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Molecular basis of disease > Nutritional anaemias > Flashcards

Nutritional anaemias Flashcards

1
Q

what is anaemia?

A

Anaemia is a condition in which the number of red blood cells (and consequently their oxygen-carrying capacity) is insufficient to meet the body’s physiological needs. / also low levels of haemoglobin

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2
Q

what are the ingredients for making RBCs

A

Vitamin B12 folic acid and iron (also cytokines and healthy bone marrow niche)

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3
Q

What are the 3 causes for anaemia

A

Failure of production of haemoglobin
Ineffective erythropoiesis (rbc production)
Decreased survival (blood loss, haemolysis, reticulocytosis)

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4
Q

What is reticulocytopenia?

A

a reticulocyte is an immature red blood cell, reticulocytopenia is a condition where there is an abnormal level of reticulocytes in the body

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5
Q

What does failure of production of haemoglobin/rbcs mean

A

it means there might not be enough ingredients resulting in hypo proliferation (not enough rbcs produced)
or it could be due to reticulocytopenia (not enough baby rbcs in the body)

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6
Q

what does ineffective erythropoiesis mean

A

decreased output of rbcs basically ineffective rbc production

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7
Q

how do we investigate anaemia

A

based on whether blood test results show rbcs are microcytic (smaller than normal) or macrocytic (bigger than normal)

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8
Q

why are macrocytic rbcs bad

A

they dont have enough nutrients

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9
Q

what causes rbcs to be macro and microcytic

A

microcytic- Iron deficiency
macrocytic- B12, folate deficiency

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10
Q

what role does iron have in blood

A

O2 transport

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11
Q

why do daily requirement for women after 51 years become the same as men

A

menopause they no longer have periods and no longer need more iron to make up for blood loss.
(pregnant women have the highest iron requirement)

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12
Q

where does most of our iron go and how

A

most of it goes to bone marrow to be carried by blood via transferrin a transport protein (some goes to muscles and liver)

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13
Q

where is iron stored

A

in the liver and can be transferred back out via transferrin

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14
Q

how many states of iron are there in the body and what form are they mostly found as in the body

A

Fe+3 (ferric state) Fe+2 (ferrous state), most of it is found as Hb (haemoglobin)

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15
Q

what are the transport and storage proteins of iron

A

ferritin
haemosiderin
found in bone marrow spleen and liver

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16
Q

how is iron absorption regulated

A

GI mucosal cells and hepcidin

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17
Q

How does hepcidin regulate iron absorption?

A

Causes ferroportin internalization and degradation decreasing the iron transfer into the blood plasma from the duodenum.

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18
Q

what are the duodenum and the jejunum

A

Duodenum- First part of the small intestine
Jejunum- middle part of the small intestine

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19
Q

how does the duodenum and jejunum regulate iron absorption

A

They contain ferroportin receptors on cells which transfer iron into the plasma where the iron binds to transferrin and is taken wherever needed

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20
Q

what cells have ferroportin receptors

A

enterocyte cells (a cell of the intestinal lining)
found in the Duodenum and Jejunum

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21
Q

What affects the amount of iron the body absorbs

A

Type of iron ingested (Heme, Ferrous, non heme)
GI acidity
Iron storage levels
Bone marrow activity

22
Q

how does hepcidin regulate iron absorption

A

it gets rid of ferroportin receptors available (by degradation and internalisation) which means iron can no longer be transferred to the plasma and cant bind to transferrin.

23
Q

how is hepcidin regulated

A

via iron conc and rbcs production demand for iron

24
Q

what happens to excess iron

A

stored as ferritin (a storage protein)

25
Q

What happens to the levels of transferrin and ferritin in iron deficiency?

A

Transferrin- increased
Ferritin- decreased

26
Q

How can we test for iron deficiency?

A

Iron binding studies

27
Q

what does low ferritin levels show and how can it be artificially increased

A

low ferritin levels mean low iron levels (i.e iron deficient)
Ferritin is part of the immune system so if you’re unwell it can be raised

28
Q

what are causes of iron deficiency

A

Blood loss (mensturation, undiagnosed GI tract blood loss, parasites)
Poor diet (can also be because of malabsorption or ^inc physiological needs)

29
Q

how is iron deficiency investigated

A

full blood count: checks Hb conc, mean cell volume, mean cell haemoglobin and reticulocyte count (baby rbc count)
blood film
BMAT (bone marrow biopsy)- very outdated

30
Q

How does Iron deficient anaemia (IDA) present under a microscope?

A

Microcytic (smaller than WBC)
Hypochromic (pale)

31
Q

what are the symptoms of IDA (iron deficiency anaemia)

A

Symptoms:
fatigue, lethargy, dizziness

Signs:
pallor of mucous membrane, bounding pulse, systolic flow murmurs, smooth tongue, koilonychias (spoon nail, the centre of the nail is depressed and starts looking like a spoon)

32
Q

Why are B12 & folate grouped together?

A

Both have similar clinical findings and are normally found together but can be isolated from one another in diagnosis

33
Q

what happens with B12 and/or folate deficiency

A

macrocytic anaemia
They have low Hb and high MCV (mean corpuscular volume, meaning bigger cell with more volume), as well as normal MCHC (mean corpuscular haemoglobin concentration).

34
Q

How do the previous symptoms (macrocytic anaemia blood results) cause anaemia?

A

Because the cells are bigger and have more volume this means they can hold more Hb in ONE cell, this gives the illusion of a healthy cell in a patient if you’re only looking at MCHC (Hb conc in a cell) since the cell is larger and has a higher capacity for Hb, however overall there is low Hb since there aren’t enough cells in the body to keep up with Hb demand meaning theres less cells overall resulting in less Hb overall causing anaemia.

35
Q

macrocytic anaemia has 2 descriptions

A

Megaloblastic- Vitamin B12 or folate deficiency, or drug related
Non-megaloblastic- every other cause

36
Q

B12 and folate sources

A

fish, meat, dairy vegetables (oil), liver
B12 folate

37
Q

What are some differences between Megaloblastic and non-megaloblastic anaemias?

A

Megaloblastic- Hyper segmented neutrophil (too many nucleus nodes in a neutrophil, normally has 3-4 where you can see up to 7 in a B12/Folate deficient patient), oval RBCs
Non-megaloblastic- has many macrocytic rbcs present but there is no uniformity to rbc size, theres just a bunch of different rbcs with no pattern in size.

38
Q

what is folate used for

A

A, T, G synthesis

39
Q

what are causes of folate deficiency

A

increased demand- breast feeding, growth spurts, cancer, rapid cell turnover, heart failure
decreased intake- diet, elderly, alcohol
decreased absorption- medicine, coeliac, jejunal resection, tropical sprue

40
Q

what is vitamin b12 essential for

A

methylation in DNA and cell metabolism
necessary for homeostasis of MMA and homocysteine

41
Q

what are some lab studies they carry out for iron

A

Fe serum- hugely variable in the day
Ferritin
Transferrin (inversely proportional to Fe stores)
Transferrin saturation- amount of transferrin that is bound to iron
Total Iron binding capacity- measurement of the capacity of transferrin to bind to iron (indirectly measures transferrin)

Difficult to carry out and is unreliable, ferritin is the most reliable measure of iron levels of a patient

42
Q

How is ferritin measurement sometimes unreliable?

A

It is also part of the immune system meaning if there is an infection or any activity of the immune system ferritin levels can be artificially boosted by such causes

43
Q

Why is transferrin inversely proportional to Fe stores

A

because the less fe available the more the body wants to transfer from the stores so they increase transferrin production to try make up for the lack of iron in the body. basically supply and demand if you think about it there was more supply so less demand now theres less supply so more demand

44
Q

How is B12 absorbed

A

In the terminal Ileum (last section of the small intestine) via intrinsic factor (a glycoprotein made in stomach parietal cells found in the stomach same cell make acid)

45
Q

what is pernicious anaemia

A

an autoimmune disease where antibodies attack either intrinsic factor or parietal cells destroying them so there is lack of B12 absorption resulting in anaemia no amount of B12 supplementation will rectify this as it wont be absorbed, you need B12 injections straight into the blood to treat this.

46
Q

What are some causes of B12 deficiency?

A

Impaired absorption- pernicious, gastrectomy/ ileal resection, parasites, zollinger-ellison syndrome
decreased intake- malnutrition, vegan diet
Congenital causes- IF receptor deficiency, folate mutation CG1 gene
inc req- Haemolysis, HIV, pregnancy, growth spurts
Medication- Alcohol, NO, metformin, PPI/H2 antagonists

47
Q

What is the difference between Iron deficient anaemia and B12 and/or folate anaemia?

A

Iron- Microcytic (smaller rbc)
Folate &/or B12- Macrocytic (enlarged rbc)

48
Q

Why are B12 & folate grouped together?

A

Both have similar clinical findings and are normally found together but can be isolated from one another in diagnosis

49
Q

What are the haematological consequences of B12 deficiency?

A

MCV- Normal or raised
Hb- Normal or low
Reticulocyte count- Low
LDH- Raised
Blood film- Macrocytes, ovalocytes, hyper segmented neutrophils
BMAT- Giant metamyelocytes, hypercellular, megaloblastic (Large immature WBCs, very unusual to need this test)
MMA- Increased

50
Q

What are some clinical consequences of B12?

A

Brain: low cognition, depression, psychosis
Neurology- sensory changes, ataxia (disorder of balance and speech), spasticity (abnormal muscle stiffness), myelopathy (compressed spine)
Infertility
cardiomyopathy
Tongue: taste impairment, glossitis
Blood: Pancytopenia (deficiency of rbc wbc and platelets)

Molecular basis of disease (14 decks)

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