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Hypersensitivity reactions (most important ) Flashcards

1
Q

Type I – Anaphylactic type, Allergy

A

In Type 1, there is release of vasoactive amines and other mediators derived from the mast cells or basophils and affecting vascular permeability and smooth muscles in various organs

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2
Q

Type I – Anaphylactic type, Allergy First encounter

A
  • Most commonly via inhalation (ex. pollen)
  • Immune response – IgE immunoglobins (antibodies) produced on
    mast cells, which contain granules filled with histamine
  • No physiological reaction
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3
Q

Type I – Anaphylactic type, Allergy second encounter

A
  • Antibodies produced from first encounter bind to the antigen
    (allergen) forming the antigen-antibody complex
  • Mast cells undergo degranulation  histamine released
  • Pathophysiological reaction
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4
Q

Histamine effects on the body

A
  • Vasodilation
  •  Bronchospasm
  •  Mucus production
  • increase permeability of blood vessels
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5
Q

Systemic anaphylaxis

A

–#1 cause of death in Type I\
– paranthyl (injection/appearance) of allergen
- Results in itching
- Hives (aka Urticaria)
- Bronchospasm
- Laryngeal edema – swelling leads to closing of the laryngeal
opening  strangulation (puncture above episternal notch)
- Abdominal cramps, diarrhea, vomiting
- Vascular (anaphylactic) shock – sudden systemic vasodilation,
blood follows gravity  no blood to brain, pass out  death

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6
Q

Local reaction

A

– reaction depends on how allergen is contacted
- Urticaria (via skin contact)
- Hay fever, AKA acute allergic conjunctivitis (via inhalation) or
acute rhinoitis
- Atopy – familial predisposition to Type I
- Atopic bronchial asthma – serious, 2 different pathological mechanisms, only 1 of which is associated with allergy
 Extrinsic bronchial asthma
o Via type I allergic reaction
o Common in kids, familial predisposition to localized
type I hypersensitivity reactions
o NOT ASSOCIATED WITH TYPE I HYPERSENSITIVITY
 Intrinsic bronchial asthma o Autoimmune
 Genetic predisposition
 Diarrhea, vomiting
 Contact allergic dermatitis - blistering

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7
Q

Type II – Antibody Dependent

A

Mediated by antibodies directed against target antigens on the surface of cells or other tissue components
 3 subtypes:
-1) Complement-Dependent Reactions
-2) Antibody-Dependent Cell-Mediated Cytotoxicity
-3) Antibody-Mediated Cellular Dysfunction

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8
Q

Complement-Dependent Reactions

A
  • Autoimmune disease – antibodies for target (self) cells
  • Cascade of complement activation
  • Complement activation via classical pathway – DIRECT LYSIS
  • Seen in glomerulonephritis
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9
Q

extrinsic bronchial asthma

A

type 1

common in kids

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10
Q

intrinsic bronchial asthma

A

NOT type 1

autoimmune

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11
Q

Complement-Dependent Reaction disorders

A

—Hemotransfusin reactions – occur with blood transfusions
where the blood types are not matched (blood types: O, A,
B, AB) 
—Erythroblastosis fetalis – 85% of people have Rh antigen
on their RBCs, Rh(+)

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12
Q

Autoimmune hemolytic anemia

A

– ex. hemosiderosis  Certain drug reactions – can lead to production of
antineutrophil antibodies  decreased neutrophils
death)

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13
Q

Pemphigus vulgaris (most common type)

A

– blister
formation in epidermis
o Pemphix = blister, bubble
o Desmosomal proteins hold/adhere cells together
o Production of antidesmosomal antibodies results
in disruption of intercellular junctions

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14
Q

type III Antibody-Dependent Cell-Mediated Cytotoxicity

A
  • Macrophages, neutrophils, eiosinophils, and natural killer (NK)
    cells are non-T and non-B lymphocytes → don’t have specific
    receptors
  • Have receptors for FC fragment of IgE (? IgG & IgM, rarely IgE)
  • Mechanism
     — Antigen-antibody complex formed (FAB fragment of IgE
    binds to target cell) 
    — Non-T/non-B cells bind to the free FC portion  cell death
  • Parasites, virus-infected cells, tumor cells
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15
Q

type III Antibody-Mediated Cellular Dysfunction

A
  • Myasthenia graves
  • Hashimoto’s Thyroiditis
  • Grave’s Disease
  • pernicious anemia
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16
Q

Myasthenia gravis

A

– progressive muscle weakness
- Antibodies against Ach receptors on the muscle prevent
muscle contraction

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17
Q

Hashimoto’s Thyroiditis

A

– most common cause of hypothyroidism
(where iodine levels in the diet are normal)
-overproduction of auto-antibodies
against TSH receptors on thyroid gland

18
Q

Graves’ Disease

A

-Autoimmune disease, more common in females 8:1 
- Overproduction of auto-antibodies that bind and
stimulate TSH receptors (mimic TSH)  overproduction of
thyroid hormones  hyperthyroidism 
-Exophthalmus – bulging eyes

19
Q

Pernicious anemia

A

Autonomic binding antibody against the intrinsic factor

receptors

20
Q

Immune Complex Mediated Type

A

hypersensitivity is Mediated by deposition of antigen-antibody (immune) complexes, followed by complement activation and accumulation of polymorphonuclear leukocytes.

21
Q

Immune Complex Mediated Type Phase 1

A

immune complex formation
 —- Antigen is present in the blood (ex. bacterium)
 —- Antigen and antibody bind to form immune complex
—- Production of antibodies

22
Q

Immune Complex Mediated Type Phase 2

A

immune complex deposition

— Immune complex attaches to the vessel wall

23
Q

Immune Complex Mediated Type Phase 3

A

complex-mediated inflammation
—- Phagocytic cells (ex. neutrophil) CANNOT engulf and phagocytize the immune complex because it is attached to the vessel wall
—- Instead the phagocyte releases proteolytic enzymes to digest the
antigen  damage to the vessel wall also occurs  vasculitis 
inflammation and narrowing of the lumen
—- Vasculitis – increases vessel permeability

24
Q

Most common sites of immune complex deposition:

A 
o  Small vessels 
o  Kidneys 
o  Joints  arthralgia
 o  Heart 
o  Skin 
o  Serousal surfaces – fibrous layers lining body cavities
---  Very sensitive to deposition
---  Results in accumulation of fluid in the cavities
25
Q

Serum sickness

A 
- Injection of serum containing antibodies and proteins from one
person into another person 
- injectee develops antibodies
against the non-self proteins 
- resulting in serum sickness 10 –
14 days post injection
26
Q

Serum sickness symptoms

A
  • fever
  • itching
  • rash
  • urticaria
  • arthralgia
  • increased lymph node size
  • vascular shock (uncommon)
27
Q

Farmer’s Lung

A
  • Inhale a large amount of antigens from hay, dust, mold
    - Leads to lung necrosis
    - Not very common
28
Q

pigeon fanciers lung

A

dung in lungs

29
Q

Type IV – Cell-Mediated Type

A

hypersensitivity reaction, Cell-mediated immune response (no antibodies or complement involved) with sensitized lymphocytes ultimately leads to cellular and tissue injury

2 subtypes:
A) Delayed Type Hypersensitivity reaction
B) T cell-mediated Cytotoxicity

30
Q

Delayed Type Hypersensitivity reaction

A

Antigen activates CD4+ T-cells of the TH1 type (TH1 type—not T h
type 2 in alergy)  production and release of cytokines 
recruitment of macrophages
-ex tuberculosis

31
Q

Mantoux reaction

A

-aka PPD test= purified protein derivative)
-Used to determine if a person has or has had TB and to
begin treatment with izoniazid if necessary

32
Q

Chronic Granulomatous Infection

A
  • most common in upper lobes of lungs
  • macrophages build a wall around the antigen
  • interferon gamma leads to epithelioid coalescence which causes giant multinucleate cells
33
Q

Contact dermatitis

A

-Poison ivy or poison oak, reaction ~ 2 days post contact 
- Chemical reaction to urushiol** (active substance) found in
the plant 
- Looks like a second degree burn – blistered

34
Q

T cell-mediated Cytotoxicity (not associated with T helper cells)

A 
-Associated w/ T8 – cytotoxic cells(don’t need antibody, immediate
response?)
Account for:
o  Antiviral immunity 
o  Antitumorous immunity
o  Graft rejection
35
Q

Neoplasia

A
36
Q

Hypoplasia

A

– inadequate development, so that the resulting tissue is immature
and functionally deficient

37
Q

Aplasia

A

– lack of organ/tissue development

38
Q

Hypertrophy

A

– cell and organ enlargement that occurs in response to an
increased demand of that tissue
o Not an increase in the number of cells
o Increase in the size of the cells
o Heart enlargement due to hypertension – increased demand on the heart
pump, enlarged myofibrils

39
Q

Metaplasia – a change of the cell type

A

o Not from normal to abnormal (pathological)
o Change from normal to normal of a different tissue type
o A more serious adaptive response, but it is reversible
o Chronic bronchitis in smokers
 Normal lung epithelial lining – composed of goblet cells (mucous-
producing cells) and columnar cells with villi; mucous traps
particles from the air and the villi remove it
 With chronic irritation from smoking, columnar cells are replaces
by squamous epithelial cells  full loss of normal function and
more vulnerable to infection

40
Q

Dysplasia

A

o Loss in the uniformity of the individual cells as well as a loss in their
architectural orientation
o More serious, but can be reversed
o Dysplasia still has some normal cells present along with pleomorphic cells
– Pleomorphism

41
Q

Pleomorphism

A

Characterized by:
o Variability in cell size and shape in contrast to the
regularity of the cell structure seen in normal tissue
o Larger, more darkly-staining nuclei, with abnormal
shape
o Increased mitosis rate
 Found in malignant tumors 
- Results from metaplasia with continuous, chronic irritation

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