Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Sem 2 - MEH > From metabolism and micolytic anaemia > Flashcards

From metabolism and micolytic anaemia Flashcards

1
Q

What are the names of the classification of anaemias in terms of the size of RBCs?

A
  • Microcytic - small
  • Macrocytic - Large
  • Normocytic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the causes of microlytic anaemias?

A

Reduced haem synthesis or reduced globin chain synthesis.

Reduced haem synthesis leads to:

  • Iron deficiency (insufficient Fe for heam synthesis -most common)
  • lead poisoning (aquired defect -lead inhibits enzymes involved inhaem synthesis)
  • Anaemia of chronic disease (Hepcidin results in functional iron deficiency)
  • Sideroblastic anaemia (inherited defect in haem synthesis)

Reduced globin chain synthesis leads to a or B thalassaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is the neumonic to help remember the causes of microcytic anaemia?

A

TAILS

T- Thalassaemia

A - Anaemia of chronic disease

I - Iron deficiency

L - Lead poisoning

S - sideroblastic anaemia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are the characteristics of erythrocytes in microcytic anaemias?

A

They are smaller than normal (microcytic)

Cells are often paler than usual (hypochromic because of lack of haem and Fe.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are the uses of Iron?

A

It is essential for all living cells.

Oxygen carrier for Hb in red cells and myoglobin in myocytes.

Co-Factor in many enzymes:

  • Cytochromes (oxidative phosphorylation)
  • Krebs cycle enzymes
  • Cytochrome P450 enzymes
  • Catalase. (protects cells from oxidative damage)

BUT, free iron is potential very toxic to cells (as fenton reaction which can produce free radicals). This means that out body has a complex regulatoru systems to ensure the safe absorbtion, transportation and utilisation of iron.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Does your body have a mechanism for excreting iron?

A

No! The body has no mechanism for exreting iron. We can only control iron absorbtion.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is the different between ferrous and ferric iron?

A

Ferrous = Fe2+ (reduced form)

Ferric = Fe3+ (oxidised form)

The body prefers ferrous iron as this is the only one we are able to absorb but most of the dietary iron in the ferric form. This

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

In what conditions does iron ger oxidised / reduced and how does iron get into the optimum form for absorbtion?

A

Fe2+ gets oxidised to Fe3+ whe there is a high (alkaline) pH

Fe3+ gets reduced to Fe2+ when there is an acidic (low) pH

The acidic environment in the stomach helps to convert ferric iron in our diet to ferrous iron which we can absorb.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are some sources of iron in our diet?

A

Haem iron (meat products) which can be readily absorbed as ferrous:

  • Liver
  • Kidney
  • Beef steak
  • Beef burger
  • Chicken
  • Duck
  • Pork chop
  • Salmon
  • Tuna

Non-heam iron which is in ferric form:

  • Fortified cereals
  • Raisins
  • Beans
  • Figs
  • Barley
  • Oats
  • Rice
  • Potatoes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Where does the absorbtion of iron occur?

A

Absorbtion of Fe is via the duodenum and upper jejunum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

How is dietary iron absorbed into the body?

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

How is Fe3+ reduced to Fe2+?

A

Thic iccurs via a ferric reductase enzyme in combination with vitamin C.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What co-transporter takes iron from the chyme and into the enterocyte?

A

DMT1 (divalent metal transporter 1) -A H+ leaves the cell as iron enters.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How is iron stored in enterocytes?

A

Iron is stored in the Fe3+ form via a protein called ferritin.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What protein allws ferrous iron to pass across the membrane and into the blood?

A

Ferroportin.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is transferrin?

A

This is a protein that traonsports two molecules of ferric iron around the body.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What protein faciltates the concersion of ferrous into ferric iron so that it can be transported around the body?

A

Haphaestin

18
Q

What factors negatively affect the absorbtion of iron from food?

A
  • Tannins (in tea)
  • Phytates (eg pulses, Chapattis)
  • Fibre
  • Antacids - as increase pH so decrease conversion of ferric to ferrous iron.
19
Q

What factors positively affect the absorbtion of iron from food? Why?

A

Vitamin C and Citrate

  • They prevent the formation of insoluble iron compunds.
  • Vit C also helps to reduce ferric to ferrous iron.
20
Q

What iron is ‘Functional’?

A

This is iron that is available for use in biological processes. (2.5/3.5g of iron in body)

  • Haemoglobin
  • Myoglobin
  • Enzymes e.g cytochromes
  • Transported irom (in serum and mainly transferrin)
21
Q

What are the ‘stored’ forms of iron?

A

Ferritin (soluble) or Haemosiderin (insoluble).

22
Q

What is ferritin?

A

This is a globular protein complex with a hollow core.

It has pores which allow iron to enter and to be released.

It is a storage capsule for iron.

23
Q

What is haemosiderin?

A
  • This aggregates clumped ferritin particles, denatured protein and lipid.
  • Accumulates in macrophages, particularly in the liver, spleen and bone marrow.
  • This apprears brown on a stain.
24
Q

How do cells take up iron?

A
  1. Fe3+ bound transferrin receptor and enters the cytosol receptor-mediated endocytosis.
  2. Fe3+ within endosome released by acidic microenvironment and reduced Fe2+
  3. The Fe2+ transported to the cytosol via DMT1
  4. Once in the cytosol, Fe2+ can be stored in ferritin, exported by ferroportin (FPN1) or taken up by motochondria for use in cytochrome enzymes.
25
Q

What percentage of our iron intake is obtained from recycling? How does this occur?

A

Over 80% of iron requirement is met from recycling damaged or senescent RBCs

Old RBCs are engulfed by macrophages (mainly those of the pleen and kupffer cells of the liver).

These macrophags the catalobise haem released from RBCs.

The amino acids are reused and iron is exported to blood (transferrin) or returned to storage pool or ferritin in macrophages.

26
Q

How is iron absorbtion regulated?

A

It depends in dietary factors, body iron stores and erthropoiesis.

The dietary iron levels are sensed by enterocytes.

Controlled by:

  • Regulation of transporters e.g. ferroportin
  • Regulation of receptors w.g. transferrin receptos and HFE protein
  • Hepcidin and cytokines
  • Crossstalk between epithelial cells and other cells like macrophages.
27
Q

What us hepcidin?

A

Hepsidin is a negative regulator of iron absorbtion. It is a peptide hormone that is synthesised by the liver and released into the bloodstream.

Hepsidin induces internalisation and degridation of the ferroportin protein.

Its synthesis is increased in iron overload and decreased by high erythropoietic activity.

It inhibits the absorbtion of iron from the gut and the release of stored iron from RE system.

28
Q

What is anaemia of chronic disease?

A
29
Q

Summarise the homeostasis of iron

A
30
Q

What are the most common causes of iron deficiency?

A
  • Insufficient iron in the diet - vegan and vegetarian diets
  • Malabsortion of iron -vegan and vegetarian diets
  • Bleeding - Menstruation, peptic ulcer
  • Increased requrment - Pregnancy, rapid growth
  • Anaemia of chronic disease - inflammatory bowel disease
31
Q

How do you treat iron diagnosis?

A

Iron deficiency is a sign not a diagnosis! Clinical diagnosis must always seek to determine the underlying reason why the patient is iron deficient.

32
Q

What groups of people have the highest iron requirement?

A

Pregnant people! pregnant people normally have an iron deficiency.

Infants, children, women of a child bearing age and the geriatric group are also at risk.

33
Q

What are the signs and symptoms of iron deficiencies?

A
  • Physiological effects of anaemia…
    • Tiredness
    • Pallor
    • Reduced exercise tolerance (due to reduced oxygen carrying capacity)
    • Cardiac - angina, palpitations, development of heart failure.
    • Increased respiratory rate
    • Headache, dizziness and light-headedness.
  • Pica (unusual cravings for non-nutritive substances eg dirt and ice)
  • Cold hands and feet
  • Epithelial changes (see picture)
34
Q

What does an FBC show during iron deficiency anaemia?

A
  • Low MCV (mean corpuscular volume)
  • Low MCHC (mean corpuscular haemoglobin concentration)
  • Often elevated platelet count
  • Normal or elevated WBCs
  • Low serum ferritin, serum iron and % transferrin saturation raised TIBC (total iron blood count)
  • Low retuculocyte Hb content (CHr)
35
Q

What are the likely peripheral blood smear results in iron deficiency anaemia?

A
  • RBCs are microcytic and hypochromic in chronic cases
  • Anisopokilocytosis: change in size and shape
  • Sometimes pencil cells and target cells.
36
Q

How do you test for iron deficiency?

A

Plasma ferritin is comonly used as an indirect marker of total iron status - reduced plasma ferritin definitively indicates iron deficiency.

BUT normal or increased ferritin does NOT exclude iron deficiency because the levels can increase with other conditions e.g. cancer and infection.

CHr (reticulocyte haemoglobin content) is recommended by NICE to test for functional iron deficiency. This is because CHr remains low during inflammatory resonses. (CHr is also low in patients with thalassaemia)

37
Q

Why do you not measure iron in the blood to test for iron deficiency?

A

Because the amount of free iron in the blood will vary remarkably during a day.

38
Q

How do you treat iron deficiency?

A
  • Dietary advice (Meat..)
  • Oral iron (with orange juice and avoid tea and pulses). BUT GI side effects so low complience.
  • Intramuscular iron injections
  • IV iron
  • Blood transfusion.

Should see an improvement of 20g/L in 3 weeks and an improvement in symptoms.

39
Q

Why is iron excess dangerous?

A

If excess iron exceeds the binding capacity of transferin it is dangerous.

This is because excess iron is deposited in organs as haemosiderin and it promotes free radical formation and organ damage.

This occurs as iron (both forms) react with hydrogen peroxide to produce redicals with cause damage to cells (lipid peroxidation, damage to proteins and damage to DNA).

It leads to transfision associated haemosiderosis or hereditary haemochromatosis

40
Q

What is transfision associated haemosiderosis?

A

This is when repeated blood transfision gives a gradual accumulation of iron.

400ml blood = 200mg iron.

Problem with transfusion dependant anaemias such as thalassaemia and sickle cell death.

Iron chelating agents such as desferrioxamine can delay but do not stop the inevitable effects of iron overload.

41
Q

What are the consequenses of transfusion associated haemosiderosis or hereditary haemochromatosis?

A

Accumulation of iron (haemosiderin) in liver, heart and endocrine organs leads to:

  • Liver cirrhosis
  • Diabetes mellitus
  • Hypogonadism
  • Cardiomaopathy
  • Arthopathy (joints)
  • Increased skin pigmentation
42
Q

What is hereditary haemochromatosis?

A
  • This is caused by an autosomal recessive diseased casued by a mutation in the HFE gene (chromosome 6)
  • HFE protein nirmally interacts with the transferrin receptor, reducing its affinity for iron-bound transferrin.
  • HFE also has a negative infuence on hepsidin. So, without HFE there is an uncontrolled intake of dietary iron.
  • Mutated HFE gene can’t bind to transferrin so the negative influence on iron uptake is lost.
  • Too much iron enters cells.
  • Iron accumulated in end organs causing damage.
  • Treat with venesection (removal of blood every few weeks).

Sem 2 - MEH (22 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions