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MedEd GKP/AB/VP > Haem - Anaemia > Flashcards

Haem - Anaemia Flashcards

1
Q

Microcytic anaemia causes?

MCV in fL?

A

Iron deficiency anaemia
Thalassaemia
Anaemia of chronic disease (can also be normocytic)

MCV <80fL

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2
Q

Normocytic anaemia causes?

MCV in fL?

A

Anaemia of chronic disease
Bone marrow failure
-aplastic anaemia

MCV 80-100fL

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3
Q

Macrocytic anaemia causes?

MCV if fL?

A 
Megaloblastic
 - folate/B12 deificency
Non megaloblastic
 - Alcohol
 - Haemolysis (raised reiticulocytes)

MCV >100fL

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4
Q

Causes of Iron Deficiency Anaemia?

A

Loss of blood - eg. GI
Incresaed demand/use of Fe - eg. pregnancy
Decreased intake of Fe - dietary (vegetarian)
Decreased absorption of Fe - eg. Coeliac

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5
Q

Clinical features of Iron def anaemia?

A

Signs of anaemia: pallor, lethargy, SOB
Atrophic glossitis, angular stomatitis
Koilonychia (spoon-shaped nails)
Conjunctival pallor

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6
Q

Iron def anaemia investigations?

A

Bloods: FBC = low iron, low ferritin

Blood film:
microcytic,
hypochromic (central pallor of >1/3 cell size), anisocytosis (size variation),
poikilocytosis (shape variation)

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7
Q

SBA key words: Iron deficiency anaemia ?

A

Low ferritin

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8
Q

SBA tip: Unexplained anemia investigation?

A

Colonoscopy = ?colorectal cancer causing blood loss?

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9
Q

Anaemia of chronic disease definition?

A

Anaemia seen in chronic conditions. Effects of inflammatory cytokines.

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10
Q

Causes of anaemia of chronic disease?

A

Infection, inflammation, malignancy:

Chronic inflammatory/autoimmune disease - Rheumatoid arthritis
Chronic infections - TB
Malignancy

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11
Q

Clinical features of anaemia of chronic disease?

A

Signs of anaemia: pallor, lethargy, SOB

Signs of underlying diesase

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12
Q

Anaemia of chronic disease investigations?

A

Bloods: FBC - low iron, NORMAL/HIGH ferritin!

Blood film: normocytic or microcytic

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13
Q

Why is ferritin normal or high in anaemia of chronic disease?

A

Ferritin is an acute phase protein.

In chronic disease it will be elevated and can mask low iron.

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14
Q

SBA key words: Anaemia of chronic disease?

A

Normal/ high ferritin

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15
Q

What kind of anaemia is aplastic anaemia?

A

Normocytic

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16
Q

Aplastic anaemia definition?

A

Anaemia caused by diminished haematopoietic precursors in the bone marrow and deficiency of all blood cell elements (pancytopaenia)

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17
Q

Causes of aplastic anaemia?

A 
Idiopathic: 
 - autoimmune mechanisms -> destruction
Acquired:
 - Drugs - anti-epileptics
 - Viral infection - Parvovirus B19
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18
Q

Clinical features of aplastic anaemia?

A

Anaemia: Pallor, Lethargy, SOB
Thrombocytopenia: Bruising, Petechiae (bleeds)
Leukopenia: increased infections

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19
Q

Aplastic anaemia investigations?

A

Bloods:

  • low Hb, normal MCV
  • low WCC, low Platelets
  • low reticulocytes

Blood film
- exclude leukaemia

Bone marrow trephine biopsy -> hypocellular marrow

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20
Q

SBA key words: Aplastic anaemia?

A

Low Hb
Low WCC
Low platelets

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21
Q

B12 deficiency anaemia causes?

A

Decreased intake - diet (vegetarians)
Decreased absorption - Crohn’s (ileal resection), Pernicious anaemia (autoantibodies against Intrinsic Factor/Parietal Cells)

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22
Q

Clinical features of B12 deficiency?

A

Peripheral neuropathy
Ataxia
Glossitis

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23
Q

B12 deficiency anaemia investigations?

A 
Bloods:
 - low Hb, high MCV, low serum B12
Blood film:
 - Macrocytes (large RBCs)
 - Megaloblastic anaemia - hypersegmented neutrophil nuclei (>5 lobes)
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24
Q

SBA key words: B12 deficiency?

A

Peripheral neuropathy

Hypersegmented neutrophils

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25
Q

Folate deficiency anaemia causes?

A

Decreased intake - alcoholics!
Increased demand - pregnancy, high cell turnover (malignancy, haemolysis)
Decreased absorption (jejunum): coeliac
Drugs: methotrexate

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26
Q

Clinical features of folate deficiency?

A

Anaemia signs: pallor, lethargy, SOB

Signs of underlying disease

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27
Q

Folate deficiency investigations?

A 
Bloods:
 - low Hb, high MCV, low serum folate
Blood film:
 - macrocytes (large RBCs)
 - megaloblastic anaemia -> Hypersegmented nuclei (>5 lobes)!
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28
Q

SBA key words: folate deficiency?

A

Alcoholics

Hypersegmented neutrophils

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29
Q

Haemolytic anemia definition?

A

Premature breakdown of RBCs which leads to shorter than 120 days life-span and anaemia

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30
Q

Causes of haemolytic anaemia

A

Hereditary and Acquired

Hereditary:

  • Membrane defects: Hereditary Spherocytosis
  • Enzyme deficiencies: G6PD Deficiency (glucose 6 phosphate dehydrogenase)
  • Haemoglobinopathies: Sickle Cell Disease, Thalassaemeia

Acquired:

  • Autoimmune
  • Drugs - penicillin, quinine
  • Infection - malaria, sepsis
  • Microangiopathic Haemolytic Anaemia MAHA - HUS, TTP, DIC
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31
Q

Definition + investigations of Hereditary Spherocytosis?

A

Oval-shaped RBCs
Inv:
- Blood film - spherocytes
- Osmotic fragility test

32
Q

SBA key words: hereditary spherocytosis?

A

Spherocytes

lol

33
Q

Triggers of G6PD deficiency?

A

Fava beans
Moth balls
Infections
Drugs - antimalarials

34
Q

G6PD deficiency investigations?

A

Blood film = Heinz bodies

35
Q

SBA key words: G6PD deficiency?

A

Fava beans
Heinz bodies
Anti-malarials

36
Q

Autoimmune Haemolytic Anaemia cause?

A

Warm/cold antibodies attach to RBCs causing their haemolysis.

Warm Antibodies IgG - agglutinate RBCs at 37C. Associated with SLE and Lymphomas

Cold Abs IgM agglutinate ar room temp or colder. Associated with infections (EBV), Lymphomas

37
Q

Autoimmune Haemolytic anaemia investigations?

A

Coomb’s test/ Direct Antigglobulin Test (DAT)

= detects antibodies

38
Q

SBA key words: Autoimmune Haemolytic Anaemia?

A

Coomb’s test/ Direct Antigglobulin Test (DAT)

Warm/cold antibodies

39
Q

Why do Microangiopathic Haemolytic Anaemias (MAHAs) cause haemolysis and anaemia (patophysiology)?

A

RBCs pass through fibrin strands deposited in small vessels -> Shearing (damage) of RBCs -> intravascular haemolysis + RBC fragmentation

40
Q

MAHA investigations?

A

Blood film: schistocytes, reticulocytes

41
Q

SBA key words: MAHA?

A

Schistocytes (fragmented RBCs)

42
Q

Features of haemolytic anaemia?

A

Anaemia: pallor, lethargy, SOB
Jaundice
Hepatosplenomegaly

43
Q

Haemolytic anaemia investigations?

A

Bloods:

  • low Hb, high unconjugated bilirubin
  • high LDL (intracellular enzyme), high reticulocytes

Urine:
- high urobillinogen (also haemoglobinuria)

Blood film:

  • reticulocytes, schistocytes
  • macrocytosis
  • specific abnormal cells - spherocytes, Sickle cells
44
Q

SBA key words: Haemolytic anaemia?

A

Schistocytes

High urobilinogen

45
Q

*Extra Q: What is urobillinogen?

A

Urobilinogen is a colourless by-product of bilirubin reduction. It is formed in the intestines by bacterial action on bilirubin. About half of the urobilinogen formed is reabsorbed and taken up via the portal vein to the liver, enters circulation and is excreted by the kidney.

**Excess info from wikipedia below (not necessary to know, but it’s a good summary of jaundice):

Increased amounts of bilirubin are formed in hemolysis, which generates increased urobilinogen in the gut. In liver disease (such as hepatitis), the intrahepatic urobilinogen cycle is inhibited also increasing urobilinogen levels. Urobilinogen is converted to the yellow pigmented urobilin apparent in urine.

The urobilinogen in the intestine is directly reduced to brown stercobilin, which gives the feces their characteristic color. It can also be reduced to stercobilinogen, which can then be further oxidized to stercobilin. This constitutes the normal “enterohepatic urobilinogen cycle”.

In biliary obstruction, below-normal amounts of conjugated bilirubin reach the intestine for conversion to urobilinogen. With limited urobilinogen available for reabsorption and excretion, the amount of urobilin found in the urine is low. High amounts of the soluble conjugated bilirubin enter the circulation where they are excreted via the kidneys. These mechanisms are responsible for the dark urine and pale stools observed in biliary obstruction.

Low urine urobilinogen may result from complete obstructive jaundice or treatment with broad-spectrum antibiotics, which destroy the intestinal bacterial flora. (Obstruction of bilirubin passage into the gut or failure of urobilinogen production in the gut.)

Low urine urobilinogen levels may result from congenital enzymatic jaundice (hyperbilirubinemia syndromes) or from treatment with drugs that acidify urine, such as ammonium chloride or ascorbic acid.

Elevated levels may indicate hemolytic anaemia (excessive breakdown of red blood cells RBC), overburdening of the liver, increased urobilinogen production, re-absorption – a large hematoma, restricted liver function, hepatic infection, poisoning or liver cirrhosis.

46
Q

Types of Microangiopathic Haemolytic Anaemias?

A

HUS, TTP, DIC

Haemolytic Uraemic Syndrome, Thrombotic Thrombocytopenic Purpura, Disseminated Intravascular Coagulation

47
Q

HUS: sign Triad?

A

Microangiopathic Haemolytic Anaemia,
Acute Renal Failure and
Thrombocytopenia

48
Q

Causes of HUS?

A

Infection - E.Coli!!!
Drugs - OCP
Malignancy

49
Q

Clinical features of HUS?

A

Anaemia - pallor
Jaundice; from haemolysis
Bruising; from thrombocytopaenia
Renal - oedema, HTN, oliguria

50
Q

Investigations for HUS?

A

Bloods:

  • anaemia; high neutrophils, low platelets
  • clotting: normal PT/APTT/fibrinogen
  • HIGH unconjugated billirubin, HIGH LDL from haemolysis

Blood film:

  • SCHISTOCYTES (fragmented rbc)
  • high RETICULOCYTES

Renal biopsy

51
Q

SBA key words: Haemolytic Uraemic Syndrome?

A

TRIAD: MAHA, Renal failure, low platelets!

52
Q

Thrombotic Thrombocytopenic Purpura: sign Pentad?

A 
MAHA
Acute renal failure
Thrombocytopaenia
Fever
Fluctuating CNS signs!
53
Q

Causes of TTP?

A

Idiopathic

54
Q

Clinical features of TTP?

A

Pallor, jaundice, bruising
Renal - oedema, HTN, oliguria
CNS - Weakness, decreased vision, fits, decreased consciousness!!!

55
Q

TTP investigations?

A

Same as HUS!
Bloods:
- anaemia, high neutrophils, low platelets
- clotting: normal PT/APTT/fibrinogen
- HIGH unconjugated billirubin, HIGH LDL from haemolysis

Blood film:

  • SCHISTOCYTES
  • high RETICULOCYTES

Renal biopsy

56
Q

SBA key words: Thrombotic Thrombocytopenic Purpura?

A

PENTAD: MAHA, Acute renal failure, low platelets, fever, fluctuating CNS

57
Q

Thalassaemia definition?

A

Group of genetic disorders characterised by reduced globin chain synthesis

58
Q

Thalassaemia aetiology?

A

Autosomal recessive genetic defects:

  • Alpha-thalassaemia - low alpha-globin chain synthesis
  • Beta-thalassaemia - defect in B-globin gene on Chr 11 -> reduced/none B-chain synthesis
    • B-Thalass. major - no B-chain synthesis
59
Q

Phenotypic Beta-Thalassaemia classification?

A

Silent carrier
Beta-thalassaemia minor (aka B-thal. trait)
Beta-thalassaemia intermedia
Beta-thalassaemia major

60
Q

Clinical features of Alpha-thalassaemia / Beta-thalassaemia trait (minor)?

A

Mild microcytic anaemia

asymptomatic

61
Q

B-thalassaemia major clinical features?

A

Presents at 3-6 months (γ-chain synthesis switches to β-chain synthesis).
Anaemia; Failure to thrive; Infections

62
Q

Thalassaemia investigations?

A

Bloods:
↓Hb; ↓MCV; Normal Ferritin

Blood Film:

  • Microcytic, Hypochromic Anaemia
  • Target Cells
  • ↑ Reticulocyte Count

Hb Electrophoresis:
↓HbA ↑HbF

63
Q

SBA key words: Thalassaemia?

A

Target cell

64
Q

Definition of sickle cell disease?

A

Chronic condition with sickling of RBCs caused by inheritance of HbS

65
Q

Sickle cell disease causes/ risk factors?

A

Autosomal recessive inherited mutation in β-globin gene.

  • Sickle Cell Anaemia = Homozygosity HbS
  • Sickle Cell Trait = Carrier of one copy of HbS

Factors precipitating sickling:
- Infection; Dehydration; Hypoxia

66
Q

Features of sickle cell disease?

A

Splenic infarction
Abdo pain
Bones - dactylitis (painful crises affecting small bones of the hand)
Lungs - SOB (“Acute Chest Syndrome” - presents like pneumonia)

67
Q

Sickle Cell Disease investigations?

A

Bloods: ↓Hb;
- Reticulocytes - ↑in haemolytic crises, ↓in Aplastic crises

Blood film:

  • Sickle Cells
  • Features of Hyposplenism: Target Cells; Howell-Jolly bodies

Hb Electrophoresis

68
Q

SBA key words: Sickle cell disease?

A 
Sickle cells (duh)
Crises
69
Q

How would you manage an acute painful crises fo SCD?

A

Oxygen
IV fluids
Analgesia - IV opiates
Antibiotics

70
Q

Management of chronic SCD?

A

Infection prophylaxis- penicillin V
Hydroxyurea - reduces crises freq. and recurrence
Red cell transfusion
Avoid precipitating factors (infection, dehydration, hypoxia)

71
Q

What are the complications of Sickle cell disease?

A

Aplastic crises (parvovirus B19 infection)
Haemolytic crises
Gallstones; cholecystitis

72
Q

What is the prognosis of SCD?

A

If well managed, survive to ~50 years

73
Q 
A 64 year old lady complains of pain in her hands. She has gross deformities of her fingers and has nodules on her elbows which she has been told are to do with the pain.
Bloods:
Hb 71 (115-180g/L)
MCV 93 (80-100fL)
WCC 5.1 (4-11 x10^9/L)

The most likely cause is:

Alcohol
Anaemia of Chronic Disease
Iron Deficiency Anaemia
Vitamin B12 Deficiency
Thalassaemia
A

Anaemia of Chronic Disease

Gross deformities of fingers and nodules on elbows indicate Rheumatoid arthritis. Bloods show normocytic anaemia.

74
Q

A 22 year old female presents to her GP complaining of tiredness at work. Upon further questioning, she reveals she has a longstanding history of heavy periods. On examination she has pale conjunctivae. The most likely cause is:

Alcohol
Anaemia of Chronic Disease
Iron Deficiency Anaemia
Vitamin B12 Deficiency
Thalassaemia
A

Iron Deficiency Anaemia

tiredness, heavy periods, pale conjunctivae - the bleeding depleted her iron stores.

75
Q 
A 40 year old woman suffers from Crohn’s Disease. She has recently been complaining that she feels weak and notices tingling in her fingers. A blood test is performed:
Hb 105 (115-180g/L)
MCV 120 (80-100fL)
WCC 300 (150-400 x10^9/L) 
The most likely explanation is:
Alcohol
Anaemia of Chronic Disease
Iron Deficiency Anaemia
Vitamin B12 Deficiency
Thalassaemia
A

Vitamin B12 Deficiency

Crohn’s - reduced absorption of B12.
Tingling - Peripheral neuropathy
Bloods - Macrocytic anaemia

76
Q

A 35 year old man travels to South Africa. On arriving, he begins his course of antimalarial tablets. A few days later, he becomes ill with shortness of breath, pallor and bloody urine. Blood tests show he is anaemic and a blood smear shows presence of Heinz Bodies. The most likely cause is:

Disseminated intravascular coagulation
Glucose-6-phosphate dehydrogenase deficiency
Haemolytic Uraemic Syndrome
Hereditary spherocytosis
Hereditary elliptocytosis
A

Glucose-6-phosphate dehydrogenase deficiency

Antimalarias - drugs triggering G6PD
Heinz bodies
anaemia

MedEd GKP/AB/VP (28 decks)

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