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Cardiovascular & Respiratory Medicine > Anaemia > Flashcards

Anaemia Flashcards

1
Q

What is anaemia

A

A reduction in the haemoglobin concentration (Hb) in the circulating blood below what is normal for a healthy person of the same age and gender as the individual (no absolute cut off)

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2
Q

What are the consequences of low Hb and what presentations are caused?

A

Low Hb= reduced oxygen around the body
1. Eyes:
- Yellowing
2. Skin:
- Paleness
- Coldness
- Yellowing
3. Resp:
- Shortness of breath
4. Muscular:
- Weakness
5. Intestinal:
- Changed stool colour
6. Central:
- fatigue
- Dizziness
- Fainting
7. Blood vessels:
- Low blood pressure
8. Heart:
- Palpitations
- Rapid heart rate
- Chest pain
- Angina
- Heart attack
9. Spleen:
- Enlargement

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3
Q

What is a blood film?

A

a sample of blood that’s spread on a glass slide which is treated with a special stain:
allows the evaluation of white blood cells (WBCs, leucocytes), red blood cells (RBCs, erythrocytes), and platelets (thrombocytes).

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4
Q

What are the 3 types of anaemia?

A
  1. Microcytic
  2. Macrocytic
  3. Normocytic
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5
Q

What is the mechanism of microcytic anaemia?

A

“Reduced haemoglobin synthesis”- Red blood cells do not grow sufficiently

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6
Q

What is the mechanism of macrocytic anaemia?

A

“Abnormal haemopoesis” (production of red blood cells):
- Reticulocytes (“baby RBCs”) are large
- Have not lost their nucleus yet
- Abnormal haemopoeisis= RBCs stay in their early stages (reduced development)

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7
Q

What is the mechanism of normocytic anaemia?

A

The red blood cells are made normally (structurally), but you have fewer number of RBCs than normal:
- RBC pooling in spleen (RBCs are being destroyed)
- Insufficient haemopoesis (not making enough no. of RBCs)
- Acute blood loss (lose the normally- structured RBCs)

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8
Q

What are the causes of microcytic anaemia?

A
  • Iron loss
  • Anaemia of chronic disease
  • Insufficient intake
  • Thalassaemia
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9
Q

How does iron lose lead to microcytic anaemia?

A

reduced raw material needed to make Hb

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10
Q

How does “anaemia of chronic kidney disease” lead to microcytic anaemia?

A

You’re eating enough iron but no taking enough to the cells (due to inflammation from the CKD); not enough iron is being used to make Hb

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11
Q

What is meant by “insufficient intake” leading to microcytic anaemia?

A

Not eating enough iron

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12
Q

How does thalassaemia lead to microcytic anaemia?

A

Mutation in the gene needed to make Hb

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13
Q

What are the causes of Macrocytic anaemia?

A
  • B12/ folate deficiency (megaloblastic anaemia)
  • Liver disease
  • Ethanol toxicity
  • Haemolytic anaemia (mild, with reticulocytosis)
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14
Q

How does B12/ folate deficiency lead to macrocytic anaemia?

A
  • B12/ folate are needed for DNA production;
  • When there is not enough, cells that are “not ready” get ‘kicked out’ (released into the bloodstream)
  • Larger than usual (still have their nucleus- are underdeveloped)
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15
Q

How does Liver disease lead to macrocytic anaemia?

A
  • Reduced absorption of vitamins needed to make RBCs
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16
Q

How does ethanol toxicity lead to macrocytic anaemia?

A

Affects the liver- reduced absorption of material/ vitamins needed for RBC production

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17
Q

How does haemolytic anaemia lead to macrocytic anaemia?

A

Haemolytic anaemia= “condition that occurs when your red blood cells are destroyed faster than they can be replaced”

You break down RBCs so much, and make so many new ones that you end up with many reticulocytes (again are much larger- underdeveloped- intake nucleus)

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18
Q

What are the causes of normocytic anemia?

A

GI bleed/ tauma
Chemotherapy
Leukaemia
Sickle cell anaemia

19
Q

How do GI bleeds/ trauma cause normocytic anaemia?

A

Increase RBC lose

20
Q

How can chemotherapy and leukaemia cause normocytic anaemia?

A

Both can damage the bone marrow (site of hematopoiesis)- in some leakeumia cases, there is no longer production of RBCs, just cancer cells

21
Q

How can sickle cell anaemia cause normocytic anaemia?

A

Blood cells are normal when they’re not sickled- you just destroy the RBCs much more rapidly beacuse of the sickling process & pooling

22
Q

What is haemolysis?

A

The increased destruction of red blood cells (reduced red cell survival)

23
Q

What are haemolytic anaemias?

A

A group of anaemias in which red cell lifespan is reduced (i.e. haemolysis that leads to a reduction in Hb)- your red blood cells are destroyed faster than they can be replaced

24
Q

What is a complication of haemolytic anaemia?

A

Haemolytic anaemia increases the levels of bilirubin in the body and can cause jaundice

25
Q

Describe the pathophysiology behind jaundice

A

NORMALLY:
1. When RBCs are engulfed by macrophages, haemoglobin is broken down into haem and globin
2. The haem is further broken down into iron and protoporphyrin
3. Protoporphyrin is further reduced to Unconjugated Bilirubin (UCB)- this is lipid soluble/ NOT water soluble
4. the UCB then binds to albumin to be transported to the liver where it gets conjugated by the enzyme UGT
5. This Conjugated Bilirubin (CB) is water soluble
6. It drains into the bile ducts and is sent to the gallbladder for storage as bile
7. When used as bile when we eat, it is excreted into the duodenum where it is converted to urobilinogen (breakdown products of urobilinogen causes pigmenetation)
ANY DISRUPTION TO THIS:
8. Causes an increase in serum UCB, CB or both
9. Leads to symptoms: yellowing of skin and eyes

26
Q

Explain the significance of an increase in unconjugated bilirubin

A

UCB accumulates in pre-hepatic jaundice (haemolytic anaemias or ineffective hematopoesis overworking the liver):
1. The liver is working out MAX to remove these RBCs (as they are underdeveloped/ faulty)
2. The liver has converted to much CB from the large amounts of UCB which can increases in the bile and can lead to the formation of gallstones
3. Also the liver will still have left over UCB (increased demands)- UCB is not water soluble and cannot be excreted leading to build up (UCB is toxic to tissues and organs such as the brain)

27
Q

Explain the significance of an increase in conjugated bilirubin

A

CB accumulates in post-hepatic jaundice (obstructive jaundice)
1. An obstruction in the bile duct (can be caused by gallstones, pancreatic and cholangio- carcinomas and liver fluke) blocks bile flow
2. This increases the pressure in the common bile duct
3. Causes the bile (containing CB) to spill out
4. Increased CB in the blood can lead to darker urine (due to its breakdown product)

28
Q

Explain the significance of an increase in conjugated bilirubin AND unconjugated bilirubin

A

Raised UCB and CB can be a sign of viral hepatitis:
1. Liver is damaged (infected) and cannot convert UCB into CB (increased build up of UCB- toxic)
2. The hepatocytes are also the cells lining the common bile duct between the duct and the blood (acts as a sort of barrier); if those cells are damaged bile can leak out of the duct into the blood= increases CB

29
Q

Compare the differences between conjugated and unconjugated bilirubin

A

Unconjugated:
- Insoluble in blood
- Largely attached to albumin in blood
- Accumulates in pre-hepatic jaundice
- Is toxic to tissues and organs such as the brain
- Cannot be excreted in the urine

Conjugated:
- Is water soluble
- Small amounts are loosely bound to albumin in blood
- Accumulates in post-hepatic jaundice
- Relatively non-toxic
- Can be excreted in the urine (causes dark urine)

30
Q

What is transferrin and ferritin? How can they aid diagnosis in suspected anaemia?

A

Ferritin is the molecule that holds/ stores iron and transferrin is the molecule that carries iron around.
The levels of ferritin and transferrin can be used to distinguish between iron deficiency anaemia and anaemia of chronic disease

31
Q

How can you differentiate between iron deficiency anaemia and anemia of chronic disease using iron studies?

A

In iron deficiency anaemia you:
- Have low ferritin (not enough iron to put into this storage protein)
- Upregulate/ have high transferrin (attempt to be efficient at moving the little iron you do have, around the body)
- Have low trans sats
- Low iron

In anaemia of chronic disease (it is the other way roound)
- You have enough iron; normal or high ferritin
- but not able to move it around the body/ into the tissues (due to the inflammation, etc); low or normal transferrin
[in ACD the inflammation also causes uprgulation of hepcidin which is regulatory protein that reduces the absorbtion of iron; contributes to the low transferrin]
- Have low trans sats
- Low iron

32
Q

What is the significance of Hb electrophoresis in iron studies?

A

Hemoglobin electrophoresis measures hemoglobin levels and looks for abnormal types of hemoglobin:
Increase in HbA2 seen in thalasaemia

33
Q

How would you assess suspected autoimmune haemolytic anaemias?

A

Use the “Direct Antiglobulin Test”:
- In pts who have developed auto ABs the auto ABs would bind to their erythrocytes
- In the lab “rabbit ABs” are made to detect the auto ABs and have fluorescent tags
- We test for/ look for these tags

34
Q

What is the difference between thalassaemia and sickle cell?

A

Sickle cell:
-Unusual genes that affect the quality and structure of haemoglobin (missing amino acid)
- Haemoglobin variants such as HbS, HbO and HbE
- normocytic anaemia

Thalassaemias:
- Unusual genes that affect the quantity of haemoglobin
- such as alpha or beta thalassaemia
- microcytic anaemia

35
Q

What would you expect to see on a blood film from inherited disorders?

A

Spherocytes

36
Q

When would you see schistocytes on a blood film?

A

“small RBC fragments”- seen when there is RBC breakdown

37
Q

What would you expect to see on a blood film for microcytic anaemia?

A

Hypochromic cells (reduced haemoglobin- large area of central pallor on RBC)

38
Q

What would you expect to see on a blood film of B12/ folate deficiency?

A

Megaloblasts

39
Q

When would you see heinz bodies on a blood film

A

“oxidised haemoglobin”- seen in G6PD deficiency

40
Q

How does G6PD deficiency cause anaemia?

A
  • G6PD enzyme is needed to generate NADPH and then Glutathione
  • Glutathione maintains/ protects the RBCs membrane
  • This deficiency is usually not severe (symptoms are not too bad)
  • but worsens when put under extra stress (e.g. illness, broad beans, drugs, etc)
  • Causes haemolysis
41
Q

What are some causes of haemolysis?

A

impairments in:
1. Integrity of the membrane: hereditary spherocytosis (membrane less strong) & autoimmune haemolytic anaemia (ABs against the membrane)
2. Haemoglobin structure and function: sickle cell anaemia
2. Ceullular metabolism: G6PD deficiency

42
Q

What is megaloblastic anaemia?

A
  • Asynchronous nucelocytotplasmic maturation (cytoplasm/ nucleus aren’t maturing correctly)
  • Due to vit B12 and folic acid deficiency
    = Macrocytic RBC often with a very high MCV
43
Q

What condition would you expect on a blood fim with too many RBCs

A

Polycythemia (too many RBCs and differently shaped RBCs)

44
Q

What would you see on a blood film of macrocytic anemia?

A
  • Very granulated lymphocytes (mast cells)
  • Blue-tinge looking RBCs (due used to stain DNA)- indicates reticulocytosis

Cardiovascular & Respiratory Medicine (14 decks)

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