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Immune System > Hypersensitivity - 1 > Flashcards

Hypersensitivity - 1 Flashcards

1
Q

Define hypersensitivity

A

the antigen specific immune responses that are either inappropriate or excessive and result in harm to the host

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2
Q

what are the two triggers for hypersensitivity

A

• Hypersensitivity to exogenous antigens
 Non infectious substances (innocuous) - pollen, hair ect
 Infectious microbes
 Drugs (Penicillin)

• Hypersensitivity to intrinsic antigens
 Infectious microbes (mimicry)
 Self antigens (auto-immunity) - this will cause chronic inflammation and host damage

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3
Q

outline the types of hypersensitivity reactions

hint A,B,C,D
what type of antigen is responsible

A
  • Type I or immediate (Allergy) - driven by IgE
  • Environmental non infectious antigens
  • Type II or antiBody mediated - organ specific/at cell surface - IgG or IgM
  • Type III or immune Complexes mediated - systemic - anitbody/antigen complex circulates in blood - IgG or IgM

• Type IV or cell mediated (Delayed)
 Environmental infectious agents and self antigens

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4
Q

what are the two common phases of hypersensitivity reactions

A

Sensitization phase
 First encounter with the antigen. Activation of APCs
and memory effector cells. A previously exposed
individual to the antigen is said to be “sensitized”

• Effector phase
 Pathologic reaction upon re-exposure to the same
antigen and activation of the memory cells of the
adaptive immunity - causing a harmful inflammatory response

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5
Q

Type II hypersensitivity

time frame
antibody type
targets
outcomes ?

A
  • Usually develops within 5-12 hr
  • Involves IgG or IgM antibodies
  • Targets cell bound antigens
  • Exogenous: Blood group antigens, Rhesus D antigens
  • Endogenous: self antigens
  • Induces different outcomes
  • Tissue/cell damage
  • Physiological change
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6
Q

outline the mechanism of a type II reaction

A

the antibody after being sensitised now produces an innapropraite immune response

bind ag/ab complex - release osponins - destroy cells via membrane pore complex and respiratoy burst macrophages

causes damage via 
compliment activaitons -
 cell lysis, 
Neutrophil recuitment - c3a,c5a
Opsonisatin - c3b

Antibody dependent cell cytotoxiticy - NK cells

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7
Q

give examples of type II hypersensitivity reactions

A

• Haemolytic disease of the newborn (HDN)
- Antigen = Rhesus D

• Transfusion reactions
- Antigen= ABO system - if given wrong blood type, ya fucked

  • Autoimmune haemolytic anaemia (warm and cold)
  • Immune thrombocytopenia Purpura
  • Goodpasture’s syndrome (kidney disease)

• Graves’ disease - receptor inappropriate stimulated
− Increased thyroid activity
− Antigen = TSH receptor

• Myasthenia gravis - receptors inappropriate blockade
− Impaired neuromuscular signalling
− Antigen = Acetylcholine receptor

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8
Q

in type II hypersensitivity the immune compliment pathway is activated - recap the compliment pathway to outline the damage it can do

this is not key - just read

A 
innate immunity - 
opsonisation
lysis of pathogens/own cells
chemotaxis
inflammation (damaging)
cell activation

Disposal -
clear immune complexes and apoptotic cells

Adaptive immunity -
Antibody response
Promotes T cell response
Eliminates of self reactive b cells 
enhance immunologic memory
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9
Q

explain the mechanism behind a heamolytic transfusion reaction (type II) a IgM type

A

Haemolytic transfusion reaction an IGM reaction
• Life-threatening condition
• Shock, kidney failure, circulatory collapse,
and death

Immune mechanism
• Incompatibility in the ABO or rhesus D antigens
• Donor RBC destroyed by recipient’s immune system
• RBC lysis induced by type II hypersensitivity involving
by the naturally occurring antibodies (IgM)

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10
Q

outline a type IgG type II immune hypersensitivity reaction

A

heamolytic disease of the newborn

involves rheus D antigen

Rh+ father - Rh- mother
Rh+ fetus (1st baby) - the rh+ antigens enter mum and sensitise - mother produces anti rh antibodies

2nd baby - the rh+ fetus - moms anti rh+ antibodies cross placenta as they are now IgG and damage fetal red blood cells

we give rhoD - blocks the rh+ of 1st baby in mother blood - mother cant detect this and so cannot develop an sensitisation so wont prodice antibodies

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11
Q

what are the thereaputic approches to type II reactions

to help the
tissue/cell damage
and
the physiological change

A

Anti-inflammatory drugs
- Complement activation

• Plasmapheresis - filter blood to remove bad antibodies
- Circulating antibodies and
inflammatory mediators

• Splenectomy
- Opsonisation/Phagocytosis

• Intravenous immunoglobulin (IVIG)
- IgG degradation

  • Correct metabolism
  • Antithyroid drugs in Graves’s disease
  • Replacement therapy
  • Pyridostigmine in Myasthenia gravis
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12
Q

what do we ise plasmapheresis for ?

A

myasthenia gravis
goodpastures syndrome
graves disease

removes the disease causing antibody
only short term relif - allows tissues time to heal

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13
Q

type III hypersensitivity

time
Involves ?
Targets
Result ?

A

Type III hypersensitivity

• Usually develops within 3-8 hr

• Involves immune complexes between
IgG or IgM and antigens

• Targets soluble antigens
 Foreign (Infection)
 Endogenous (self antigens)

• Tissue damage caused by the deposition
of immune complexes in host tissues

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14
Q

Type III hypersensitivity :

key factors affecting Immune complex pathogenesis

A

Complex size (IC is immune complex)
 Small and large size ICs cleared
 Intermediate size ICs - probelm

• Host response
 Low affinity antibody
 Complement deficiency

• Local tissue factors
 Haemodynamic factors
 Physicochemical factors

these lead to intermediate IC deposition in the joints, kidneys, small vessels, Skin
causing multi system disease

these intermediate IC then cause compliment activation which is innapropriate - neutrophils recritued - inflammation and self tissue destruction - release enzymes and ROS

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15
Q

give three examples of type III reactions

A
  • Rheumatoid arthritis (self-antigen)
  • Antigen = Fc portion of IgG (75%) - yup antigen is part of its antibody
  • Articular and extra-articular features
  • Episodes of inflammation/remission
• Poor prognosis factors (not important)
 <30 year-old
 High-titre of RF
 Female
 DR4 allele
 Joint erosions
  • Glomerulonephritis (infectious)
  • Bacterial endocarditis
  • Hepatitis B infection

Systemic lupus erythematosus
• Antigen = Ds-DNA
• Most prevalent immune complexes disease
• Ratio female:male (9:1)
• 40-60% patients with cardiac, respiratory, renal, joint and neurological features
• Repeated miscarriage
• Every patient is unique!!!!!!

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16
Q

give some SLE symptoms

A 
fever, photosensitivity
malar rash
ulcers in mouth 
fatigue
muscle aches
inflammation - pleura and pericardium
joint arthritis
poor circulation to fingers and toes (rauynards)
17
Q

type IV hypersensitivity -

time
involves?
Subtypes?

A

Usually develops within 24-72hr

• Involves lymphocytes and macrophages

  • Different subtypes (clinical outcomes)
  • Contact hypersensitivity
  • Tuberculin hypersensitivity
  • Granulomatous hypersensitivity
18
Q

what is the pathogenisis of type IV hypersensitivity

A

sensitisation phase
APCs- macrophages - present pathogen antigen to TH cells
effector phase - TH1 - activate macrophages - cause damage

19
Q

examples of contact hypersensitivity

A

Contact hypersensitivity
• Occurs 48-72 hr postexposure

  • Epidermal reaction
  • Require endogenous proteins

• Examples
o Nickel
o Poison ivy
o Organic chemicals

20
Q

examples of granulomatous hypersensitivity

A 
Granulomatous hypersensitivity
• Occurs 21-48 days post-exposure
• Tissue damage
• Examples:
o Tuberculosis
o Leprosy (tuberculoid)
o Schistosomiasis
o Sarcoidosis
21
Q

examples of tuberculin hypersensitivity

A

Tuberculin hypersensitivity
Occurs 48-72hr
Dermal reaction

22
Q

Diseases caused by Type IV hypersensitivity to endogenous antigens

A

Pancreatic Islet cells:
o Insulin-dependent diabetes mellitus

• Thyroid gland:
o Hashimoto’s thyroiditis

• Fc portion of IgG:
o Rheumatoid arthritis

23
Q

try explain the difference in mechanism and result in graves and hashimotos

check against lec 1 picture slide - better than writing it up

A

do it

24
Q

outline therapy for Type III and IV hypersensitivity

A 
Anti-inflammatory drugs
• Non-steroidals
• Corticosteroids (oral prednisolone)
• Second drugs as steroid-sparing agents (<10 mg oral steroid)
 Azathioprine
 Mycophenolate mofetil
 Cyclophosphamide

Monoclonal antibodies
• B Cells and T cells
• Cytokine network
• APCs

Immune System (7 decks)

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