Anaemia Flashcards

1
Q

Define anaemia.

A
  • a haemoglobin concentration lower than normal range.
  • not a diagnosis on its own but a manifestation of an underlying disease and cause important to establish.
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2
Q

name a few signs and symptoms of anaemia.

A
  • signs of insufficient O2 delivery to tissues.
  • symptoms : SOB, palpitations, headache, lethargic.
  • signs : Pallor, tachycardia, hypotension, systolic flow murmur, tachypnoea ( high RR).
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3
Q

what are some specific sign associated with anaemia, that may lead you to a diagnosis.

A
  • Koilonychia ( spoon shaped nails) : iron deficiency.
  • Angular stomatitis ( mouth corners inflamed) : iron deficiency.
  • Glossitis ( inflamed, depapilation of tongue) : Vit B12 deficiency.
  • Abnormal facial bones : thalassaemia.
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4
Q

why might anaemia develop?
break it down to RBC in BM, vessels, removal by spleen.

A
  • BM : reduced erythropoiesis, abnormal haem, abnormal globin chains.
  • Vessels : abnormal RBC, mechanical damage, abnormal metabolism.
  • Spleen : increased removal by reticuloendothelial.
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5
Q

what might cause reduced or dysfunctional erythropoeisis?

A
  • lack of production of EPO by kidney, in CKD.
  • marrow unable to respond to EPO, after chemo/infection.
  • marrow infiltrated by cancer cells or fibrous tissue.
  • chronic diseases like rheumatoid arthritis where iron is not made available for marrow.
  • myelodysplatic syndromes where abnormal clones of stem cells reduce capacity to make RBC + WBC.
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6
Q

why might defects in haemoglobin synthesis cause anaemia?

A
  • SIDEROBLASTIC ANAEMIA : defects in haem synthesis pathway.
  • insufficient iron in diet : iron deficiency anaemia.
  • anaemia in chronic disease as functional iron deficient.
  • mutations in globin chains in HB ( alpha/beta thalassaemia, sickle cell disease ).
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7
Q

how might abnormal structure and mechanical damage to RBC lead to haemolytic anaemia?

A

*inherited
- mutation in gene coding for plasma membrane cytoskeleton interactions.
- less flexible and more easily damaged and removed.

*acquired
- shear stress through defective heart valves.
- cell snagging on fibrin strands in small vessels with clots.
- heat burns or osmotic damage.

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8
Q

what defects in RBC metabolism can cause anaemia?

A
  • G6PDH deficiency : cross-linking of HB and Heinz bodies, removed by spleen.
  • Pyruvate kinase deficiency so glycolysis affected and RBC deficient in ATP and undergo haemolysis.
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9
Q

how might excessive bleeding cause anaemia?

A
  • acute blood loss, like injury.
  • chronic blood loss : heavy menstrual bleeding, haemorrhoids, GI bleeds, kidney or bladder tumours.
    *treated with NSAID anti-inflammatory drugs.
    *IRON LOST FROM BODY NOT RECYCLED!
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10
Q

how might the reticuloendothelial system play a part in anaemia development?

A
  • damage in vessels, autoimmune haemolytic anaemias cause abnormal RBC so destroyed.
  • by spleen leading to splenomegaly as working harder. NEVER NORMAL TO PALPATE SPLEEN below costal margin.
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11
Q

how might myelofibrosis cause anaemia?

A
  • due to proliferative haemotopoietic stem cells.
  • little space for haemotopoeisis.
  • progenitor cells spill out of marrow into liver and spleen leading to extra-medullary haemopoeisis, so enlarged.
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12
Q

how might thalassemia cause anaemias?

A
  • decreased or absent alpha or beta globin chain production.
  • imbalance in composition of A2B2 so defective microcytic hypochromic RBC.
  • severity depends on type.
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13
Q

what are reticulocytes and why are they important?

A
  • immature RBC just released to blood, no nucleus and eliminate remaining mitochondria.
  • 1% of all RBC, matures in 1 day.
  • shows if marrow is capable of responding to conditions like anaemia, you’d expect high count to replenish.
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14
Q

what would microcytic/ macrocytic/ normocytic RBC indicate?

A
  • microcytic : thalassaemia, chronic disease anaemia, iron deficiency, lead poisoning.
  • macrocytic : vit B12, folate, liver disease.
  • normocytic : BM failure.
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15
Q

what are the types of macrocytic anaemias?

A
  • megaloblastic : DNA synthesis interfered and nucleus development retarded cell division delayed so large.
    eg: Vit B12/ folate deficiency
  • macronormoblastic erythropoiesis : cytoplasm retained and erythroblasts larger than normal.
    eg : liver disease, alcohol toxicity.
  • stress erythropoiesis : high reticulocytes and larger, high level of erythropoetin so expanded.
    eg: recovery from haemorrhage, haemolytic anaemia.
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16
Q

why is folate important?

A
  • abundant in green leafy veg, absorbed by duodenum and jejunum.
  • converted to tetrahydrofolate and taken up by liver as stores.
    *carbons for other reactions like nucleotide base synthesis for DNA and RNA.
    *FOLIC ACID IN PREGNANCY to prevent neural tube defects.
17
Q

what causes folate deficiency and what are the symptoms?

A
  • causes : poor diet, increased requirement like pregnancy or anaemias, disease of absorption sites, drugs that inhibit converting to store, alcoholism, liver disease.
  • symptoms : anaemia related, diarrhoea, muscle weakness.
18
Q

why is vitamin B12 essential?
PRODUCED BY BACTERIA.

A
  • essential co-factor in DNA synthesis.
  • required for erythropoiesis.
  • essential for normal CNS development.
    *largely obtained by animal origin as produced by commensal bacteria.
19
Q

how is Vit B12 absorped?

A
  • binds to haptocorrin in saliva and is digested by pancreatic proteases.
  • released B12 binds to intrinsic factor which binds to cubam receptor which is up-taken into enterocytes,
  • then eventually bound to transcobalamin transported around blood stream and stored in liver.
    *stores enough for 3-6 years.
20
Q

what causes vitamin B12 deficiency and what are the symptoms?
name some severe complications around it?

A
  • dietary deficiencies, lack of intrinsic factors, ileum affected, chemical inactivation of B12, parasitic infection.
  • symptoms : related to anaemia, diarrhoea, parasthesia, irritability, disturbed vision.
  • affects nervous system, focal demyelination, reversible peripheral neuropathy, degeneration of cord in posterior and lateral columns of spinal cord.
21
Q

how does B12 and folate deficiency lead to megaloblastic anaemia?

A
  • ultimately a thymidine deficiency, uracil instead, DNA repair enzymes detect and repair.
  • results in asynchronous maturation between nuclei and cytoplasm (nucleus not fully mature and cytoplasm rate normal )
22
Q

how do you treat Vit B12 and folate deficiencies?

A
  • folate : oral folic acid.
  • B12 : hydroxycobalamine intramuscular in perinicious anaemia, other causes : oral cyanocobalamine.
23
Q

what could cause microcytic anaemia?
( smaller than normal, hypochromic)

TAILS

A
  • reduced haem synthesis : Iron deficiency, Lead poisoning inhibiting enzymes involved in haem synthesis, Anaemia of chronic disease, Sideblastic anaemia inherited.
  • reduced globin chain synthesis : in alpha/ beta Thalessaemia.
24
Q

what is anaemia of chronic disease?

A
  • inflammatory conditions causing release of cytokines which increases Hepcidin production, inhibits EPO.
  • this decreases iron release, RBC making and iron absorption at gut.