. Glossitis - beefy red sore tongue
  4. Angular cheilosis
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19
Q

What neurological sx does B12 deficiency cause?

A

paraesthesia, peripheral neuropathy

neuropsychiatric - irritability depression, psychosis

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20
Q

What is the management of symptomatic vitamin B12 deficiency?

A

If severe - IM cyanocobalamin or hydroxocobalamin (these are both vit B12 injections) + folic acid

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21
Q

What is the management of asymptomatic b12 deficiency?

A
  1. Dietary supplementation + multivits
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22
Q

what is pernicious anaemia?

A

autoimmune condition in which atrophic gastritis leads to lack of IF secretion from parietal cells in the stomach

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23
Q

In what groups of ppl is pernicious anaemia more common?

A

females
>40yrs
blood group A

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24
Q

what other conditions is pernicious anaemia associated w?

A

thyroid disease
vitiligo
Addisons

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25
Q

what are the features of pernicious anaemia?

A 
lethargy 
weakness
SOB
paraesthesia
mild jaundice, diarrhoea, sore tongue
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26
Q

What is the treatment of pernicious anaemia?

A

If due to malabsorption - vit B12 injections - hydroxocobalamin
If due to diet - oral B12 after initial IM course

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27
Q

What are the causes of folate deficiency?

A
  1. Poor intake - found in green leafy veg, legumes and fruit nd fortified cereals etc
  2. Malabsorption - tropical sprue, coeliac, intestinal resection
  3. Increased demand - pregnancy, increase cell turnover
  4. Increased loss - chronic dialysis, chronic haemolytic disease
  5. Alcoholism
  6. Drugs
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28
Q

What drugs cause folate deficiency/

A 
sulfasalazine 
trimethoprim 
methotrexate
pyrimethamine
anticonvulsants - phenytoin
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29
Q

What is usually seen on blood film in b12 and folate deficiency?

A

microcytic anaemia and hyperhsegmented neutrophils

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30
Q

Where is folate usually absorbed?

A

duodenum/proximal jejunum

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31
Q

What is folate also known as?

A

vitamin B9

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32
Q

What are normal body stores of folate and how long do they last?

A

10-12mg lasting 4 months

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33
Q

What is the main difference between vitamin B12 deficiency and folate deficiency?

A

folate deficiency isn’t associated w neurological sx

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34
Q

Why should you not give folate treatment until you’ve excluded vitamin B12 deficiency?

A

can worsen neuropathy - can precipitate/worsen subacute combined degeneration of the spinal cord

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35
Q

What are the signs and sx of folate deficiency?

A
  1. May be asymptomatic
  2. Anaemia sx - pallor, fatigue, SOB, anorexia, headache
  3. Glossitis
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36
Q

What are causes of increased cell turnover?

A

haemolysis
malignancy
inflammatory disease
renal dialysis

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37
Q

What is the treatment of folate deficiency?

A

Rx underlying cause
Folic acid tablets daily for 4ms
PLUS B12 supplement

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38
Q

What is the function of folate?

A 
essential for DNA synthesis 
fetal development (neural tube defects)
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39
Q

How does folate deficiency cause anaemia?

A

impairment of DNA synthesis -> delayed nuclear maturation -> large rbcs + decreased rbc production in BM

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40
Q

What is haemolysis?

A

premature breakdown of rbc’s

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41
Q

Where can haemolysis occur in the body?

A
  1. Intravascular

2. Extravascular -reticuloendothelial system i.e. macrophages of liver, spleen + BM

42
Q

Why does haemolysis not always result in anaemia?

A

compensatory increase in red cell production by BM

43
Q

Why may haemolysis cause a macrocytic anaemia?

A

Reticulocytes are released prematurely which are larger than mature cells

44
Q

What are the causes of haemolytic anaemia?

A
  1. RBC membrane defects - hereditary spherocytosis
  2. Enzyme defects - G6PD deficiency
  3. Haemoglobinopathies - thalassaemia, sickle cell disease
  4. Autoimmune haemolytic anaemia
45
Q

What are the features of haemolytic anaemia?

A 
High serum unconjugated bilirubin 
high urinary urobilinogen
high faecal stercobilinogen
splenomegaly 
BM expansion
Reticulocytosis
46
Q

What is the pattern of inheritance of hereditary spherocytosis? (HS)

A

autosomal dominant

47
Q

Explain the pathophysiology behind HS

A

Deficiency in the structural protein spectrin
Cells are spherocytic - more rigid and less deformable
Unable to pass through splenic microcirculation and trapped in the spleen -> shortened lifespan + destroyed via extravascular haemolysis

48
Q

How does HS present?

A

Jaundice at birth
Splenomegaly
Failure to thrive
Chronic - formation of gallstones

49
Q

What investigations would u do for HS?

A
  1. Blood film - spherocytes and reticulocytes
  2. FBC - anaemia + increased reticulocytes + MCHC
  3. Raised serum bilirubin + urinary urobilinogen
  4. Negative Coombs test
50
Q

What other condition is associated w spherocytes?

A

autoimmune haemolytic anaemia

51
Q

What is the treatment of HS?

A

Folate replacement

Splenectomy

52
Q

What is the inheritance pattern of G6PDD? who does it affect most?

A

x linked - males

africans, mediterranean, Middle East and SE asia

53
Q

Explain the pathophysiology of G6PDD, give the function of G6PD

A

↓ G6PD -> ↓ glutathione → increased red cell susceptibility to oxidative stress

54
Q

Where is the gene for G6PD?

A

chromosome Xq28

55
Q

How do patients w G6PD usually present?

A

Usually asymptomatic unless they get an oxidative crisis due to reduction in glutathione production
Chronic haemolytic anaemia - gallstones
Neonatal jaundice

56
Q

What are the causes of an oxidative crisis in G6PDD?

A
  1. acute drug induced:
    - aspirin
    - antimalarials
    - abx (sulphonamides, nitrofurantoin, chloramphenicol)
    - dapsone
    - quinidine
  2. Ingesting fava beans
57
Q

How would someone present in an attack w G6PDD?

A

rapid anaemia

jaundice

58
Q

What investigations would you do in G6PDD?

A
  1. Film - bite and blister cells

2. G6PD levels - low, may be normal after attack

59
Q

What is the treatment of G6PDD?

A
  1. Stop cause
  2. Blood transfusion
  3. avoid henna use!
60
Q

What is the pattern of inheritance in sickle cell anaemia? (SCA)

A

Autosomal recessive

61
Q

What is the pathology underlying SCA?

A

Synthesis of abnormal Hb chain - HbS

62
Q

Who is more commonly affected in SCA?

A

African

63
Q

What is the chance of being. a carrier (heterozygous) of SCA?

A

50%

64
Q

Explain the pathophysiology of SCA

A

AA substitution in gene coding for beta chain (valine replaces glutamine) -> production of HbS rather than HbA
HbS polymerises when deoxygenated, rbcs deform -> sickle cells, fragile and haemolyse + block small vessels

65
Q

What is sickle cell trait? What is a benefit of having it?

A

those who are heterozygous for sickle cell (HbAS) - no disability
+ve - protects from falciparum malaria

66
Q

What things can precipitate sickling?

A 
infection
dehydration
cold
acidosis
hypoxia
67
Q

What does sickling result in?

A

shortened rbc survival -> haemolysis
impaired passage of cells through the microcirculation leading to obstruction of small vessels and tissue infarction and this impaired pain

68
Q

How does a person w sickle cell trait tend to present?

A

sx free w no disability

69
Q

When will a person w sickle cell trait present w symptoms?

A

hypoxia e.g. unpressurised aircraft, anaesthesia

70
Q

What crises can occur as a result of SCA/

A
  1. Vaso-occlusive ‘painful’ crisis
  2. Aplastic crisis
  3. Acute chest syndrome
  4. Aplastic crisis
71
Q

How do vaso-occlusive crises present in children?

A

acute pain in the hand and feet -> dactylitis due to vaso-occlusion of the small vessels and avascular necrosis of the bone marrow

72
Q

How can vaso-occlusive crises present in adults?

A

pain in the long bones e.g. femur, spine, ribs and pelvis due to avascular necrosis of theBM

73
Q

How can vaso-occlusive crises present neurologically?

A

CNS infarcts -> stroke seizures or cognitive defects

74
Q

What is acute chest syndrome?

A

vaso-occlusive crisis of the pulmonary vasculature

75
Q

what causes acute chest syndrome?

A

infection (clam, mycoplasma, strep pneumoniae)
fat embolism from necrotic BM
pulmonary infarction - due to sequestration in the pulmonary vasculature

76
Q

How does acute chest syndrome present?

A

SOB
chest pain
hypoxia

77
Q

What causes pulmonary hypertension in SCA? what is the definition?

A

Mean pulmonary artery pressure >25mmHg

Damage from repeated chest crises and repeated thromboembolism and intravascular haemolysis

78
Q

What causes aplastic crises in SCA? how does it do this? What is the rx?

A

parvovirus B19
invades proliferating erythroid progenitors -> rapid fall in Hb w no reticulocytes in the peripheral blood due to failure of erythropoeisis in the BM,
Rx: transfusion

79
Q

What are sequestration crises? why does it affect children more?

A

splenic sequestration leads to acute painful splenomegaly w acute fall in Hb, affects children more as spleen is atrophic in adults

80
Q

What is the treatment of sequestration crises?

A

urgent transfusion

81
Q

What are the long term effects of SCA on bones?

A

Bones are common sites for vaso-occlusive crises resulting in chronic infarcts
Avascular necrosis of the hips and shoulders, vertebrae compression, shortening of bones in hands and feet
Osteomyelitis due to staph. aureus, staph pneumonia and salmonella

82
Q

What are the long term cardiac complications of SCA>

A

Cardiomegaly
arrhythmias
iron overload cardiomyopathy
MI

83
Q

What are the long term neurological complications of SCA?

A

TIA
fits
cerebral infarction
coma

84
Q

What are the long term hepatic complications of SCA?

A

chronic hepatomegaly and liver dysfunction due t trapping of liver cells

85
Q

What are the long term renal complications from SCA/?

A

chronic tubulointerstitial nephritis

86
Q

what are the long term eye complications of SCA?

A

retinopathy
vitreous haemorrhage
retinal detachments

87
Q

What investigations would you do for SCA?

A
  1. FBC - Hb 60-80, raised reticulocytes
  2. Blood film - sickle cells
  3. Sickle solubility test - +ve
  4. Hb electrophoresis - 80-95% HbS, absent HbA
88
Q

How is SCA screened for in the newborn?

A

neonatal blood spot screening “Guthrie” test at 5-9 days of life

89
Q

What test is diagnostic for SCA?

A

Hb electrophoresis

90
Q

What is the treatment of ongoing chronic sickle cell disease?

A
  1. Analgesia
  2. Hydroxycarbamide to help w disease severity
  3. Prophylaxis + prompt rx of infections
  4. FOLIC ACID to all haemolytic pts
  5. BM transplant
91
Q

What is the rx of a vaso-occlusive crisis?

A
  1. Analgesia
  2. antihistamine as opioids cause pruritus
  3. rx precipitating cause eg. correct acidosis, warm pt
92
Q

What is the rx of acute chest syndrome?

A
  1. O2 + incentive spirometry
  2. Analgesia
  3. Antihistamine
  4. Broad spec abx
  5. transfusion
93
Q

When are blood transfusions indicated in the rx of SCA?

A 
ACS
Acute anaemia due to acute splenic sequestration
Aplastic crisis
Stroke 
HF
94
Q

How can autoimmune haemolytic anaemia (AIHA) be divided?

A
  1. Warm
  2. Cold
    depends on what temperature the abs best cause haemolysis
95
Q

What is AIHA?

A

abs are directed against rbcs causing extravascular haemolytic and spherocytosis

96
Q

What is warm AIHA?

A

ab (usually IgG) causes haemolysis best at body temp,

97
Q

What are the causes of warm AIHA?

A

autoimmune disease: e.g. systemic lupus erythematosus*

neoplasia: e.g. lymphoma, CLL
drugs: e.g. methyldopa

98
Q

What is cold AIHA? what is the usual ab? How does it present?

A

ab - IgM
Haemolysis usually at 4C
More commonly intravascular
Sx of raynauds and acrocyanosis

99
Q

What usually causes cold AIHA

A

infection - mycoplasma, EBV

100
Q

What is rx of warm AIHA

A

Steroids
immunosuppressants
+/-splenectomy

Haematology (18 decks)

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