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Haem/Immuno > Haem pathlology > Flashcards

Haem pathlology Flashcards

1
Q

Anaemia

A

Haemoglobin level below normal for age and sex of the patient

Not a diagnosis but a feature of underlying pathology

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2
Q

Clinical features of anaemia

A

Pallor
Pale conjuctiva
Tachycardia
Increased pulse pressure

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3
Q

Symptoms of anaemia

A 
Weakness
Fatigue
Lethargy
Dizziness
Headache
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4
Q

Severity of anaemia

A

Hb level
Rate of development
Age of the patient
Degree of physiological compensation

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5
Q

Anaemia causes

A

Decreased red cell production

  • Bone marrow
  • Reduced EPO
  • Reduced DNA synthesis
  • Reduced Hb synthesis
  • Chronic disease

Increased red cell loss

  • Blood loss
  • Haemolysis
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6
Q

Testosterone in erythropoiesis

A

Drives erythropoiesis

Males have higher RBC count than females

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7
Q

Three types of anaemia

A

Microcytic (Low MCV, Low MCH)
Macrocytic (High MCV)
Normocytic

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8
Q

MCH

A

“Mean cell hemoglobin” (MCH), is the average mass of hemoglobin per red blood cell in a sample of blood

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9
Q

MCV

A

Mean corpuscular volume (MCV) is the average volume of red cells

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10
Q

Microcytic anaemia

A

Iron deficiency
Chronic disease anaemia
Thalassaemia

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11
Q

Macrocytic anaemia

A 
Megaloblastic
Liver disease
Alcohol
Pregnancy
Hypothyroidism
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12
Q

Normocytic

A

Blood loss
Chronic disease
Renal failure
Haemolytic anaemias

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13
Q

Ferritin

A

Major storage protein of iron

Levels are proportional to the iron stores

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14
Q

Transferrin

A

Major transport protein of iron

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15
Q

Transferrin receptor

A

Cells absorb iron through internalisation of the transferrin bound to the transferrin receptor

**These levels increase in iron deficiency

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16
Q

Ferroportin

A

Transports iron across cell membranes to the plasma

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17
Q

What is the transporter on enterocytes

A

DMT1

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18
Q

Useful iron versus stored iron

A

Useful is Fe2+

Stored is Fe3+

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19
Q

Three main causes of iron deficiency

A

Decreased absorption
Increased use
Blood loss

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20
Q

How much iron is absorbed daily

A

1 mg

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21
Q

Blood film of iron deficiency anaemia

A

Hypochromic cells
Pencil cells
Microcytic
Low Hb

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22
Q

Low ferritin

A

Equals iron deficiency

*Careful in inflammation

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23
Q

Management

A

Oral iron therapy- safe, cheap, effective

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24
Q

Oral iron

A

Iron is best absorbed as ferrous salt
Ascorbic acid given to enhance absorption

150-200 mg/day

Keep going until ferritin stores are replenished

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25
Q

Adverse effects of oral iron

A

Nausea
Constipation
Diarrhoea
Abdominal pain

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26
Q

Where in the body is iron absorbed

A

Duodenum and proximal jejunum

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27
Q

Failure to respond to oral iron therapy

A

Malabsorption
Poor compliance
Ongoing blood loss

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28
Q

Parenteral iron therapy

A

For patients unable to tolerate oral iron or non-compliant, high rate of loss

Products- Iron polymaltose (Ferrosig) and Iron carboxymaltose (Ferrinject)

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29
Q

Anaemia of inflammation

A

Blunted EPO response
Decreased red cell survival
Impaired absorption of iron due to hepcidin

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30
Q

Hepcidin

A

Released by liver in inflammation, causes internalisation and degradation of ferroportin

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31
Q

Management of anaemia of inflammation

A

Does not respond to oral iron

Combination of IV iron and EPO

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32
Q

B thalassaemia major

A

Cannot produce any B globin
a globin precipitates and damages developing erythroid cells and breakdown of cells occurs in the bone marrow
Ineffective erythropoiesis and shortened red cell survival leading to severe transfusion dependent anaemia

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33
Q

Hb Barts/Hydrops fetalis

A

Cannot produce a globin

High affinity for oxygen, very poor oxygen delivery to tissues

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34
Q

HbH disease

A

Loss of three alpha genes, hypochromic microcytic anaemia

Unstable and precipitates causing damage to red cell membrane

35
Q

Megaloblastocsis

A

Large oval shaped cells with immature nucleus
Increased erythroid activity

Occur in vitamin B12 or folate deficiency

36
Q

Blood film in megaloblastic anaemia

A

Low reticulocyte count
Megaloblastic changes
Hypersegmented neutrophils
Severe cases- low platelets and white cells

37
Q

Two reactions Vit B12 is needed for

A

1) Methylmalonyl mutase reaction (maintaining myelin in CNS)

2) Methionine synthetase reaction (DNA synthesis)

38
Q

B12 deficiency reasons

A 
Decreased dietary intake
Decreased absorption 
Intestinal problems
Increased excretion
Increased demand
39
Q

Clinical features in B12 deficiency

A 
Pallor due to anaemia
Glossitis
GI disturbances
Weight loss
Psychiatric and neurological problems
40
Q

Haemolysis

A

Increased red blood cell destruction and subsequent reduced red blood cell lifespan

41
Q

Clinical features of haemolysis

A

Increased RBC destruction
Increased bilirubin
Increased lactate dehydrogenase
Dark urine

42
Q

Causes of RBC destruction

A

Intrinsic

  • Spherocytosis, elliptocytosis
  • Hb- thalassaemia, sickle cell anaemia
  • Enzyme- G6PD deficiency, PK deficiency

Extrinsic

  • Trauma
  • Infection (Malaria)
  • Autoimmune haemolytic anaemia
43
Q

Autoimmune haemolytic anaemia

A

Production of auto-antibodies against RBC causing haemolysis

44
Q

What test is used to detect Autoimmune haemolytic anaemia

A

Coombs test (Positive direct antiglobulin test DAT)

45
Q

Two subtypes of antibodies in Autoimmue haemolytic anaemia

A

IgG (Warm)

C3d (Cold)

46
Q

Secondary causes of AIHA

A

Infection
Recent transfusion
Lymphoproliferative diseases
Medication or drug induced

47
Q

Therapy for AIHA

A

Warm- steroids (prednisolone and dexamethasone)

Cold- Rituximab

48
Q

Microangiopathic haemolytic anaemia

A

Red cell fragmentation

Causes:
Mechanical trauma
DIC
Drug induced

49
Q

Primary vs Secondary haemostasis

A

Primary- vWF

Secondary- coagulation cascade

50
Q

Endothelial injury

A

Platelets go to the site and bind to subendothelial collagen to initiate primary closure of the vessel wall defect
TF combines with factor VII. FVIIa-TF activate other clotthing proteins to produce thrombin which converts fibrinogen to fibrin to stabilise the clot

51
Q

What causes bleeding

A

Abnormalities of vasculature
Defects of primary haemostasis
Defects of secondary haemostasis
Accelerated breakdown of clot

52
Q

Platelet disorders

A

Quantitative
Qualitative
Both

53
Q

Causes of thrombocyopaenia

A

Congenital disorders

Acquired

  • Impaired bone marrow production (leukaemia, myelodysplasia)
  • Increased platelet destruction (Sepsis, DIC, ITP, autoimmune conditions, Pre-eclampsia)
  • Hypersplenism
  • Drug induced
54
Q

Immune thrombocytopaenia purpura

A

Increased platelet destruction
Inhibition of megakaryocyte platelet production through IgG antibodies

Petechiae, epitaxis, bleeding gums

55
Q

Platelet function in haemostasis

A

Platelets bind to surface receptors (GP1b through vWF and GPVI to collagen)
They then change shape
Express GPIIb/IIIa
Produce ADP/TxA2 to recruit more platelets to produce platelet plug

56
Q

Abnormal platelet function

A

Congenital

  • GP-Ib-IX-V- Bernard Soulier syndrome
  • GPIIb/IIIa- Glanzmann thrombocytpaenia

Acquired

  • Aspirin
  • Clopidogrel
  • Dipyridimole
57
Q

Bleeding disorders causes

A

Congenital

  • Haemophilia (A is FVIII, B is FIX)
  • vWF disease

Acquired

  • Liver disease
  • Renal problems
58
Q

Principles of mixing studies

A

Prolonged APTT or PT—–> Mix 50:50 patients plasma

  • –> if normal (clotting factor deficiency)
  • –> if not normal (clotting factor inhibitor)
59
Q

vWF disease

A

Three types of vWD

1) Reduced vWF
2) Reduced function of vWF
3) Both leading to severe deficiency

60
Q

Management of vWD

A

1) Desmopressin (release of vWF from stored granules)
2) Tranexamic acid tablets (stabilise fibrin clot)
3) Biostate (product with FVIII and vWF)

61
Q

Vitamin K deficiency

A

Prolonged APTT and PT but normal fibrinogen

Because Vit K important for activation of 2,7,9,10

62
Q

Why should all babies receive IM vit K at birth?

A

Vitamin K is ommitted at delivery

63
Q

Disseminated intravascular coagulation (DIC)

A

Systemic process where blood is exposed to pro-coagulant factor
Leading to widespread coagulation, massive thrombin generation, depletion of clotting factors

64
Q

Causes of DIC

A

Sepsis
Pregnancy
Snake bite

65
Q

Clinical presentation for DIC

A

Bleeding
Renal dysfunction
Shock
Hepatic dysfunction

66
Q

Lab test findings for DIC

A

Prolonged APTT
Reduced fibrinogen
Low platelets
Raised D-dimers

67
Q

Heparin causes what in lab tests

A

Prolonged APTT

68
Q

Warfarin causes what in lab tests

A

Prolonged PT

69
Q

Virchow’s triad

A

Abnormal blood flow
Hypercoagubility
Endothelial injury

70
Q

Venous thromboembolism

A

Venous thromboembolism (VTE) is the formation of blood clots in the vein. When a clot forms in a deep vein, usually in the leg, it is called a deep vein thrombosis or DVT

71
Q

Risk factors for VTE

A

Acquired

  • Pregnancy
  • Obesity
  • Hospitalisation
  • Oestrogen therapy

Inherited

  • Antithrombin deficiency
  • Protein C/S deficiency
72
Q

Natural inhibitors of coagulation

A 
Antithrombin (on X)
Protein C (on V)

Protein S- activates protein C

73
Q

Antithrombin

A

Major inhibitor of Factor Xa

Works slowly without heparin but fast with heparin

74
Q

Protein C

A

Needs to be activated
Activated Protein C inactivates Factor V and VIIIa
Markedly enhanced effect due to Protein S

75
Q

Protein S

A

Important in Protein C system

Acquired deficiency in pregnancy, OCP, liver disease, certain drugs, HIV infection

76
Q

Factor V Leiden

A

Point mutation (Arg to Glu) where there is protein C resistance and protein C is unable to inactivate factor V

77
Q

D-dimer

A

Plasmin breaks down cross-linked fibrin to D-dimers

Useful for VTE, DVT, DIC, infection, trauma

78
Q

Why use D-Dimer?

A

Can exclude DVT/PT but not diagnose it

**High NPV but low PPV

79
Q

Diagnosis of PE

A

Imaging
D-Dimer
V/Q scan

80
Q

Warfarin

A

Blocks vitamin K epoxide reductase

81
Q

Transfusion indications

A

Hb<70g/L

Raises it by 10g/L

82
Q

Other blood products

A

Platelets
Fresh frozen plasma
Cryoprecipitate

83
Q

Fresh frozen plasma

A

For clotting factors
Fibrinogen
vWF

84
Q

Cryoprecipitate

A

Thawing FPP leaves a precipitate rich in fibrinogen.

Has 10x as fibrinogen

Haem/Immuno (3 decks)

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