Nutritional Anaemia Flashcards

1
Q

What is Anaemia

A

RBC number + O2 carrying-capacity insufficient to meet physiological needs

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2
Q

What does insufficient O2 C-C result in

A

↓[Hb] (w/insuff. RBC)

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3
Q

Anaemia cause

A

Lack of ingredients body acquires from food = iron, B12 + folate deficiency

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4
Q

Erythropoiesis requires what

A

Erythropoiesis, requires B12, folic acid, DNA, iron, hg synthesis

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5
Q

Erythropoiesis process

A

Process, decr. O2 detected by kidneys
EP secreted + binds to receptors that will become RBC
Haemocytoblast (stem cell) to proerythroblast to erythroblast (polychromatic) by EP stim
Then normoblast, nucleus expelled to form reticulocyte = erythrocyte in circulation

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6
Q

Anaemias due to what - 3 categories

A

= 1. failure of prod. - hypoproliferation (not enough RBC, BM present) = reticulocytopenia

  1. ineffective erythropoiesis
  2. Decreased survival = blood loss, haemolysis, reticulocytosis = if anemic, BM will be trying to catch up so early RBCs will be pushed out – if not enough RCyte, BM can’t produce enough RBCs​
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7
Q

What is iron and describe its uses

A

Iron = most abundant trace element, needed for O2 transport

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8
Q

Iron excretion description

A

No natural excreting method for iron, take in vitamin C, body uses what it needs then excretes it out​,

If you take in too much, body has no natural way of losing it = blood loss and desquamation​ ​

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9
Q

Iron composition

A

Ferric = 3+, ferrous = 2+, most iron in body as circulating Hb.

Remainder as storage/transport proteins = ferritin + hemosiderin (cells of liver, spleen + BM)

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10
Q

Describe iron absorption

A

Iron absorption = regulated by GI mucosal cells and hepcidin,

duodenum & proximal jejunum via ferroportin receptors on enterocytes +

transferred into plasma and binds to transferrin then binds to transferrin receptors on RBC precursors in BM,

if excess = ferritin, iron deficiency = incr. transferrin and decr. in ferritin stores

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11
Q

Reticulocyte count use

A

Adds further clue as to failure of production or increased losses

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12
Q

What effects absorption levels

A

Ferrous ions best absorbed + other foods
GI acidity
State of iron storage levels
BM activity ​

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13
Q

Hepcidin function

A

Ferroportin internalization and degradation =

↓ iron transfer into blood plasma from duodenum,

↓ in macrophages in recycling senescent erythrocytes

↓ iron-storing hepatocytes

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14
Q

Hepcidin regulation

A

[iron] in plasma/liver + by erythropoietic demand for iron

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15
Q

What is ferritin

A

Primary storage protein & providing reserve, Water soluble

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16
Q

What is transferrin saturation

A

Ratio of serum iron and total iron binding capacity – % of transferrin binding sites occupied by iron

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17
Q

What is transferrin

A

Glycoprotein made by liver,

Production inversely proportional to Fe stores. Vital for Fe transport.

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18
Q

What is total iron binding capacity

A

Measurement of the capacity of transferrin to bind iron​

Indirect measurement of transferrin

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19
Q

Lab results in iron deficiency anaemia

A

Ferritin = low
TF sats = low
TIBC = high
Serum iron = low/normal

20
Q

Iron deficiency causes

A

Causes = diet, malabsorption, incr. phys needs, blood loss, menstruation, GI tract loss, parasites

21
Q

Iron deficiency investigations

A

FBC: Hb, MCV, MCH, Reticulocyte count​
Iron Studies: Ferritin, Transferrin Saturation​
Blood film

22
Q

Description of stages in development of IDA

A

Percentage sats of transferrin w/iron and free erythrocyte protoporphyrin values do not become abnormal until tissue stores are depleted of iron

↓in the [Hb] occurs when iron is unavailable for haem synthesis

MCV/MCH is not abnormal for several months after tissue stores are depleted of iron

23
Q

Hypochromic microcytic anemia

A

Red cells that are in general much smaller than a neutrophil, with marked anisocytosis (variation of the red cell size) and hypochromia (area of central pallor of red cells that is larger than normal, indicating a low MCHC).​

Microcytosis = size defnining ​

Hypochromia = colour ​

Hypochromic microcytic anemia

24
Q

Iron deficiency anaemia symptoms

A

Fatigue, lethargy, and dizziness​

25
Q

Iron deficiency anaemia signs

A
Pallor of mucous membranes, ​
Bounding pulse, ​
Systolic flow murmurs, ​
Smooth tongue, 
koilonychias (spoon nails)
26
Q

Macrocytic Anaemia​ = Hb, MCV, MCHC

A

Low Hb and high MCV with normal MCHC ​

27
Q

Megaloblastic macrocytic anaemia cause

A

Vitamin B12/Folic acid deficiency​
Drug-related ​
(interference with B12/FA metabolism)

28
Q

Nonmegaloblastic macrocytic anaemia cause

A
Alcoholism 
Hypothyroidism​
Liver disease​
Myelodysplastic syndromes​
Reticulocytosis (haemolysis)
29
Q

B12/folate needed for

A

Final maturation of RBC and DNA synth.

Thymidine triphosphate synthesis

30
Q

Megaloblastic vs. non megaloblastic

A

M = anemia results from inhibition of DNA synthesis during red blood cell production (can’t move to M phase)

N = are those in which no impairment of DNA synthesis occurs

31
Q

Folate function

A

Folate necessary for DNA Synthesis:​

Adenosine, guanine and thymidine synthesis

32
Q

Folate deficiency causes - 3 categories w/examples

A

Increased demand = Pregnancy / Breast feeding, infancy and growth spurts, Haemolysis & rapid cell turnover: e.g. SCD, disseminated cancer, urinary losses: e.g. heart failure

Decreased Intake​ = ​diet, age, chronic alcohol intake

Decreased absorption = medication (folate antagonists), coeliac, jejunal resection + tropical sprue

33
Q

Effect of alcohol on bone marrow

A

Alcohol 2 way effect on BM – direct toxin (macrocytosis) or interferes w/folate pathway = make pt’s folate def.​

34
Q

B12 function

A

Essential co-factor for methylation in DNA and cell metabolism​

Intracellular conversion to 2 active coenzymes necessary for the homeostasis of methylmalonic acid (MMA) and homocysteine

35
Q

What does B12 require

A

Requires the presence of Intrinsic Factor for absorption in terminal ileum​

IF made in Parietal Cells in stomach​

Transcobalamin II and Transcobalamin I transport vitB12 to tissues

Can’t absorb B12 w/out it

36
Q

B12 deficiency causes - 5 categories w/examples

A
Impaired​ absorption​:
Pernicious Anaemia​
Gastrectomy or ileal resection​
Zollinger-Ellison syndrome​
Parasites​

Decreased intake:
Malnutrition
Vegan diet

Congenital causes:
Intrinsic factor receptor deficiency​
Cobalamin mutation ​= C-G-1 gene

Increased requirements:
Haemolysis​
HIV​
Pregnancy​
Growth Spurts​
Medication:
Alcohol​
NO​
PPI, H2 antagonists​
Metformin​
37
Q

Haematological consequences

A

MCV = Normal or raised​
= Megaloblastic anaemia​, Ineffective erythropoiesis
Hb​ = Normal or low​
RetCount = low
LDH = raised = intramedullary haemolysis
Blood film = Macrocytes, ovalocytes, hypersegmented neuts
BMAT = Hypercellular, megaloblastic, giant metamyelocytes = Unusual to need​
MMA = increased = not standard lab test

38
Q

Effect on cells when B12 low

A

Fragmented cells

39
Q

Clinical consequences of nutritional anaemia

A
Brain: cognition, depression, psychosis​
Neurology: myelopathy, sensory changes, ataxia, spasticity (SACDC)​
Infertility​
Cardiac cardiomyopathy​
Tongue: glossitis, taste impairment​
Blood: Pancytopenia
40
Q

Pernicious anaemia features

A

Autoimmune disorder​
Lack of IF ​
Lack of ​B12 absorption

41
Q

Pernicious anaemia mechanism

A

Develops AB against IF – against cells or IF itself = consequence same = no IF

42
Q

Why is oral B12 ineffective for pernicious anaemia

A

Even if oral B12 administered = cant absorb, injections needed to overcome that pathway​

43
Q

Treatments for anaemia

A

Treat the underlying cause **
Iron – diet, oral, parenteral iron supplementation, stopping the bleeding​
Folic Acid – oral supplements​
B12 – oral vs intramuscular treatment

44
Q

Diagnosis if normal/low MCV

A

If high ferritin = acute/chronic illness

If low ferritin = iron deficiency, GI/gynae blood loss

45
Q

Diagnosis if high MCV

A

If high B12 = MPD+
If normal B12 = alcohol = liver
If low B12 = GPC (anti-gastric parietal cell antibody/IF antibodies = pernicious anaemia
If low B12/folate = dietry deficiency = malabsorbtion