Hypersensitivity reactions (most important ) Flashcards
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
Serum sickness
- 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
Serum sickness symptoms
- fever
- itching
- rash
- urticaria
- arthralgia
- increased lymph node size
- vascular shock (uncommon)
Farmer’s Lung
- Inhale a large amount of antigens from hay, dust, mold
- Leads to lung necrosis
- Not very common
pigeon fanciers lung
dung in lungs
Type IV – Cell-Mediated Type
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
Delayed Type Hypersensitivity reaction
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
Mantoux reaction
-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
Chronic Granulomatous Infection
- 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
Contact dermatitis
-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
T cell-mediated Cytotoxicity (not associated with T helper cells)
-Associated w/ T8 – cytotoxic cells(don’t need antibody, immediate response?) Account for: o Antiviral immunity o Antitumorous immunity o Graft rejection
Neoplasia
Hypoplasia
– inadequate development, so that the resulting tissue is immature
and functionally deficient
Aplasia
– lack of organ/tissue development
Hypertrophy
– 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
Metaplasia – a change of the cell type
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
Dysplasia
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
Pleomorphism
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
