nutritional anaemia Flashcards

1
Q

definition of anaemia

A

no. of RBCs (consequently the O2 carrying capacity) is insufficient to meet the bodies physiological needs

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2
Q

haemoglobin

A

iron containing O2 transport metalloprotein within RBCs

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3
Q

components of blood

A

RBCs, platelets, WBCs

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4
Q

example of difference in Hb levels when diagnosing anaemia

A

differs in age, gender, physiological state e.g. pregnant

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5
Q

eythropoesis

A

maturation of RBC from erythropoietic stem cell

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6
Q

what is required for normal erythropoiesis to take place?

A

vitamin B12 & folic acid, DNA synthesis, Iron, Hb synthesis

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7
Q

3 main mechanisms of action of anaemia

A
  1. Failure of production (hypoproliferation, reticulocytopenic)
  2. Ineffective Erythropoiesis
  3. Decreased survival (haemolysis, reticulocytosis)
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8
Q

Reticulocytopenic

A

Abnormal decrease of reticulocytes in the body. Reticulocytes are new, immature red blood cells.

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9
Q

Reticulocytosis

A

Increase in reticulocytes

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10
Q

Haemolysis

A

Rupture or destruction of RBCs

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11
Q

Mean Cell Volume (MCV)

A

describes average RBC size

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12
Q

Microcytic

A

small, hypochromic RBCs

- e.g. iron deficiency, thalassaemia, anaemia of chronic disease

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13
Q

Normocytic

A

normal sized RBCs, but a low number
- e.g. anaemia of chronic disease, aplastic anaemia, chronic renal failure, bone marrow infiltrations sickle cell disease

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14
Q

Macrocytic

A

large sized RBCs

- e.g. B12/Folate deficiency, Myelodisplasia, Alcohol/Drug induced, Liver disease, Myxoedema

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15
Q

Nutritional Anaemia

A

Anaemia caused by lack of essential ingredients that the body requires, e.g. Iron, Folate & B12 deficiency

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16
Q

where is iron absorbed?

A

duodenum

17
Q

what is transferrin?

A

Transferrins are iron-binding blood plasma glycoproteins that control the level of free iron (Fe) in biological fluids.

18
Q

what is Ferritin?

A

storage of iron: when there is excess iron (will be low in iron deficiency)

19
Q

how is iron absorption regulated?

A

by hepcidin, via ferroportin receptors on enterocytes

20
Q

Action of hepcidin

A

degrades ferroportin, decreasing iron transfer from blood plasma from duodenum

21
Q

causes of iron deficiency

A
  • not enough in diet, malabsorption

- excess loss, e.g. blood loss

22
Q

normochromic

A

normal concentration, but insufficient number of RBCs

23
Q

symptoms of iron deficiency anaemia

A

fatigue, lethargy & laziness

24
Q

signs of iron deficiency anaemia

A

pallor of mucous membranes, bounding pulse, systolic flow murmurs, smooth tongue, koilonchias

25
Q

megaloblastic macrocytic anaemia

A

vitamin b12/folate deficiency: RBCs larger than normal

26
Q

nonmegaloblastic macrocytic anaemia

A

no impairment of DNA synthesis: due to alcoholism, hypothyroidism, liver disease

27
Q

source of B12

A

animal & dairy produce

28
Q

source of folate

A

vegetables, liver

29
Q

importance of vitamin B12 & folic acid

A

final maturation of RBC and DNA synthesis, for thymidine triphosphate synthesis

30
Q

peripheral smear of B12 & Folic acid deficiency

A

macroovalocytes & hypersegmented neutrophils

31
Q

folate uses

A

Adenosine, guanine and thymidine synthesis

32
Q

vitamin B12 uses

A

Essential co-factor for methylation in DNA and cell metabolism

33
Q

how is vitamin B12 absorbed

A

requires the presence of intrinsic factor for absorption in the terminal ileum
(IF is made in parietal cells in the stomach)

34
Q

how is vitamin B12 transported

A

Transcobalamin II and Transcobalamin I transport vitB12 to tissues

35
Q

clinical consequences of VitB12 & Folic acid deficiency

A
Brain: cognition, depression, psychosis
Neurology: myelopathy, sensory changes, ataxia, spasticity (SACDC)
Infertility
Cardiac cardiomyopathy
Tongue: glossitis, taste impairment
Blood: Pancytopenia
36
Q

what is pernicious anaemia?

A

autoimmune disoder, with a lack of IF - reduced B12 absorption
IF antibodies

37
Q

treatments for anaemia

A

Iron – diet, oral, parenteral iron supplementatin, stopping the bleeding

Folic Acid – oral supplements

B12 – oral vs intramuscular treatment