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Anaemia Flashcards

1
Q

What is shown by an increase in unconjugated bilirubin

A

prehepatic/hepatic jaundice

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2
Q

How does bilirubin become conjugated

A

Bilirubin in the blood is bound to albumin (unconjugated). It is converted to conjugated bilirubin when entering the liver

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3
Q

What are some of the complications associated with a higher bilirubin?

A

Jaundice, Obstructive gall stones

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4
Q

What is hereditary spherocytosis?

A

Inherited disruption of vertical linkages in RBC cell membrane (ankyrin), -> spherocytes

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5
Q

What blood cells would you see in a blood film of hereditary spherocytosis?

A

Spherocytes, Cells with no central pallor, Reticulocytes

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6
Q

Why would you see reticulocytes in a blood film?

A

Compensatory effect - as more blood cells get destroyed, early forms of rbcs (reticulocytes) are released from the bone marrow prematurely to do some of the oxygen delivering

seen as polychromatic (blue tinge) cells

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7
Q

What causes raised bilirubin

A

RBC breakdown

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8
Q

What is haemolysis

A

^ destruction of RBC

due to intrinsic RBC abnormality
due to extrinsic factors acting on RBC

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9
Q

What is haemolytic anaemia

A

Haemolysis -> red. Hb

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10
Q

How to treat haemolytic anaemia

A

Folic acid (aid rq for erythropoeisis)
Splenectomy (^RBC lifespan)

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11
Q

Presentation of px with conjugated bilirubin

A

Pigment gallstones
Obstructive jaundice - block common bile duct

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12
Q

Difference btw unconjugated and conjugated bilirubin

A

Unconjugated bilirubin:
insoluble in blood - bound to albumin
Pre-hepatic jaundice
Toxic (to the brain)
Cannot be excreted via urine

Conjugated bilirubin:
Water soluble
small amounts loosely bound to albumin
post-hepatic jaundice (issues w/ bile duct/gallbladder)
Relatively non-toxic
Excreted in urine -> dark

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13
Q

Mechanism of anaemia
PPLS

A

Production (red. RBC/Hb prod by the bone marrow)
Pooling (Splenomegaly)
Loss of blood from the body
Survival (haemolysis).

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14
Q

What is DAT and how does it work

A

Direct Antiglobulin test
In solution coloured rabbit AB to identify whether blood contains autoantibodies (binds autoAB)

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15
Q

What does AIHA stand for and what are its causes

A

Autoimmune Haemolytic anaemia
idiopathic, SLE, lymphoma

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16
Q

What lab evidence would point towards haemolysis

A

^ LDH (lactate dehydrogenase)
Unconjugated hyperbilirubinemia (show prehepatic issue)
red. haptoglobulins (breakdown free Hb in liver)

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17
Q

What is the bone marrows response to haemolysis

A

Reticulocytosis

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18
Q

What causes aq haemolytic anaemia (HA)

A

Defect in the RBC environment (plasma, vasculature)

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19
Q

Non-immune environmental factors leading to aq HA

A

Haemolytic uraemic syndrome - AKI
Malaria - microbe
Snake venom
drugs - oxidant damage

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20
Q

Immune mediated factors leading to aq HA

A

Autoimmune
Alloimmune (post transfusion)

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21
Q

How can you differentiate between AIHA and hereditary spherocytosis?

A

DAT test - positive in AIHA

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22
Q

What inherited defects can affect RBC

A

Hereditary spherocytosis - membrane
Sickle cell anaemia - Hb
G6PD deficiency - Pentose shunt dysfunction

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23
Q

What is the purpose of the HMP Shunt?

A

Forms Glutathione and protects RBC from oxidant damage

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24
Q

What enzyme is critical in the HMP shunt that if deficient can lead to haemolytic anaemia?

A

G6PD

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25
Q

What can you see in a blood film for someone with G6PD deficiency?

A

Evidence of oxidant damage:
Bite cells w/ no central pallor
Heinz bodies - denatured Hb
Ghost cells

26
Q

What does the presence of ghost cells show?

A

Intravascular Haemolysis

27
Q

What advice would you give patients with G6PD deficiency?

A

Avoid oxidant drugs, broad beans, naphthalene (in cigarette smoke), protect against infection

28
Q

Two types of HA

A

Inherited HA - abnormal membrane/Hb/enzymes
Acquired HA - extrinsic factors: microbes/chemicals/drugs

29
Q

Where are the two locations that haemolysis can occur?

A

Intravascular - within blood vessels (acute damage to RBC)
Extravascular - in spleen or liver (due to removal)

30
Q

What evidence would point towards HA

A

Morphologically abnormal RBC
^ RBC breakdown - ^bilirubin/red. haptoglobin
^ Bone marrow activity - ^MCV due to reticulocytes

31
Q

Blood film abnormalities with iron deficiency anaemia

A

Microcytic (red. MCV)
Hypochromic (red. MCHC)
low ferritin/iron

32
Q

Clinical signs of iron deficiency anaemia

A

Koilonychia - bent nails
Glossitis - inflammation of the tongue
Angular stomatitis - inflamed corners of the mouth

33
Q

Causes of iron deficiency

A

^ loss - menstrual, GI
insufficient iron - dietary, malabsoption (coeliac)
^ iron rq - pregnancy

34
Q

What conditions cause microcytic anaemia

A

Haem Synthesis Defect (iron deficiency, chronic disease)
Globin Synthesis Defect (alpha and beta thalassaemia)

35
Q

What conditions lead to macrocytic anaemia?

A

B12 and folate deficiency
Liver disease
Drugs affecting DNA synthesis

36
Q

What cells would be macrocytic and polychromatic?

A

Reticulocytes

37
Q

What conditions lead to normocytic anaemia?

A

Recent blood loss - GI haemorrhage
Bone marrow failure (leukaemia/chemo),
Splenic Sequestration - hypersplenism

38
Q

What are the symptoms of iron deficiency anaemia?

A

Tiredness, lethargy, breathlessness at rest, peripheral oedema

39
Q

What is ferritin?

A

Stores of iron in the body

40
Q

What is transferrin?

A

plasma transport protein

41
Q

What is hepcidin?

A

Protein that inhibits Fe absorption/transport from the gut

released in response to xs ferritin
suppressed by EPO

42
Q

What questions would you ask someone with iron deficiency anaemia?

A

Diet (vegan), Gastrointestinal Symptoms (bowels, indigestion, dysphagia), Menstrual History, Weight Loss, Medication (NSAIDs)

43
Q

How do you treat iron deficiency anaemia?

A

Iron Replacement Therapy (Ferrous Sulphate)

44
Q

What is shown in the blood film with high ESR

A

Rouleaux - stacks of RBC (looks like coins)
When plasma protein conc is high

45
Q

What are some causes of anaemia of chronic disease?

A

Infections - TB, HIV
Rheumatoid/ autoimmune
Malignancy

46
Q

How does chronic disease lead to anaemia?

A

Inflammatory responses ^ hepcidin production whilst also red. transferrin production
-> less Fe abs from gut / high ferritin

47
Q

What are the key differences in ferritin/transferrin/transferrin saturation between iron deficiency anaemia and anaemia of chronic disease?

A

IRON - low ferritin (high in chronic) / high transferrin (low in chronic) / low transferrin saturation (normal in chronic)

48
Q

What is pernicious anaemia?

A

Anaemia from deficiency of vitamin B12

49
Q

What is poikilocytosis?

A

Variation in RBC shape

50
Q

What does the term megaloblastic anaemia refer to?

A

Macrocytic anaemia caused by B12 or folate deficiency

51
Q

What is a megaloblast and what are the features of it?

A

Abnormal erythroblast in the bone marrow - macrocytic, asynchronous nucleocytoplasmic maturation. It is NOT a reticulocyte

nucleus hypersegmentation

52
Q

What are B12/folic acid rq for

A

Dna synthesis

53
Q

What are some causes of B12 deficiency?

A

Dietary, Gastric (gastrectomy, autoimmune), Bowel (Crohn’s)

54
Q

How would you treat each cause of b12 deficiency?

A

Dietary - oral supplements,
Gastric & Bowel - IM Hydroxocobalamin Injection

55
Q

What are some causes of folate deficiency?

A

Red. Availability (diet, malabsorption - coeliac)
^ Demand (pregnancy, haemolysis)

56
Q

How would you treat these causes of folate deficiency?

A

Oral supplements

57
Q

Neurological disorders associated with B12/folate deficiency

A

Vit B12- Dementia, spinal cord degeneration
Folate - developmental neural tube defects

58
Q

How does the body absorb B12

A

Cleared from food using HCL forms B12-IF (parietal cells)
B12-IF absorbed into ileum where it binds receptors

59
Q

How does the body absorb folic acid

A

Absorbed into the duo/jej of the SI

60
Q
A

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