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Molecular Basis Of Disease > Nutritional Anaemias > Flashcards

Nutritional Anaemias Flashcards

1
Q

What is an anaemia?

A
  • Anaemia is the defiency of red blood cells and/ or haemoglobin concentration within the blood meaning the oxygen-carrying capacity is insufficient to meet the body’s physiological needs
  • Anaemia = ‹ RBC or ‹ Hb conc. in blood -> insufficient 02 carrying capacity
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2
Q

What is the role of haemoglobin (Hb) in RBCs?

A
  • Hb = Iron containing oxygen transport metalloprotein within RBCs
  • Therefore Reduction of haemoglobin in blood = (reduction in oxygen carrying capacity) = anaemia
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3
Q

State the main components of blood?

A
  • RBCs
  • Platelets
  • WBCs: Monocyte, lymphocytes, eosinophil, basophil and nuetrophil
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4
Q

What are the main factors used for the diagnosis of anaemia?

A
  • Hb levels
  • Age
  • Gender
  • Side note: Anaemia is found more likely in pregnant women or during menstruation
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5
Q

Define erythropoesis

A

Erythropoeisis - Maturation of RBCs (RBCs are formed + matured in the bone marrow)

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6
Q

State the factors required for normal erythropoeisis? (5)

A
  • Factors required:
  • Vitamin B12 & folic acid: DNA synthesis
  • Iron: Haemoglobin synthesis
  • Vitamins
  • Cytokines (erythropoeitin): Erythropoitein = a hormone secreted by the kidneys that increases the rate of production of red blood cells in response to falling levels of oxygen in the tissues
  • Healthy bone marrow environment
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7
Q

State the 3 major mechanisms of action which can lead to anaemia?

A
    1. Failure of Production: hypoproliferation Reticulocytopenic
  • a. Bone marrow prodcues reticulocytes (developing RBCs)
  • b. Hypo. -> BM doesn’t have sufficient factors -> decreased production of reticulocytes (sign of anaemia)
    1. Ineffective Erythropoiesis
    1. Decreased Survival: Blood loss, Haemolysis, reticulocytosis
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8
Q

Define haemolysis and reticulocytosis

A
  • Haemolysis: Destruction of red blood cells
  • Reticulocytosis: Increase in reticulocyte production due to BM using up factors for Blood cell production to compensate for anaemia
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9
Q

State the 3 types of classification of anaemia and state the additional factor which may indicate the potential mechanism for cause?

A
  • Based on MCV (mean cell volume) - average size of RBC
  • Microcytic (smaller than average range)
  • Normocytic (within normal range)
  • Macrocytic (larger than average range)
  • Reticulocyte count then adds further clue as to failure of production or increased losses
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10
Q

State 3 causes of microcytic anaemia?

A
  • Iron deficiency (heme deficiency)
  • Thalassamia (globin deficiency)
  • Anaemia of Chronic Disease
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11
Q

State 5 causes of normocytic anaemia?

A
  • Anaemia chronic disease
  • Aplastic anaemia
  • Chronic renal failure
  • Bone marrow infiltration
  • Sickle cell disease
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12
Q

State 5 causes of macrocytic anaemia?

A
  • B12/folate deficency
  • Myelodysplasia
  • Alcohol induced
  • Drug induced
  • Liver disease
  • Myxoedema
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13
Q

What is nutritional anemia and state 3 deficiencies which lead to this?

A
  • Anaemia caused by lack of essential ingredients that the body acquires from food sources
  • Iron deficiency
  • Vitamin B12 deficiency
  • Folate deficiency
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14
Q

What is the role of iron in the body and state the factors which determine the daily requirement of iron for erythropoiesis?

A
  • Iron role = Essential for 02 transport (part of Hb)
  • Iron required for erythropoiesis factors = gender + physiological needs (greater for pregnant and during menstruation)
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15
Q

How does iron intake differ between vegan and meat diets?

A
  • Recommended intake assumes 75% of iron is from heme iron sources (meats, seafood) - as it contains blood.
  • Non-heme iron absorption is lower for those consuming vegetarian diets, for whom iron requirement is approximately 2-fold greater
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16
Q

Describe the sites of iron distribution including site of iron absorption, sites sent to and areas of iron loss? VD

A

Iron cannot be excreted

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17
Q

Describe the 2 forms of iron and how they can be found within the body?

A
  • Stable forms of iron: Ferric states (3+) and Ferrous states (2+)
  • Sites of Fe in body: Most iron is in the body as circulating Hb
  • A. Hb: 4 haem groups, 4 globin chains able to bind 4 02
  • (2). Remainder as storage and transport proteins
  • A. ferritin (major one) and haemosiderin
  • B. Found in cells of liver, spleen and bone marrow
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18
Q

State how iron absorption occurs describing the regulation and site?

A
  • Regulated by Gl mucosal cells and hepcidin in duodenum & proximal jejunum: Hepcidin = Hepcidin is an iron-regulating peptide hormone made in the liver.
  • Via ferroportin receptors on enterocytes (cells of the intestine)
  • Transferred into plasma and binds to transferrin (transport protein)
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19
Q

State the factors which affect the rate of iron absorption?

A
  • Type of iron ingested: Heme, ferrous (red meat, > than non-heme). Ferric forms Heme iron makes up 10-20% of dietary iron
  • Other foods
  • GI acidity
  • State of iron storage levels
  • Bone marrow activity
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20
Q

State the role of hepcidin in iron regulation?

A
  • The iron-regulatory hormone hepcidin and its receptor and iron channel ferroportin control the dietary absorption, storage, and tissue distribution of iron…
  • Hepcidin 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.
  • Hepcidin is feedback regulated by iron concentrations in plasma and the liver and by erythropoietic demand for iron.”
21
Q

Describe what occurs once iron transported from the enterocytes and how these will differ during iron deficiency?

A
  • Either into plasma or if excess iron stored as ferritin
  • In plasma: attaches to transferrin and then transported to bone marrow binds to transferrin receptors on BC precursors
  • Iron deficency: Decreased ferritin stores + increased transferrin
22
Q

State 5 factors and describe them as used to investigate iron levels in labs?

A
  • Serum Fe: Hugely variable during the day
  • Ferritin: Primary storage protein & providing reserve, water soluble
  • Transferrin Saturation: Ratio of serum iron and total iron binding capacity - Revealing %age of transferrin binding sites that have been occupied by iron
  • Transferrin: Made by liver, Production inversely proportional to Fe stores. Vital for Fe transport
  • Total iron binding capacity: Measurements of the capacity of transferrin to bind iron. It is an indirect measurement of transferrin
23
Q

State how ferritin, TF saturation, Total Iron Binding Capacity and serum iron levels (low, normal or high) will be during iron deficiency anaemia?

A
  • Ferritin = Low
  • TF saturation = Low
  • TIBC = high
  • Serum iron = Low/normal
24
Q

State causes of iron defiency (5)?

A
  • Not enough iron in: Poor diet, Malabsorption (difficulty in digestion of nutrients), Increased physiological needs
  • Losing too much iron: Blood loss, Menstruation, GI tract loss, Paraistes (parasites)
25
Q

State the 4 investigations that should be performed to help diagnose iron deficiency?

A
    1. FBC (full blood count): Hb, MCV, MCH (mean cell haemoglobin), Reticulocyte count
    1. Iron Studies: Ferritin, Transferrin Saturation
    1. Blood film: Examination of blood cells using microscope
    1. ?BMAT and Iron stores: BMAT = bone marrow biopsies - not really done as too invasive
26
Q

How does IDA normally start with and generally how does the stages of IDA go?

A
  • IDA is initally normocytic (cytic = size) and normochromic (chromic = conc. of Hb in RBCs
  • Produces dark layer depending on Hb count)
  • VD
27
Q

What is the most common cause of Iron Deficiency Anaemia in men and women?

A
  • Blood loss from the Gl tract: Men + postmenopausal women
  • Excessive menstrual losses: Premenopausal women
28
Q

State 3 symptoms of Iron Deficiency Anaemia?

A
  • Fatigue
  • Lethargy
  • Dizziness
29
Q

State 5 signs of Iron Deficiency Anaemia?

A
  • Pallor of mucous membranes,
  • Bounding pulse
  • Systolic flow murmurs
  • Smooth tongue
  • Koilonychias (spoon nails)
30
Q

Why are B12 and folate defiency commonly referred to each other and what type of anamia does it result in?

A
  • Both have very similar laboratory finding and clinical symptoms
  • Can be found together or as isolated pathologies
  • Results in Macrocytic Anaemia: Low Hb and high MCV with normal MCHC
31
Q

State the 2 types of macrocytic anaemia and state examples that cause them?

A
  • Megaloblastic: Low reticulocyte count. Vitamin B12/Folic acid deficiency, Drug-related (interference with B12/FA metabolism)
  • Non-megaloblastic: Alcoholism ++, Hypothyroidism, Liver disease, Myelodysplastic syndromes, Reticulocytosis (haemolysis)
32
Q

What is it called when anaemia occurs in the presence of macrocytosis and hyper segmented neutrophils?

A
  • Anemia occurring in the presence of macrocytosis and hypersegmented neutrophils is known as megaloblastic anaemia
  • The absence of hypersegmented neutrophils characterizes non-megaloblastic anemia.
33
Q

State the source, effect of cooking, absorption site and average body store of vitamin B12 and folate?

A
  • Basically B12 required less as its stored for much longer
  • VD
34
Q

State another term for vitamin B12 and state the uses of vitamin B12 and folate (3)

A
  • Vitamin B12 = cobalamin
  • Both important for the final maturation of BC, synthesis of DNA and thymidine triphosphate synthesis
35
Q

State the megaloblastic characteristics of blood cell film seen in Vit. B12 and folic acid deficiency?

A

Characterised on peripheral smear via macroovalocytes and hypersegmented neutrophils VD

36
Q

What is folate necessary for?

A

DNA synthesis: Adenosine, guanine and thymidine synthesis

37
Q

State the 3 major reasons why folate defiency occurs?

A
  • Increased demand
  • Decreased intake
  • Decreased absorption
38
Q

State 5 causes of increased demand leading to folate defiency?

A
  • Pregnancy/breast feeding
  • Infancy and growth spurt
  • Haemolysis and rapid cell turnover e.g. SCD
  • Disseminated cancer -> cancer that has spread throughout the body
  • Urinary losses e.g. heart failure
39
Q

State 3 causes of decreased intake leading to folate defiency?

A
  • Poor diet
  • Elderly
  • Chronic alcohol intake
40
Q

State 4 causes of decreased absorption leading to folate
defiency?

A
  • Medication (folate antagonists)
  • Coeliac
  • Jejunal resection
  • Tropical sprue (small intestine can’t absorb properly)
41
Q

What is the role of vitamin B12 and state the conversion required?

A
  • Role: 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
  • Defiency of B12 = 1 MMA
  • DNA methylation is essential for silencing retroviral elements, regulating tissue-specific gene expression, genomic imprinting, and X chromosome inactivation
  • Importantly, DNA methylation in different genomic regions may exert different influences on gene activities based on the underlying genetic sequence.
42
Q

State 3 animal sources of B12?

A
  • Fish
  • Meat
  • Dairy
43
Q

How is B12 absorped into the terminal ileum?

A
  • Requires the presence of Intrinsic Factor for absoprtion in terminal ileum
  • IF made in Parietal Cells in stomach
  • Transcobalamin II and Transcobalamin I transport vitB12 to tissues for absorption to occur
44
Q

State major causes of B12 defiency?

A
  • Impaired absorption = pernicious anemia, zollinger-ellison syndrome. Pernicious anaemia is an autoimmune condition that affects your stomach
  • Decreased intake
  • Congenital causes - IF receptor defiency, Cb mutation
  • Increased requirements
  • Medications -> metoformin
45
Q

State the level or what can be seen in MCV, Hb, reticulocyte count, LDH, Blood film, BMAT and MMA in B12 deficiency?

A

VD

46
Q

State clinical consequences of B12 defiency in terms of the brain, tongue and blood, neurology

A
  • Brain: cognition, depression, psychosis
  • Neurology: myelopathy, sensory changes, ataxia, spasticity (SACDC)
  • Infertility
  • Cardiac cardiomyopathy
  • Tongue: glossitis, taste impairment: Glossitis is a problem in which the tongue is swollen and inflamed, This often makes the surface of the tongue appear smooth.
  • Blood: Pancytopenia - deficiency of all three cellular components of the blood (red cells, white cells, and platelets).
47
Q

What is pernicious anaemia?

A
  • Autoimmune disorder
  • Lack of Intrinsic factor
  • Lack of B12 absorption
  • Gastric Parietal cell antibodies
  • IF antibodies
48
Q

State the treatment for iron, folic acid and B12?

A
  • Iron: diet, oral, parenteral iron supplementation, stopping the bleeding
  • Folic Acid: oral supplements
  • B12: oral vs intramuscular treatment

Molecular Basis Of Disease (30 decks)

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