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103 theme 2 > Anaemia > Flashcards

Anaemia Flashcards

1
Q

what is anaemia

A

Haemoglobin (Hb) concentration falls below defined level (outside normal range)
Units of Hb are g/L

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2
Q

what is the clinical consequence of anaemia

A

Clinical consequence: insufficient O2 delivery

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3
Q

what causes anaemia

A

low Hb content
low Red blood cells (RBCs)
Altered Hb does not carry sufficient O2
synthesis, consumption, bleeding or sequestering

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4
Q

what are the normal ranges of haemoglobin for pregnant women and children

A

110-160 g/L

Pregnancy - produce more plasma so more abc dilution

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5
Q

what are the normal ranges of haemoglobin for women and men

A

women 115-165 g/L

men 130-180 g/L

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6
Q

how many RBCs per litre

A

4x10^12/L
5litres of blood and 50 million, million red cells
make approx 5 million per second

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7
Q

what is the haematocrit

A

percentage of red cells after centrifugation

40-45%

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8
Q

what are the symptoms of anaemia

A 
Lethargy, fatigue
Shortness of breath
(At rest vs On exertion?)
Palpitations
Headache
Worse symtoms if acute onset
Acute bleed / haemolysis
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9
Q

what are the signs of anaemia

A

Skin pallor
Pale conjunctivae
Tachypnoea
Tachycardia

Koilonychia

  • spoon shaped nails
  • iron deficiency
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10
Q

how does inadequate synthesis cause anaemia

A

Deficiency in necessary components
Iron, B12, folic acid

Bone Marrow Dysfunction / Infiltration
e.g., myelodysplasia or aplastic anaemia

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11
Q

how does blood loss or consumption cause anaemia

A

Bleeding

Haemolytic
(Increased red cell destruction
Shortened RBC lifespan)

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12
Q

how can anaemia be classified

A

Size of red cell

Acute or chronic

Underlying aetiology

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13
Q

what is the most common type of anaemia

A

iron deficiency in uk and globally

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14
Q

what causes iron deficiency

A

Bleeding (esp. occult)
Nutritional deficiency
Increased requirements

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15
Q

how is iron deficiency confirmed

A 
with iron studies:
Ferritin (measure of iron stores) low
Serum Fe low
Transferrin high 
Transferrin saturation % low
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16
Q

what is iron deficiency not

A

a diagnosis in itself and should always prompt other investigations to establish underlying cause

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17
Q

what are the diagnostic tests for iron

A

serum ferritin
serum iron
serum transferrin
% transferrin saturation

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18
Q

what is serum ferritin

A

Storage form of iron

Low = iron deficient (high = iron overload or reactive)

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19
Q

what is serum iron

A

Labile in blood, so reflects recent intake of iron

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20
Q

what is serum transferrin

A

Carrier molecule for iron from gut to stores
Homeostatically goes up if iron is deficient
Reflects total iron binding capacity (TIBC) of the blood

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21
Q

what is % transferrin saturation

A

Sensitive measure of iron status
Reflects proportion of transferrin with iron bound
Low TF saturation indicates iron deficiency

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22
Q

how can bleeding cause iron deficiency

A 
Occult gastro-intestinal blood loss:
GI Malignancy (never miss this)
GI peptic ulceration
Menstrual
Renal tract
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23
Q

how can inadequate intake cause iron deficiency

A

Dietary deficiency:
Vegan/vegetarian diet
Malabsorption:
Coeliac and Crohn’s disease

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24
Q

how does increased requirement cause iron deficiency

A

pregnancy

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25
Q

how is anaemia caused by chronic disease

A

caused by chronic inflammation and seen in conditions such as connective tissue disease, malignancy, and chronic infection such as TB

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26
Q

how does mean corpuscular volume categorise size of red blood cell

A

This is the size of red blood cells (mean cell volume)

Normally about 80-100fL

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27
Q

how does mitcrocytic (small) categorise size of red blood cell

A

Iron deficiency (acquired) - hypo chromic
Inherited disorders of haemoglobin (beta-thalassaemia trait)
a/B imbalance, abnormal Hb electrophoresis but normal ferritin

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28
Q

how does macrocytic (large) categorise size of red blood cell

A

B12 and folate deficiency (needed for synthesis of nucleotides) - megaloblastic
Myelodysplasia (causes defective erythropoiesis)

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29
Q

how does normocytic anaemia categorise size of red blood cell

A

Anaemia of chronic disease
Acute haemorrhage
Renal failure (caused by low erythropoietin levels)

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30
Q

why are blood films used

A

Easy, quick, useful

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31
Q

what can a blood film be used to diagnose

A 
haematinic deficiency (microcytic/macrocytic, hypochromic, anisopoikilocytosis)
haemoglobinopathy (sickled cells, haemolysis, polychromasia)
other abnormalities (white cells, platelets, leukaemic cells)
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32
Q

what is RBC lifespan

A

Red cell lifespan:

approx 100 days in the circulation

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33
Q

how is reticulocyte count done

A

Can be calculated on a blood film using a stain to detect RNA
Usually measured by flow cytometry based on size and colour
Typically ~1% but can be >10% in haemolysis e.g., sickle cell disease
Causes polychromasia on a blood film (large blue-ish red cells)

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34
Q

what does reticulocyte count indicate

A

Indicates rate of production of RBCs by bone marrow
Low during precursor deficiencies (e.g. iron)
Low if bone marrow is infiltrated
High in chronic bleeding
High in haemolysis

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35
Q

what is reticulocyte count useful for

A

Reticulocyte count useful to monitor response to treatment

Red cell production driven by erythropoietin from kidney

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36
Q

how do blood cells appear on a blood film in iron deficiency

A

Hypochromia

Microcytosis

Pencil Cells

Target Cells

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37
Q

what history should be taken in suspected anaemia

A

Dietary history
Travel History
Ethnic Origin
Family History

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38
Q

what symptoms indicate anaemia in a history

A 
GI Symptoms
Dyspepsia / Reflux
Change in bowel habit (?melaena)
Weight loss?
Menstrual History ?menorrhagia
Bowel history ?coeliac / Crohn’s disease
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39
Q

how is megaloblastic anaemia (B12 and folate) seen morphologically

A 
Macrocytic red cells (MCV > 100)
Hypersegmented neutrophils (more than 4 nuclear lobes)
40
Q

what is pernicious anaemia

A

B12 deficiency

41
Q

what causes pernicious anaemia

A

Autoimmune – parietal cell loss
Deficiency of intrinsic factor
Cannot absorb B12 in terminal ileum where IF receptors are located
Check for autoantibodies
against intrinsic factor or gastric parietal cells
Treat with B12 injections
load initially with 5 doses alternate days, then every 3 months

42
Q

what are other causes of pernicious anaemia

A

Dietary
Strict vegans (B12 found in diary produce)
Supplement with oral B12

Malabsorption:
Coeliac disease and Crohn’s disease
Post gastric / ileal surgery

43
Q

how is folate deficiency caused

A

Dietary – common

Malabsorption
Coeliac
Crohn’s disease

Excess Utilisation
Chronic haemolysis
Pregnancy

Alcohol

Drugs
Phenytoin
Methotrexate

44
Q

what is the most common cause of anaemia in hospitalised patients

A

anaemia of chronic disease

45
Q

what are common causes of anaemia of chronic disease

A

Chronic inflammation
Chronic infection e.g. TB

Auto-immune conditions
e.g. rheumatoid arthritis

Cancer

Renal failure (also causes low EPO level)

46
Q

how does poor utilisation of iron in the body cause CD anaemia

A

Iron is stuck in macrophages of the reticuloendothelial system
There is poor mobilisation of the iron from the stores into the erythroblasts

47
Q

how does dysregulation of iron homeostasis in the body cause CD anaemia

A

Decreased transferrin
Increased ferritin (acute phase reactant)
Increased hepcidin

48
Q

how does Impaired proliferation of erythroid progenitors in the body cause CD anaemia

A

Blunted response to EPO (erythropoietin)

Iron is functionally unavailable

49
Q

what causes sickle cell disease

A

Point mutation in the beta globin gene causing HbS (sickle Hb)
leads to Increased turnover of red cells = survival approx 20 days due to haemolysis
Raised reticulocytes >10%

50
Q

what is sickle cell crisis

A

Triggered by low blood O2 level
Vaso-occlusive due to sickling in the vessels
Causes ischaemia leading to pain, necrosis and potential organ damage

51
Q

how is sickle cell disease managed

A

Analgesics, hydration, transfusion

compensated by 2,3DPG to move oxygen dissociation curve to the right

52
Q

what characterised sickle cell disease

A

Genetic, autosomal recessive
Sub-Saharan Africa
Shortened life expectancy (42 for men and 46 for women without good management)

53
Q

what is the mechanism of sickle cell disease

A

Increased mechanical fragility resulting in shortened lifespan (6-10 days)
The rigidity of sickle cells results in increased viscosity with occlusion of small blood vessels
Adhesion of sickle cells to endothelium

54
Q

what is thalassemia

A

Insufficient production of normal Hb
Imbalance of alpha and beta chains
Inherited autosomal recessive
Either alpha or beta thalassaemia

55
Q

what are the clinical features of thalassemia

A

enlarged spleen, liver, and heart

bones may be misshapen (frontal bossing)

56
Q

what are the two types of thalassemia

A

Beta-thal major (homozygous) = disease - requires life-long transfusions
Beta-thal minor (heterozygous) = carrier (aka Beta-thal trait) - clinically healthy

57
Q

where is beta thalassemia found

A

Family history
Trait vs disease
Distribution as per malaria

58
Q

how is beta thalassemia diagnosed

A 
characteristic indices
Microcytic
Hypochromic
Hb electrophoresis
Blood Film
59
Q

what are the diseases of bone marrow infiltration

A

leukaemia
lymphoma
myeloma

60
Q

what are the symptoms of leukaemia

A

Non-specific symptoms

Bone marrow failure

61
Q

what are the symptoms of lymphoma

A

Lymphadenopathy

Weight loss

62
Q

what are the symptoms of myeloma

A

Anaemia
Hypercalcaemia
Renal Failure
Bone lesions

63
Q

how is bone marrow infiltration diagnosed

A

Bone marrow sample obtained from iliac crest:
aspirate film for morphology of cells
trephine biopsy for histological section

64
Q

when does acute anaemia need a transfusion

A

Acute > chronic
guided by symptoms rather than Hb level
make blood with haematinic therapy?
If not, then transfuse for symptoms (usually if Hb <80g/L)

65
Q

what are the signs of acute chronic haemorrhage

A

Haematemesis (vomiting blood)

Melaena (darkened stools)

66
Q

how is chronic anaemia managed

A

Treat the underlying cause:
Iron supplementation (oral ferrous sulphate 3 months)
Folic acid (oral folate for 3 months)
B12 (load initially then injections every 3 months)

67
Q

how is chronic anaemia treated in patients with haemodialysis or kidney failure

A

Erythropoietin (EPO) weekly sub-cut injections

68
Q

what are long term causes for transfusion in chronic anaemia

A 
Iron overload (iron deposition in organs)
Allo-antibodies (to foreign red cells)
69
Q

what is the world wide impact of anaemia

A

increased risk of morbidity in children

impaired physical and cognitive development

poor pregnancy outcome

contributes to 20% of all maternal deaths

reduced work productivity in adults

70
Q

what is anaemia of chronic disease

A

Normal-sized cells
Iron trapped inside macrophages
Cancer, inflammation, rheumatoid arthritis
Normal/raised ferritin, normal/low transferrin
Raised hepcidin (and inflammatory proteins)

71
Q

what is anaemia due to renal failure

A

Lack of erythropoietin (low serum Epo level)
Red cell hormone produced by kidney
Treat with recombinant Epo (weekly sc injection)

72
Q

what is bone marrow failure

A

Not making enough red cells
Reticulocyte count is low
Haematinics are normal

Can be congenital
rare bone marrow failure states

73
Q

how can bone marrow failure be acquired

A

three causes:

1) Marrow is empty (aplastic anaemia)
2) Marrow is full (infiltration e.g. leukaemia)
3) Marrow is not working (e.g. dysplasia)

74
Q

what is the main causes for haemolysis

A

Inherited:
Membrane problems
Haemoglobin problems
Metabolic problems

Acquired:
Immune (antibodies)
Non-immune (direct damage)

75
Q

how can inherited red cell issues be membrane problems

A

Membrane problems
e.g. hereditary spherocytosis or elliptocytosis
Red cells are spherical, not biconcave
Splenectomy can help (may need cholecystectomy for gallstones also)

76
Q

what is haemoglobinopathy

A

inherited issues eg sickle cell disease (wrong type of Hb)

e.g. thalassaemia (not enough Hb)

77
Q

what are metabolic red blood cell issues

A

e.g. G6PD deficiency
X-linked recessive, males, Afro-Caribbean
Must avoid fava beans, legumes, certain antimalarials and antibiotics

78
Q

what are acquired red cell problems

A

Immune i.e. antibody-mediated (spherocytes)
Autoimmune (warm IgG vs. cold IgM)
Alloimmune (red cell transfusion reaction)

Non-immune (red cell fragments)
Heart valves (mechanical)
DIC (very sick patients - sepsis, metastatic cancer)
MAHA (microangiopathic haemolytic anaemia)

79
Q

how can haemolysis be diagnosed

A

inherited?
haemolysis screen
Direct anti-globulin test (DAT or Coomb’s test)
Bilirubin level – is patient jaundiced?
Blood film – are there spherocytes? fragments?
LDH level – goes up in haemolysis
Reticulocyte count – goes up in haemolysis
Haptoglobins – levels go down in serum (binds free Hb)
Haemoglobinuria = free Hb in urine (dark colour)
Urine dipstick shows urobilinogen (colourless)

80
Q

what are the main causes of bleeding

A

bowel
menstrual
cancer

81
Q

what is sequestering

A 
Internal bleeding
E.g. trauma or vascular rupture
Abdomen
Thorax
Tissues
or due to
Big spleen (hypersplenism)
82
Q

what causes HbS

A

Substitution of valine for glutamic acid at 6th amino acid position (qualitative change)
deoxygenation, HbS forms parallel aggregates
Valine substitution stabilises this conformational change causing sickling (aggregate formation)
Red cell shape is deformed into sickle shape

83
Q

how is sickle cell disease inherited

A

Inherit 1 copy of  globin gene from each parent
If only 1 HbS gene inherited = sickle cell trait
This is generally asymptomatic
If both parents have sickle trait, then there is a 25% chance of the offspring inheriting both sickle genes
HbC is genetic variant of sickle Hb (6th aa, lysine)
SC disease clinically very similar to SS disease

84
Q

what are the clinical features of sickle cell in babies

A

Presentation in infancy (baby protected by HbF)
Anaemia and jaundice
Dactylitis, epiphyseal damage can result in shortening of the digits
Splenic sequestration only in children
Classical vaso-occlusive crises
Pneumococcal septicemia

85
Q

how can sickle cell anaemia present as clinical complications

A 
Chest syndrome
SOB
Pleuritic chest pain
Patchy shadowing on CXR
Progressive hypoxia and fever
Brain syndrome
Presents as stroke
Aplastic crisis
Associated with parvovirus infection
86
Q

how does sickle cell present on a blood film

A

Sickle cells
Polychromasia
Howell-Jolly bodies
Nucleated RBCs

87
Q

how is sickle cell anaemia diagnosed

A

positive sickle cell solubility test (less soluble)

haemoglobin electrophoresis

88
Q

how can sickle cell be managed

A 
Antenatal screening
In high prevalence areas
But variable clinical course
Prophylaxis against infections
Penicillin prophylaxis
Vaccination
pneumovax / meningovax / haemophilus (HIB)
Prevention of crises
Avoid infections, hypoxia, dehydration
89
Q

how can sickle cell crisis be managed

A 
Exclude underlying infection
Intravenous fluids
Oxygen
Analgesia
NSAID’s
Opiates
Avoid pethidine (seizures and addiction)
Antibiotics
Monitor FBC and reticulocyte count
90
Q

how can stroke be prevented in sickle cell

A

Transcranial doppler predictive of stroke
If blood flow >200cm/sec the risk of stroke is significantly increased
Risk reduced by exchange transfusion
Aim to reduce HbS level to below 30%
Hydroxyurea is an alternative if unable to transfuse

91
Q

how is exchange transfusion done

A 
Manually or with cell separator machine
Aim to reduce HbS level to <30%
Blood-match ABO/Rhesus/Kell/Sickle neg
Indications:
Chest syndrome
Stroke
Major surgery
Recurrent severe crises
Priapism
92
Q

what are complications for sickle cell

A 
Sepsis
Bone infarcts 
Avascular necrosis of femoral/humoral heads
Gallstones (pigment stones)
Proliferative retinopathy
Osteomyelitis (Salmonella)
Papillary necrosis/renal failure
Leg ulcers
93
Q

what are new treatments for sickle cell disease

A

Hydroxyurea reduced frequency of crises, chest syndrome and transfusions

94
Q

what is hydroxyurea

A

Also known as hydroxycarbamide
Leads to reactivation of gamma globin locus in patients
Results in increased production of fetal Hb (HbF)
Results in reduced sickling of red cells
Also, reduction in WCC and platelets
Reduction in frequency of crises

95
Q

what is HPFH (hereditary persistence of fatal Hb

A

HbF levels over 20%
These patients have fewer crises and a milder clinical phenotype
Understanding the biology might allow new therapies to be developed to increase HbF

96
Q

what is allogeneic SCT

A 
Potentially curative
Survival 90-95%, 80-85% cured
Patients usually below 16 years
History of stroke, recurrent chest syndrome or severe painful crises
Infertility likely
5-10% risk of chronic GvHD

103 theme 2 (7 decks)

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