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Immunology > Hypersensitivity Clinical Correlations > Flashcards

Hypersensitivity Clinical Correlations Flashcards

1
Q

Hypersensitivity reactions

A

Excessive, undesirable reaction produced by the normal immune system

  • exaggerated and harmful response
  • mild to life threatening
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2
Q

Sensitizaiton

A

Initial exposure to an antigen

- subsequent exposure to the same antigen results in hypersensitivity

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3
Q

Type 1

A

Immediate!

  • minor symptoms to death
  • present 15-30 min after antigen exposure
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4
Q

Type 1 - phase 1

A

Sensitization

  • antigens encountered at mucosal and cutaneous surfaces
  • IgE production to inital encounter
  • asymptomatic
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5
Q

Type 1 - phase 1 example

A 
DC within the bronchial epithelium encounters an inhaled antigen
--> DC travels to lymph node to signal Th2 --> IL-4, 13 induces a humoral response --> B cells are directed to a class switch to IgE production --> IgE binds to tissue mast cells, where they reside at mucosal/cutaneous surfaces at the original site of encounter = sensitization
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6
Q

Type 1 - phase 1 summary

A
  • mediated by IgE

- primary cellular component is the mast cell

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7
Q

Type 1 - phase 2

A

Re-exposure

  • exposure to the same allergen = cross linking (occurs when antigen is bound by 2 or more IgE)
  • initiates signal pathway in mast cells and triggers degranulation
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8
Q

Mast cell degranulation

A

Release of cytokines (IL-4,5,6 and inflammatory mediators)

- results in pruritus, bronchoconstriction, and vasodilation

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9
Q

Type 1 active substances

A
  • histamine!
  • heparin
  • leukotrienes
  • prostaglandin D2
  • platelet activating factor
  • eosinophil chemotactic factor
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10
Q

Clinical consequence of mast cell degranulation

A

Immediate hypersensitivity (occurs within 15-20 min)

  • vasodilation/vascular permeability = tissue edema
  • bronchoconstriction (smooth muscle contraction)
  • interaction with local nerves = pruritis
  • platelet aggregation
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11
Q

Type 1 - late phase

A

Occurs 4-24 hrs after antigen exposure

- recruitment of eosinophils and macrophages into the tissue

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12
Q

Presence of ______ is the hallmark of type 1 hypersensitivity

A

Eosinophils!

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13
Q

Majority of type 1 reactions are ______

A

Localized

  • skin: dermatitis
  • respiratory: asthma, allergic rhinitis
  • intestinal tract: food allergy
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14
Q

Type 1 - systemic reactions

A

Often involve drugs or insect stings

- causes anaphylactic reaction

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15
Q

Anaphylactic reaction signs

A
  • bronchoconstriction and dyspnea
  • hypotension
  • tachycardia
  • vomiting/diarrhea
  • dizziness
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16
Q

Anaphylactic reaction treatment

A
  • epinephrine
  • fluids
  • oxygen
  • antihistamines
  • steroids
  • supportive care
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17
Q

Feline Asthma

A

Lower airway disease, limiting airflow due to reduced airway diameter

  • airway inflammation
  • accumulating airway mucus
  • airway smooth muscle contraction
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18
Q

What 2 cells play an important role in feline asthma?

A

Interactions between T cells and eosinophils

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19
Q

Feline asthma treatment

A

Need to address inflammation and bronchoconstriction

- steroids and bronchodilators

20
Q

Adverse vaccine reactions

A

Due to IgE mediated degranulation of mast cells located in the skin = histamine and leukotriene release to deeper skin layers
- causes angioedema, urticaria, and pruritis

21
Q

Type 2 hypersensitivity

A

Aka cytotoxic or antibody mediated hypersensitivity

  • affects variety of organs
  • involves destruction of a target cell and the sensitization is to an antigen displayed on the surface of that target cell
22
Q

Type 2 - antibody production

A

Produced to endogenous antigens or exogenous substances (haptens) which attach to cell membranes and cause subsequent tissue damage
- mediated by IgG or IgM (with or without complement involvement)

23
Q

Type 2 - pathophysiology

A

Rapid destruction occurs via activation of classical complement pathway and formation of MAC
- takes longer when target cell destruction involves NK cell destruction or macrophage phagocytosis of the antibody dependent cell mediated pathway

24
Q

Type 2 - examples

A
  • IMHA
  • transfusion reactions
  • myasthenia gravis
  • pemphigus
25
Q

IMHA

A

Antibodies coat RBC and induce destruction

  • leads to severe damage by antibodies and complement = intravascular hemolysis
  • macrophages recognize Fc portion of antibody and remove the targeted RBC
26
Q

Intravascular hemolysis leads to _____ and ______

A

Hemoglobinemia and hemoglobinuria

- build up of hemoglobin due to RBC destruction

27
Q

Extravascular hemolysis

A

Destruction of RBCs by spleen/liver macrophages

28
Q

What is the hallmark of IMHA?

A

Autoagglutination

29
Q

How do you treat IMHA?

A

Immunosuppressive medications

30
Q

Blood transfusion in cats

A

Type A
- no or low levels of pre-formed anti-B alloantibodies
Type B
- high levels of pre-formed anti-A alloantibodies

31
Q

Type A cat receiving type B blood

A

Minor risk, but possible for transfusion reactions

32
Q

Type B cat receiving type A blood

A

Much greater risk for transfusion reaction

33
Q

Myasthenia gravis

A

Generalized muscle weakness that worsens with exercise, and megaesophagus

  • antibodies against Ach receptors
  • treat with cholinesterase inhibitors
34
Q

Pemphigus foliaceus

A

Most common autoimmune disease of dogs

  • causes lethargy, febrile, lymphadenopathy
  • widespread distribution over head, face, ears
  • treat with immunosuppressive steroids
35
Q

Type 3 hypersensitivity

A

Immune complex hypersensitivity

- formation of soluble immune complexes in the blood and subsequent tissue deposition and tissue damage

36
Q

Type 3 - pathophysiology

A

Excessive production of antigen specific IgG antibody with sensitization
- re - exposure causes antibody binding to antigen in circulation and formation of antigen/antibody complexes

37
Q

Immune complexes are comprised of

A

Antibodies, antigens, platelets, and neutrophils

38
Q

Type 3 - signs

A

Occur once immune complexes are deposited into tissues

  • inflammatory response
  • complement activation
  • recruitment of inflammatory cells to site of inflammation (neutrophils and macrophages)
39
Q

Where do the immune complexes deposit?

A

Within the walls of the capillaries of differing tissues

  • kidneys
  • skin
  • joints
40
Q

Vasculitis

A

Complement fixation and triggering of inflammatory pathways within the vascular walls
- leads to: joint pain, cutaneous lesions, and protein losing nephropathy

41
Q

Type 3 - cause

A

Antigenic cause is often not determined

- idiopathic or immune-mediated

42
Q

Immune-mediated polyarthritis

A

Inflammatory disease where microbial organisms cannot be cultured from the joints and where the immune system plays an important role in the pathogenesis

43
Q

Type 4 hypersensitivity

A

Cell mediated, or “delayed” type

  • prolonged onset of action (24-72 hrs)
  • sensitization leads to generation of antigen specific T lymphocytes (Th1)
44
Q

Type 4 - pathophysiology

A

Subsequent exposure leads to activation of sensitized Th1 cells and movement to site of exposure
- release of cytokines and recruitment of inflammatory cells (macrophages, Th cells, Tc cells)

45
Q

What causes direct damage in type 4?

A

Cytotoxic T cells

- recruited by helper T cells

46
Q

What is the most significant type 4 manifestation?

A

Contact allergy

- inappropriate inflammatory response at cutaneous site of challenge

Immunology (28 decks)

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