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Phase 3a - GP > Haematology > Flashcards

Haematology Flashcards

1
Q

Where is iron mainly absorbed in the intestine?

A

Duodenum and jejunum

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2
Q

Describe how iron is absorbed and how deficiency occurs?

A

Fe requires stomach acid → keeps iron soluble ferrous (Fe2+) form → less acid = changes to insoluble ferric (Fe3+) form.

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3
Q

What can affect iron absorption and cause iron deficiency?

A

Inadequate iron absorption → meds like PPI can interfere with Fe absorption, infl. of duodenum or jejunum like coeliac or Crohn’s disease.

Dietary insufficiency → MC in children.

Loss of iron → heavy menstruation.

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4
Q

What is ferritin? When is extra ferritin released?

A

The form that iron takes when it is deposited and stored in cells.

Extra ferritin is released from cells when there is inflammation, such as with infection or cancer.

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5
Q

Sx of Fe deficiency anaemia?

A

General anaemia sx +
Brittle hair and nails
Koilonychia (spoon shaped nails)
Angular stomatitis ( ulceration around mouth corners)
Atrophic glossitis (enlarged tongue)

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6
Q

Ix + results for Fe deficiency anaemia?

A

FBC - Low MCV
Blood film - target cells + Howell Jolly bodies
Fe studies - low: serum Fe, ferritin, transferrin
Colonoscopy/oesophagogastroduodenoscopy (OGD) for malignancy.

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7
Q

Tx of Fe deficiency anaemia?

A

Oral Fe → Ferrous sulphate or ferrous fumarate.

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8
Q

What are the SE of oral iron?

A

Constipation and black coloured stools.

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9
Q

Describe structure of haemoglobin

A

two alpha-globin and two beta-globin chains

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10
Q

What is thalassaemia?

A

Genetic defect in protein chains that make up Hb (defects in both alpha and beta - globin chains).

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11
Q

How does splenomegaly occur in thalassaemia?

A

Px w/thalassaemia → fragile RBCs → breakdown easily → haemolytic anaemia → spleen filters blood and removes old cells → therefore collects destroyed RBCs → splenomegaly

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12
Q

Sx of thalassaemia

A

Fatigue
Pallor
Jaundice
Gallstones
Splenomegaly
Poor growth and development

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13
Q

Ix of thalassaemia

A

FBC - low MCV
Raised ferritin - iron overload
Hb electrophoresis

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14
Q

How would iron overload occur in thalassaemia?

A

Inefficient production of RBCs due to low Hb levels leads to:
1. Increased iron absorption in the gastrointestinal tract
2. Blood transfusions → maintain adequate Hb levels

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15
Q

What kind of genetic inheritance are both alpha and beta thalassaemia?

A

Autosomal recessive

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16
Q

Which chromosome do gene mutations occur in alpha thalassaemia?

A

Chromosome 16 - has 4 alpha genes
In alpha thalassaemia mutation (gene deletion) occurs in one of the alpha genes.

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17
Q

What does each of the following stand for and what does it consist of?
1. HbA
2. HbA2
3. HbF
4. HbH

A
  1. Adult Hb (2 alpha, 2 beta)
  2. Minor component of HbA (2 alpha, 2 delta)
  3. Fetal Hb (2 alpha, 2 gamma)
  4. Abnormal Hb form where mutation of alpha Hb chains leads to excess beta chains (4 beta no alpha)
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18
Q

In alpha thalassaemia gene deletion occurs. What is the name when these occur + Sx:
1 gene deletion
2 gene deletion
3 gene deletion
4 gene deletion

A

1 - Silent carrier/ aSx
2 - Alpha thalassaemic trait - mild anaemia Sx
3 - HbH hemotetrameres - moderately severe anaemia
4 - Hb Bart’s - hydrops fetalis - in utero HF → baby dies in utero

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19
Q

At birth how much do HbF and HbA account for in Hb and when does the Hb mostly transition to HbA?

A

At birth:
HbF - 80%
HbA - 20%

By 6 months mostly HbA

20
Q

Tx of alpha/beta thalassaemia?

A

Blood transfusions
Splenectomy may be performed
Bone marrow transplant
iron chelation - remove excess Fe from body

21
Q

Which chromosome do gene mutations occur in beta thalassaemia?

A

Chromosome 11

22
Q

In beta thalassaemia mutation occurs. What is the name when these occur + Sx:
1 normal + 1 reduced/absent beta
1 reduced + 1 absent or 2 reduced beta
2 absent beta (no functioning beta)

A
  1. Thalassaemia minor (trait) - aSx, carrier
  2. Thalassaemia intermedia - marked anaemia sx
  3. Thalassaemia major - abnormal features:
    Frontal bossing (prominent forehead)
    Enlarged maxilla (prominent cheekbones)
    Depressed nasal bridge (flat nose)
    Protruding upper teeth
23
Q

What is sickle cell anaemia?

A

Genetic condition that causes sickle (crescent) shaped red blood cells.

24
Q

Describe pathophysiology of sickle cell anaemia

A

Patients with sickle-cell disease → abnormal variant haemoglobin S (HbS). HbS results in sickle-shaped red blood cells → more fragile as S.A low → less efficient + causes clotting

25
Q

What kind of genetic inheritance is sickle cell anaemia?

A

Autosomal recessive.

26
Q

Why is sickle cell anaemia most common in countries with malaria?

A

As it increases antimalarial properties → likely to survive malaria + reduces malaria severity.

27
Q

Sx of sickle cell anaemia

A

General anaemia sx +
jaundice
splenic sequestrations (cells get trapped)
cognitive defects → children
Pul htn + chronic lung disease

28
Q

Ix for sickle cell anaemia

A

Heel prick test - new born screening
FBC + blood film ( normal MCV + sickled RBCs)
GS - Hb electrophoresis

29
Q

Tx of sickle cell crisis + chronic sickle cell

A

Crisis (acute exacerbation):
High flow O2
IV fluids
Analgesia

Chronic:
Hydroxycarbamide (stimulates HbF)
Blood transfusions - severe anaemia
Bone marrow transplant
Antibiotic prophylaxis to protect against infection

30
Q

Why would using hydroxycarbamide which increases HbF help treat sickle cell anaemia?

A

Foetal haemoglobin does not lead to the sickling of red blood cells (unlike HbS). It reduces the frequency of vaso-occlusive crises, improves anaemia and may extend lifespan.

31
Q

What is hereditary spherocytosis?

A

Condition where the red blood cells are sphere shaped, making them fragile and easily destroyed when passing through the spleen.

32
Q

What kind of genetic inheritance is hereditary spherocytosis?

A

Autosomal dominant

33
Q

Sx of hereditary spherocytosis?

A

Jaundice
Anaemia
Gallstones
Splenomegaly

34
Q

What kind of virus can patients with hereditary spherocytosis develop and what causes it?

A

Infection with parvovirus causes aplastic crisis which presents with increased anaemia, haemolysis and jaundice

35
Q

Ix of hereditary spherocytosis + results?

A

FBC + Blood film - (inc. reticulocytes + spherocytes + coombs test -ve)

36
Q

What is G6PD deficiency?

A

A condition where there is a defect in the G6PD enzyme normally found in all cells in the body. This leads to haemolysis - RBC damage

37
Q

Where is G6PD deficiency commonly found + what are the RF?

A

Mediterranean, Middle Eastern and African patients.
RF - infections, medications (nitrofurantoin) or fava beans (broad beans), henna

38
Q

What is the inheritance pattern of G6PD deficiency?

A

X-linked recessive

39
Q

Sx of G6PD deficiency?

A

Neonatal jaundice or intermittent jaundice - in response to triggers
Anaemia Sx
Gallstones
Splenomegaly

40
Q

Ix for G6PD deficiency + results

A

FBC + blood films - (Heinz bodies + bite cells)

41
Q

What are medications that reduce B12 absorption?

A

PPI and metformin

42
Q

Where is B12 absorbed in the gut?

A

Distal ileum

43
Q

What sx can a lack of B12 cause?

A

Peripheral neuropathy, with numbness or paraesthesia (pins and needles)
Lemon yellow skin *
Loss of vibration sense
Loss of proprioception
Visual changes
Mood and cognitive changes

44
Q

Ix for pernicious anaemia + results?

A

Bloods - presence of:
Intrinsic factor antibodies (1st line)
Gastric parietal cell antibodies (less helpful)

45
Q

Tx of pernicious anaemia?

A

Intramuscular hydroxocobalamin - B12 injections

46
Q

What’s important to look out for when treating both B12 and folate deficiency?

A

Treat B12 deficiency first as giving px folic acid when they have B12 deficiency can further deplete B12 lead to subacute combined degeneration of the cord + severe neurological problems.

47
Q

Where in the gut is folate absorbed?

A

Jejunum

Phase 3a - GP (15 decks)

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