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Immune Flashcards

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1
Q

Hypersensitivity

A

antigen sensitive responses that result in inappropriate or excessive immune response, leading to harm to host

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2
Q

exogenous antigens

A

non-infective substances

e.g. peanuts, infectious microbes or drugs e.g. penicillin

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3
Q

intrinsic antigens

A

infectious microbes (mimicry) or self antigens (auto immunity)

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4
Q

properties of all hypersensitivity reactions

A 
sensitisation phase (1st encounter, triggers APC activation + memory cells, no clinical effects)
effector phase (pathological reaction upon re-exposure to antigen, memory cells and AB production, notable clinical manifestation)
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5
Q

Type 1 hypersensitivity

A

allergy
IgE
immediate response (<30 mins), local or systemic

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6
Q

Type 1 hypersensitivity mechanism

A

activation of TH2
activation of IgE
1st exposure - memory cell production
2nd exposure - IgE cross linking -> mast cell degranulation -> mediators released

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7
Q

Type 1 HS

Mediators

A

Tryptase
histamine
leukotrienes
platelet activating factor

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8
Q

Type 1 HS

tryptase

A

remodels CT matrix

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9
Q

type 1 HS

histamine

A

toxic to parasites

increases vascular permeability + smooth muscle contraction

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10
Q

type 1 HS

leukotrienes

A

(C4/D4/E5)

increases smooth muscle contraction, vascular permeability + mucus production

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11
Q

type 1 HS

platelet activating factor

A

attracts leucocytes

increases lipid mediator production (leukotrienes) + activates neutrophils, eosinophils + platelets

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12
Q

type 1 HS

characterised by

A

increased vascular permeability
vasodilation
bronchial constriction

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13
Q

type 1 HS

presentation

A

urticaria - rash (activation of mast cells in epidermis)

angioedema - mast cell activation in deep dermis

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14
Q

anaphylaxis

A 
type 1 HS
systemic mast cell activation
hypotension
CVS collapse
generalised urticaria
angioedema
breathing problems
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15
Q

anaphylaxis treatment

A 
IM adrenaline (epipen)
multiple doses may be required

(reverses peripheral vasodilation, airway obstruction and mast cell activation, alleviates hypotension, reduces oedema, +ve inotropic effect)

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16
Q

allergen desensitisation / immunotherapy

A

increasing doses of allergen extracts over years by injection / sublingual drops
very effective in bee + wasp anaphylaxis

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17
Q

Xoliar

A

anti-IgE monoclonal antibody

to control severe asthma

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18
Q

type 2 HS

A

antibody mediated (IgG/IgM
develops in 5-12 hours
IgG/IgM antibodies target cell bound antigens
exogenous - blood group / Rhesus D antigens
endogenous - self antigens (autoimmunity)

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19
Q

type 2 HS

mechanism

A

IgG/IgM -> tissue damage by complement activation ->
cell lysis ->
opsonisation + neutrophil activation + natural killer cell activation
also cause physiological change by receptor stimulation/blockade

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20
Q

type 2 HS

treatment

A

anti-inflammatory drugs
splenectomy (prevents opsonisation/phagocytosis)
plasmapheresis (filters blood to remove ABs, myasthenia gravis/Graves)
IV immunoglobulin (causes IgG degradation)
replacement therapy (e.g. pyridostigmine inhibits ACh esterase in MG)

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21
Q

Myasthenia gravis

A

autoimmune destruction of nicotinic ACh receptors at NMJ
weakness of skeletal muscle + fatigue
treatment -> pyridostigmine (acetylcholinesterase inhibiotr) with immunosupressants e.g. prednisone

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22
Q

Haemolytic disease of the newborn (HDN)

A

occurs in newborn
Rhesus -ve mother has a 2nd Rhesus +ve baby
IgG antibodies cross placenta to fetus -> haemolysis

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23
Q

HDN

1st vs 2nd baby

A

1st Rh+ baby - sensitisation
maternal and foetal blood don’t mix until birth -> triggers IgG
2nd Rh+ baby - effector phase
ABs present in mother’s blood against Rh+, cross placenta

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24
Q

HDN

treatment

A

RhoGAM (anti-Rhesus D antibody)
given to all Rh- mothers to prevent HDN (after birth of Rh+ child)
binds to + removes Rh+ blood cells in blood stream -> mother doesn’t make ABs to Rh+ cells

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25
blood types
``` +/- = Rhesus D antigen O = no antigen / A + B antibodies A = A antigen / B antibody B = B antigen / A antibody AB = A + B antigens / no antibodies - must have - cannot give the antigen if they have the antibody ```
26
universal blood donor
O-
27
type 3 HS
immune complex (IgG/IgM) develops 3-8 hrs IgG/IgM forms immune complexes with soluble antigens damages tissues by deposition in joints, kidney, small vessels, skin
28
type 3 HS | factors affecting level of damage
complex size - large cleared by opsonisation, small complexes cleared by reticuloendothelial system, intermediate complexes not cleared host response - low affinity antibody / complement deficiency tissue factors - filtration / BP
29
Systemic lupus erythematous
autoimmune inflammation of connective tissue affecting CNS, renal, joints, resp system, CNS high risk of repeated miscarriage
30
opsonisation
makes a foreign cell more susceptible to phagocytosis | molecules chemically modified to have stronger interactions with cell surface receptors on phagocytes + antibodies
31
type 4 HS
``` cell mediated develops in 24-72 hrs (delayed) activation of TH1 sensitises body 2nd exposure - TH1 activates lymphocytes + macrophages to cause: contact hypersensitivity granulomatous hypersensitivity tuberculin hypersensitivity ```
32
contact hypersensitivity
type 4 HS | epidermal reaction to nickel/ivy/chemicals in 24-48 hrs
33
granulomatous hypersensitivity
type 4 HS occurs in 21-48 days post exposure e.g. TB, leprosy, schistosomiasis, sarcoidosis
34
tuberculin hypersensitivity
type 4 HS Mantoux test 48-72 hrs dermal reaction
35
Hashimoto's disease
type 4 HS autoimmune attack of thyroid gland activation of TH1 -> lymphocyte + macrophage damage of thyroid causes hypothyroidism
36
type 3 / 4 HS treatment
NSAIDs corticosteroids - e.g. prednisolone steroid sparing agents - e.g. aziathioprine/mycophenolate mofetil/cyclophosphamide monoclonal antibiotics
37
TB antibiotics
6 months - rifampicin + isoniazid | 2 months - pyrazinamide + ethambutol
38
allergen
any substance stimulating production of IgE or a cellular immune response
39
sensitisation
the production of IgE antibodies (detected by serum IgE assay) after repeated exposure to antigen
40
allergy
a hypersensitivity (type 1) reaction initiated by specific immunological mechanisms IgE mediated - e.g. peanut allergy non-IgE mediated - e.g. milk allergy
41
atopy
tendency to produce IgE antibodies in response to ordinary exposure to potential allergens normally triad of asthma, eczema, allergic rhinitis (hayfever)
42
anaphylaxis
a serious allergic reaction with bronchial, laryngeal and cardiovascular involvement that is rapid in onset and can cause death
43
food allergy subdivisions
IgE mediated - immediate (5-30 min) | non-IgE mediated - delayed onset (hrs-days), occurs in infancy or early childhood
44
food allergy | IgE mediated presentation
skin - pruritis, erythema, acute urticaria, facial angioedema GI - nausea + vomiting resp - wheeze, dysponea CVS (rare) - pallor, drowsiness, hypotension
45
food allergy | IgE mediated foods
``` milk + eggs (can resolve before adulthood) peanuts tree nuts fish shelfish fruit/vegetables pollen food syndrome ```
46
food allergy | non-IgE mediated presentation
skin - pruritis GI - food refusal, abdo pain, diarrhoea/constipation, blood/mucus in stool proctocolitis enterocolitis eosinophilic oesophagitis food protein induced enterocolitis syndrome
47
proctocolitis
non-IgE mediated | mucus + blood stained stools in otherwise asymptomatic infants (breast milk allergy)
48
enterocolitis
non-IgE mediated | multiple GI symptoms (milk/egg/wheat allergy)
49
eosinophilic oesophagitis
non-IgE mediated | oesophageal inflammation and scarring, dysphagia, vomiting, reflux and food impaction (milk/egg/wheat allergy)
50
food protein induced enterocolitis syndrome
non-IgE mediated infants profuse vomiting leading to pallor, lethargy and possibly shock +/- diarrhoea (milk/soya/wheat/rice/meat allergy)
51
food allergy | non-IgE mediated foods
``` milk soya wheat rice oats can resolve by school age ```
52
milk allergy | presentation
always presents by 12 months old, symptoms can be present weeks after ingestion immediate/IgE mediated (40%) - presents with typical allergy symptoms (wheeze, urticaria, diarrhoea, vomiting) but can cause anaphylaxis delayed/non-IgE mediated (60%) - presents with mainly GI symptoms and can be misdiagnosed as GORD/colic
53
milk allergy | treatment
extensive hydrolysed formula (based on milk, can help tolerance) 2nd line - amino acid or soya formula, then at 9-12 months begin milk reintroduction
54
food allergy | diagnosis
serum specific IgE skin prick tests (response of skin mast cells to allergens) oral food challenge (small amounts of allergen ingested in controlled environment) level of IgE in blood or response to skin prick test predicts likelihood of allergy, it DOESN'T correlate with severity of allergy
55
food allergy | management
dietary exclusion allergy action plan 2 x EpiPens (carry)
56
autoimmunity
an immune response against the host due loss of immunological tolerance of self antigen
57
autoimmune disease
disease caused by tissue damage or disturbed physiological responses due to an autoimmune response
58
types of autoimmune disease
organ specific - one or multiple self antigens within one single organ or tissue non organ specific - widely distributed self antigens throughout body
59
hypersensitivity is autoreactive T cell driven
cytotoxic T cells + macrophages
60
types of autoantibody driven
primary autoantibodies secondary autoantibodies IgG transfer
61
primary autoantibodies
rare/pathogenic | e.g. anti-TSHR in Graves / anti-acetylcholine receptor in myasthenia gravis / anti-anti-GBM antibodies in Goodpastures
62
secondary autoantibodies
appear later in disease e.g. anti-nuclear antibodies in SLE / anti-gastric parietal cells in pernicious anaemia / anti-thyroid peroxidase in Hashimotos / anti-RF in rheumatoid arthritis
63
non-organ specific autoimmune diseases
autoimmune haemolytic anaemia - red blood cells antigens rheumatoid arthritis - rheumatoid factor (Fc portion of the IgG antibody) systemic lupus erythematosus (SLE) - double stranded DNA (dsDNA) + other nuclear proteins (histones) Sjogren's syndrome - nuclear antigens (Ro and La)
64
autoimmunity occurs due to
breakdown of central tolerance (thymus fails to delete autoreactive T cells) breakdown of peripheral tolerance (regulatory T cell defects / altered self antigens / impaired immunoglobulin) activation of autoreactive B cells
65
autoimmunity triggered by
genetics (increased risk with MHC variation) hormonal factors = increased risk if female/post puberty infection e.g. strep pyogenes to rheumatic fever drugs e.g. D. pencillamine to myasthenia gravis, SLE + anti GBM
66
autoimmunity | treatments
plasmapheresis - myasthenia gravis / anti GBM / graves disease immunosupressive drugs - e.g. ciclosporin / methotrexate anti-inflammatory drugs replacement therapy surgery - e.g. thyroidectomy / splenectomy monoclonal antibodies e.g. tocilizumab
67
Hashimoto's thyroiditis
type IV hypersensitivity reaction anti-thyroid peroxidase antibodies (secondary autoantibodies) lead to hypothyroidism presentation - fatigue, bradycardia, constipation, weight gain, hoarse voice diagnosis - low T3/T4, high TSH, presence of anti-thyroid peroxidase antibodies treatment - levothyroxine (yearly TSH monitoring)
68
Graves disease
type II hypersensitivity thyroid stimulating immunoglobulin bind to TSH receptor hyperthyroidism presentation - fatigue, weight gain, exophthalmos, heat intolerance diagnosis - high T3/T4, low TSH, presence of thyroid stimulating immunoglobulin (TSI) treatment - antithyroid drugs, plasmapheresis or radioactive iodine/surgery
69
Addison's disease
type II-IV hypersensitivity reaction (involving antibody + cell mediated destruction) steroid-21-hydroxylase antibodies alongside cytotoxic T cells attack adrenal cortex -> adrenal insufficiency presentation - fatigue, hyperpigmentation, depression, sexual dysfunction, hypoglycaemia diagnosis - high ACTH, presence of steroid-21-hydroxylase antibodies treatment - lifelong glucocorticoid replacement (ACTH triggers cortisol release from adrenal cortex)
70
Myasthenia gravis
type II hypersensitivity reaction ACh receptor antibodies attack ACh receptors at NMJ skeletal muscle weakness treatment - acetylcholinesterase inhibitors, immunosupressants
71
Rheumatoid arthritis
type IV hypersensitivity reaction rheumatoid factor antibodies -> inflammation and joint destruction presentation: joint - pain, stiffness, swelling (worse in morning) malaise / weight loss treatment - DMARDs + steroids
72
Systemic lupus erythematosus (SLE)
type III hypersensitivity reaction antibodies to dsDNA and histones -> multisystem disease RF - female, FHx, Afro-carribean>south Asian>caucasian presentation: hands - Raynauds, joint pain + swelling head - alopecia, malor rash trunk - myalgia, pericardial pain, pleuritic chest pain, photosensitivity other - renal abnormalities, neurological symptoms (e.g. depression) treatment - patient education + DMARDs (e.g. hydroxychloroquine) + steroids (e.g. prednisolone) severe cases - IV cyclophosphamide (chemotherapy / suppress immune system)

Clinical Conditions (14 decks)

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