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Immune System > Hypersensitivity > Flashcards

Hypersensitivity Flashcards

1
Q

4 signs of immunodeficiency

A

SPUR

Severe infection - life threatening
Persistent - even with antibiotics
Unusual - organism or location of infection
Recurrent

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2
Q

Causes of immunodeficiency

A 
HIV
Asplenic
Malnutrition - main cause 
Diabetes 
Organ transplant
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3
Q

Hypersensitivity

A

Inappropriate or excessive antigen specific immune response that results in harm to the host

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4
Q

Types of hypersensitivity triggers

A

Exogenous:

  • allergens e.g. pollen, dust
  • infectious microbes - sepsis
  • drugs - Steve -Johnson syndrome

Intrinsic:

  • host antigens (autoimmune)
  • infectious microbes - mimicry
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5
Q

Mimicry

A

The antigen of the pathogen has a similar structure to the host therefore the immune response attacks the pathogen and the host

E.g. rheumatic fever

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6
Q

Which triggers are harder to remove

A

Intrinsic antigens - therefore causes chronic inflammation as harder to eradicate

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7
Q

Type I hypersensitivity

A

Trigger: environmental, non infectious antigens
Mechanism: Immediate allergy response
Antibody: IgE

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8
Q

Type II hypersensitivity reaction

A

Trigger:

  • exogenous - blood group antigens (transfusion), rhesus D antigens (HDN)
  • endogenous - self antigens

Mechanism: antibody mediated immune response

Antibody: IgG or IgM

Target: membrane bound antigens in tissue and cell surfaces

Outcome:

  • tissue or cell damage
  • physiological change e.g Grave’s disease

Time: develops within 5 -12 hours

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9
Q

Type III hypersensitivity reaction

A

Trigger:
Exogenous- infection
Endogenous - self antigen

Mechanisms: immune complexes circulate in the blood and deposit in host tissue causing infection

Antibody: IgG and IgM

Target: soluble antigens

Time: 3-8hrs

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10
Q

Type IV hypersensitivity infection

A

Trigger: environmental infectious agents and self antigens

Mechanism: cell mediated delayed response

Antibody: are involved but predominantly lymphocytes and macrophages

Time: 1-3 days

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11
Q

Sensitisation phase of hypersensitivity

A

First encounter with the antigen

Activated antigen presenting cells and memory effector cells

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12
Q

Effector phase

A

Re-exposure to the same antigen
Causes a pathological reaction
Activates memory cells of the adaptive immune response

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13
Q

Type II hypersensitivity mechanism

A
  1. Antibody binds to antigens on the cell surface
  2. Activates the compliment cascade
    - cell lysis by macrophages
    - neutrophil activation and recruitment - C3a and C5a
    - opsonisation - C3b
  3. Also activate antibody dependent cell cytotoxicity by NK cells
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14
Q

Diseases caused by Type II hypersensitivity reactions

A

Autoimmune haemolytic anaemia
Immune thrombocytopenia purpura
Goodpasture’s syndrome - nephritic syndrome

Grave’s disease - hyperthyroidism as antibody stimulates the TSH receptor continuously

Myasthenia gravis - antibodies against acetylcholine receptors, impairs neuromuscular signalling causing paralysis and weakness

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15
Q

Difference between IgM and IgG

A

IgM antibodies are larger

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16
Q

Haemolytic transfusion reaction consequences

A

Life threatening
Can cause shock
Kidney failure

17
Q

Immune mechanism of haemolytic transfusion reaction

A

Incompatibility in the ABO or rhesus D antigens
Therefore donor RBCs are destroyed by recipient’s immune response
Caused by IgM

18
Q

Blood types and antibodies

A

A - anti B
B - anti A
AB - none
O - anti A and anti B

Rhesus +ve - no antibodies against rhesus D antigens
Rhesus -ve - antibodies against rhesus D antigens

19
Q

Haemolytic disease of the newborn (HDN)

A

Father - rhesus positive
Mother - rhesus negative - has rhesus D antibodies
Child - rhesus positive - has Rhesus D antigens

  1. Some foetal RBCs cross the placenta and enter the maternal circulation in the third trimester of the first trimester. Therefore the mother becomes sensitised and produces IgG
  2. In subsequent pregnancies as already sensitised, IgG crosses tube placenta and binds to the foetal rhesus D antigens causing haemolytic disease of the newborn
20
Q

How to treat haemolytic disease of the newborn

A

Give Rhogam to the mother to prevent sensitisation

Rhogam contains antibodies against rhesus D antigens therefore the mother does not need to create its own IgG and become sensitised

21
Q

Treatment of type II hypersensitivity reactions

A

Anti- inflammatory drugs:

  • prevent complement activation
  • cytotoxic and can cause serious side effects

Plasmapheresis:

  • separate platelets and haematocrit
  • remove the inappropriate antibodies and inflammatory mediators
  • introduce plasma back into the circulation with supportive fluid

Splenectomy - reduces opsonisation and phagocytosis

Intravenous immunoglobulin (IVIG)
- igG degradation

Grave’s - Anti thyroid drugs or thyroidectomy
Myasthenia gravis - pyridostigmine - increases Ach in the neuromuscular junction

22
Q

Key factors affecting type III hypersensitivity

A

Complex size:

  • small and large immune complexes are cleared
  • intermediate immune complexes are difficult to clear

Host response:

  • low affinity antibody
  • complement deficiency - can cause immune complex type III hypersensitivity disease as less immune complexes reach the liver to be degraded

Local tissue factor:

  • haemodynamic factors
  • physio chemical factors
23
Q

Where do immune complexes deposit usually

A

Joints
Kidney
Small vessels - where birfucates
Skin

  • multisystem disease
24
Q

Immune complexes

A

Small IC - cleared by monocytes and macrophages
Large IC - cleared once opsonised

Intermediate IC

  • deposits in tissues and activates the complement cascade
  • causes neutrophil chemotaxis - C5a
  • neutrophils adhere to the cell surface and degranulate releasing cytotoxic substances e.g ROS
25
Q

Type III hypersensitivity reaction diseases

A 
Rheumatoid arthritis 
Glomerulonephritis 
Bacterial endocarditis 
Hepatitis B 
Systemic lupus erythematous
26
Q

Rheumatoid arthritis

A

Autoimmune disease against the Fc portion of IgG

Causes symmetrical, peripheral inflammation of the joints

27
Q

Who has a poor prognosis of rheumatoid arthritis?

A 
Under 30s
High titres of rheumatoid factor 
Female
DR4 allele
Joint erosions
28
Q

Glomerulonephritis

A
  1. Sustained and prolonged production of the microbe causes immune complex formation
  2. Deposited in the kidney causing glomerulonephritis
29
Q

SLE

A

Most prevalent immune complex disease
Antigen: Double stranded DNA
Every patient has a different presentation as a variety of systemic effects

30
Q

SLE ratio of females to males

A

Females: male = 9:1

31
Q

Sub types of type IV hypersensitivity

A

Contact hypersensitivity
Tuberculin hypersensitivity
Granulomatous hypersensitivity

32
Q

Type IV hypersensitivity mechanism

A

Sensitisation phase:

  1. Antigen presenting cells e.g. macrophages trigger TH1
  2. TH1 stimulates Cd8 and cytotoxic T lymphocytes

Effector phase:

  1. TH1 remember the pathogen antigen which triggered inflammatory mediators e.g IL2,3 and 8 and activate macrophages
  2. Causes a clinical manifestation and removes pathogen
33
Q

Contact hypersensitivity

A

Caused by exogenous antigens e.g.

  • nickel
  • poison ivy
  • organic chemicals

Occurs 2 - 3 days after exposure
Epidermal reaction
Requires endogenous proteins to stimulate TH1

34
Q

Granulomatous hypersensitivity

A

21 -48 days post exposure
Causes tissue damage

Examples:

  • tuberculosis
  • tuberculoid leprosy
  • schistosomiasis
  • sarcoidosis
35
Q

Anti TNF

A

Potent
May rupture granuloma
Therefore test for TB first

36
Q

Diseases caused by type IV hypersensitivity endogenous antigens

A

Pancreatic islet cells:
- insulin dependent diabetes mellitus

Thyroid gland:
- Hashimoto’s thyroiditis - hypothyroidism

FC portion of IgG:
- rheumatoid arthritis

37
Q

Anti- inflammatory drugs

A
  • NSAIDs - nephrotoxic
  • corticosteroids - oral prednisone - inhibits immune response
  • steroid sparing drugs:
    > azathioprine
    > mycophenolate mofetil
    > cyclophosphamide

Immune System (6 decks)

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