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Haem/Immuno > Immuno pathology > Flashcards

Immuno pathology Flashcards

1
Q

Bone marrow biopsy

A

Aspirate- cells

Trephine- tissues

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2
Q

B symptoms

A

Weight loss > 10%
Fever >38.5
Night sweats

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3
Q

Joske’s Law

A

The more of the three cell lineages that are numerically abnormal, the more likely it is to be an intrinsic marrow disorder

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4
Q

Spectrum of haematological disorders

A

Aplasia –> Dys/Hypoplasia –> Hyperplasia –> Neoplasia

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5
Q

Aplastic anaemia- causes and treatment

A

Pancytopaenia

Causes:

  • Drugs
  • Irradiation
  • Viruses
  • Thymoma

Treatment:

  • Immunosuppression
  • BM transplant
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6
Q

Myelodysplasia- what is it and treatment

A

Low peripheral blood count
Abnormal cell morphology
5-20% blasts
Risk of progression to AML

Treatment:

  • RBC Transfusion
  • Antibiotics

AZACITIDINE (promotes myeloid differentiation)
LENALIDOMIDE

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7
Q

Myeloproliferative disorders

A

Overproduction of blood cells- usually through one cell lineage- generally normal cellular morphology

Fatigue, headaches, weight loss, night sweats and can progress to AML

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8
Q

Myeloproliferative disorders- three conditions

A

1) Polycythaemia vera
2) Essential thrombocythaemia
3) Myelofibrosis

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9
Q

PV

A

Too many red cells
Either relative or true
Under true either primary or secondary

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10
Q

Polycythaemia vera treatment

A

Venesection
Aspirin
Hydroxyurea

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11
Q

Essential thrombocythaemia

A

Too many platelets
>1000 sometimes

Film has thrombocytosis and giant cells

Treatment:
Aspirin
Hydorxyurea
Anagleride

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12
Q

Chronic myeloid leukaemia

A

Myeloproliferative disorder with high neutrophil count
Philadelphia chromosome
Imatinib treatment

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13
Q

Acute leukaemia

A

Too many white cells in the blood (>20% blasts)
ALL more common in children
AML more common in adults

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14
Q

Acute promyelocytic leukaemia

A

Abnormal myelocytes with excess granules

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15
Q

Treatment of acute leukaemias

A

Acute myeloid

  • Cytosine arabinoside
  • Etoposide

Acute lymphoid

  • Prednisolone
  • MTX
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16
Q

Which lymphoma type are chemo resistant?

A

T cell

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17
Q

Which viral infection can increase the risk of NHL

A

EBV

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18
Q

Investigations for lymphoma

A

Fine needle aspiration
Core biopsy
Open biopsy

And,
Blood tests
PET
Imaging

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19
Q

Commonest lymphoma

A

Follicular B-cell lymphoma

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20
Q

Follicular B-cell lymphoma

A

Commonest
Indolent relapsing course
Bcl-2 over-expression

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21
Q

Diffuse large B-cell lymphoma

A

Commonest agressive lymphoma

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22
Q

Burkitt’s lymphoma

A

EBV

Rapidly growing masses in the head, neck or abdomen

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23
Q

Hodgkin’s lymphoma

A

“Reed-Sternberg cells”
B-cell lymphoma not over-expressing B cell surface antigens

Hallmark is high levels of cytokines produced eliciting a vigorous inflammatory response

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24
Q

Multiple myeloma

A

Cancer of the immune system (plasma cells)
Plasma cells acquire a mutation that leads to them producing an abnormal protein that can lead to bone absorption, anaemia and renal impairment

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25
Q

Monoclonal gammopathy of uncertain significance

A

Plasma cells producing abnormal proteins

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26
Q

Multiple myeloma isotypes

A

IgG
IgA
Light chain

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27
Q

Renal disease is multiple myeloma

A

Light chain cast neuropathy
Dehydration
Hypercalcaemia
Amyloidosis

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28
Q

Amyloid light chain (AL) Amyloidosis

A

Abnormal folding of the light chain- produced by plasma cells in the bone marrow

Misfolded light chain –> Aggregation –> Direct tissue toxicity or organ damage due to fibril accumulation

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29
Q

Screening tests for multiple myeloma

A

Protein electrophoresis
Immunofixation
Serum free light chains

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30
Q

What can be used to differentiate clonal from reactive sybtypes of lymphoproliferative disorders

A

Flow cytometry

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31
Q

Chronic lymphocytic leukaemia

A

Clonal
Reactive

Accumulation of small, mature lymphocytes in the blood, lymph nodes and BM

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32
Q

Most common adult leukaemia

A

Chronic lymphocytic leukaemia

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33
Q

CLL vs SLL

A

CLL has more blood and BM involvement compared to SLL
CLL: B cell >5x10(9)
SLL B cell <5x10(9)

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34
Q

Monoclonal B cell lymphocytosis

A

B cell <5x10(9) in the peripheral blood

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35
Q

CLL sequelae

A

Impaired cell mediated and humoral responses leading to increased risk of infection
Risk of progression to a high grade lymphoma

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36
Q

Primary immunodeficiency

A

Inherent problems of the immune system

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37
Q

DiGeorge syndrome

A

Heterozygous chromosomal deletion affecting chromosome 22

Abnormal faces
Hypocalcaemia
Absence or partial thymus
Cardiac abnormalities

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38
Q

What problem is shared in B cell defects?

A

Impaired defence against encapsulated bacteria

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39
Q

Two main problems of B cell defects

A

1) X-agammaglobulinaemia

2) Common variable immunodeficiency disorder

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40
Q

XLA

A

No B cells are produced due to a defect in BTK gene
Problems arise after maternal antibodies fade
Scarring lung diseases are common

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41
Q

CVID

A

Problems with antibody production
IgA deficiency or other antibody deficiency
Diagnosis- deficiency of at least two isotypes

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42
Q

Defects with T and B cells

A

SCID- severe combined immunodeficiency disorder

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43
Q

Defects of phagocytes

A

Chronic granulomatous disease

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44
Q

Which infections are common with which defect

A

T and B cell- systemic
Antibodies- URTI, LRTI, GI
Phagocytes- Resp, skin
Complement- systemic, meningitis

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45
Q

Investigations for immune defects

A

FBC
Lymphocyte subsets
Functional Ab
Functional neutrophil

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46
Q

What is the most common cause of over-activity or underactivity in endocrine organs

A

Autoimmunity

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47
Q

Hallmarks of autoimmunity

A

1) Auto-antibodies in tissues
2) Auto-reactive T cells
3) Lymphocytes, plasma cells and macrophages in tissues
4) Germinal centres in tissues

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48
Q

Causes of thyroid toxicosis

A

Graves disease
Toxic hyper-functioning multi-nodular goitre
Toxic adenoma

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49
Q

How is iodine used to test for thyrotoxicosis

A

Greater uptake of iodine by the thyroid if there is an adenoma present as the rest of the gland is switched off

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50
Q

Graves disease

A

Autoantibodies to TSH receptor leading to hyperactivity and growth

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51
Q

Symptoms and signs of Graves disease

A 
Weight loss
Loss of appetite
Nervousness
Loose stools
Sweating

Enlarged thyroid
Fast pulse rate
Tremor

**Basically, over-activation of sympathetic NS

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52
Q

Eye signs in Graves disease

A

Stare
Lid-lag
Proptosis

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53
Q

Lab diagnosis in Graves disease

A

High T4, low TSH

54
Q

Therapy for Graves disease

A 
Ablative therapy (surgical thyroidectomy)
Anti-thyroid drugs
55
Q

Atrophic thyroiditis

A

Chronic autoimmune inflammation that results in thyroid failure
Most common cause of primary hypothyroidism
Antibodies to thyroid peroxidase and thyroglobulin

56
Q

Which antibody is common in hypothyroidism

A

Thyroid peroxidase antibody

57
Q

Addisonian pernicious anaemia

A

Malabsorption of vitamin B12 due to antibodies to gastric parietal cells leading to lack of intrinsic factor

58
Q

Coeliac disease

A

Autoimmunity to tissue transglutaminase (hence, hypersensitivity to gluten)

59
Q

Process of autoimmunity in coeliac disease

A

Gluten –> Gliadin (Glutamine and Proline) –> tissue transglutaminase removes amine from glutamine –> the remaining then goes and binds to HLADQ2 –> presented to T cells –> T cell and antibody response against gliadin as well as tissue transglutaminase

60
Q

Coeliac disease effects

A

Diarrhoea
Weight loss
Nutritional deficiencies
Osteoporosis

61
Q

What are the antibodies directed against in Autoimmune thyroiditis

A

Thyroglobulin

Thyroid peroxidase

62
Q

SLE pathological changes in different organs

A

Skin- Malar rash, discoid rash, oral ulcers
Joints- Arthritis
Lungs and Heart- Pleuritis and pericarditis
Kidney- glomerulonephritis
Blood- Low WBC, platelets, haemolytic anaemia
Immune system- Anti dsDNA
Immune system- ANA

63
Q

Autoantigens in SLE

A

Cell surface
Cytoplasmic
Nuclear
Extra-cellular

64
Q

Sjogren’s syndrome

A

Systemic chronic inflammatory disorder characterised by lymphocytic infiltrates in exocrine organs
Produces Sicca symptoms- dry eyes, dry mouth and other connective tissue disorders

65
Q

Scleroderma

A

Fibrous thickening of wall of blood vessels in the small intestine and elsewhere
Raynaud’s phenomenon

66
Q

Raynaud’s phenomenon

A

Sharply demarcated digital artery spasm and narrowing
Blue- slow flow in dilated venules
Red- capillary dilation in anoxic tissue

67
Q

Mixed connective tissue disease

A

Term used to describe features of SLE, polymyositis, systemic sclerosis, Raynaud’s joint pain

68
Q

Poly/Dermatomyositis

A

Symmetrical weakness of limb girdle muscles

Muscle fibre necrosis, phagocytosis and regeneration

69
Q

Jo-1 syndrome

A

Major- myositis and pulmonary fibrosis

Minor- Raynaud’s tenosynovitis etc

70
Q

Henoch-Schonlein purpura

A

Multi-system small vessel mediated vasculitis

71
Q

What diagnostic test for small vessel vasculitis

A

Skin biopsy to diagnose fibrinoid necrosis

72
Q

Diagnostic tests for small vessel vasculitis

A

Skin biopsy
Anti-neutrophil cytoplasmic antibody
Anti-proteinase 3
Anti-myeloperoxidase

73
Q

Necrotising vasculitis of medium vessels

A

Medium arteriolies (

74
Q

Pathophysiology of vasculitis

A

Immune complexes form and deposit in subendothelium, overwhelm the reticuloendothelial system, activate complement, recruit and degranulate neutrophils

75
Q

Mixed cryoglobulinaemia

A

Immune complex mediated vasculitis
Small vessel vasculitis
Associated with cryoprecipitate
HCV infection (80%)

76
Q

Treatment of mixed cryoglobulinaemia

A

Treatment of underlying HCV infection

Immunosuppression

77
Q

Anti-neutrophil cytoplasmic antibody

A

Antibodies directed against neutrophilic granules causing activation, sequesteration and degranulation in small vessels

78
Q

Treatment of ANCA associated vasculitis

A

Prednisolone
Cyclophosphamide
Rituximab
Plasmapheresis

79
Q

Examples of different types of vasculitis

A

Small vessel

  • Henoch-Schonlein purpura
  • Mixed cryoglobulinaemia

Medium vessel
- Polyarteritis nodosa

Large vessel
- Giant cell arteritis

80
Q

Polyarteritis nodosa

A

Medium vessel vasculitis

Primary or associated with HepB or HepC

81
Q

Diagnosis of polyarteritis nodosa

A

Biopsy

Angiography

82
Q

Large cell primary vasculitis

A

Chronic, persistent inflammatory condition with infiltrates within arteries with 3 distinct layers and well developed elastic membranes

83
Q

Histopathology of giant cell arteritis

A

Narrowed lumen
Intimal expansion
Pan-arteritis
Multi-nucleated giant cells

84
Q

Treatment of giant cell arteritis

A

High dose corticosteroids tapered over 18-24 months

Low dose aspirin

85
Q

Secondary immunodeficiency disorders

A

Deficiency or dysfunction of immune cells caused by infection, disease or medical treatments

86
Q

CMV disease

A

Can occur after solid organ transplantation

87
Q

Progressive multifocal leukoencephalopathy

A

Reactivation of JC virus infection
Cause lesions on the myelin sheath leading to loss of coordination and weakness

Natalizumab therapy

88
Q

Rarer causes of secondary cellular immunodeficiency

A

Idiopathic CD4 lymphopaenia

Autoantibodies to IFNy

89
Q

Six immune-related transfusion complications

A

1) Acute haemolytic transfusion reaction
2) Delayed haemolytic transfusion reaction
3) Hypersensitivity
4) Febrile non-transfusion related reaction
5) Graft-versus-host disease
6) Transfusion related acute lung injury

90
Q

Secondary hypogammaglobulinaemia

A

After haematological malignancy or

Solid organ transplantation

91
Q

Treatment of secondary hypogammaglobulinaemia

A

Immunoglobin therapy

92
Q

Causes of asplenia

A

Congenital asplenia

Splenectomy

93
Q

Causes of hyposplenia

A

Sickle cell disease
Coeliac disease
Lupus

94
Q

Thymoma associated immune dysfunction

A

B cell deficiency
Cellular immunodeficiency
Autoimmune disease
Lichen planus

95
Q

Allergy

A

Harmful, misguided and excessive immune response to antigens

96
Q

Allergic rhinitis

A

Inflammation of the nasal mucose due to hypersensitivity to environmental antigens

97
Q

Asthma

A

Chronic inflammatory disorder of the airways

98
Q

Symptoms of asthma

A

Wheezing
Chest tightness
Breathlessness
Cough

99
Q

Pathogenesis of asthma

A

Airflow limitation –> Chronic mucus plug formation –> Airway remodelling

Three components:
Infiltration of cells –> Change in resident cells –> Change in non-cellular components

100
Q

Three hypotheses for raise in asthma

A

1) Hygiene hypothesis
2) Microbiota hypothesis
3) Biodiversity hypothesis

101
Q

Which subset of T cells are produced in chronic allergic response

A

Th2 cells

102
Q

What prevents default Type 2 immunity to environmental antigen at birth?

A

APC maturation

103
Q

Early and late allergic response

A 
Early- B cells class switch
Late- Chemokines produced and migration of eosinophils
104
Q

Urticaria

A

Red, raised, itchy rash resulting from vasodilation, increased blood flow and increased vascular permeability

105
Q

Angioedema

A

Similar as urticaria but involves the submucosa, deeper reticular dermis and subcutaneous tissue

106
Q

Difference between urticaria and angioedema

A

Urticaria swellings subside in 8-12 hours

Angioedema swellings continue for days

107
Q

Urticaria treatment

A

Anti-histamines

108
Q

Allergen specific immunotherapy

A

Subcutaneous and Sublingual

Subcutaneous

  • More evidence for asthma and allergic rhinitis
  • Multi-allergens

Sub-lingual

  • Effective for allergic rhinitis
  • Single allergen
109
Q

Allergic contact dermatitis

A

Allergen induced delayed hypersensitivity immune response

110
Q

Pathogenesis of allergic contact dermatitis

A

Allergen –> engulfed by APCs –> Presented to naive T cells –> Sensitised CD4+ and CD8+ cells

Re-exposure –> (12-48 hours later) –> Causes reaction in sensitised individual

111
Q

Diagnosis of allergic contact dermatitis

A

Patch testing

112
Q

Three mediators released from mast cells

A

Histamine
Leukotrienes
Prostaglandins

113
Q

Drug hypersensitivity

A

Type B drug reaction
Immediate (<1 hour), Accelerated (1-<72 hours) and Late (>72 hours)
Usually requires prior drug exposure or unsuspected cross-reactivity

114
Q

Approaches to penicillin allergy

A 
Amoxycillin
Skin testing (gold standard)
Penicillin challenge (administer a small dose)
115
Q

Oral penicillin desensitisation protocol

A

Small doses of penicillin given every 15 minutes, patient observed for 30 minutes and then full therapeutic dose given

116
Q

What do most cross-reactivity reactions occur with in terms of penicillin and cephalosporins

A

With 1st generation cephalosporins

117
Q

Delayed drug hypersensitivity

A

Occurs after several days to weeks

Often due to drug-viral interactions

118
Q

DRESS, DIHS and SCAR

A

DRESS- Drug reaction with eosinophilia and systemic symptoms

DIHS- Drug induced hypersensitivity reaction

SCAR- Severe cutaneous adverse reaction

119
Q

Sepsis cascade

A

Toxins produced –> Trigger the innate immune system –> inflammatory cascade –> systemic activation –> organ circulation –> multi-organ failure

120
Q

What has nosocomial causative agents for bacteraemia shifted to?

A

Gram positives (MRSA)

121
Q

Classic signs and symptoms of bacteraemia

A 
Fever
Rigors
Chills
Hypothermia
Delirium, agitation
Acute renal failure
122
Q

What score is used for sepsis

A

SOFA score

123
Q

Sepsis, rapid identification is necessary- what methods are used?

A

MALDI-TOF
FISH
PCR

124
Q

Treatment of sepsis

A

Antibiotics (identify the organism fast, start with broad spectrum)
Drainage of infected fluid
Support- IV fluid, glycaemic control
Glucocorticoids to curb inflammation

125
Q

Toll-like receptors

A

Found on intracellular vesicles of dendritic cells and macrophages.
Activates NFkB to induce pro-inflammatory cytokines and chemotactic factors

126
Q

NOD like receptors

A

Expressed in cytoplasm of the cells routinely exposed to bacteria
Have a NOD protein
Loss of the NOD protein- Crohn’s disease
Also activate NFkB

**NAPL3 is an example

127
Q

Muckel-Wells Familal Cold inflammatory syndrome

A

Two types of periodic fever syndrome

Due to inappropriate expression of NAPL3 inflammasome

128
Q

Corticosteroids

A

Act by increasing the expression of anti-inflammatory genes and suppression of pro-inflammatory genes

129
Q

Complement function

A

Host defence against infection
Links innate to adaptive immune system
Disposal of waste

130
Q

How can acute lupus flare be identified

A

Low C3 and C4

131
Q

Two functions of T-reg cells

A

1) Inhibit T-cell activation

2) T-cell effector function

132
Q

Four different types of angioedema

A

1) Allergy
2) Drug induced
3) Hereditary
4) C1 esterase inhibitor gene

Haem/Immuno (3 decks)

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