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Molecules and Cells II > Hypersensitivity Types II and III > Flashcards

Hypersensitivity Types II and III Flashcards

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Organic Chemistry 101 flashcards
1
Q

Erythroblastosis fetalis also known as

A

Hemolytic disease of the newborn (HDNB)

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2
Q

Speed of Hypersensitivities from fastest to slowest

A

Type 1- Type II-Type III-Type IV

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3
Q

•Type II hypersensitivity represents damage resulting when the ____________immune system becomes directed against self.

A

Humoral

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4
Q

IgM antibodies in plasma that cross-react with blood group antigens not present on an individual’s own RBCs are called ____________

A

isohemagglutinins

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5
Q

Arthus reactions

A

Hypersensitivity Type III

Can be induced by insect bites, inhalation of fungal or animal protein

Characterized by local and sometimes severe inflammation of blood vessels

A local reaction

  • Intradermal injection of Ag induces Abs, which form Ag-Ab complexes in the skin
    • Initiates an inlammatory reaction that peaks approximately 4 to 10 hrs post injection
    • Inflammation is characterized by swelling and localized bleeding, followed by fibrin deposition
    • Edema, necrosis, and activation of complement
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6
Q

Hypersensitivity Type III

Immune Relationship

Mechanism of tissue injury

Presentation

A

Immune Relationship

  • Immune Complex mediated
    • Antigen-antibody complexes form
    • Antigens can be self or foreign

Mechanism of tissue injury

  • Complexes are filtered out of circulation and deposited in healthy tissue and capillary beds
  • Neutrophils attracted and complement activated by Ab-Ag complex
  • Neutrophils release lysosomal enzymes
  • Healthy tissue damaged

Presentation

  • Widespread molbility of Ab-Ag complexes allows for vasculitis and system manifestations
    • Compared to type II with generally localized reactions
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7
Q

Diabetes Type II

A

Hypersensitivity Type II NonCytotoxic

Anti-Insulin receptor antibody

  • Inhibits binding of insulin
    • Hyperglycemia
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8
Q

•Rh- individual may have Abs against Rh antigen, but usually only after 1st exposure to Rh Ag called ____________

A

Sensitization

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9
Q

Pernicious anemia

A

Hypersensitivity Type II Noncytotoxic

Low Intrinsic factor

  • Secreted from parietal cells of the stomach
  • Necessary for the absorption of vitamin B12

Anti-intrinsic factor Ab

  • Inhibits binding of IF of gastric parietal cells to receptor
    • Leads to neautralization of IF
    • Decreased vitamin B12 absorption; macrocytic anemia and hypersegmented neutrophils

Resection of terminal ileum

Intestinal infections

  • Diphyllobothrium latum
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10
Q

Hypersensitivity Type II

A
  • Type II hypersensitivity represents damage resulting when the humoral immune system becomes directed against self.
  • The mechanisms of type II hypersensitivity are those of antibody effector function.
  • Antibodies may bind specifically to tissue antigens
  • In both cases, the deposited antibodies induce inflammation, leading to tissue injury.
  • Type II is cy-2-toxic
  • Ab and complement lead to MAC
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11
Q

Idiopathic thrombocytopenic purpura

A

Anti-platelet Abs (IgG) bind to platelets triggering complement cascade resulting in the formation of MAC and cell lysis.

When platelets are depleted, clotting abnormalities occur, resulting in petechia and ecchymoses seen in the patient.

Type II Cytotoxic hypersensitivity

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12
Q

Serum sickness

A

Hypersensitivity Type III

Most is caused by drugs (like beta-lactams, sulfa drugs, anti-venin) acting as haptens

Abs to the foreign proteins are produced, complex formed and deposited in membranes, fix complement and lead to tissue damage

  • Activate/consume C3 and result in decreased serum levels of C3

Fever, urticaria, arthralgias, proteinuria, lymphadenopathy

Usually self-limited, and will resolve with withdrawal of the offending agent

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13
Q

Hypersensitivity Type III reactions

A

Involve Abs against soluble Ags circulating in the serum

  • Type III, immune complex of 3 things stuck together
    • Ag-Ab-complement

Un-cleared immune complexes

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14
Q

Acute rheumatic fever

A

Hypersensitivity Cytotoxic Type II

An autoimmune disease that follows untreated pharyngeal streptoccocal infection

Ab against streptococcal cell wall binds healthy tissue

  • Heart and joint inflammation

Risks include right-sided heart disease

  • Secondary to valvular dysfunction
  • Most often mitral stenosis
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15
Q

Systemic Lupus Erythematosis

A

Hypersensitivity Type III

Anti-dsDNA, anti-Sm, anti Rho Abs in complex with Ag

  • Butterfly facial rash
  • Nephritis
  • Arthritis
  • Vasculitis
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16
Q

Type of effector mechanisms. Types I, II, and III are ________ mediated. Type IV is _______ mediated.

A

Antibody; cell

17
Q

Bullous pemphigoid

A

Hypersensitivity Cytotoxic Type II

Patients with bullous pemphigold are generally elderly

Auto Abs against the basement membrane of the epidermis

  • Speration of epidermis from basement membrane
  • Results in formation of tense and intact blisters
    • Subepidermal
    • Less fragile, intact, don’t rupture
18
Q

Prevention/ Treatment of Hemolytic Disease of the Newborn (Erthroblastosis fetalis)

A
  • RhoGAM (anti-RhD IgG) given to mother at 28 weeks withinin 72 hours of delivery, which prevents mother from developing B cell memory of RhD
  • For severe reactions, fetus can be given an intrauterine blood-exchange transfusion to replace fetal Rh+ red blood cells with Rh- cells.
  • In less severe cases, a blood-exhange transfusion is not given until after birth, primarily to remove bilirubin
    • Infant is also exposed to low amounts of UV light to break down the bilirubin and prevent cerebral damage
    • The mother can also be treated during the pregnancy by plasmapheresis
      • A cell separation machine is used to separate the mother’s blood into two fractions: cell and plasma
      • The plasma containing the anti-Rh Ab is discarded, and the cells are reinfused into the mother in an albumin or fresh plasma solution
19
Q

Rheumatoid arthritis

A

Hypersensitivity Type III

Anti-IgM Fc region antibody complex with antigen

  • joint pain, decrease in range of motion
  • Destruction of cartilage and bone
    *
20
Q

Rh is present in around ______ % of the population.

A

85

21
Q

Hypersensitivity pneumonitis

A

Hypersensitivity Type III

Inhaled dust forms an Ab-Ag complex

“Farmer’s lung”

Tests

  • Bronchoalveolar lavage
  • Pulmonary function test
  • High resolution computed tomography
22
Q

Hypersensitivity Type II

  • Immune Relationship
  • Mechanism of Tissue Injury
  • Presentation
A

•Immune relationship

  • Ab mediated
    • IgM, IgG bind to antigen
    • complement activation
    • results in lysis via MAC or phagocytosis
  • Effector cells
    • cytotoxic
    • PMN (Neutrophils), macrophages, NK cells

Mechanism of tissue injury

•Abs lead to disease via 3 different processes

  • activation of complement or opsonization
  • recruitment of neutrophils and macrophages that incite tissue damage
  • interfere with normal receptor function

Presentation

  • Disease localized to specific tissues where Abs are present
23
Q

Graves’ disease

A

Type II Hypersensitivity NonCytotoxic

Anti-TSH receptor Ab

  • Stimulation of cell-surface receptors (stimulates T3 and T4 release)
    • Hyperthyroid followed by hypothyroid

Most common cause of hyperthyroidism

Female Dominant

  • HLA-B8- DR3 association

Often incited during stress

Complications stress-induced catecholamine surge

  • May be fatal by arrhythmia

Pregnancy complications

  • anti-TSH receptor antibodies may cross placenta and produce hyperthyroidism in the fetus
24
Q

___________ can induce all 4 types of hypersensitivity with various clinical manifestations. What manifestations are seen in each type?

A

Penicillin

Type I: Urticaria, systemic anaphylaxis

Type II: Hemolytic anemia

Type III: Serum sickness, glometulonephritis

Type IV: Contact dermitis

25
Q

Poststreptococcal glomerulonephritis

A

Hypersensitivity Type III

Anti-streptococcal glomerulonephritis

Nephritis

  • Lumpy Bumpy pattern” on immunofluorescence staining
  • Large complexes
  • Puffy face and tea-colored urine

High titers of antistreptolysin O and anti-DNAase B antibodies and low levels of C3

26
Q

Pemphigus vulgaris

A

Hypersensitivity Cytotoxic Type II

Mainly adults ages of 30 and 60

Affects the skin and mucous membranes

Auto Abs against the connections between epidermal cells

Auto Abs against desmoglein 1 and/ or 3 in the epidermis and inhibit its adhesive function, which lead to disruption of the intercellular junctions

  • Results in very superficial, intraepidermal, fragile bullae (burst easily)

Patients often present first with oral bullae and ulcerations, and later develop bullae on the skin

27
Q

What test can be used to test Erythroblastosis fetalis?

A

Direct Coombs test: detects Ab that are directly bound to patients RBCs (Test and Rh+ infant of an Rh- mother)

Indirect Coombs test: detects free Abs in serum, detects Abs that can adhere to other RBCs (Test an Rh- woman for Rh+ Abs)

28
Q

What are the immune mediators for each type of hypersensitivity?

A

Type I- IgE

Type II- IgG or IgM

Type III- Immune complexes

Type IV- Delayed Type Hypersensitivities

29
Q

Hypersensitivity Type II Non-cytotoxic Disorders

A

Graves’ Disease

Myastenia gravis

Pernicious anemia

Type II Diabetes

30
Q

Goodpasture’s syndrome

A

Type II Cytotoxic hypersensitivity

Immune system mistakenly attacks collagen in the tiny air sacs in the lungs and the filtering units (glomeruli) of the kidneys

  • Anti-type IV collagen Ab

Lung alveoli

  • Coughing up blood, dry cough, shortness of breath

Kidney glomeruli

  • Nephritis
  • Linear deposits
  • Blood urine, burning sensation when urinating, nausea and vomiting, pale skin

Symptoms

  • Often develop quickly over days or weeks
  • Loss of appetite
  • Fatigue
  • Weakness
  • Swelling (edema) in any area of the body, especially in the legs
31
Q

Hypersensitivity Type III

A

Serum sickness

Artus reaction

Systemic lupus erythematosis

Polyarteritis nodosa

Poststreptococcal glomerulonephritis

32
Q

Hypersensitivity Type II Cytotoxic Disorders

A
  • Autoimmune hemolytic anemia
  • Acute hemolytic transfusion reactions
  • Erythroblastosis fetalis [Hemolytic disease of the newborn (HDNB)]
  • Idiopathic thrombocytopenic purpura
  • Goodpasture’s syndrome
  • Pemphigus vulgaris
  • Bullous pemphigoid
  • Rheumatic fever
33
Q

Autoimmune Hemolytic Anemia

A

Type II Cytotoxic Hypersensitivity

  • Certain antibiotics (e.g., penicillin, cephalosporins, and streptomycin), and drugs (e.g., ibuprofen and naproxen), can be absorbed non specifically by proteins on RBC membranes, forming a drug protein complex and induce formation of Anti-RBC Abs .
  • These Anti-RBC Abs bind to the absorbed drug on RBCs, inducing complement-mediated lysis (destruction of RBC) and thus progressive anemia.
  • When the drug is withdrawn, the hemolytic anemia disappears.
34
Q

Myasthenia gravis

A

Hypersensitivity Type II Noncytotoxic

Anti-acetylcholine receptor antibody

  • Inhibits muscle stimulation
    • Muscle Weakness and paralysis
35
Q

H antigen (type O blood) adds a __________

A antigen (type A blood) adds ___________ to the H antigen

B antigen (type B blood) adds ____________ to the H antigen

A

fucose

galactosamine (N-gal)

galactose (Gal)

36
Q

Polyarteritis nodosa

A

Hypersensitivity Type III

Deposition of complexes in medium sized arteries

Blood vessel inflammation causing injury to organ systems

Symptoms: Generally ill and fatigued, have fevers, loss of appetite and weight

37
Q

Which is dominant Rh+ or Rh-?

A

Rh+

Molecules and Cells II (14 decks)

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