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MEH > 5 MEH > Flashcards

5 MEH Flashcards

1
Q

Anaemia can develop from reduced erythropoiesis, why might this occur?

A
  1. Kidney not making EPO in response to hypoxic blood, so no stimulus on bone marrow to make RBCs
  2. Empty bone marrow, so unable to respond to EPO sitmulus
  3. Marrow infiltrated by cancer cells or fibrous tissue so normal haematopoietic cell are reduced
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2
Q

How can parvovirus infection induce anaemia?

A

Parvovirus diminishes bone marrow, so unable to respond to EPO stimulus

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3
Q

In which 3 clinical conditions is Anaemia of chronic disease ACD commonly seen?

A
  1. Inflammatory conditions EG. Rheumatoid arthritis, Inflam. bowel disease (Crohns/Ulc.colitis), SLE
  2. Chronic infection Eg. TB
  3. Bronchiectasis
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4
Q

Is anaemia of chronic disease an iron deficiency?

A

No! Iron is present but stuck in macrophages! So bone marrow can’t use it for erythropoiesis, there is a lack of FUNCTIONAL iron

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5
Q

How are ferritin levels altered in anaemia of chronic disease?

A

Ferritin is increased! ie. it is NOT an iron deficiency!

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6
Q

Is there a treatment for anaemia of chronic disease?

A

No, there is no specific treatment, must treat the underlying cause

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7
Q

what sort of disease is anaemia of chronic disease?

A

It is dyserythropoiesis due to various causes.

  • inflammatory conditions
  • chronic infections such as TB
  • bronchiectasis
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8
Q

What are myelodysplastic syndromes?

A

They are a type of dyserythropoiesis.

  • production of abnormal clones of marrow stem cells.
  • the red cell are defective and large (macrocytic anaemia develops)
  • because cells are defective, they are prematurely destroyed the RES and so progressive anaemia develops
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9
Q

Is there any point giving iron as a treatment to patients with myelodysplastic syndromes?

A

No. We need to give them red blood cells. These patients have the iron for production, only the production of blood cells is faulty.
Myelodysplastic syndromes are treated by chronic transfusion of red cells.

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10
Q

What is the difference between anaemia of chronic disease and iron deficiency?

A

Anaemia of chronic disease ACD is a lak of functional iron. The iron is present but it is stuck in macrophages.
Whreas is iron deficiency, there is a lack of iron from underabsorption or overuse.

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11
Q

Deficiencies in which building blocks for DNA synthesis can lead to anaemia? (2)

A
  1. Folate

2. Vitamin B12

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12
Q

A deficiency in Folate of vitamin B12 can lead to which type of anaemia?

A

Megaloblastic anaemia

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13
Q

Why are RBC of megaloblastic anaemic patient huge?

A

Both B12 and folate are necessary for nuclear divisions and nuclear maturation. When deficient, nuclear maturation and cell divisions lag behind cytoplasm development. This lead to LARGE RED CELL PRECURSORS with inappropriately LARGE NUCLEI, and open chromatin.
The mature cells are also large leading to macrocytic anaemia.

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14
Q

How is B12 synthesised?

A

By microorganisms.

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15
Q

How do humans acquire vitamin B12?

A

By eating foods of animal origin, leading to a large excess of B12 in the diet of meat eaters.

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16
Q

Who is likely to be B12 deficient?

A

Vegetarians and vegans because B12 is acquired through eating foods of animal origin.

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17
Q

Who is receiving an excess of B12?

A

Meat eater

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18
Q

What is intrinsic factor IF?

A

Intrinsic factor is a glycoprotein produced by parietal cells in the stomach and will combine to B12.
The IF-B12 complex then bonds in the ileum leading to absorption of B12 and destruction of IF.

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19
Q

Where is B12 absorbed?

A

In the ileum

20
Q

In the portal blood, B12 binds to which plasma protein?

A

Transcobalamin

21
Q

What is transcobalamin?

A

Transcobalamin is a plasma protein that binds to B12 in the portal blod and delivers B12 to the bone marrow and other tissues.

22
Q

From which 4 causes could B12 deficiency arise?

A
  1. Dietary B12 deficiency; vegetarians, vegans
  2. Intrinsic factor deficiency; Pernicious anaemia is an autoimmune disease that targets parietal cells, the producers of intrinsic factor.
  3. IF-B12 complex binds in the ileum; so Crohn’s disease, ideal resection or tropical spruce will affect B12 absorption
  4. Transcobalamin deficiency; it normally delivers B12 to bone marrow and tissues
23
Q

Which of B12 or folate is importantly stocked and so takes a long time to be deficient?

A

B12 is stocked! Takes ages to become deficient. It takes years f being a vegan to be B12 deficient, but only a very short time to be folate deficient.

24
Q

Where does folate absorption occur?

A

In the duodenum and jejunum.

25
Q

In which foods is folate present?

A

Folate is present in most foods, yeast, liver and especially in leafy greens

26
Q

Dietary folates are all converted ino one compound, this is?

A

MethylTHF

27
Q

What is methylTHF?

A

It is the compound into which all folates are converted.

MethylTHF circulates in plasma nd is needed throughout th body for DNA synthesis

28
Q

What can folate deficiency result from?

A
  1. Dietary deficiency. Or increased use during pregnancy, or severe skin diseases
  2. Duodenum and jejunum: proximal small bowel disease such as Coeliac/Crohns
  3. MethylTHF: drug which inhibit conversion of folates
  4. Alcoholism, urinary loss of folate, etc.
29
Q

Vit B12 is also associated with diseases of which system?

A

Neurological diseases,

  • focal demyelination
  • depression
  • dementia
30
Q

Which diseases affecting haemoglobin synthesis result in anaemia? (2)

A
  1. Thalassaemia - reduced rate of synthesis of normal a- or b- globin chains
  2. Sickle cell - synth of abnormal b-globin
31
Q

What mutation causes sickle cell disease?

A
  • point mutation: substitution of valine for glutamine
  • position 6 in the b-chain
  • HbSS: homozygous sickle cell anaemia
  • HbS: carrier, confers protection against malaria, with only mild symptoms of anaemia
32
Q

What are thalassaemias?

A

They are genetic disorders with varied expression worldwide: S. Asian, Meditranean anf Far east.
They are defined by a relative excess of one globin chain (a or b) contributes to the defective nature of the red cell.
- most red cells are destroyed in the bone marrow before they even reach circulation
- other RBCs are excessively degraded within the spleen

33
Q

What is the consequence of thalassaemia on the liver?

A

Hepatomegaly, as the liver tries to compensate for the lack of RBCs in the blood = extramedullary haemopoiesis

34
Q

Why are skeletal abnormalities seen in patients with thalassaemia?

A

Because of extramedullary haemopoiesis.

Haemopoiesis expands into bone cortex, therefore impairing growth an causing skeletal abnormalities.

35
Q

What is the major cause of premature death in thalassaemic patients?

A

IRON OVERLOAD!

  • excessive absorption of dietary iron due to ineffective haematopoiesis
  • repeated blood transfusions required to treat the anaemia
36
Q

What treatment is recommended for thalassaemic patients?

A
  1. Transfusions
  2. Iron chelating agents
  3. Folic acid
  4. Holistic care. Cardiology, endocrinology, psychological
37
Q

What is the difference between b-thalassaemia minor and b-thalassaemia major?

A

The difference between minor and major is the number of inherited “ill” genes.

  • minor: only 1 ill gene, so heterozygous
  • major: 2 ill genes, so homozygous
38
Q

What do RBCs look like in thalassaemia?

A
  • hypochromic
  • microcytic
    => due to low levels of intracellular haemoglobin
39
Q

There are 2 majored cell enzyme defects that can lead to anaemia, these are:

A
  1. Glucose-6-phosphate dehydrogenase deficiency

2. Pyruvate kinase deficiency

40
Q

Why can glucose-6-phosphate dehydrogenase deficiency lead to anaemia?

A

G6P is an important enzyme of the pentose pathway.
The pentose pathway is one of the ways RBCs get energy.
But G6P is also involved in protecting from oxidative stress by glutathione production. SO if less glutathione, then less protection against oxidative stress, so BCs ar damaged and degraded.
Most patients are asymptomatic!
But abnormal haemolytic in G6PDH deficiency can have symptoms such as: prolonged jaundice at birth, haemolytic crises (broad beans!)

41
Q

Why can pyruvate kinase deficiency lead to anaemia?

A

Pyruvate kinase is the last enzyme of glycolysis.
If this enzyme is deficient, then completion of glycolysis is blocked. Therefore, all products past the block are deficient in the RBC, including ATP and pyruvate.
=> all active processes needing ATP come to a halt.
=> RBCs are destroyed

42
Q

What is autoimmune haemolytic anaemia?

A

It is a condition in which autoantibodies (Ig protein produced by own B lymphocytes) bind to the red cell membrane proteins.

43
Q

What is warm autoimmune haemolytic anaemia?

A

It is mediated by IgGs, maximally active at 37°c

44
Q

What is cold autoimmune haemolytic anaemia?

A

It is mediated by IgMs, maximally active at 4°c.

here IgMs are directed at body’s own red cells.

45
Q

What is polycythaemia?

A

Too many red cells

  • diagnosis: high hematocrit or raised cell mass
  • it is a group of varied disorders with an increase in circulating red cells that are typified by a persistently raised hematocrit
46
Q

What is polycythaemia vera?

A
  • it is an erythrocytosis, ie an increase in concentraiton of RBCs., that is Absolute ad primary.
  • absolute = increase in red cell mass that is not due to a decrease in plasma volume.
  • primary = NOT driven by EPO production.

Polycythaemia vera is. significant cause of arterial thrombosis, ends thrombosis, priorities, gout etc.

47
Q

What is the treatment of polycythaemia vera?

A

Venesection to maintain Hct to <0.45
Aspirin 75mg
Possibly drugs if venesection poorly tolerated, splenomegaly or other signs or progression.

MEH (4 decks)

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