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Pathophysiology > Alterations of the Immune system > Flashcards

Alterations of the Immune system Flashcards

1
Q

Immune disorders

A
  • hypersensitivity
  • autoimmune disease
  • immunodeficiency
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2
Q

Hypersensitivity definition

A

-Inappropriate or excessive immune response to antigens

allergies = excessive

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3
Q

Autoimmune disease definition

A

when the immune response mistakenly targets normal body cells and tissues
-inappropriate

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4
Q

Immunodeficiency definition

A
  • the immune system fails to develop normally or is blocked in some way
  • not working
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5
Q

Hypersensitivity reactions

A
  • an exaggerated immune response that causes inflammation (more than needed) and results in the injury of healthy tissue
  • atopic person
  • repeated exposure to relatively large doses of allergen is required to produce sensitization of the individual (genetic tendency)
  • there are for interrelated mechanisms
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6
Q

Atopic person

A

individual who is predisposed to form specific IgE antibodies to antigens that do not affect most people (allergic person)

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7
Q

Hypersensitivity Types

A
  • Type I: immediate IgE-mediated reactions (allergy) B cells
  • Type II: antibody- mediated reactions (tissue specific reactions)
  • Type III: immune complex-mediated reactions (autoimmune)
  • Type IV: delayed hypersensitivity (cell-mediated reactions) T cells
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8
Q

Mechanism of Type I

A
  • IgE-mediated reactions
  • immediate hypersensitivity, usually in response to an environmental allergen
  • an “allergen” is an antigen that causes allergies
  • allergic individuals must first be sensitized to the allergen
  • chemical mediators of inflammation (major player is Histamine)
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9
Q

Sensitizaiton

A
  • 2 steps
    1. contact with the allergen causes formation of a specific IgE antibody
    2. IgE attaches to cell membrane of mast cells
  • later when the sensitized person is exposed to the same allergen, the allergen attaches to the IgE (just takes time)
  • union of allergen and IgE causes the mast cell to degranulate and release chemical mediators of inflammation, especially histamine
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10
Q

Histamine

A
  • contracts bronchial smooth muscles (bronchoconstriction or bronchospasm)
  • vasodilation and increased vascular permeability (swelling, due to leaky blood vessels)
  • increases respiratory mucus secretions
  • produces itching sensation (have chemoattractants
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11
Q

Atopy

A
  • atopic individuals tend to produce higher concentrations of IgE and to have more IgE receptors on their mast cells
  • IL4 (interleukin 4 and chemical mediator of inflammation) causes plasma cells to switch from making IgG to making IgE
  • atopic people make 10 x IL4 > normal people
  • atopy is a reaction to inhaled allergens; often referred to as “hay fever” (pollen, cat dander, dust mites, etc)
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12
Q

Examples of Type I Hypersensitivity

A
  • Atopy
  • Bronchial asthma
  • Urticaria (hives)
  • Atopic dermatitis
  • Anaphylaxis
  • Gastrointestinal (food) allergy
  • drug allergies
  • different responses in different places based on HI receptors
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13
Q

Atopy

A
  • allergic rhinitis, allergic conjunctivitis

- common allergens: cat dander, pollen, dust mites

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14
Q

Bronchial asthma

A
  • histamine -> bronchospasm, inflammation, increased mucus secretion
  • not all asthma is due to allergies
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15
Q

Uticaria

A
  • hives
  • -> severe itching, raised, red rash
  • not all hives are due to allergy
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16
Q

Atopic Dermatitis

A
  • Eczema
  • refers to any itchy red rash that weeps or oozes serum and may become crusty
  • not all eczema is due to allergies
17
Q

Anaphylaxis

A
  • severe, potentially life-threatening allergic reaction
  • -> selling of throat and larynx, respiratory distress, decreased blood pressure, shock and death
  • there can also be mild cases and localized cases
18
Q

Gastrointestinal (food) allergy

A
  • vomiting, diarrhea, abdominal pain, and/or anaphylaxis
  • may be a food, product of food breakdown, additive, or preservative in the food
  • some people claim to have “food allergies” are actually intolerances due to the lack of a digestive enzyme (dif. allergies have dif. runs at dif. levels)
19
Q

Drug allergies

A

-some are true allergies, but other so called “drug allergies” are side effects and not true allergies

20
Q

Treatment of Type I reactions

A
  • antihistamines
  • cromolyn drugs
  • desensitization
21
Q

antihistamines

A
  • bind with histamine before it can reach its receptors
  • has no effect on all other chemical mediators of inflammation
  • still have inflammation
22
Q

cromolyn drugs

A

prevent mast cell degranulation

23
Q

desensitization

A
  • allergy-shots
  • causes formation of specific IgA and IgG antibodies against the allergen
  • IgA and IgG combine with the allergen before it can attach to the IgE on the mast cells and trigger degranulation (“race”)
24
Q

Mechanism of Type II reactions

A
  • tissue-specific
  • antibodies are formed against a specific antigen that is located in only one tissue
  • these cells care then destroyed by phagocytosis
  • Non-autoimmune Type II reactions:
  • transfusion reactions (mismatched blood types)
  • hemolytic disease of the newborn (Rh incompatibility)
  • Autoimmune type II reactions:
  • a person’s immune system makes antibodies against one of its own normal tissues
25
Q

Type II: Ab vs. RBCs

A

chronic hemolytic anemia

26
Q

Type II: Ab vs. platelets (thrombocytes)

A

thrombocytopenia purpura

27
Q

Type II: Ab vs. myelin

A

multiple sclerosis

28
Q

Type II: Ab vs. beta cells of pancreas

A

diabetes mellitus type 1

29
Q

Type II: Ab vs. throid tissue

A

autoimmune throiditis

30
Q

Type II: Ab vs. ACh receptors on skeletal muscle

A

myasthenia gravis

31
Q

Mechanism of Type III

A

Immune Complex Mediated Injury

  • antibodies are formed vs. a soluble antigen in the serum
  • causes circulating antigen-antibody complexes
  • the largest complexes form when there is equivalence
  • these complexes can get deposited in many different places “sticks”
  • location of deposition will determine the symptoms
32
Q

harmful effects due to complement activation

A
  • complement is chemotactic to neutrophils
  • large amounts of lysosomal enzymes are released
  • results in tissue damage where the complex gets stuck
  • the phagocyte can’t completely surround the Ag/Ab complex, so their enzymes damage surrounding tissues (“innocent bystanders”)
33
Q

Examples of Type III

A
  • immune complex glomerulonephritis
  • rheumatoid arthritis
  • rheumatic fever: develops post Group A beta-hemolytic streptococcal infection; a small % of these patients develop rheumatic heart disease (anti-bodies bind to heart cells)
  • systemic lupus erythematosus
  • ulcerative colitis
34
Q

Mechanism of Type IV

A

Delayed Hypersensitivity

  • symptoms have slow onset: 24-48 hrs. after exposure
  • T lymphocytes, not antibodies, are responsible for tissue injury
  • reason for delay= time necessary for sensitized T cells to accumulate at site and generate an inflammatory reaction
  • T cells release chemical mediators of inflammation, attack and destroy cellular targets directly
35
Q

clinical examples of type IV

A
  • contact dermatitis: -> inflammation only at point of contact (immediate reactions are usually more widespread)
  • posion ivy/poison oak: a specific type of contact dermatitis
  • graft rejection: grafts contain foreign antigens
  • need to inhibit recipient’s immune system

Pathophysiology (11 decks)

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