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NA Flashcards

1
Q

Define anaemia

A

→the number of red blood cells (and consequently their oxygen-carrying capacity) is insufficient to meet the body’s physiologic needs

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2
Q

What is insufficient oxygen carrying capacity due to?

A

→reduced haemoglobin concentration as seen with insufficient RBC

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3
Q

How many chains are found in Hb?

A

→alpha=2

→beta=2

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4
Q

What are the basic requirements for normal erythropoeisis?

A 
→Vitamin B12 & folic acid
→Iron
→vitamins
→cytokines
→healthy bone marrow environment
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5
Q

Why is VitB12 and folic acid needed for erythropoiesis?

A

→DNA synthesis

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6
Q

Why is iron needed for erythropoeisis?

A

→Hb synthesis
→Essential for O2 transport
→Most abundant trace element in body

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7
Q

What are the three mechanisms of action that leads to anaemia?

A

→hypoproliferation
Reticulocytopenic
→Ineffective Erythropoiesis
→Decreased Survival

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8
Q

Give three examples of microcytic anaemias

A

→Iron deficiency
→Thalassemia
→anaemia of chronic disease

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9
Q

What is thalassaemia due to?

A

→globin deficiency

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10
Q

Give examples of normocytic diseases

A 
→anaemic chrocinc disease
→aplastic anaemia
→chronic renal failure
→bone marrow infiltration
→SCD
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11
Q

Give examples of macrocytic diseases

A 
→b12 deficiency
→folate deficiency
→myelodysplasia
→alcohol/drug induced
→liver disease
→myxoedema
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12
Q

What does reticulocyte count inform on?

A

→whether marrow can actually make cells

→adds further clue as to failure of production or increased losses

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13
Q

What is nutritional anaemia?

A

→Anaemia caused by lack of essential ingredients that the body acquires from food sources

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14
Q

What deficiencies are found in nutritional anaemias?

A

→Iron deficiency
→Vitamin B12 deficiency
→Folate deficiency

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15
Q

What are foods that are rich in iron?

A

→Meats
→seafood
→vegetables
→wheat

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16
Q

How does iron absorption differ between meat eaters and vegetarians?

A

→Non-heme iron absorption is lower for those consuming vegetarian diets, for whom iron requirement is approximately 2-fold greater.

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17
Q

How is excess iron dealt with?

A

→regulation is at absorption level, not excreted is an essential component of cytochromes, oxygen-binding molecules

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18
Q

Where is dietary iron absorbed?

A

→predominantly in the duodenum

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19
Q

How does iron circulate?

A

→bound to plasma transferrin and accumulate within cells in the form of ferritin

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20
Q

How is 2/3 of the iron in the body incorporated?

A

→incorporated into haemoglobin in developing erythroid precursors and mature red cells

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21
Q

Which other cells is iron found in?

A

→hepatocytes and reticuloendothelial macrophages

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22
Q

What do reticuloendothelial macrophages do?

A

→ingest senescent red cells,
→catabolise haemoglobin to scavenge iron,
→load the iron onto transferrin for reuse

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23
Q

How many states of iron are in the body?

A

→ferric states- 3+

→ferrous states- 2+

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24
Q

Where are ferrritin and haemosiderin found?

A

→liver
→spleen
→bone marrow

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25
Q

How is iron regulated?

A

→Regulated by GI mucosal cells and hepcidin

26
Q

How is iron absorbed?

A

→Via ferroportin receptors on enterocytes

→Transferred into plasma and binds to transferrin

27
Q

What affects absorption activity?

A

→GI acidity,
→state of iron storage levels
→bone marrow

28
Q

What is hepcidin?

A

→iron-regulatory hormone hepcidin and its receptor and iron channel ferroportin control the dietary absorption, storage, and tissue distribution of iron

29
Q

What does hepcidin do to ferroportin?

A

→causes ferroportin internalization and degradation, thereby decreasing iron transfer into blood plasma from the duodenum, from macrophages involved in recycling senescent erythrocytes, and from iron-storing hepatocytes

30
Q

How is hepcidin feedback regulated?

A

→by iron concentrations in plasma

→the liver and by erythropoietic demand for iron.

31
Q

What do transferrin bind to in the bone marrow?

A

→receptors on RBC precursors

32
Q

What is the relationship between transferrin and Fe store levels?

A

→inversely proportional to Fe stores

33
Q

What is an indirect measurement of transferrin in the lab?

A

→total iron binding capacity

34
Q

Why is ferritin an unreliable measure?

A

→part of immune system and can be raised in immune response

35
Q

What is TIBC levels like in iron deficiency anaemia?

A

→high

36
Q

What studies are involved in iron deficiency investigations?

A

→FBC: Hb, MCV, MCH, Reticulocyte count
→Iron Studies: Ferritin, Transferrin Saturation
→blood film

37
Q

Which test is most sensitive indicator of mild iron deficiency?

A

→serum ferritin

38
Q

What is anisocytosis?

A

→variation of red cell size

39
Q

What is the most common cause of IDA in adult men and postmenopausal women?

A

→Blood loss from the GI tract

40
Q

What are the sigs for IDA?

A

→pallor of mucous membranes,
→Bounding pulse, systolic flow murmurs,
→Smooth tongue, koilonychias

41
Q

What type of anaemia is consistent with B12 and folate deficiency?

A

→macrocytic anaemia

→Low Hb and high MCV with normal MCHC

42
Q

What is the reticulocyte count like in megablastic macrocytic anaemia?

A

→low

43
Q

What are the causes of megablastic macrocytic anaemia?

A

→Vitamin B12/Folic acid deficiency

→Drug-related eg methotrexate (interference with B12/FA metabolism)

44
Q

What are the causes of nonmegaloblastic macrocytic anaemia?

A 
→Alcoholism ++
→Hypothyroidism
→Liver disease
→Myelodysplastic syndromes
→Reticulocytosis (haemolysis)
45
Q

Where is B12 and folate absorbed?

A

→B12= ileum via IF

→folate=duodenum and jejunum

46
Q

How long is the average body store for B12 and folate?

A

→B12=2-4 years

→folate=3-4 months

47
Q

How much does cooking affect B12 and folate?

A

→10-30% loss for B12

→60-90% loss after cooking

48
Q

What is another name for B12?

A

→cobalamin

49
Q

Why is B12 and folic acid important?

A

→Both important for the final maturation of RBC and for synthesis of DNA
→Both needed for thymidine triphosphate synthesis

50
Q

What are the characteristics of megaloblastic on peripheral smears?

A

→macroovalocytes and hypersegmented neutrophils

51
Q

What are the causes of increased demand leading to folate deficiency?

A

→Infancy and growth spurts
→Haemolysis & rapid cell turnover: eg SCD
→Disseminated Cancer
→Urinary losses: eg heart failure

52
Q

What are the causes of decreased absorption in folate deficiency?

A

→folate antagonists
→jejunal resection
→tropical sprue

53
Q

What is B12 essential for?

A

→methylation in DNA and cell metabolism
→Intracellular conversion to 2 active coenzymes necessary for the homeostasis of methylmalonic acid (MMA) and homocysteine

54
Q

How is IF made?

A

→Parietal Cells in stomach

55
Q

What molecules transport B12 to tissues?

A

→Transcobalamin II and Transcobalamin I

56
Q

What is pernicious anaemia?

A

→Lack of IF
Lack of b12 absorption
Autoimmune- IF antibodies

57
Q

What are the causes of impaired absorption is B12 deficiency?

A

→pernicious anaemia
→Gastrectomy or ileal resection
→Zollinger-Ellison syndrome
→parasites

58
Q

What are some congenital causes of B12 deficiency?

A

→IF

→cobalamin mutation

59
Q

What are some haemotological consequences of B12 deficiencies?

A

→low ret count
→low/normal Hb
→raised LDH

60
Q

What are the clinical consequences of B12 deficiency?

A 
→Neurology: myelopathy, sensory changes, ataxia, spasticity (SACDC)
→infertility
→Brain: cognition, depression, psychosis
→Tongue: glossitis, taste impairment
→Blood: Pancytopenia
61
Q

What are treatments for B12 and folate deficiency?

A

→Folic Acid – oral supplements

B12 – oral vs intramuscular treatment

Dysfunction (29 decks)

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