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Dermatology & Haematology > Anaemia > Flashcards

Anaemia Flashcards

1
Q

How long do RBCs live?

A

120 days

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2
Q

What hormone stimulates RBC production? Where is it released?

A

EPO: erythropoietin

Mostly the renal cortex, but 10% comes from the liver

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3
Q

What is a reticulocyte?

What is ferritin?
What is haemosiderin? Which is soluble and which isn’t?

A

Immature RBCs

Ferritin is protein + iron (soluble)

Haemosiderin is fragmented ferritin
(insoluble)

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4
Q

What is the structure of haemoglobin?

How many oxygen molecules can one Hb carry?

A

Two alpha chains
Two beta chains
4 Haem groups each containing iron atom

4 oxygen molecules, one on each haem group

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5
Q

Causes of microcytic and macrocytic anaemia?

A

Microcytic:
Iron deficiency
Chronic disease
Thalassaemia

Macrocytic:
B12 deficiency
Folate deficiency
Alcohol excess
Bone marrow failure
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6
Q

What causes iron deficiency anaemia?

A

Blood loss (GI, gynaecological)

Malabsorption: coeliac disease

High demand: pregnancy

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7
Q

Symptoms of iron deficiency anaemia?

A 
Fatigue
Dyspnoea
Angina
Palpitations
Glossitis
Pruritus
Headache
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8
Q

What investigations would you do for iron deficiency anaemia?

A

Bloods:

  • FBC, ferritin
  • blood film
  • LFTs

Investigate underlying causes:

  • OGD
  • Colonoscopy
  • Gynae investigations
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9
Q

What would the FBC and blood film show in iron deficiency anaemia?

A

Microcytic
Hypochromic

Ferritin low
Transferrin high

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10
Q

Management of iron deficiency anaemia?

What are the side effects?

A

Ferrous sulphate 200mg BD or TDS

Black stools, nausea, reflux

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11
Q

What two types of macrocytic anaemia are there? Explain and give examples.

A

Megaloblastic: impaired DNA synthesis resulting in bigger cell
- B12 and folate deficiency

Non-megaloblastic: fatty deposits in cell

  • alcohol excess
  • hypothyroid
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12
Q

What is folate’s other name?

In what foods are B12 and folate found?

A

Vitamin B9

B12: animal sources, fortified foods
Folate: green veg, cereal

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13
Q

Where and how is B12 absorbed?

A

Combines with intrinsic factor in the stomach and is absorbed in the terminal ileum

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14
Q

How long does B12 deficiency take to manifest?

What about folate?

A

B12 takes years
Hepatic stores of B12 take years to empty.

Folate takes months as liver stores are smaller

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15
Q

What causes B12 deficiency?

A

Pernicious anaemia (80% cases)

IBD
GI surgery
H. pylori
Dietary

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16
Q

What is a serious complication of B12 deficiency?

A

Subacute spinal cord degeneration

Symmetrical dorsal column loss

  • peripheral neuropathy initially
  • UMN signs later
  • lower limbs more affected
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17
Q

How and where is folate absorbed?

A

Absorbed in the duodenum / jejunum

18
Q

What is the link between B12 and folate?

A

Folate depends on B12 for activation

19
Q

What causes folate deficiency?

A

Alcohol excess
Dietary
Malabsorption
Drugs

20
Q

Your patient has macrocytic anaemia. How can you differentiate between B12 and folate deficiency?

A

Check folate levels in serum and RBCs

B12 deficiency: LOW red cell folate, NORMAL serum folate

Folate: LOW red cell folate and LOW serum folate

21
Q

What is pernicious anaemia? What vitamin deficiency does it cause any why?

A

Autoimmune disease that attacks the parietal cells in the stomach

Parietal cells produce intrinsic factor

So reduced intrinsic factor means reduced B12 absorption

22
Q

Who gets pernicious anaemia?

Which conditions are associated with pernicious anaemia?

A

Commonly women over 60

Vitiligo
Hypothyroidism
Addison’s
Type I diabetes

23
Q

Clinical features of pernicious anaemia?

A

Anaemia symptoms

  • Fatigue
  • Anorexia
  • Weight loss

Diarrhoea
Dyspepsia
Jaundice

24
Q

Investigations for pernicious anaemia?

A

Bloods:

  • FBC
  • Blood film
  • Serum B12 and folate
  • anti-IF
  • anti-parietal cell

Bone marrow aspirate

25
Q

Management of pernicious anaemia?

What should you not give and why?

A

B12 injections

Folate injections, because of the risk of severe neuropathy

26
Q

What are the possible complications of pernicious anaemia?

A

Gastric carcinoma
Gastric polyps

Neurological damage if left untreated: fatigue, depression, memory loss

Iron deficiency

27
Q

What is haemolytic anaemia?

A

Abnormal breakdown of RBCs

28
Q

What are some causes of haemolytic anaemia?

A

Hereditary erythrocyte defects:

  • Spherocytosis
  • G6PD deficiency
  • Pyruvate kinase deficiency
  • Sickle cell
Autoimmune
Transfusion
Malaria
DIC
Myelofibrosis
29
Q

What is spherocytosis?

Pathophysiology
Inheritance

A

Production of abnormal RBCs

They are sphere shaped rather than biconcave

They’re called spherocytes

Caused by a defect in the proteins of the RBC cytoskeleton

Autosomal dominant

They have normal oxygen carrying capacity but they are more fragile and mistaken for old RBCs by the spleen and thus destroyed

30
Q

In which anaemias are spherocytes seen?

A

All haemolytic anaemias have some spherocytes

But in spherocytosis there are only spherocytes

31
Q

What’s the treatment of spherocytosis?

A

Splenectomy or partial splenectomy

So the spleen can’t destroy all the spherocytes

32
Q

Investigations of spherocytosis? What would the results be?

A

FBC: hyperchromia

Blood film: RBCs look small and don’t have pale middle as they’re not biconcave
Reticulocytosis

Osmotic fragility test: spherocytes rupture easily in solutions less concentrated than the inside of the RBC

33
Q

What’s the osmotic fragility test? Which blood disorder does it detect? How does it work?

A

Detects spherocytosis

It relies on the fact that spherocytes will rupture easily in solutions less concentrated than themselves

34
Q

What is G6PD deficiency?

Pathophysiology
Inheritance

A

G6PD is an X-linked recessive inborn error of metabolism

Glucose-6-phosphate dehydrogenase is an enzyme that protects RBCs from breakdown triggered by infections, drugs or foods (fava beans)

Only when there is a trigger does haemolysis and therefore symptoms occur

35
Q

What are some triggers for a haemolytic crisis in G6PD deficiency?

A

Illness especially infections

Drugs

Fava beans (broad beans)

DKA
AKI

36
Q

Investigations for G6PD deficiency? What would the results be?

A

FBC

Blood film:

  • Macrocytic anaemia
  • Reticulocytosis

G6PD enzyme assay

37
Q

List the hereditary erythrocyte defects?

A

G6PD deficiency
Hereditary spherocytosis
Pyruvate Kinase deficiency

38
Q

What is pyruvate kinase deficiency?
Pathophysiology
Inheritance

A

Autosomal recessive
But can also be acquired secondary to leukaemia

Deficiency of an enzyme which limits RBC ATP production

39
Q

Investigations of pyruvate kinase deficiency? What will they show?

A

FBC and blood film: macrocytic anaemia, retculocytosis

LFTs: bilirubin high

40
Q

Management of pyruvate kinase deficiency?

A

Transfusion
Splenectomy may help with symptoms
Bone marrow transplant

41
Q

Management of G6PD deficiency?

A

Avoid triggers

Splenectomy can help

Dermatology & Haematology (8 decks)

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