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HLB > Anaemia > Flashcards

Anaemia Flashcards

1
Q

What type of deficiency are pencil cells associated with

A

iron

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2
Q

Reticulocytes

A
  • new RBCs (1 day old)
  • indicates the rate of production of
    RBCs by the marrow ***
  • can be used to monitor progress of
    treatment; demonstrates that more
    RBCs are being produced in
    response to replacement
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3
Q

Anaemia is like money (4 reasons):

A

not making enough = synthesis problem

spending too much = consumption

been lost = bleeding

hidden away = sequestered (but will
come back)

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4
Q

anaemia definition

A

condition that arises when there is a deficiency in the number of red blood cells and or the haemoglobin in circulation

not a diagnosis

WHO def = Hb<130g/L men and <120 female

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5
Q

Anaemia Symtpoms:

A
  • lethargy
  • shortness of breath
  • palpitations
  • headache
  • non-specifically unwell
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6
Q

Anaemia Signs:

A
  • pallor
  • pale conjunctivae
  • tachypnoea
  • tachycardia
  • changes to hair and nails: brittle, Koilonychia (spoon shaped nails)
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7
Q

20% of all maternal deaths are due to

A

anaemia either during or after pregnancy

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8
Q

B12 and folate important for —– which starts eryhtropoeisis

A

dna replication

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9
Q

Reticulocytes causes “—–” on blood film

A

polychromasia
large bluish red cells

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10
Q

Reticulocytes are measured by

A

flow cytometry (counts the cells with RNA)

usually around 1%

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11
Q

If reticulocyte count is low

A
  • precursor deficiency or bone
    marrow failure
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12
Q

If reticulocyte count is high

A

in chronic bleeding or haemolysis

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13
Q

RBC normal shape? Relies on (3)?

A
  • biconcave
  • specific cytoskeletal proteins
  • normal enzymes (pyruvate kinase)
  • normal type and amount of Hb
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14
Q

RBC life span?

A
  • relatively short
  • 120 days
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15
Q

RBCs carry millions of Hb molecules. Each Hb molecule has

A

4 goblin proteins
2 alpha and 2 beta

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16
Q

Haematocrit

A
  • volume percentage of RBC in blood
  • RBC make up the major component
    of blood
  • gives an idea of the proportion of
    the mass of RBCs that make up the
    whole blood pool
  • dervied result (not measured
    directly)
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17
Q

MCH

A

mean cell haemoglobin
average amount (mass) of Hb in the average cell (derived)

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18
Q

MCV

A

mean corpuscular volume
volume of the average RBC
measured using a red cell distribution width RDW

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19
Q

the greater the RDW

A

the greater the variation in the size of the cells

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20
Q

Investigations in Anaemia:

A
  • full blood count: haemoglobin,
    platelet, haematocrit, MCV, MCH,
    neutrophils
  • blood film = direct inspection of
    size and shape
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21
Q

Sequestration definition (anaemia)

A

iron is trapped in macrophages as a result of chronic inflammation meaning supply of iron to RBC becomes limited

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22
Q

Why do we get anaemic? Problem with synthesis:

A
  • deficiency of a building block of
    RBC/Hb eg: iron/B12/folate
  • bone marrow failure: leukaemia,
    aplastic anaemia
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23
Q

Why do we get anaemic? Consumption problem:

A
  • premature destruction of RBCs
    (haemolysis) because the body
    knows they are damaged due to:
    - inherited problems with Hb eg
    sickle cell, thalassemia
    - acquired haemolysis eg
    autoimmune (mechanical heart
    valve)
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24
Q

Why do we get anaemic? Sequestration/ bleeding anaemic problems?

A
  • bleeding from somewhere in the
    body: bowel perforation, heavy
    periods
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25
Q

Establishing the cause of anaemia 4 steps:

A
  • MCV: microcytic, normo, macro?
  • causes for micro, normo, macro
  • clues in history and rest of FBC
  • what further tests would help?
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26
Q

Establishing the cause of anaemia: Step One:

A
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27
Q

Establishing the cause of anaemia: Step 2:

A
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28
Q

Establishing the cause of anaemia: Step 3:

A
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29
Q

Establishing the cause of anaemia: Step 4:

A
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30
Q

Problems with Synthesis: Iron Deficiency:

  • is
  • population
  • broad categories of causes (3)
A
  • not enough iron = small, pale cells:
    MICROCYTIC & hypochromic
  • most common
  • causes: bleeding, nutritino
    deficiency, increased requirements
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31
Q

Diagnostic Tests for Iron deficiency (problems with synthesis):

A
  • Serum Iron:
    - labile, so reflects recent intake
    of iron
  • Serum Ferratin:
    - storage form of iron
    - low = iron deficient
    - high = overload/chronic dis
  • Serum Transferrin:
    - carrier molecule for iron in the
    blood
    - homeostatically UP if iron
    deficient
    - similar to total iron binding
    capacity
  • % Transferrin saturation:
    - sensitive measure of iron
    status
    - low = iron deficient
    - high = iron overload
32
Q

Depth into 3 broad causes of iron deficiency:

A
  • Blood loss: menstrual, OCCULT GI
    MALIGNANCY, stomach wall
    ulceration
  • Dietary: malabsorption, poor diet,
    vegan/veg
  • increased requirements: pregnancy
33
Q

what does this blood film show

A

insert

34
Q

Problems with synthesis: B12 deficiency: how is B12 absorbed?

A
  • B12 (cobalmin) in food
  • binds to intrinsic factor (IF)*** from
    gastric parietal cells
  • transported to terminal ileum for
    absorption
35
Q

Problems with synthesis: B12 deficiency: causes (6):

A
  • genetic abnormalities (rare)
  • meds: protein pump inhibitors
    (omneprazole), metformin
  • infections: fish tapeworm, H pylori
  • dietary: strict vegans, pregnancy
    increases requirements
  • malabsorption
  • autoimmune
36
Q

Problems with synthesis: B12 deficiency: malabsorption as a cause:

A
  • post grastric or ileal surgery y
  • removal of parietal cells decreases
    intrinsic factor production
  • Crohn’s disease (inflammatory
    bowel disease due to decreased
    B12/IF absorption
37
Q

Problems with synthesis: B12 deficiency: autoimmune causes:

A
  • Pernicious anaemia
  • check for auto-antibodies to IF
  • routine testing not recommended
  • leads to deficiency of IF
  • can not absorb B12 in terminal
    ileum
38
Q

Problems with synthesis: B12 deficiency: treatment:

A
  • oral replacement may be sufficient
    in dietary or med related
  • for pernicious anaemia or
    absorptive problem: B12 injections
    (load and then every 3 months)
  • both B12 and folate deficient, B12 must be replaced first because sudden replacement of folate in someone who is also B12 deficient, can drop B12 even lower and hasten subacute GI combined degeneration of the cord
39
Q

Megaloblastic anaemia:

A
  • B12/folate deficiency most
    common cause
  • bone marrow produces large RBC
  • often low WBC and platelets
  • sufficient iron for Hb
  • sufficient precursors for cell growth
  • INSUFFICIENT PRECURSORS FOR
    CELL DIVISION
40
Q

clinical manifestations of B12 deficiency

A

insert table

41
Q

sub-acute combined degeneration of the cord

A
  • very rare
  • progressive demyelination of dorsal and lateral columns of the spinal cord
  • due to severe B12 deficiency
  • presents:
    - altered sensation: vibration
    - numbness/tingling
    - weakness
    - ataxia and gait disturbance
42
Q

Red cells are microcytic, hypochromic and show anisopoikilocytosis

A
  • small pale different shapes and size and some long thin like pencils
  • iron deficiency
43
Q

Problems with synthesis: Folate Deficiency: causes:

A
  • dietary
  • malabsorption: Coeliac, Crohns
  • excessive utilisation: chronic haemolysis, pregnancy
  • alcohol
  • drugs: phenytoin, methotrexate
44
Q

Management of sub-acute combined degeneration of the cord:

A

replace B12

45
Q

What is the most common anaemia in hospitalised patients?

A

anaemia of chronic disease

46
Q

Common causes of chronic disease anaemia:

A
  • chronic inflammation
  • auto-immune: rheumatoid arthiritis
  • chronic infection; TB
  • cancer
  • chronic kidney disease
  • advancing age
47
Q

Iron deficient anaemia vs anaemic of chronic disease

A

insert table

48
Q

Anaemia of chronic disease: poor utilisation of iron:

A

-*** iron is stuck in the macrophages of the RE system, can not be mobilised into erythroblasts
- decreased transferrin

49
Q

Anaemia of chronic disease: impaired proliferation of erythrooid progenitors:

A
    • blunted response to erythropoietin
  • IRON UNAVAILBLE
50
Q

Anaemia of chronic disease is a cause of which type of anaemia

A

normocytic

51
Q

Problems in synthesis: Bone marrow failure:

A
  • not making enough haematopoeitic cells
  • RETICULOCYTES LOW
  • haematinics are normal
52
Q

3 causes of bone marrow failure as a problem in synthesis for anaemmia

A
  • marrow not working myelodysplasia
  • marrow is full of other things (infiltration eg leukeamia)
  • marrow is empty (aplastic anaemia)
53
Q

Diagnosis of bone marrow failure as a problem of synthesis (anaemia)

A
  • myelodysplastic syndrome
  • not effectively working maymore, weary
  • low blood counts lead to fatigue, infections, bleeding
54
Q

Management of bone marrow failure as a problem of synthesis (anaemia)

A
  • supportive
  • chemotherapy in some cases
  • bone marrow transplant if young
55
Q

Anaemia: Excess consumption of RBCs: causes

A
  • haemolysis = red cell breakdown
  • inherited: membrane, Hb, metabolic problems
  • acquired: immune 9antibodies, non-immune (direct damage)
56
Q

Symtpoms and signs of haemolysis

A

insert

57
Q

Inherited red cell problems are what type of mutation

A

recessive

58
Q

Qualitative inherited red cell problem

A

wrong type of haemoglobin produced

59
Q

Quantitative inherited red cell problem

A

not enough haemoglobin produced

60
Q

Combine inherited red cell problem

A

mix of quant and qaul (HbS Beta Thal)

61
Q

Sickle Cell Disease:
- type of mutation
- life expectancy
- RBC turnover
- reticulocyte count
- triggers
- diagnosis
- management

A
  • autosomal recessive
  • shortened life expectancy
  • point mutation in beta gobulin gene
  • increased RBC turnover (20 days) because body tries to compensate for removing damaged RBCs from circulation
  • reticulocytes raised 10%
  • many triggers, vaso-occlusive: ischaemia, pain, chest crisis, organ failure
  • HIGH PERFORMANCE LIQUID CHROMOTAGROPHY
    management: analgesics, hydration, transfusion, red cell exchange
62
Q

Sickle Cell Disease vs Trait:

A
  • mutated sickle haemoglobin HbS:
    - forms long filamentous strands
    - insoluble at low O2 tension
    - RBC inflexible and sticky = CRISIS
  • sickel cell trait:
    - heterozygous for HbS and HbA
    - much lower risk of crisis
    - RESISTANCE TO MALARIA INFECTION
63
Q

Haemolysis screen results

A

insert

64
Q

Sickle cell trait diagram

A

insert

65
Q

sickle cell diagram

A

insert

66
Q

sickle cell disease chromatography

A

insert

67
Q

Thalassaemia:

A
  • 4 alpha genes and 2 beta genes and can inherit mutations in the alpha genes or beta genes or both
  • alpha thalessemia, beta thalassaemia
  • leads to less or no HbA production
  • most mutations are deletions
  • affects people of mediterranean, south asian, south east asiam, middle eastern
68
Q

Iron deficient anaemai vs thalassemia

A
69
Q

Alpha Thalassemia

A
  • problems arise due to genertic mutations that lead to ABSENT alpha chains
70
Q

Alpha Thalassemia

A
  • problems arise due to genertic mutations that lead to ABSENT alpha chains
71
Q

hydrops fetalis

A

alpha thalessamia
no alpha chains
fatal

72
Q

Iron deficient anaemia vs thalassemia:

A
  • insert side
  • thalassemia is very microcytic and hypochromic
  • if not anaemic at all then thalassemia
  • life long family history?
  • high iron number in thalassemia
  • thalassemia: no pencil cells, RDW
73
Q

Thalassemia can have associated anaemia, but also not be associated

True or False

A

True

74
Q

Inherited Red cell problems: enzymopathies:

A
  • G6PD
  • pyruvate kinase
  • if these enzymes are deficient then under the influence or certain triggers or insults in food, medicine, oxidative haemolysis can occurr causing Hb to precipitate out, then cells rejoin forming blister cells
75
Q

G6PD deficiency

A

x linked recessive (males)
- due to fava beans causing oxidative crisis
- drugs like aspirin, anti malarials
- management = support, avoid oxidative stress

76
Q

To differentiate between acquired disorders using haemolysis

A
  • immune will have DAT positive
  • non-immune DAT negative

HLB (49 decks)

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