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MICRO / PARA (DUMP) > HYPERSENSITIVITY RXN Micro LE2 > Flashcards

HYPERSENSITIVITY RXN Micro LE2 Flashcards

1
Q

Which type of hypersensitivity involves IgE antibodies reacting to allergens?
a) Type I
b) Type II
c) Type III
d) Type IV

A

a) Type I
Rationale: Type I hypersensitivity, also known as immediate/anaphylactic hypersensitivity, involves IgE antibodies reacting to allergens, binding to mast cells and eosinophils via the Fc receptor.

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2
Q

Which cell undergoes degranulation upon subsequent exposure to the allergen in Type I hypersensitivity?
a) T-cells
b) Neutrophils
c) Mast cells
d) B-cells

A

c) Mast cells
Rationale: In Type I hypersensitivity, upon subsequent exposure to the allergen, fixed IgE becomes cross-linked, causing mast cells to undergo degranulation.

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3
Q

Histamine primarily contributes to which effect during an allergic reaction?
a) Platelet aggregation
b) Vasodilation
c) Antibody production
d) Phagocytosis

A

b) Vasodilation
Rationale: Histamine is the primary mediator for Type 1 reactions and causes vasodilation, increased capillary permeability, and smooth muscle contraction.

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4
Q

Which drug can be used to counteract the effects of histamine during an allergic reaction?
a) Ibuprofen
b) Epinephrine
c) Antihistamine
d) Insulin

A

c) Antihistamine
Rationale: Antihistamine drugs can block histamine receptor sites, thereby counteracting the effects of histamine during an allergic reaction.

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5
Q

Which substance promotes platelet aggregation during Type I hypersensitivity reactions?
a) Histamine
b) Prostaglandin
c) Thromboxane
d) Epinephrine

A

c) Thromboxane
Rationale: Thromboxanes, during Type I hypersensitivity reactions, promote platelet aggregation.

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6
Q

Which type of hypersensitivity is most prevalent?
a) Type I
b) Type II
c) Type III
d) Type IV

A

a) Type I
Rationale: Type I hypersensitivity is mentioned as the most prevalent type of allergy.

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7
Q

What is the main goal of treatment for Type I hypersensitivity reactions?
a) Stimulate immune response
b) Increase antibody production
c) Counteract the mediators’ effects
d) Promote mast cell degranulation

A

c) Counteract the mediators’ effects
Rationale: The main goal of treatment for Type I hypersensitivity reactions is to counteract the effects of mediators like histamine.

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8
Q

Which is NOT a treatment for Type I hypersensitivity reactions?
a) Epinephrine
b) Antihistamines
c) Corticosteroids
d) Vitamin C

A

d) Vitamin C
Rationale: The treatments for Type I hypersensitivity reactions include epinephrine, antihistamines, and corticosteroids. Vitamin C is not mentioned as a treatment.

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9
Q

What is the genetic predisposition towards certain allergic reactions called?
a) Hypoactivity
b) Atrophy
c) Atopy
d) Anaphylaxis

A

c) Atopy
Rationale: Atopy refers to the strong genetic predisposition towards certain allergic reactions.

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10
Q

Which allergic reaction is characterized by high IgE levels?
a) Atopy
b) Anaphylaxis
c) Eczema
d) Urticaria

A

a) Atopy
Rationale: Atopy is associated with elevated IgE levels and a genetic predisposition towards certain allergies.

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11
Q

Which is a symptom of atopy?
a) Bronchospasm
b) Hay fever
c) Thrombocytopenia
d) Anemia

A

b) Hay fever
Rationale: Hay fever is one of the symptoms of atopy, along with other allergic reactions like asthma, eczema, and urticaria.

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12
Q

Which pathway does prostaglandin originate from?
a) Arachidonic acid via the lipoxygenase pathway
b) Arachidonic acid via the cyclooxygenase pathway
c) Glycolysis
d) Krebs cycle

A

b) Arachidonic acid via the cyclooxygenase pathway
Rationale: Prostaglandin is derived from arachidonic acid via the cyclooxygenase pathway.

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13
Q

How are most allergens in Type I hypersensitivity identified?
a) Blood tests
b) MRI scans
c) Skin tests
d) Urine tests

A

c) Skin tests
Rationale: Allergens causing Type I hypersensitivity reactions are often identified using skin tests, such as injection, patch, or scratch tests.

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14
Q

Which cell contains histamine in a preformed state?
a) Neutrophils
b) Lymphocytes
c) Platelets
d) Monocytes

A

c) Platelets
Rationale: Histamine exists in a preformed state in platelets as well as in the granules of mast cells and eosinophils.

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15
Q

Which secondary mediator is involved in Type I hypersensitivity reactions?
a) Hemoglobin
b) Insulin
c) IL-4
d) Progesterone

A

c) IL-4
Rationale: Alongside cytokines like TNF-a, IL-4 acts as a secondary mediator in Type I hypersensitivity reactions.

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16
Q

Which type of hypersensitivity involves cell surface antigens reacting with antibodies?
a) Type I
b) Type II
c) Type III
d) Type IV

A

b) Type II
Rationale: Type II hypersensitivity, also known as antibody-mediated hypersensitivity, involves cell surface antigens reacting with antibodies.

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17
Q

Which antibody is primarily involved in binding to cell surface antigens in Type II hypersensitivity?
a) IgA
b) IgE
c) IgG
d) IgM

A

c) IgG
Rationale: In Type II hypersensitivity, IgG antibodies play a significant role by binding to cell surface antigens.

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18
Q

What can the interaction of antibodies with cell surface antigens in Type II hypersensitivity activate?
a) Phagocytosis
b) Complement system
c) Natural killer cells
d) B-cell proliferation

A

b) Complement system
Rationale: In Type II hypersensitivity, the interaction of antibodies with cell surface antigens can activate the complement system, potentially leading to complement-mediated lysis.

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19
Q

Which drug, when bound to red blood cell surfaces, can trigger antibody formation leading to hemolysis?
a) Aspirin
b) Ibuprofen
c) Penicillin
d) Metformin

A

c) Penicillin
Rationale: Penicillin can bind to proteins on red blood cell surfaces, triggering the formation of antibodies that can lead to hemolysis.

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20
Q

Which pathogen induces antibodies that cross-react with red cell antigens, causing hemolytic anemia?
a) Escherichia coli
b) Staphylococcus aureus
c) Mycoplasma pneumoniae
d) Salmonella typhi

A

c) Mycoplasma pneumoniae
Rationale: Mycoplasma pneumoniae can induce antibodies that cross-react with red cell antigens, resulting in hemolytic anemia.

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21
Q

In Rheumatic Fever, antibodies against which bacteria cross-react with cardiac tissue?
a) Group A streptococci
b) Group B streptococci
c) Group C streptococci
d) Group D streptococci

A

a) Group A streptococci
Rationale: In Rheumatic Fever, antibodies generated against group A streptococci cross-react with cardiac tissue, potentially causing damage.

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22
Q

In which syndrome are antibodies formed against the basement membranes of the kidney and lung?
a) Sjögren’s Syndrome
b) Goodpasture’s Syndrome
c) Guillain-Barré Syndrome
d) Turner Syndrome

A

b) Goodpasture’s Syndrome
Rationale: In Goodpasture’s Syndrome, antibodies target the basement membranes of both the kidney and lung, potentially causing severe damage.

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23
Q

In Graves’ Disease, an autoantibody binds to which receptor leading to hyperthyroidism?
a) Insulin receptor
b) Adrenaline receptor
c) Thyroid-stimulating hormone (TSH) receptor
d) Growth hormone receptor

A

c) Thyroid-stimulating hormone (TSH) receptor
Rationale: In Graves’ Disease, an autoantibody binds to the TSH receptor, which results in the stimulation of the thyroid and consequently, hyperthyroidism.

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24
Q

What is the primary result of complement-mediated lysis in Type II hypersensitivity?
a) Vasodilation
b) Antibody formation
c) Cell death
d) Inflammation

A

c) Cell death
Rationale: Complement-mediated lysis, which can occur in Type II hypersensitivity, leads to the destruction or death of cells.

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25
Q

Which condition involves antibodies cross-reacting with cardiac tissue?
a) Rheumatoid Arthritis
b) Rheumatic Fever
c) Osteoarthritis
d) Myasthenia Gravis

A

b) Rheumatic Fever
Rationale: In Rheumatic Fever, antibodies against group A streptococci cross-react with cardiac tissue, which can cause damage.

26
Q

Which of the following diseases is NOT related to Type II hypersensitivity?
a) Graves’ Disease
b) Goodpasture’s Syndrome
c) Rheumatic Fever
d) Celiac Disease

A

d) Celiac Disease
Rationale: Celiac Disease is related to an immune response to gluten ingestion and is not directly related to the mechanisms of Type II hypersensitivity, unlike the other options provided.

27
Q

Which hypersensitivity type is often associated with transfusion reactions?
a) Type I
b) Type II
c) Type III
d) Type IV

A

b) Type II
Rationale: Type II hypersensitivity reactions include ABO transfusion reactions, where the wrong blood type is transfused, leading to an immune response against the mismatched blood.

28
Q

What can penicillin potentially cause when attached to red blood cells?
a) Vasoconstriction
b) Hemolysis
c) Increased platelet count
d) Leukopenia

A

b) Hemolysis
Rationale: When penicillin attaches to red blood cell surfaces, it can trigger antibody formation leading to hemolysis or destruction of the red blood cells.

29
Q

Which organ is primarily affected by the autoantibody binding in Graves’ Disease?
a) Liver
b) Pancreas
c) Thyroid
d) Kidney

A

c) Thyroid
Rationale: In Graves’ Disease, an autoantibody binds to the TSH receptor, stimulating the thyroid and leading to hyperthyroidism.

30
Q

In Type II hypersensitivity, what is the result of the antibody binding to cell surface antigens?
a) Activation of T-cells
b) Stimulation of B-cells
c) Activation of the complement system
d) Suppression of the immune response

A

c) Activation of the complement system
Rationale: In Type II hypersensitivity, when antibodies bind to cell surface antigens, it can activate the complement system, potentially leading to complement-mediated lysis.

31
Q
  1. Type III hypersensitivity reactions are primarily driven by:
    a) T-cell mediated reactions
    b) Immediate IgE responses
    c) Persistent antigen-antibody complexes
    d) Direct antibody-mediated cellular damage
A

c) Persistent antigen-antibody complexes
Rationale: Type III hypersensitivity is caused by antigen-antibody immune complexes that are not promptly removed, leading to their deposition in tissues and subsequent damage.

32
Q
  1. In the context of Acute Post Streptococcal Glomerulonephritis, which component is notably deposited at the glomerular basement?
    a) IgA
    b) IgE
    c) C3
    d) C5
A

c) C3
Rationale: The disease features lumpy deposits of immunoglobulins and the complement component C3 in the glomerular basement.

33
Q
  1. The Arthus Reaction is characterized by:
    a) A delayed inflammatory response peaking in weeks
    b) Erythema and edema peaking within 3-8 hours
    c) Immediate respiratory distress
    d) Chronic joint pain
A

b) Erythema and edema peaking within 3-8 hours
Rationale: The Arthus reaction involves a localized inflammatory response characterized by skin erythema and swelling that intensifies within 3-8 hours.

34
Q
  1. Serum sickness historically arose from passive immunization using serums derived from:
    a) Pigs
    b) Sheep
    c) Horses
    d) Goats
A

c) Horses
Rationale: Serum sickness was a result of passive immunization using animal serums, especially from horses or cows.

35
Q
  1. In Rheumatoid Arthritis, which antibody is prominently involved?
    a) Anti-DNA
    b) Anti-M protein
    c) Rheumatoid factor
    d) Anti-nucleosome
A

c) Rheumatoid factor
Rationale: Rheumatoid Arthritis features the antibody known as the “rheumatoid factor” that targets IgG.

36
Q
  1. The main organ affected in SLE due to immune complex deposition is:
    a) Liver
    b) Heart
    c) Kidney
    d) Lung
A

c) Kidney
Rationale: Though SLE can impact multiple organs, the kidneys face the most significant damage due to immune complex deposition.

37
Q
  1. What results from the lingering antigen-antibody complexes in Type III hypersensitivity?
    a) Inhibition of polymorphonuclear cells
    b) Attraction of polymorphonuclear cells leading to tissue damage
    c) Enhanced B-cell production
    d) Immediate mast cell degranulation
A

b) Attraction of polymorphonuclear cells leading to tissue damage
Rationale: In Type III hypersensitivity, the lingering antigen-antibody complexes attract polymorphonuclear cells to the deposition sites, causing tissue damage.

38
Q
  1. Which infection can potentially lead to Acute Post Streptococcal Glomerulonephritis?
    a) Group B streptococci
    b) Nephritogenic E. coli
    c) Group A hemolytic streptococci
    d) Staphylococcus aureus
A

c) Group A hemolytic streptococci
Rationale: Onset of Acute Post Streptococcal Glomerulonephritis occurs post-infection by group A hemolytic streptococci, especially strains with nephritogenic properties.

39
Q
  1. Which reaction involves a hemorrhagic necrotic lesion that might ulcerate?
    a) Serum sickness
    b) Rheumatoid Arthritis
    c) Arthus Reaction
    d) SLE flare
A

c) Arthus Reaction
Rationale: The Arthus Reaction leads to a localized inflammatory response with hemorrhagic, necrotic lesions that might ulcerate.

40
Q
  1. In Systemic Lupus Erythematosus (SLE), the antibodies primarily target:
    a) Cell wall M protein
    b) DNA and nucleohistones
    c) IgG
    d) Glomerular basement
A

b) DNA and nucleohistones
Rationale: In SLE, the antibodies predominantly target DNA and nucleohistones found in most body cells.

41
Q
  1. Type III hypersensitivity reactions are often linked with the deposition of immune complexes in:
    a) Lymph nodes
    b) Blood plasma
    c) Tissues
    d) Bone marrow
A

c) Tissues
Rationale: Type III hypersensitivity arises when lingering antigen-antibody immune complexes deposit in tissues, leading to subsequent damage.

42
Q
  1. In Rheumatoid Arthritis, where does immune complex deposition primarily occur?
    a) Liver tissues
    b) Inflamed joint membranes
    c) Cardiac muscles
    d) Lung alveoli
A

b) Inflamed joint membranes
Rationale: In Rheumatoid Arthritis, immune complexes mainly deposit in the membranes of inflamed joints.

43
Q
  1. Maurice Arthus is best known for demonstrating which hypersensitivity reaction?
    a) Serum sickness
    b) Anaphylactic shock
    c) Arthus Reaction
    d) Post transfusion reaction
A

c) Arthus Reaction
Rationale: The Arthus Reaction is named after Maurice Arthus due to his experiments demonstrating this localized inflammatory response in rabbits.

44
Q
  1. The primary mechanism of tissue damage in Type III hypersensitivity is through the activation and attraction of:
    a) Macrophages
    b) T-lymphocytes
    c) B-lymphocytes
    d) Polymorphonuclear cells
A

d) Polymorphonuclear cells
Rationale: In Type III hypersensitivity, the activated complement due to antigen-antibody complex deposition attracts polymorphonuclear cells, causing tissue damage.

45
Q
  1. Which condition can be a result of a previous infection with certain strains of group A streptococcus containing M protein in their cell wall?
    a) Serum sickness
    b) Rheumatoid Arthritis
    c) Acute Post Streptococcal Glomerulonephritis
    d) Grave’s Disease
A

c) Acute Post Streptococcal Glomerulonephritis
Rationale: Acute Post Streptococcal Glomerulonephritis primarily affects individuals after respiratory infections caused by specific strains of group A streptococcus that contain M protein in their cell wall.

46
Q

Which type of hypersensitivity involves specifically sensitized T lymphocytes?

A) Type I
B) Type II
C) Type III
D) Type IV

A

D) Type IV
Rationale: Type IV hypersensitivity is a cell-mediated response involving sensitized T lymphocytes that activate macrophages, leading to inflammation.

47
Q

In contact hypersensitivity, what duration after contact with the antigen does the reaction typically begin?

A) Immediately
B) 6-8 hours
C) 12-48 hours
D) 2-3 days

A

C) 12-48 hours
Rationale: For contact hypersensitivity, the response typically begins 12-48 hours after contact with the offending agent.

48
Q

Which test is utilized to identify the offending antigen in contact hypersensitivity?

A) Blood test
B) Urine test
C) Patch testing
D) Intradermal test

A

C) Patch testing
Rationale: Patch testing is used to determine the specific antigen causing the reaction in contact hypersensitivity.

49
Q

Which type of hypersensitivity has a delayed response, beginning 2-3 days after antigen contact?

A) Type I
B) Type II
C) Type III
D) Type IV

A

D) Type IV
Rationale: Type IV hypersensitivity is characterized by a delayed response, starting 2-3 days post-antigen contact.

50
Q

Which cell functions as the antigen-presenting cell in contact hypersensitivity?

A) Neutrophil
B) B lymphocyte
C) Langerhans cell
D) Macrophage

A

C) Langerhans cell
Rationale: In contact hypersensitivity, the Langerhans cell in the epidermis acts as the antigen-presenting cell.

51
Q

Which of the following can cause erythema, itching, vesication, or eczema within 12-48 hours upon skin contact in sensitized individuals?

A) Tuberculin
B) Nickel
C) Blood transfusion
D) Intradermal injection

A

B) Nickel
Rationale: Nickel is one of the agents listed under contact hypersensitivity that can trigger skin reactions in sensitized individuals.

52
Q

A negative TST test in the context of leprosy suggests:

A) Tuberculoid leprosy
B) Lepromatous leprosy
C) Active tuberculosis
D) Past tuberculosis exposure

A

: B) Lepromatous leprosy
Rationale: A negative test in leprosy indicates lepromatous leprosy, which is characterized by weak cell-mediated immunity.

53
Q

Which type of hypersensitivity reaction is initiated by T lymphocytes that activate macrophages?

A) Type I
B) Type II
C) Type III
D) Type IV

A

D) Type IV
Rationale: Type IV hypersensitivity involves T lymphocytes that activate macrophages, leading to inflammation.

54
Q

A positive TST test in leprosy is indicative of:

A) Lepromatous leprosy
B) Tuberculoid leprosy
C) Past tuberculosis exposure
D) Current tuberculosis

A

B) Tuberculoid leprosy
Rationale: In leprosy, a positive TST points to tuberculoid leprosy, indicating active cell-mediated immunity.

55
Q

Which chemical is NOT associated with contact hypersensitivity?

A) Formaldehyde
B) Sulfonamides
C) Tuberculin
D) Nickel

A

C) Tuberculin
Rationale: Tuberculin is associated with the tuberculin skin test (TST) for tuberculosis exposure or infection, not contact hypersensitivity.

56
Q

Which of the following statements about Type IV hypersensitivity is true?
A) It involves antibody-antigen reactions.
B) It is an immediate hypersensitivity reaction.
C) It is mediated by T lymphocytes.
D) It begins immediately after antigen contact.

A

C) It is mediated by T lymphocytes.
Rationale: Type IV hypersensitivity is cell-mediated and involves specifically sensitized T lymphocytes.

57
Q

The antigen-presenting cell in contact hypersensitivity interacts primarily with:
A) CD8 T cells
B) CD4 TH1 cells
C) B cells
D) Natural Killer cells

A

B) CD4 TH1 cells
Rationale: In contact hypersensitivity, the antigen-presenting Langerhans cell in the epidermis interacts with CD4 TH1 cells to trigger a response.

58
Q

In which hypersensitivity type is the response usually delayed, starting 2-3 days after antigen exposure?
A) Type I
B) Type II
C) Type III
D) Type IV

A

D) Type IV
Rationale: Type IV hypersensitivity is characterized by a delayed response, which typically starts 2-3 days post-antigen contact.

59
Q

Poison ivy can lead to which type of hypersensitivity?
A) Type I
B) Type II
C) Type III
D) Type IV

A

D) Type IV
Rationale: Contact with agents like poison ivy can trigger Type IV hypersensitivity, causing skin reactions in sensitized individuals.

60
Q

Which of the following reactions typically peaks within 3-8 hours of antigen exposure?
A) Arthus reaction
B) Tuberculin reaction
C) Serum sickness
D) Rheumatoid arthritis

A

A) Arthus reaction
Rationale: The Arthus reaction is characterized by erythema and edema that peak within 3-8 hours after antigen exposure.

MICRO / PARA (DUMP) (12 decks)

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