HYPERSENSITIVITY RXN Micro LE2

Question 1

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

Answer 1

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.

Question 2

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

Answer 2

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.

Question 3

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

Answer 3

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

Question 4

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

Answer 4

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

Question 5

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

Answer 5

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

Question 6

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

Answer 6

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

Question 7

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

Answer 7

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.

Question 8

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

Answer 8

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

Question 9

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

Answer 9

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

Question 10

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

Answer 10

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

Question 11

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

Answer 11

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

Question 12

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

Answer 12

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

Question 13

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

Answer 13

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

Question 14

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

Answer 14

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

Question 15

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

Answer 15

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

Question 16

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

Answer 16

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

Question 17

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

Answer 17

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

Question 18

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

Answer 18

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.

Question 19

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

Answer 19

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

Question 20

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

Answer 20

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

Question 21

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

Answer 21

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

Question 22

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

Answer 22

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

Question 23

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

Answer 23

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.

Question 24

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

Answer 24

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

Question 25

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

Answer 25

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

Question 26

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

Answer 26

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.

Question 27

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

Answer 27

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.

Question 28

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

Answer 28

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.

Question 29

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

Answer 29

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

Question 30

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

Answer 30

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.

Question 31

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

Answer 31

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.

Question 32

2. 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

Answer 32

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

Question 33

3. 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

Answer 33

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.

Question 34

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

Answer 34

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

Question 35

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

Answer 35

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

Question 36

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

Answer 36

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

Question 37

7. 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

Answer 37

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.

Question 38

8. 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

Answer 38

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.

Question 39

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

Answer 39

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

Question 40

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

Answer 40

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

Question 41

11. 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

Answer 41

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

Question 42

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

Answer 42

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

Question 43

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

Answer 43

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

Question 44

14. 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

Answer 44

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

Question 45

15. 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

Answer 45

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.

Question 46

Which type of hypersensitivity involves specifically sensitized T lymphocytes? A) Type I B) Type II C) Type III D) Type IV

Answer 46

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

Question 47

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

Answer 47

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

Question 48

Which test is utilized to identify the offending antigen in contact hypersensitivity? A) Blood test B) Urine test C) Patch testing D) Intradermal test

Answer 48

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

Question 49

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

Answer 49

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

Question 50

Which cell functions as the antigen-presenting cell in contact hypersensitivity? A) Neutrophil B) B lymphocyte C) Langerhans cell D) Macrophage

Answer 50

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

Question 51

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

Answer 51

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

Question 52

A negative TST test in the context of leprosy suggests: A) Tuberculoid leprosy B) Lepromatous leprosy C) Active tuberculosis D) Past tuberculosis exposure

Answer 52

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

Question 53

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

Answer 53

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

Question 54

A positive TST test in leprosy is indicative of: A) Lepromatous leprosy B) Tuberculoid leprosy C) Past tuberculosis exposure D) Current tuberculosis

Answer 54

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

Question 55

Which chemical is NOT associated with contact hypersensitivity? A) Formaldehyde B) Sulfonamides C) Tuberculin D) Nickel

Answer 55

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

Question 56

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.

Answer 56

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

Question 57

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

Answer 57

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.

Question 58

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

Answer 58

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

Question 59

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

Answer 59

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

Question 60

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

Answer 60

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