Hypersensitivity reactions (most important ) Flashcards
(41 cards)
Type I – Anaphylactic type, Allergy
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
Type I – Anaphylactic type, Allergy First encounter
- Most commonly via inhalation (ex. pollen)
- Immune response – IgE immunoglobins (antibodies) produced on
mast cells, which contain granules filled with histamine - No physiological reaction
Type I – Anaphylactic type, Allergy second encounter
- Antibodies produced from first encounter bind to the antigen
(allergen) forming the antigen-antibody complex - Mast cells undergo degranulation histamine released
- Pathophysiological reaction
Histamine effects on the body
- Vasodilation
- Bronchospasm
- Mucus production
- increase permeability of blood vessels
Systemic anaphylaxis
–#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
Local reaction
– 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
Type II – Antibody Dependent
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
Complement-Dependent Reactions
- Autoimmune disease – antibodies for target (self) cells
- Cascade of complement activation
- Complement activation via classical pathway – DIRECT LYSIS
- Seen in glomerulonephritis
extrinsic bronchial asthma
type 1
common in kids
intrinsic bronchial asthma
NOT type 1
autoimmune
Complement-Dependent Reaction disorders
—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(+)
Autoimmune hemolytic anemia
– ex. hemosiderosis Certain drug reactions – can lead to production of
antineutrophil antibodies decreased neutrophils
death)
Pemphigus vulgaris (most common type)
– 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
type III Antibody-Dependent Cell-Mediated Cytotoxicity
- 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
type III Antibody-Mediated Cellular Dysfunction
- Myasthenia graves
- Hashimoto’s Thyroiditis
- Grave’s Disease
- pernicious anemia
Myasthenia gravis
– progressive muscle weakness
- Antibodies against Ach receptors on the muscle prevent
muscle contraction
Hashimoto’s Thyroiditis
– most common cause of hypothyroidism
(where iodine levels in the diet are normal)
-overproduction of auto-antibodies
against TSH receptors on thyroid gland
Graves’ Disease
-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
Pernicious anemia
Autonomic binding antibody against the intrinsic factor
receptors
Immune Complex Mediated Type
hypersensitivity is Mediated by deposition of antigen-antibody (immune) complexes, followed by complement activation and accumulation of polymorphonuclear leukocytes.
Immune Complex Mediated Type Phase 1
immune complex formation
—- Antigen is present in the blood (ex. bacterium)
—- Antigen and antibody bind to form immune complex
—- Production of antibodies
Immune Complex Mediated Type Phase 2
immune complex deposition
— Immune complex attaches to the vessel wall
Immune Complex Mediated Type Phase 3
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
Most common sites of immune complex deposition:
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