LESSON 1: HYPERSENSITIVITY REACTIONS Flashcards by Zari Ami

State of unresponsiveness to a specific antigen in an effort to
prevent destruction from overreactivity of the immune system

Immune tolerance

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ability of immune system to recognize
= NOT RESPOND against self produced antigens

self tolerance

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failed self tolerance =

autoimmune disease

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immune system actively
AVOIDS RESPONDING to external antigens

induced tolerance

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failed induced tolerance =

hypersensitivity reactions

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EXCESSIEVE and INAPPROPRIATE immune response = damaged host tissue resulting from
prolonged or repeated antigen exposure

Hypersensitivity reaction

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end result of hypersensitivity reaction

damaged host cells, tissue and organs

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All hypersensitivity reactions are consequences of ? = tissue damage

adaptive immune response

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4 general types of hypersensitivity reaction

type 1: immediate or anaphylactic
type 2: cytotoxic
type 3: immune complex
type 4: delayed or cell-mediated

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types of hypersensitivity reaction that are ANTIBODY MEDIATED = faster onset of signs and symptoms

type 1,2,3

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Antigens that stimulate allergies; mostly proteins that naturally triggers an immune
response

allergens

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factors that are instrumental in the manifestation
of an allergy

genetic background
environment

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COMPONENTS OF THE IMMUNE SYSTEM INVOLVED IN TYPE I
HYPERSENSITIVITY REACTION

IgE
Mast cells
Basophils
Eosinophils
T helper 2 cells
Cytokines and chemokines (IL-4, IL-5, IL-13)

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TYPE I IMMEDIATE OR ANAPHYLACTIC HYPERSENSITIVITY

Antibody mediator

IgE

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TYPE I IMMEDIATE OR ANAPHYLACTIC HYPERSENSITIVITY

Antigen involved

soluble antigens

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TYPE I IMMEDIATE OR ANAPHYLACTIC HYPERSENSITIVITY

cellular mediators

mast cells and basophils

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TYPE I IMMEDIATE OR ANAPHYLACTIC HYPERSENSITIVITY

chemical mediators

histamine

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TYPE I IMMEDIATE OR ANAPHYLACTIC HYPERSENSITIVITY

mechanism

CROSS LINKING OF (2) IGE antibodies on mast
cells/basophils and the RELEASE OF HISTAMINE

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causes the manifestation of
the signs and symptoms of Type I Hypersensitivity
reactions

release of HISTAMINE

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TYPE I IMMEDIATE OR ANAPHYLACTIC HYPERSENSITIVITY

Clinical states

Hay fever
Asthma
Food allergies
Anaphylactic shock

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Involves the second or subsequent exposure to the
same antigen; stage that causes damage to the host cell

Effector Stage / Reaction Phase

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Involves the first exposure to the antigen

sensitization stage

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TYPE I IMMEDIATE OR ANAPHYLACTIC HYPERSENSITIVITY

Sensitization stage: Allergen enters the body through ?

Direct contact
Inhalation
Ingestion
Puncture

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cause the mast cells and basophils to undergo
degranulation

crosslinking of IgE

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Expresses Fc Epsilon receptors (FcERI) = why IgE has the greatest affinity to mast cells

mast cells

Antibody isotype involved in allergy disorders/parasite immunity

IgE

Tetrameric receptor complex that binds specifically to the Fc portion of the epsilon heavy chain of your IgE

FcERI

MECHANISM OF TYPE I HYPERSENSITIVITY REACTION where APC migrates to present processed antigen to the naive T helper cells

lymph nodes

MECHANISM OF TYPE I HYPERSENSITIVITY REACTION migrate to the target site to which the allergen first entered; attach to the receptor site of the APC → start to secrete large amounts of cytokines

T helper 2 cell

Allows differentiation of B cells into IgE producing plasma cells

IL-4 and IL-5

MECHANISM OF TYPE I HYPERSENSITIVITY REACTION allow successful attachment of IgE into the mast cell and basophils

FCeRI

releases Interleukin 4, Interleukin 13 and Interleukin 5.

T helper 2

causes T helper cells to DIFFERENTIATE into T helper 2 cells

IL-4

enhances MUCUS production of epithelial cells

IL-13

recruit EOSINOPHILS from the bone marrow to the site of infection

IL-5

PATHOGENESIS OF TYPE 1 HYPERSENSITIVITY bronchi of the lungs

bronchochostriction

PATHOGENESIS OF TYPE 1 HYPERSENSITIVITY intestine

(!) Bowel Peristalsis (due to increased peristaltic movement) (2) Diarrhea (attempt to dilute food) (3) Epigastric pain (increased prod of HCl)

PATHOGENESIS OF TYPE 1 HYPERSENSITIVITY blood vessel

vasodilation permeability = hypotension

fluid will accumulate underneath the skin showing skin manifestation is called

urticaria

PATHOGENESIS OF TYPE 1 HYPERSENSITIVITY nerves

pruritus/itching

TYPE 1: LOCALIZED HYPERSENSITIVITY REACTIONS also known as?

atopy

TYPE 1: LOCALIZED HYPERSENSITIVITY REACTIONS examples of atopy

asthma allergic rhinitis (hay fever) atopic dermatitis

Reaction affects the entire body; exterme allergic reactions

SYSTEMIC HYPERSENSITIVITY REACTIONS

Severe type of allergic reaction that involves airway obstruction and circulatory collapse

anaphylaxis

drugs for anaphylaxis

penicillin

SYSTEMIC HYPERSENSITIVITY REACTIONS clinical picture

- decrease in BP = SHOCK - bronchospasm, cyanosis, edema and urticaria = respiratory distress

TREATMENT OF TYPE I HYPERSENSITIVITY REACTIONS localized HSR

antihistamine

TREATMENT OF TYPE I HYPERSENSITIVITY REACTIONS systemic HSR

(1) epinephrine (2) corticosteroids (mmunosuppresant) (3) antihistamine

TREATMENT OF TYPE I HYPERSENSITIVITY REACTIONS Address the decrease in the blood pressure; reverse the symptoms of decreasing blood pressure

epinephrine

Type II: Cytotoxic Hypersensitivity Reaction Antibody mediator

IgG and IgM

Type II: Cytotoxic Hypersensitivity Reaction Antigens involved

cell-bound

Type II: Cytotoxic Hypersensitivity Reaction End result when the complement system is triggered by the activation of classical pathway

Membrane Attack Complex (MAC) = cause the lysis of the cell

Type II: Cytotoxic Hypersensitivity Reaction Substance used for opsonization; used to coat the cell surface and enhance the phagocytic activity of macrophage which leads to lysis

C3B

Type II: Cytotoxic Hypersensitivity Reaction Cellular mediators

macrophages

Type II: Cytotoxic Hypersensitivity Reaction chemical mediators

complement proteins

Type II: Cytotoxic Hypersensitivity Reaction mechanism

IgG and IgM bind to epitopes -> promote opsonization, complement mediated lysis, and ADCC

These Type 2 Hypersensitivity reactions are triggered by antigens present on the cell surface, which are?

Self-antigen Modified/Altered self-antigen Alloantigen

THREE MAIN MECHANISM OF TYPE II HYPERSENSITIVITY REACTION

Complement activation Opsonization Antibody-Dependent Cell-Mediated Cytotoxicity (ADCC)

end result here is the destruction of Red Blood Cell due to transfusion incompatibility

hemolytic transfusion reactions

Reasons why Hemolytic Disease of the Newborn occurs

ABO incompatibility Rh incompatibility

HEMOLYTIC DISEASE OF THE NEWBORN Antibodies are naturally occurring

ABO blood group

HEMOLYTIC DISEASE OF THE NEWBORN does not have naturally occurring antibodies; requires exposure to the antigen

Rh blood group

HEMOLYTIC DISEASE OF THE NEWBORN acts as a barrier where Rh antigen of the baby will not go to the mother

placenta

HEMOLYTIC DISEASE OF THE NEWBORN Administered To Prevent Antibody Formation

Rhesus Immune Globulin Injection (Rhogam injection)

HEMOLYTIC DISEASE OF THE NEWBORN An intramuscular injection is given when ?

■ At 28 weeks into the pregnancy. ■ Within 72 hours of birth of a confirmed Rh positive baby.

Anemia that results from lack of intrinsic factor

pernicious anemia

Disease that is characterized by the presence of autoantibodies in the form of IgG and IgM; autoantibodies will lead to the DESTRUCTION OF THE PARIETAL CELLS

PERNICOUS ANEMIA

PARIETAL CELLS of the stomach produces ?

HCl and intrinsic factor

Pernicious Anemia absent intrinsic factor will cause?

not absorbed VitB12

Antibodies attack the BASEMENT MEMBRANE in lungs and kidneys → leading to bleeding from the lungs and kidney failure

GOODPASTURE SYNDROME

GOODPASTURE SYNDROME Circulating antibodies are directed against the collagen of the part of the kidney known as ?

Glomerular Basement Membrane (GBM)

Circulating antibodies directed at KIDNEY will result to what kind of disease?

Acute or Rapidly Progressive Glomerulonephritis

resuling condition if the circulating antibodies also attack the collagen of the air sacs of the LUNG (alveoli)

Pulmonary Hemorrhage

TWO MANIFESTATIONS present in patient→ probable diagnosis would be the Goodpasture syndrome.

hemoptysis hematuria

Hypersensitivity reaction against Streptococcus pyogenes

ACUTE RHEUMATIC FEVER

causative agent for tonsillitis

Streptococcus pyogenes

what organ has an antigen w a similar structure to M protein of S. pyogenes

human heart

ACUTE RHEUMATIC FEVER attacking the heart due to its similar structure w S. pyogenes M protein will lead to ?

destructction of the MITRAL VALVE of the heart = Rheumatic heart disease or Acute Rheumatic Fever.

Autoimmune disorder caused by an antibody-mediated blockade of NEUROMUSCULAR TRANSMISSION resulting in SKELETAL MUSCLE WEAKNESS

Myasthenia Gravis

MYASTHENIA GRAVIS autoimmune attack occurs when autoantibodies form against the - at the -

nicotinic acetylcholine postsynaptic receptors ; neuromuscular junction of skeletal muscles

autoimmune disorder that is characterized by the production of autoantibodies against the acetylcholine receptors found in the muscle.

myasthenia gravis

MYASTHENIA GRAVIS Binding of antibodies (Ab) to the ACh receptors → in people with myasthenia gravis → leads to the MANIFESTATION OF ?

paralysis

Graves' disease is an autoimmune disease characterized by ?

hyperthyroidism

GRAVES’ DISEASE – controls the metabolic rate of the body

thyroid gland

GRAVES’ DISEASE – responds to the drop in metabolic rate

hypothalamus

GRAVES’ DISEASE – responsible in increasing/correcting the metabolic rate

T3 and T4

GRAVES’ DISEASE stimulates thyroid gland to release t3 and T4

TSH (thyroid-stimulating hormone)

autoimmune disease characterized by autoantibodies binding to TSH receptors → stimulates hormone synthesis → OVERPRODUCTION OF THYROID HORMONES

GRAVES' DISEASE

DIABETES MELLITUS TYPE 2 (DM 2) Adult-onset diabetes, is a form of diabetes that is characterized by ?

increased blood sugar insulin resistance

DIABETES MELLITUS TYPE 2 (DM 2) the presence of autoantibodies binding to insulin receptors, preventing insulin to bind to the receptor → inability of the cell to absorb glucose WILL CAUSE WHAT CONDITION

hyperglycermia (increased glucose in the blood)

TYPE III HYPERSENSITIVITY: IMMUNE COMPLEX HYPERSENSITIVITY REACTION Antibody mediators

IgG and IgM

TYPE III HYPERSENSITIVITY: IMMUNE COMPLEX HYPERSENSITIVITY REACTION Antigen involved

Soluble bound antigens

TYPE III HYPERSENSITIVITY: IMMUNE COMPLEX HYPERSENSITIVITY REACTION Cellular mediators

Neutrophils

TYPE III HYPERSENSITIVITY: IMMUNE COMPLEX HYPERSENSITIVITY REACTION Chemical mediators

complement proteins

TYPE III HYPERSENSITIVITY: IMMUNE COMPLEX HYPERSENSITIVITY REACTION Mechanism

ANTIGEN-ANTIBODY complexes in tissues activate complement and attract neutrophils that release LYTIC MOLECULES

unremoved immune complexes can be deposited on the following preferred sites

Blood bessels Glomerules of the kidney Joints Skin

TYPE III HYPERSENSITIVITY: s IMMUNE COMPLEX HYPERSENSITIVITY REACTION Most preferred site of complex deposition since

GLOMERULUS OF THE KIDNEY

TYPE III HYPERSENSITIVITY: s IMMUNE COMPLEX HYPERSENSITIVITY REACTION byproducts of the complement system and a powerful chemotaxin, will recruit more neutrophils toward the area where the immune complex are deposited

C5A

2 TYPES OF TYPE III HYPERSENSITIVITY REACTION

Local: Arthus reaction Systemic: Serum sickness

Discovered Arthus reaction

Nicolas Maurice Arthus in 1903

Caused by SUBCUTANEOUS or INTRADERMAL introduction of soluble antigen which later forms immune complexes

Arthus reaction

ARTHUS REACTION immune complexes deposited in the blood vessels can cause

vasculitis necrosis

ARTHUS REACTION antibody formed upon repeated administration of horse serum into the rabbit

high levels of IgG

PATHOPHYSIOLOGY OF ARTHUS REACTION Time period of severe pain, swelling, induration, edema, hemorrhage, and occasionally by necrosis

4-12 hours

Arthus reactions (type III hypersensitivity reactions) are rarely reported after vaccination and can occur after - and -

TETANUS toxoid-containing or DIPTHERIA toxoid-containing vaccines

Autoantibody formation against the soluble antigens of the host (DNA, histones, nucleolar antigens and RNA)

SYSTEMIC LUPUS ERYTHEMATOSUS (SLE)

SLE is characteried by

production of antibodies against NUCLEIC ACID and their associated proteins

SYSTEMIC LUPUS ERYTHEMATOSUS (SLE) anti-DNA complexes are deposited in different tissues in the body, such as ?

skin joints glomerulus serous membranes

SYSTEMIC LUPUS ERYTHEMATOSUS (SLE) Skin: characteristic - is seen along the bridge of the nose and cheek

butterfly rash

SYSTEMIC LUPUS ERYTHEMATOSUS (SLE) Joints

Non-Erosive inflammation with no to little deformity of the joints

SYSTEMIC LUPUS ERYTHEMATOSUS (SLE) GLOMERULUS

Kidney damage

most affected organ in cases of SLE

kidney

SYSTEMIC LUPUS ERYTHEMATOSUS (SLE) SEROUS MEMBRANES: most common affected body cavity in cases of SLE

pericardial and pleural cavities

POST-STREPTOCOCCAL GLOMERULONEPHRITIS occurs after - of untreated Streptococcal infection of the pharynx and skin

1-4 weeks

S. pyogenes infection in the pharynx

Streptococcal pharyngitis

S. pyogenes skin infection

Impetigo

Autoimmune disorder that may affect many organs but primarily attacks the JOINTS

RHEUMATOID ARTHRITIS

RHEUMATOID ARTHRITIS caused by autoantibodies formed againts - in the blood

citrullinated proteins

abnormal stiffening and immobility of a joint due to the fusion of the bones

ankylosis

allows for distal end of bones of the joints to glide smoothly, no friction

articular cartilage

TYPE IV. CELL-MEDIATED/DELAYED-TYPED HYPERSENSITIVITY Antibody mediator

none

TYPE IV. CELL-MEDIATED/DELAYED-TYPED HYPERSENSITIVITY Antigen involved

SOLUBLE and CELL-BOUND

TYPE IV. CELL-MEDIATED/DELAYED-TYPED HYPERSENSITIVITY Cellular mediators

T HELPER 1 CELLS and MACROPHAGES

TYPE IV. CELL-MEDIATED/DELAYED-TYPED HYPERSENSITIVITY Chemical mediators

cytokines

TYPE IV. CELL-MEDIATED/DELAYED-TYPED HYPERSENSITIVITY Mechanism

Released of mediators by SENSITIZED T CELLS provoke tissue destruction by MONONUCLEAR cells

PATHOPHYSIOLOGY OF TYPE IV HYPERSENSITIVITY Reaction will be evident in - (time)

24-72 hours

chemicals that bind in the glycoproteins present in the skin cells (poison ivy)

urushiol

condition caused by contact w poison iyivy

contact dermatitis

TYPE IV. CELL-MEDIATED/DELAYED-TYPED HYPERSENSITIVITY act on the T helper cells = T helper cells will transform into a T helper 1

IL-12

TYPE IV. CELL-MEDIATED/DELAYED-TYPED HYPERSENSITIVITY T HELPER 1 functions to release -

IFN-gamma

TYPE IV. CELL-MEDIATED/DELAYED-TYPED HYPERSENSITIVITY Act on to recruit more macrophages toward the site of infection

IFN-gamma

TYPE IV. CELL-MEDIATED/DELAYED-TYPED HYPERSENSITIVITY recruited macrophages will release -

lysosomal enzymes and reactive oxygen species

TYPE IV. CELL-MEDIATED/DELAYED-TYPED HYPERSENSITIVITY Skin lesions (poison ivy contact): responsible for causing the skin lesions or tissue damage

Recruited macrophages

Occurs due an exposure to nickel metal

CONTACT DERMATITIS - NICKEL

Other causes of Contact Dermatitis

○ Bleach and Detergents ○ Shampoos ○ Rubber ○ Latex gloves

Skin disorder that causes skin cells to multiply up to 10 times faster than normal

psorriasis

commonsnites of psoriasis

elbows lumbosacral areas galns penis

MULTIPLE SCLEROSIS

Autoimmune demyelinating diseases caused by immune responses (t cells & macrophages) directed against the component of the myelin sheath of the neurons in the central nervous system

cause the destruction of the certain areas of the myelin sheath of the axons of the nerves from the central nervous system.

cytokins

Characterized by the absence of insulin

DIABETES MELLITUS TYPE 1

Qualitative skin test done to screen in vivo sensitization by M. Tuberculosis

Mantoux test

Mantoux test Antigen introduced through intradermal route

PPD purified derivative protein

Mantoux test >15 mm

Positive

Mantoux test <15 mm

Negative

LESSON 1: HYPERSENSITIVITY REACTIONS Flashcards

(144 cards)