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MEH > Session 4 anaemias > Flashcards

Session 4 anaemias Flashcards

1
Q

Why are RBC’s in megaloblastic anaemia so big?

A

Cytoplasm develops before nuclear maturation and cell division occur
(lots of cytoplasm, large nuclei and open chromatin)

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2
Q

In femtolitres, how big is an RBC in macrocytic anaemia?

A

> 100 fl

normal: 80-100 fl

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3
Q

What neurological symptoms can a B12 deficiency cause?

A

dementia, depression

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4
Q

Where are the spleen and liver in abdomen?

A

Liver - upper right

Spleen - upper left

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5
Q

Which system removes old red blood cells?

Which particular organ of this system?

A

Reticuloendothelial system

spleen

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6
Q

Where does extramedullary haematopoiesis take place?

A

liver > hepatomegaly
spleen > splenomegaly
bone cortex > skeletal deformities

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7
Q

Why is bilirubin high in haemolytic anaemia?

A

Spleen removes RBC’s

metabolises haem to bilirubin

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8
Q

What is myelofibrosis?

How can you diagnose it?

A

Condition where fat cells for the bone marrow are replaced by fibrotic tissue (less haematopoiesis)

Tear shaped RBC’s
Splenomegaly (extramedullay haematopoiesis)

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9
Q

Why is there raised lactate dehydrogenase in haemolytic anaemia?

A

Enzyme in RBC’s released when they lyse

interconverts between pyruvate and lactate

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10
Q

Intravascular vs extravascular haemolytic anameia?

A

intra- in vessels

extra- RES (in spleen or liver by macrophages)

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11
Q

Which proteins are deficient in hereditary spherocytosis?

A

ankyrin / protein 4.2

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12
Q

Which mutation occurs in sickle cell anaemia?

A

glutamate to valine on beta chain of haemoglobin

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13
Q

How do sickle cell RBC’s behave in deoxygenated conditions?

When is this exacerbated?

A

polymerise irreversibly (occlude vessels > MI/ stroke)

cold and infection

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14
Q

What are thalassemias?

A

Reduced rate of alpha/ beta chain synthesis in haemoglobin

Hb A - x2 alpha chains, x2 beta chains

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15
Q

Give 4 causes of macrocytic anaemias?

A
  • B12/ folate deficiency
  • alcoholism (folate deficiency)
  • liver disease (less B12/ folate storage)
  • reticulocytosis
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16
Q

3 causes of microcytic anaemias?

Why are the cells so small?

A

Iron deficiency
Anaemia of chronic disease (sometimes)
Thalassaemia

Reduced rate of haemoglobin synthesis

17
Q

What is sideroblastic anaemia?

A

type of microcytic anaemia

inherited defects in haem synthesis pathway

18
Q

How does lead poisoning cause microcytic anaemia?

A

Inhibits enzymes in the haem synthesis pathway

19
Q

In what form is iron absorbed?

A

Ferrous, Fe2+ (more readily available in haem iron)

20
Q

Why is free iron toxic to cells?

A

Catalyses reactions which produce ROS

21
Q

How is haem iron absorbed from the duodenum?

A

Haem iron (fe2+) transported in to the enterocyte
Haem oxidase degrades haem to release the free ferrous iron
Transported into the blood via ferroportin
Binds transferrin as FE3+

22
Q

How is non-haem iron absorbed from the intestine?

A

Ferric (Fe3+) reduced to Fe2+ by DcytB (duodenal cytochrome B)
Fe2+ carried into the cell by DMT1 (divalent metal transporter 1)

23
Q

Which liver peptide is the main regulator of iron absorption?

A

Hepcidin

  • Binds ferroportin causing its degradation
  • inhibits transcription of DMT1
24
Q

Which foods, vitamins and drugs affect iron absorption?

A

Tannins (tea) and phylates (chapattis and pulses) inhibit iron absorption bu binding non-haem iron

Antacids inhibit iron absorption

Vitamin C aids iron absorption
(helps reduce fe3+ to fe2+)

25
Q

What happens to absorbed iron?

A

Taken up by bone marrow for eythropoiesis or stored in macrophages (RES)

26
Q

Ferritin is the soluble cellular iron store.

What is the insoluble cellular iron store?

A

Haemosiderin

27
Q

Long standing iron deficiency can cause what changes to the mouth and nails?

A

inflammation at the corners of the mouth- angular cheilitis

spoon nails- koilonychia

28
Q

What is Plummer vinson syndrome?

A

Syndrome of long standing iron deficiency

dysphagia is one effect- difficulty swallowing

29
Q

What is hereditary haemochromatosis?

How do you treat it?

A

Excess iron in the tissues and organs due to a defect in the HFE protein which interacts with the transferrin receptor

Therapeutic phlebotomy to get the iron out

30
Q

Which organs / tissues are damaged first in hereditary haemochromatosis?

A 
pancreas- diabetes
liver- cirrhosis
adrenal glands - adrenal insufficiency 
heart - heart failure 
joints- arthritis

MEH (9 decks)

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