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CLS > Immunity > Flashcards

Immunity Flashcards

1
Q

What types of hypersensitivity are there

A

Type 1 - igE antibodies
Type 2 -igG
Type 3 -immune complex formation
Type 4 -cell mediated (delayed)

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2
Q

Describe type 1 hypersensitivity

A

Atopic allergy

Mast cells activated (de granulation and release of mediators) by binding of 2 igE on allergens

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3
Q

What is the mechanism behind type 1 hypersensitivity

A

Antigen presenting cell uptake and present via MHC class ii
TH2 cell interact with CD4 T cell via cytokines
T cell produces igE antibodies
They bind to the antigen on second exposure and activate the mast cell

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4
Q

What do the mediators released by mast cells do

A

Pharmacological- blood vessels, airways, cell infiltration and accumulation
Clinical effects- hay fever, asthma, eczema, anaphylaxis

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5
Q

Define atopic

A

Allergy due to hypersensitivity- Have higher evens of igE in serum- genetically predisposed

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6
Q

What do mast cells release

A

Preformed mediators- histamine, heparin and tryptase
Newly formed- arachiodonic acid (mins)
Prostaglandins, leukotrienes, cytokines (hours)

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7
Q

What are the types of hypersensitivity in terms as what things are recognised

A

Foreign- self damaging-allergy/hypersensitivity

Self- self damaging-autoimmunity/ hypersensitivity

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8
Q

Name five type 1 hypersensitivity responses and what is the response in each

A

Systemic anaphylaxis- oedema, tracheal occlusion and increased vascular permeability, circulatory collapse, death
Acute urticaria- local increase in blood flow increased vascular permeability, itch
Allergic rhinitis- oedema of nasal muscosa and irritation
Asthma- bronchial construction and increased mucus production, airway inflammation
Food allergy- vomiting diarrhoea, pruritis, urticaria, anaphylaxis

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9
Q

What are be staged reactions to skin tests

A

Immediate- igE
Immediate and late- igE and T cells
Delayed- TH1 cells
Eczematous- igE and TH2 cells

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10
Q

What is type 2 hypersensitivity

A

Cell of membrane reactive- igG igA and igM - neutrophils and complement

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11
Q

Name some type 2 allergies

A

Allergic haemolytic anaemia blood transfusion reactions

Haemolytic disease of the newborn

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12
Q

Name some type 2 autoimmunities

A 
Autoimmune he's militia anaemia
Autoimmune thrombocytopenia
Pemphigold 
Good pastures disease
Myasthenia gravis
Graves' disease
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13
Q

Explain rhesus haemolytic disease of the newborn

A

Rhesus d negative mother has a rhesus d positive fetus
Rhesus d antigens mix with mothers blood ( at birth?)
Mother makes igG antibodies against them
New rhesus d postitive baby, igG antibodies cross the placenta and attack babies red blood cells

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14
Q

How is rhesus haemolytic disease avoided

A

Mother given rhesus prophylaxis- anti- d antibodies

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15
Q

What is type 3 hypersensitivity

A

Antibody mediated- ineffective removal of immune complexes

Involved igG igA igM, neutrophils and complement

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16
Q

Give examples of type 3 allergy and type 3 autoimmunity

A

Allergy- dermatitis, herpetoformis, allergic alveolitis

Autoimmunity- systemic lupus, erythematosus, rheumatoid arthritis

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17
Q

Explain normal removal of immune complexes

A

Usually removed via liver ( hepatic macrophages) too many produced- not removed or can become lodged in parts of the body

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18
Q

What is type 4 hypersensitivity

A 
Cell mediated 
Involved T cells 
Th cells
Macrophages
Cytotoxic T cells
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19
Q

Give examples of type 4 allergy and type 4 autoimmunity

A

Allergy- contact dermatitis, acute graft rejection, Tb, leprosy
Autoimmunity- thyroiditis, adrenalitis (addisons) gastritis ( pernicious aneamia) type1 diabetes melluitis

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20
Q

What do macrophages become in type 4 hypersensitivity

A

Multincleated giant cells

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21
Q

What are the three types of leprosy

A

Tuberculoid, borderline and lepromatous

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22
Q

Define autoimmunity

A

Damage to self tissues triggered by an adaptive immune response to the bodies own tissue components ( auto antigens)

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23
Q

How can autoimmunity be categorised

A

Organ specific eg MS

Systemic disease eg rheumatoid arthritis

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24
Q

What hypersensitivities can be autoimmune

A

2 3 and 4

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25
Q

What is Graves’ disease

A

Type 2 hypersensitivity autoimmunity.
Autoimmune B cells make Autoantibodies that stimulate TSH receptors- overstimulation of thyroid follicular cells without any negative feedback control
= hyperthyroidism, goitre, weight loss, nervousness, palpitations and irritable

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26
Q

What is the danger of someone with Graves’ disease when they are pregnant
What is the treatment

A

Anti-TSHR antibodies cross the placenta and cause the newborn to also suffer from Graves’ disease
Anti-TSHR antibodies cures the disease

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27
Q

What is graves ophthalmopathy

A

Inflammation of connective tissue behind eyes= swelling
Production of mucopolysaccharides
Protrusion of eyeballs

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28
Q

What is pre-tibial myxoedema

A

Swelling of ankles

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29
Q

What is Hashimoto’s thyroiditis

A

Autoimmune destruction of thyroid tissue
Massive infiltration of lymphocytes to the thyroid
Causes hypothyroidism- weight gain/depression/fatigue

30
Q

How can you detect Hashimoto’s thyroiditis

A

Autoantibodies produced to thyroid per oxidase and thyroglobulin, can be detected in blood/serum samples

31
Q

Explain pernicious anaemia

A

Autoimmune destruction of gastric parietal cells type 4 autoimmunity.
Production of autoantibodies for intrinsic factor IF. Stops IF binding to vitamin b12 in ileum so can’t absorb.
B12 needed for nucleotide synthesis so no DNA = no replication especially important in fast replicating cells ie RBC

32
Q

Explain type 1 diabetes

A

Insulting producing beta cells in islets of langerhans attacked and destroyed by autoreactive T cells. Leave alpha and gamma in tact

33
Q

Explain myasthenia gravis

A

(Type 2) Autoantibodies inhibit Ach receptors expressed on muscle cells ( at neuromuscular junction) blocks binding and induces internalisation and degradation of receptors

34
Q

Explain autoimmune haemolytic anaemia

A

Autoantibodies (type 2) opsonise erythrocytes, activating complement and flagging for destruction by phagocytes

35
Q

What is good pastures disease

A

Autoantibodies ( type 2) bind to glomerular basement membranes, activate complement and neutrophils = tissue damage and eventually kidney failure
Can also be to alveoli basement membrane

36
Q

What is pemphigus vulgaris

A

Autoantibodies bind to intracellular substance of epidermis of skin= blistering skin reaction

37
Q

What is systemic lupus erythematosus

A

Immune complexes of DNA/ anti-DNA in blood are deposited in the glomeruli= irregular staining pattern
Tissue damage in the kidney glomeruli, skin, joints, CNS

38
Q

explain rheumatoid arthritis

A

Immune complexes formed by rheumatoid factors

IgM and igG autoantibodies - joint damage

39
Q

What is the classification of immune deficiency

A

Primary- inherited or congenital
Secondary- congenital or acquired
Component - adaptive (antibody/cell mediated/ combined)
Innate (complement/phagocytes/NK cells)

40
Q

What are the different infections that can characterise immunodeficiency

A

Fungi and viruses- T cells
Bacteria - antibody, classical complement, terminal complement and phagocytes
Abscesses - phagocytes

41
Q

Which antibody defect ( primary or secondary) is more common in adults

A

Primary

42
Q

Which antibody deficiency (1• or 2• ) is lymphoproliferative

A

Secondary

43
Q

Which antibody deficiency is underdiagnosed

A

Primary

44
Q

What can antibody defects be secondary to

A

Lymphoproliferative
Renal/gut loss of igG
Malnutrition
Drugs

45
Q

What are the primary causes of antibody deficiency

A 
Hyper igM syndrome 
X limbed agammaglobulinaemia 
Common variable immune deficiency 
IgA deficiency 
IgG deficiency
46
Q

What is common with and antibody deficiency

A 
Bacterial infections ( ears, sinus, chest) 
Giardia gut infection
Permanent damage esp. If diagnosis is delayed
47
Q

What are other complications of antibody deficiency

A

Enteroviral infection
malignancy
Autoimmunity

48
Q

What is Di George syndrome

A

T cell defect, primary immunodeficiency
Defective development of thymus and other tissue in face/neck/chest due to defective 3rd and 4th pharyngeal arches
= fungal and viral infections

49
Q

What is AIDS defined as

A

HIV with appearance of opportunistic infections

50
Q

How does HIV infect T cells

A

Bind to cd4 molecules

51
Q

What are the early symptoms of HIV

A

Persistent generalised lymphadenopathy

52
Q

How is HIV transmitted

A

Sexual/ blood contact

53
Q

How is HIV diagnosed

A

Detection of anti-HIV antibodies in serum

54
Q

What is sever combined immunodeficiency

A

Primary immunodeficiency inherited stem cell defect lack of function of b and T cells
Susceptible to essentially all types of infectious agents
Fatal is untreated ( bone marrow transplant)

55
Q

What causes primary neutrophil defects

A

Kostmanns, cyclical neutropenia

56
Q

What causes secondary neutrophil defects

A

Leukaemia
Cancer chemotherapy
Infections

57
Q

What is leucocyte adages ion define u due to

A

Lack of production of integrins adhesion molecules

58
Q

What is chronic granulomatous disease

A

Defects in enzymes involved in generation of reactive oxygen species ( needed to kill phagocytosed infection)

59
Q

What is recurrent neisserial infections a feature of

A

Complement defieciency - alternative and membrane attack pathways

60
Q

What are immunodeficiencies secondary to

A

Iatrogenic ( immunosuppressive treatment or radiation or surgery)
Malignancies ( leukaemia, lymphoma, myeloma)
Some infections- HIV, chronic malaria, measels
Malnutrition
Protein losing diseases
Chronic diseases ( renal)
Burns

61
Q

What is acute appendicitis caused by

A

Lumen obstruction and bacterial infection

62
Q

What does acute appendicitis spread to become when it perforates

A

General peritonitis

63
Q

What are some outcomes of lobar pneumonia

A 
Death in acute phase 
Death during resolution 
Successful resolution
Abscess formation
Organisation of exudate- lung fibrosis
64
Q

What can neisserial infection cause

A

Meningitis
Septicaemia
Pneumonia
Arthritis

65
Q

What is an acute superficial folliculitis

A

Zits

66
Q

What are the signs of inflammation

A

Calor- heat
Pain- dolor
Rubor- redness
Tumor- swelling

67
Q

What is osteomyelitis

A

Come infection almost always causes by bacteria and can destroy the bone

68
Q

What do a high pulse and bp often indicate

A

Infection

69
Q

What types of TB are there

A

Primary
Miliary ( spread in blood)
fibrocaseous
Tuberculosis bronchopneumonia

70
Q

What are five causes of granulomatous infection

A

Mycobacterium infection
Insoluble organic material ( endogenous/ exogenous)
Insoluble inorganic material (endogenous (urate) exogenous (silica))
Sarcoidosis
Fungal infection

CLS (12 decks)

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