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*Medicine: Haematology > Microcytic anaemia > Flashcards

Microcytic anaemia Flashcards

1
Q

What is anaemia?

A
  • functionally defined as an insufficient red cell mass to adequately deliver oxygen to peripheral tissues
  • generally considered to be present when the Hb conc is below lower limit of 95% ref range for the population
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2
Q

What are the main cells in blood?

A
  • Red blood cells
  • White blood cells
  • Platelets
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3
Q

What are the cellular components of blood derived from?

A
  • bone marrow, where maturation occurs
  • from multipotent haematopoetic stem cell
  • these HSCs -> turn into any blood cell + self renew
  • haemopoesis = formation of blood cells
  • erythropoietin is an important growth factor for RBCs
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4
Q

What are reticulocytes?

A
  • young red cells recently released from bone marrow
  • just lost their nucleus
  • do however still contain some mRNA to synthesise Hb
  • larger than mature red cells
  • represent around 0.5-2.5% of circulating RBCs
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5
Q

How do RBCs survive without mitochondria?

A
  • survive via cytoplasmic enzymes
  • involved in metabolism including glycolysis
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6
Q

What is haemoglobin?

A
  • iron containing oxygen transport metalloprotein
  • within RBCs
  • reduction in Hb = anaemia
  • globular protein w/ quaternary structure
  • 4 polypeptide subunits; 2 alpha + 2 beta chains
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7
Q

Normal erythropoiesis refers to red blood cell production. What does maturation of red blood cells require?

A
  • vitamin B12 + folic acid : DNA synthesis
  • iron : haemoglobin synthesis
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8
Q

What are possible signs and symptoms of anaemia?

A
  • fatigue + loss of energy
  • dyspnoea on exertion
  • faintness
  • palpitations
  • headache
  • tinnitus
  • anorexia
  • pallor
  • koilonychia, angular stomatitis, abdo discomfort
  • hyperdynamic circulation - tachycardia, flow murmurs
  • angina (if pre-existing coronary artery disease)
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9
Q

What is the main diagnostic test for anaemia?

A

FBC - most common blood test, assess number and size of cells found in blood, look for:

  • Hb: conc of Hb
  • Hct: % of blood vol as RBC
  • MCV: avd size of RBC
  • MHC: avg Hb content of RBC
  • MCHC: calc measure of Hb conc in given RBCs
  • RDW: range of deviation around RBC size
  • Reticulocyte count
  • Blood film: microscopy
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10
Q

What do you look for in microscopy (blood film)?

A
  • SIZE (big, small, normal)
  • SHAPE (fragments, tear drops, spiculated, ovalocyte, spherocyte, elliptocyte)
  • COLOUR (pale, normal, polychromasia)
  • INCLUSIONS (howell-jolly bodies, nuclear remnants, malarial parasites, basophilic stippling)
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11
Q

What Hb levels suggest anaemia in men and women?

A
  • Men
    • normal: >130
    • mild: 110-129
    • moderate: 80-109
    • severe: <80
      ​
  • Women
    • normal: >120
    • mild: 110-119
    • moderate: 80-109
    • severe: <80
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12
Q

What additional tests are done to find cause of anaemia?

A
  • WBC + platelet count
  • Reticulocyte count
  • Iron studies (ferritin, serum Fe, TIBC)
  • Haematinic levels (B12/folate)
  • BMAT - iron stains
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13
Q

If the reticulocyte count is normal/decreased, then there is an inappropriate marrow response suggesting we look at MCV and determine the cause of anaemia. What if there is an increased reticulocyte count?

A
  • suggest appropriate marrow response
  • either hamolysis or blood loss
  • haemolytic anaemia can be extrinsic or intrinsic to RBC
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14
Q

How is anaemia classified?

A
  • causes of anaemia classified according to measurement of RBC size
  • using mean corpuscular volume (MCV)
  • gives average volume of RBCs in blood sample
  • microcytic (small cells), normocytic (normal), macrocytic (large cells)
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15
Q

What are common causes for microcytic anaemia, where there is a reduce MCV suggesting small RBCs?

A
  • Iron deficiency (haeme deficiency)
  • Thalassaemia trait (globin deficiency)
  • Anaemia of chronic disease ‘late’
  • Lead
  • Sideroblastic anaemia (low protoporphyrin)
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16
Q

What are causes of normocytic anaemia (normal MCV)?

A
  • anaemia of chronic disease ‘early’
  • bone marrow hypo/aplasia
  • chronic renal failure/low EPO
17
Q

What are causes of macrocytic anaemia (inc MCV)?

A
  • B12 deficiency
  • Folate deficiency
  • Myelodysplasia
  • Drug induced (eg methotrexate)
  • Liver disease/alcohol
  • Hypothyroidism
  • Smoking
18
Q

How do Hb and MCV values change from birth to adulthood?

A
  • (kind of) U shaped for both
  • Hb decrement (much higher at birth) referrred to as physiologic anaemia of infancy
  • occurs as part of normal physiologic adaptation from relatively hypoxic intrautarine existence -> well-oxygenated extrauterine environment
  • fetal erythropoiesis is replaced -> MCV decreases from birth to 1 year of age
  • after 1 year, normal childhood Hb + MCV values remain considerably lower than those occurring in adolescents + adults
  • adult levels reached at puberty
  • higher Hb levels in males - effects of androgens on erythropoiesis?
19
Q

Why do we need iron?

A
  • essential of O2 transport
  • essential component of cytochromes
  • most abundant trace element in body
  • daily requirement for iron for erythropoeisis
  • varies depending on gender + physiological needs
20
Q

What foods are rich in iron?

A
  • meats: liver, beef, lamb, ham, turkey, chicken, veal, pork
  • seafood: shrimp, dried cod, mackerel, tuna, sardines, haddock
  • vegetables: spinach, beet greens, sweet pot, peas, broc, kale
  • breads + cereals: white bread, macaroni, bran, oat, corn, rye
  • fruits: prunes, watermelon, dried apricots/peaches, strawberries, raisins, dates, figs
  • others: eggs, dried peas, corn syrup, maple syrup, lentils
21
Q

Where is dietary iron predominantly absorbed?

A

Duodenum

22
Q

How is iron distributed in the adult body?

A
  • Fe3+ ions circulate bound to plasma transferrin
  • accumulate within cells in form of ferritin
  • stored iron can be mobilised for reuse
  • more than 2/3rds of body’s iron content is incorporated into Hb in developing erythroid precursors + mature red cells
  • most of remaining body iron found in hepatocytes + reticuloendothelial macrophages, which serve as storage deposits
  • reticuloendothelial macrophages ingest senescent RBCs, carabolise Hb to scavenge iron + load iron onto transferrin for reuse
  • iron metabolism is controlled by absorption rather than excretion, iron is only lost through blood loss or loss of cells
23
Q

What is the stable form of iron and where is most of it found?

A
  • > 1 stable form of iron: Fe2+ and Fe3+
  • Most iron in body as circulating Hb
  • Remainder as storage + transport proteins
    • ferritin + haemosiderin
    • found in cells of liver, spleen + bone marrow
24
Q

Describe iron absorption

A
  • regulated by GI mucosal cells mechanism
  • max absorption in duodenum + prox jejunum
  • via ferroportin receptors
  • amount absorbed depends on type ingested
  • heme, ferrous (meat) > than non-heme, ferric forms (cereals)
  • heme iron makes up 10-20% of dietary iron
  • other foods, GI acidity, state of iron storage levels + bone marrow activity affect absorption
25
Q

Discuss the role of hepcidin in iron regulation

A
  • iron regulatory hormone hepcidin + its receptor and iron channel ferroportin control dietary absorption, storage + tissue distribution of iron
  • hepcidin causes ferroportin internalisation 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 + the liver and by erythropoietic demand for iron
26
Q

Describe iron transport and storage

A
  • iron transported from enterocytes
  • then either into plasma or stored as ferritin
  • once attached to transferrin, binds to transferrin receptors on RBC precursors
  • a state of iron deficiency will see reduced ferritin stores + then increased transferrin
27
Q

Is ferritin water soluble?

A

Yes, it is the primary storage protein and providing reserve.

28
Q

What does transferrin saturation tell us?

A
  • ratio of serum iron and total iron binding capacity​
  • revealing % of transferrin binding sites that have been occupied by iron
29
Q

Where is transferrin made and why is it important?

A
  • made by liver
  • production inversely proportional to iron stores
  • vital for iron transport
  • uptake of iron from protein needs transferrin to be attached to the cell via the transferrin receptor
30
Q

What is TIBC and when is it high/low?

A
  • total iron binding capacity
  • measurement of capacity of transferrin to bind iron
  • an indirect measurement of transferrin (the iron transport protein)
  • TIBC is technically easier to measure in lab than transferrin levels directly
  • in IDA: TIBC is high - more transferrin produced aiming to transport more iron to tissues in need
  • in ACD: TIBC is low - less transferrin produced (but more ferritin), aim to reduce availability of iron for pathogens - mainly regulated by increased hepcidin production
31
Q

What are causes of iron deficiency?

A

1) Not enough in:

  • poor diet
  • malabsorption eg. coeliac
  • inc physiological needs eg. pregnancy
    ​

2) Losing too much:

  • blood loss
  • menstruation, GI tract loss, parasites - infestation of gut by hookworm
32
Q

What are lab investigations for iron deficiency?

A
  • FBC: Hb, MCV, MCH, reticulocyte count
  • Iron studies: ferritin, transferrin sats, TIBC
  • blood film
  • ?BMAT + iron stores
33
Q

As iron deficiency anaemia develops, how do the lab findings change?

A
  • occurs in several stages
  • initially IDA is normocytic + normochromic
  • serum ferritin is most sensitive lab indicator of mild iron def
  • serum ferritin decreases as IDA progresses
    • 60 -> 20 -> <12
  • transferrin sats + free erythryocyte protoporhyrin values do not become abnormal until tissue stores are depleted of iron
  • a decrease in Hb conc occurs when iron is unavailable for haem synthesis
  • MCV and MCH do not become abnormal for several months after tissue stores depleted of iron
34
Q

What are the lab results in iron deficiency anaemia for:

  • ferritin
  • transferrin saturation
  • TIBC
  • serum iron
A
  • ferritin - LOW
  • TF sat - LOW
  • TIBC - HIGH
  • serum iron - LOW / NORMAL
35
Q

What is angular stomatitis?

A

Inflammation of corners of mouth

36
Q

What is atrophic glossitis?

A
  • sore inflammed tongue
  • where papillae on dorsal surface are lost
  • leaving smooth erythematous surface
37
Q

What are the BSG guidelines for management of IDA?

A
  • upper + lower GI investigations in all postmenopausal female and all male patients
  • all pts should be screened for coeliac disease
  • colonoscopy is preferred to CT colography + barium enema
  • h. pylori should be eradicated if present
  • faecal occult blood testing is of no benefit
  • rectal exam is seldom contributory + may be postponed until colonoscopy
  • urine testing for blood is important

*Medicine: Haematology (5 decks)

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