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IMMUNOLOGY II > LECTURE 1 (Hypersensitivity) > Flashcards

LECTURE 1 (Hypersensitivity) Flashcards

1
Q

What is Hypersensitivity?

A

An immune response that causes disease and is exaggerated or inappropriate

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2
Q

What do all hypersensitivities have in common?

A
  • First contact with antigen “sensitises” the host (generation of immune response + formation of antibodies and memory cells)
  • Second contact -> hypersensitivity (patients develop symptoms from overreaction of immune response)
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3
Q

What are the four types of hypersensitivity reactions?

A

TYPE I, II, III and IV

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4
Q

Describe the TYPE I hypersensitivity reaction

A

also known as “allergies”

  • Immediate reaction to an antigen (occur within minutes)
  • Patients have pre-formed IgE antibodies (from primary exposure)
  • Antibodies are bound to MAST CELLS -> antigen binds and cross links IgE antibodies -> Mast cell degranulation (releases contents into tissues -> symptoms)
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5
Q

Describe TYPE I hypersensitivity immunology

A
  • Susceptible individuals make IgE to antigens whereas normal people do not (IgG does NOT trigger hypersensitivity response)
  • IgE results from B cell class switching driven by Th2 cells (humour response)
  • IL-4 is a KEY CYTOKINE for IgE production
  • IgE does not lead to a complement reaction
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6
Q

What are the TYPE I symptoms?

A
  • Skin = Urticaria (hives)
  • Respiratory tract = Rhinitis/wheezing (asthma)
  • Eyes = Conjunctivitis (itchy, red & watery)
  • GI tract = diarrhoea
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7
Q

What is Anaphylaxis?

A

A systemic type I hypersensitivity reaction

SYMPTOMS:
- Itching, diffuse hives/erythema
- Respiratory distress from bronchoconstriction
- Hoarseness (caused by laryngeal swelling/edema)
- Vomiting, cramps, diarrhoea
- Shock and death

TREATMENT:
- Epinephrine (vasoconstrict -> increase BP & dilate bronchioles)

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8
Q

What is Atopy?

A

A genetic tendency to localised hypersensitivity developing symptoms such as Urticaria (hives), rhinitis and asthma

Additional information: There is usually a positive family history of a similar reaction

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9
Q

What are some TYPE I examples?

A
  • Asthma
  • Penicillin drug allergy
  • Seasonal allergies (allergic rhinitis)
  • Allergic conjunctivitis
  • Peanut/shellfish allergy
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10
Q

What is the difference between TYPE I Early symptoms and Late symptoms?

A

EARLY SYMPTOMS
- occur within minutes
- caused by degranulation of cells -> release pre-formed mediators (histamine)
- caused by synthesis/release of leukotrienes & prostaglandins
- edema, redness & itching

LATE SYMPTOMS
- 6 hours later
- synthesis/release of cytokines -> leads to influx of inflammatory cells (neutrophils, eosinophils)
- induration of skin (area of hardness in skin)

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11
Q

What are the Type I mediators?

A

HISTAMINE
- vasodilation (warmth)
- increased permeability of venules (swelling)
- smooth muscle contraction (bronchospasm)

LEUKOTRIENES, PROSTAGLANDINS & THROMBOXANES
- derived from arachidonic acid
- produced in early & late phase of hypersensitivity reactions

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12
Q

How are Eicosanoids formed?

A

1) Lipids (cell membranes) are acted on by PHOSPHOLIPASE A2 to form ARACHIDONIC ACID
2) Arachidonic acid is acted on by LIPOXYGENASE to form LEUKOTRIENES + acted on by CYCLOOXYGENASE to form THROMBOXANES & PROSTAGLANDINS

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13
Q

What are the effects of PGE2 (prostaglandin)?

A
  • Redness (caused by vasodilation)
  • Edema (increasing vascular permeability)
  • Fever (increasing set temp in hypothalamus)
  • Pain (sensitise nerves)
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14
Q

What are the effects of PGD2 (prostaglandin)?

A
  • Bronchoconstriction
  • Draws Eosinophils into sites of TYPE I hypersensitivity reactions
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15
Q

What are the effects of LTC4/LTD4 (leukotrienes)?

A
  • Vasoconstriction
  • Bronchoconstriction
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16
Q

What are the effects of LTB4 (leukotrienes)?

A

Draws in neutrophils and eosinophils to sites of TYPE I hypersensitivity reactions

17
Q

What is ECF-A (Eosinophil chemotactic factor of anaphylaxis)?

A
  • TYPE I mediator
  • preformed in mast cells
  • attracts eosinophils in allergic reactions (some are pro-inflammatory)
18
Q

What are some other TYPE I mediators?

A
  • Serotonin (preformed in mast cells -> causes vasodilation)
  • Platelet activating factors (causes bronchoconstriction)
  • Natural proteases (e.g chymase, tryptase) released by mast cells that dissolve proteins
  • Heparin (released by mast cells -> anticoagulant)
19
Q

Describe allergy testing for IgE

A

Allergy testing for IgE to an allergen is done to see if a patient is sensitised to a particular substance

HOW IT WORKS
- pinprick/puncture of skin
- intradermal injection
POSITIVE RESPONSE: wheal formation (red, swollen mark)

20
Q

Describe densitisation for IgE

A

Patients are desensitised to allergens if their response is dangerous or life threatening (sometimes done when pt needs drugs they really need for a condition)

HOW IT WORKS
1) gradually administer increasing amounts of allergen
2) Response changes IgE -> IgG
3) IgG antibodies can “block” mediator release by mast cells (“modified Th2 response”)

21
Q

Describe the TYPE II hypersensitivity reactions

A

also known as “auto-immune reactions”

  • Antibodies (IgG/IgM) are directed against tissue antigens and bind to normal structures
  • Three mechanisms of tissue/cell damage (Phagocytosis, Complement-mediated lysis & Antibody-dependent cytotoxicity)
22
Q

Describe the three mechanisms of tissue/cell damage in TYPE II reactions

A
  • Phagocytosis (antibodies bind to cells -> cells consumed by phagocytosis -> phagocytes recognise Fc receptors on IgG antibodies or C3b receptors from complement pathway)
  • Complement cascade (IgG or IgM can trigger CLASSIC COMPLEMENT CASCADE -> form MAC -> cell death)
  • ADCC (natural killer cells bind Fc portion of IgG -> release contents -> destroy cells and tissues)
23
Q

What are some TYPE II samples?

A
  • Rheumatic fever (strep antibodies cross-react with cardiac myocytes -> myocardial damage/damage to heart valves)
  • Exposure to wrong blood type (RBC lysis by circulating IgG -> can cause ERYTHROBLASTOSIS FETALIS)
  • Autoimmune haemolytic anemia (methyldopa and penicillin = drugs bind to surface of RBCs, mycoplasma pneumonia = induces RBC antibodies)
  • Pemphigus vulgaris = antibodies against desmosomes in epidermis
  • Goodpasture syndrome (nephritic syndrome + pulmonary haemorrhage caused by antibodies against TYPE IV collagen)
  • Myasthenia gravis (antibodies against ACh receptors
24
Q

Describe TYPE III hypersensitivity reactions

A

Occur when Antigen-antibody (usually with IgG) complexes form -> activates complement cascade -> tissue/cell damage

TWO WAYS IN WHICH REACTIONS OCCUR
- Serum sickness (generalised)
- Arthus reaction (localised)

25
Q

What is the difference between TYPE II and TYPE III hypersensitivity reactions?

A

TYPE II = antibodies directly attack tissues or cells
TYPE III = antibodies bind to small antigens and then deposit in the tissues as an antibody-antigen complex

26
Q

What is Serum sickness?

A

A form of type III hypersensitivity reaction

  • Immune complexes in plasma cause SYSTEMIC DISEASE (usually IgG/IgM since complement activators)
  • Immune complexes deposit in various tissues (skin, kidneys and joints)
  • Once deposited, trigger an immune response by complement activation -> trigger activation of macrophages and neutrophils (via Fc receptors)
27
Q

What are the symptoms of Serum sickness?

A
  • Urticaria or palpable purpura (from complex deposition on skin)
  • Low serum complement levels (immune complexes consume complement proteins)
  • Elevated sedimentation rate (from inflammation)
  • Diffuse lymphadenopathy
  • Acute glomerulonephritis (from complex deposition in kidneys)
  • Lupus
28
Q

What are some examples of “classic serum sickness”?

A
  • Rabies/tetanus anti-toxin
  • Rarely penicillin (drug acts as a “hapten” -> a small molecule that elicits an immune response -> antibodies can be formed and bind to penicillin and deposit in tissues)
  • Monoclonal antibodies (rituximab, infliximab)
29
Q

What is Arthus reaction?

A

A form of type III hypersensitivity reaction

  • form antigen-antibody complexes in local tissue (usually on skin)
  • Injection of antigen -> preformed antibodies in plasma/tissue will bind the antigen and form immune complexes LOCALLY
  • Local immune complexes form 4-10 hours after injection -> once bound, complement activation, oedema and necrosis occur
  • Can identify using IMMUNOFLUORESCENT STAINING (antibodies + complement in vessel wall -> deposited in the tissue and are causing the reaction)
30
Q

What is the difference between TYPE I hypersensitivity reaction and Arthus reaction?

A

TYPE I reactions = occur within minutes and are caused by Mast cells and IgE antibodies

Arthur reactions = takes a few hours for immune complexes to bind -> once bound, complement activation, oedema and necrosis occur

31
Q

Why is Arthus reaction faster than Serum sickness?

A

Since in Arthus reaction, antibodies are already present (antibodies made during the previous injections of the antigen)

32
Q

What are some examples of Arthus reaction?

A
  • Reported with skin injections (e.g Tetanus, Hep B vaccines) -> exposure of antigen to already existing antibodies might cause binding at site of skin injection -> swelling, redness at site hours after injection
  • Hypersensitivity pneuminitis (patients with “farmer’s lung” have circulating antibodies -> inhale environmental antigens -> bind to tissue of lung -> cause Arthus reaction)
33
Q

Describe TYPE IV hypersensitivity reactions

A
  • Cell-mediated reaction
  • Does not involve any antibodies at all
  • Memory T-cell immune response
34
Q

Describe an example of TYPE IV reaction

A

PPD test (for tuberculosis)

Administer a small amount of Tuberculin protein under the skin -> patients previously exposed to Tuberculosis will have memory T-cells that can recognise the Tuberculin antigen -> antigen presented by Antigen presenting cells (MHC II) where memory CD4 T-cells can recognise and respond -> Th1 response (cell-mediated response) -> IFN-gamma secreted (activate macrophages) + IL-12 secreted from macrophages which stimulates Th1 cells -> redness + induration 24 to 72 hours later

35
Q

TYPE IV hypersensitivity reactions are similar to what?

A

Immune responses to many pathogens (e.g mycobacteria, fungi)

36
Q

Which diseases are examples of TYPE IV hypersensitivity reactions?

A
  • Contact dermatitis (e.g poison ivy) = chemicals attach to skin cells -> CD8 T-cells recognise those cells and attack skin cells -> erythema and itching -> occurs 12 to 48 hours after exposure
  • Multiple Sclerosis (type IV reactions to myelin basic protein lead to demyelination)

IMMUNOLOGY II (14 decks)

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