Session 4 - Anemia and Iron Deficiency Flashcards

1
Q

define anemia

A

a lower than the normal level of haemoglobin in the blood

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2
Q

draw a diagram for the life of a RBC, with the potential issues that can cause anemia

A

bone marrow - issues in
erythropoeisis -
reduced ertyropeoisis - negative feed back loop normal in erythopoeisis but chronic kidney diseases sops kidney EPO production or empty bone marrow - aplastic anmeia, Parovirus infection, Cancer in bone marrow, means abnormal heamopoetic cell reduction

myelofibirosis - reduciton in eyrthropoeisis, vibrotic marrow and tear drop polikocytosis

Dyserythroposis - anemia of chonic disease/inflammation - Fe not released, reduced RBC life span, marrow is not responding to EPO - renal disease, infalmmatory conditions like rheumatoid arthritis , IFB - chrons disease, Chronic infections and myleodisplastic syndrome - marrow produced abnormal cells

haemoglobin synthesis - defects - a lack of iron from iron deficiency or anemia of chronic disease, B12/folate deficiency (megaloblastic anemia) - mutations - thallasemia and sickle cell

Peripheral RBC - issues in

structure - Memebrane - spherocytosis/eplitocytosis - issues with ankyrin binding ect
mechanical damage - heart valve stenosis shears RBC’s
MAHA - microangiopathies
DIC
Burns

metabolism - Red cell enzyme defects can lead to anemia - G6PDH deficiency and pyruvate kinase deficiency

Loss of Red Cells - Stabbed, RTA ect

Removal - issues with
RES (reticuloendothelial system) - splenomegaly, hyposplenism lead to excess RBC removal
Autoimmune heamolytic anemias - autoantibodies attach to RBC and remove them inccorectly

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3
Q

draw a table to show evaluation of anemia

A

refer to session 4 lec 2 to see the diagrams

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4
Q

what is some evidence of heamolysis in a FBC

A

high retic count

High LDH - from lysed RBC’s
High Billirubin - excess RBC destruction

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5
Q

what is the anacronym for Anemia with a low reticuloctye count and a low MCV

A

TAILS

Thallasemia
Anemia of chronic disease
Iron deficiency
Lead poisoning
Sideroblastic anemia - inherited

a microcytic and hypochromic RBC is seen

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6
Q

what are the causes for Anemia with a low reticuloctye count and a high MCV

A

Vit B12/folate deficiency
Alcohol
liver disease
myeloidisplasia

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7
Q

what are the causes for Anemia with a low reticuloctye count and a norm MCV

A

primary bone marrow failure - rare
aplastic anaemia

secondary bone marrow failure -
Anaemia of chronic disease
HIV infection

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8
Q

outline through skketeches and recall the role of B12 and folate deficiency and how this can cause anemaia

name good sources of B12 and folate and also how to treat

A

check the lec notes

Key words

haptocrrin binds B12
paraetial cells - intrinsic factor (perincious anemia is autoimmune and targets these cells, prevents B12 absorbition from gut)
binds B12

IF receptors in ileum

folate absorbed in duodenum and jejunum

homocystine (toxic) —–> methianone

via Vit B12 via converion of folic acid —-> active Tetrahydrofolate (THF)

so deficiency in one gives a functional deficiency in the other

both THF and Methionone are key buliding blocks in biosythesis

also key maker of thymidyalte/thymie for DNA - if it is low we use uracil

cell removes bad DNA, so DNA grows slow why cytoplasm grows at a normal rate - megaloblastic anaemia - macrocytic Red cells, ansiopolikocytosis tear drops

give folic acid and diet chenged for B12

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9
Q

what are the two types of iron, and why is this important

where is iron absorbed in the body, what affects it

A

ferrous - 2+ and ferric - 3+

we cannot absorb ferric iron, we must convert it via reductase of which Vit C is a cofactor which assist absorption

Tannines in Tea inhibits iron absorption from the gut which occurs in the duodenum and jejunum

citrate and vit c help absorption

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10
Q

draw a diagram for the dietary absortion of iron and its subsequent precessing in the body with names receptors and horomnes that affect it

A

check against session 4 lec 2

ie hephaestin, ferroprotin, transferrin, hepcidin, DMT1 ect

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11
Q

how is iron stored in the body ?

A

Ferretin - globular protein where iron is stores in center, exits through pores

Heamosiderin - aggeregates of ferretin
accumulates in machrophages, liver and spleen

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12
Q

where is our main source of iron from ?

how do we regulate iron absorption

A

mostly recycled, the rest from diet

comes from recycling of RBC by splenic macrophages and kupfer cells of the liver

iron uptake is regulated by regulating the receptors and transpoters expression, such as ferroportin, transferrin recptor, HFE protein ect

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13
Q

how does hepicidin alter iron uptake

A

it inhbits ferroportin transferring iron into blood stream

hepcidin synthesis is increased by iron overload
reduced by high erythropoetic activity

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14
Q

draw a diagram to explain how anemia of chronic disease works

include conditions which cause it

A

check session 4 lec 2

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15
Q

what are common causes of iron deficiency

A
vegan diet
pregnancy 
growth spurts in kids
menstruation
anemia of chronic disease - inflammatory bowel disease
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16
Q

what are the signs and symptoms of iron deficiency ?

A
Tiredness
Pallor
reduced exercise tolerance
light headed, breathless
headache 
angina
17
Q

what does iron def look life on a blood film

how do we test for it ?

how would you treat it ?

A

a microcytic and hypochromic RBC is seen
low MCV and low MCHC

see ansiopolkicytosis

we test plasma ferretin levels or reduced plasma ferretin levels

dietary advice
oral supplements
intramuscular injections

18
Q

what is the problem with iron excess ?

what are the two conditions ?

A
  • Excess iron deposited in organs as haemosiderin
  • Iron promotes free radical formation & organ damage

Damage to proteins and Damage to DNA

Transfusion associated haemosiderosis
Repeated blood transfusions give gradual accumulation of iron
• Problem with transfusion dependent anaemias such as thalassaemia & sickle cell anaemia
• Iron chelating agents such as desferrioxamine can delay but do not stop inevitable effects of iron overload

Hereditary haemochromostosis (HH)
Autosomal recessive disease caused by mutation in HFE gene
• Mutated HFE cant bind to transferrin so the negative influence on iron uptake is lost
• Too much iron enters cells
• Iron accumulates in end organs causing damage
• Treat with regular venesection

both cause :
Liver cirrhosis
Diabetes mellitus
Hypogonadism
Cardiomyopathy
Arthropathy
Increased skin
pigmentation