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Haematology > Anaemia > Flashcards

Anaemia Flashcards

1
Q

Anaemia definition

A

a condition in which there is a deficiency of red cells or of haemoglobin in the blood, resulting in pallor and weariness

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2
Q

Signs of anaemia

A

Koilonychia - spooning of the nails Atrophic glossitis - smooth flat tongue Angular stomatitis - cracks at te corner of the mouth Oesophageal web - plumer vision syndrome Pallor (eg conjunctivae) Increased cardiac output a. angina b. flow murmurs c. palpitations d cardiac failur

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3
Q

Symptoms of anaemia

A

Due to decreased oxygen-carrying capacity: -Fatige -dyspnoea palpitations headache tinnitus

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4
Q

Classifcations of anaemia

A

Anaemias may be due to either decreased production or increased loss of RBCs 1. Macrocytic- large erythrocytes 2. Microcytic - smalle erythrocytes 3. Normocytic - normal-sized cells

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5
Q

Causes of Normocytic anaemia

A

Normocytic normochromic

First step look for

  • -MCV = 80-95 femtolittres
  • -MCH >26pigograms
  1. Acute blood loss 2. Anaemia of chronic disease 3. Bone marrow failire e.g post chemo, infiltration by carcinoma 4. Renal failure 5. Hypothyroidism 6. Haemolysis 7. Pregnancy
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6
Q

Causes of Macrocytic anaemias

A

Macrocytic

First step look for

    • MCV >95fl

Megaloblastic: -Vit B12 deficiency -Folate deficiency

Normoblastic: -Alcohol excess or liver disease -Reticulocytosis - Cytotoxic - Myelodysplastic syndromes -Hypothyroidisi

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7
Q

Normal MCV

A

76-96 fl

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8
Q

Anaemias which dont fit into the above classification

A

Haemolytic anaemias

  • may be macrocytic or normocytic

Anaemia of chronic diseae can be either:

  • RBC indices that are normocytic and normochromic suggest ACD of fairly recent onset.
  • RBC indices and blood smear that are microcytic and hypochromic suggest ACD has been present some weeks or months
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9
Q

Iron deficiency Anaemia transferrin levels

A
  • 30% saturated with transferrin
  • IDA liver responds to reduced levels, increased trasnferrin, saturation falls - 15%
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10
Q

Three phases of iron deficiency anaemia development

A

Develops gradually over three phases 1. Low serum ferritin always indicated low RES iron stores 2. Iron lost first from RES iron stores, before Hb falls – latent iron deficiency 3. The process continues Iron becomes - iron availablty to red cells is reduced and patient develops iron deficiency anaemia

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11
Q

Problem with serum ferritin

A

Acute phase protein In presence of tissue inflammation IDA can occur with normal serum ferritin levels (Rhuematoid arthiris and IBD)

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12
Q

Causes of iron deficiency anaemia

A
  1. Dietary- premature neonates and adolescent females 2. Malabsorption 3. Blood los Golden rule - IDA in males & post menopausal females is due to GI blood loss until proven otherwise - Young women; menstrual blood loss or pregnancy - GI investigations only for GI symptoms or positive FOBs
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13
Q

Treatment of iron deficiency anaemia

A
  • Treatment of IDA is iron replacement & not blood transfusion - Ferrous Sulphate -200mg tabs o 200mg = 60mg elemental iron - Ferrous Gluconate 300mg tabs (switch to this if GI toxicity) o 300mg = 36mg elemental iron - IV iron; can give 1G over 2-3 hours. Hb rises no quicker than oral replacement. - Main uses: o Intolerant of oral iron o Compliance o Renal anaemia & Epo replacement - Discover cause
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14
Q

Anaemia of Chronic disease (ACD) causes

A

Failure of iron utilisation Iron trapped in RES Common In hospitlaised patients Causes - THREE FOLD -infection -Inleammation -Neoplasia

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15
Q

Anaemia of chronic renal failure

A

is Anaemia of chronic disease + fialure of kidneys to produce EPO

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16
Q

Lab values of Anaemia of chronic disease

A

MCV/MCH is normal or decreased

Cells may be normochormic normocytic or hypochromic microcytic RBCs ESR - raised

Ferritin - N or increased

Iron - decreased (chemokine release)

TIBC - decreasd (liver does not respond by increasing transferrin levels)

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17
Q

Blood film of Anaemia of chronic disease

A

RBC roleux

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18
Q

Pathophysiology of ACD

A
  • RES Iron blockade; iron trapped in macrophages - Reduced Epo response - Depressed marrow activity; cytokine marrow depression
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19
Q

Treatment of ACD

A

-treat underlying disorder

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20
Q

Role of B12/ Folate?

A
  • Essential for DNA synthesis and nuclear maturation - Required for all dividing cells, deficiency noted first in red cells - Deficiency results in megaloblastic anaemia inititally, but will effect other organs
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21
Q

B12 os involved in which two processes?

A
  • B12 (Cobalamin) necessary for 2 processes o Methylation of homocysteine to methionine o Methylmalonyl-CoA isomerisation
22
Q

Dietary sources of B12

A

o Synthesised solely by microorganisms o Meat (esp liver and kidney), small amount in dairy products o Normal Western diet 5-30ug/day

23
Q

Daily requirements of B12

A

1 ug/day

24
Q

Process of B12 absorption

A
  • B12 ingested (in form of animal protein) -gastric parietal cells produces intrinsic factor - B12 binds to intrinsic factor (made by gastric parietal cells in funfus/ body of stomach) -IF-B12 complex binds to cubulin (receptor in the ileum) - B12 moves through the ileum and is absorbed via transcobalmin
25
Q

Total loss and stores of vitamin B12 ?

A
  • Loss o 1-2ug/d in urine/faeces - Stores – 3-4 years
26
Q

Dietary sources of folate

A

Green veg (destroyed by cooking unlike B12

27
Q

Stores of folate

A
  • Stores – Few days only – Quickly used up if increased demand (ie increased cell turnover)
28
Q

Absorption of folate

A
  • Absorption – most small bowel. No carrier molecule required
29
Q

pathophysiology of folate deficiency

A
  • Dietary folates absorbed in small intestine - B12 required for conversion - Results in disparity in rate of synthesis of the precursors of DNA - Abnormality of cell division - megaloblastic anaemia
30
Q

Tissues affected by b12 or folate deficiency

A

All rapidly growing, DNA synthesising cells B12 or folate deficiency - Bone marrow - Epithelial surfaces – mouth, stomach, small intestine, urinary, female genital tracts

31
Q

Blood abnormalities of b12 deficiency

A

Megablastic anaemia (leucopenia, thrombocytopenia)

32
Q

Neurological manifestations of b12 deficiencys

A

o Bilateral peripheral neuropathy or demyelination of the posterior and pyramidal tracts of spinal cord o Biochemical basis inclear- likely related to problem with homocysteine –> methionine

33
Q

Blood abnormalites of folate deficency

A

Megaloblastic anaemia (leucopenia, thrombocytopenia)

34
Q

Growing fetus abnormalities of folate deficiency?

A

1st 12 weeks – deficiency can cause neural tube defects

35
Q

Signs/symptoms of b12/folate deficency

A

Symptoms of anaemia/cytopenia - Tired- macrocytic/megagolastic anaemia (common) - Easy bruising – thrombocytopenic Mild jaundice - Lemon yellow tinit- haemolysis Neurological problems - Nerve distrbances as a result of B12 def - Subacute combined degeneration of cord

36
Q

Causes of any defieicny

A
  • Intake - Absorption - Utilisation - Loss
37
Q

Pathopysiology of b12 deficiencys

A
  • Pernicious anaemia –> Problem producing IF, problem with gastric parietal cells - Gastrectomy/achlorhyda – acid content of stomach - Terminal ileum problem o Crohn’s o Resection
38
Q

Causes of folate deficencys

A
  • Dietary - Extensive small bowel disease o Coeliac/severe crohsn - Increased cell turnover o Haemolysis (cannot recycle folate) o Severe skin disorders o Pregnancy
39
Q

Other causes of macrocytosis

A
  • Reticulocytosis o 20% bigger than the average mature red cell - Cell wall abnormality (lipids) o Alcohol o Liver disease o Hypothyroidism (poorly understood) - With anaemia o Bone marrow failure syndromes
40
Q

What are haemoglobinoathies

A

Problem with globin chain Inherited conditions: - Relative lack of normal globin chains due to absent genes (thalassaemias) - Variant (abnormal) globin chain eg sickle cell disease

41
Q

Severity of haemoglobinopathies depends on?

A
  • Amount of abnormal haemoglobin - Type of abnormal haemoglobin - Ameliorating factors
42
Q

Haemoglobin production process?

A
  • Globin chains produced on ribosomes - Control of production is mainly at the transcription level and depends on the availability of haem - Beta globin gene - On chromosome 11 o Epsilon, gamma, delta, beta o 1 beta gene - 2 beta chains per molecule - Alpha globin gene cluster – on chromosome 16 o Zeta 2, zeta 1 – important in fetal life o Alpha 2 and alpha 1 – important in childhood Remember 2 chromosome 11 with two beta genes, two chromosome 16 with 4 alpha genes
43
Q

Which types of haemoglobin are important pre- birth and after birth

A
  • HBa – adult, switched on shortly after birth - HbF – important pre birth (2 alpha and 2 gamma)
44
Q

Thalassemias

A

relative lack of globin genes 4 alpha globin genes (on 2 ch16) 2 beta globin gnees (on 2 Ch11)

45
Q

Types of alpha thalassaemias

A

Alpha + thal –> Missing one gene – mild microcytosis Homozygous alpha + thal or alpha zero thal - Missing two genes – microcytosis, increased red cell count and sometimes very mild (asymptomatic) anaemia HBH disease- Missing three genes – significant anaemia (Hb approx. 75g/l) and bizzare shaped small red cells Alpha thal major -Missing four genes – incompatible with life (need alpha chains for fetal haemoglobin)

46
Q

Causes of microcytic anaemia

A

Tells us that the red cells aren’t making enough haemoglobin First step -MCV

47
Q

Pathogenesis of sickle cell disease

A

“Abnormal beta chains in haemoglobin leading to HbS producion, HBS becomes insoluble and leads to cell sickling in hypoxic concentration Chromosome 11 Single aminoacid substitution on B globin gene at position 6 Glutamine>valine = HbS Glutamine >lysins = HBC

48
Q

Problem with sickle cell disease

A

cant bend and block blood vessels Reduced red cell survival (haemolysis 10-20days) vaso-occlusion (tissue hypoxia) Multisytem disease

49
Q

Multi-system effects of sickle cell

A

SICKLE MNEMONIC Stroke/swelling of hands and feet/spleen problems (hyposplenic) Infections/infarctions Crises (painful)/ Cholesthiasis/Chest syndrome Kidney disease Liver disease/Lung problem s Erections sustanained /Eye problems

50
Q

Treatment of sickle cell disease

A
  1. prevent crisis a. hydration, analgasia, early intervention b. Prophylactic vaccination and antibiotics 2. prompt management of crises -oxygen, fluids, analgaesia, antibiotics, specialist care -trasnfusion/red cell exchange 3. Bone marrow transplant in children

Haematology (11 decks)

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