Test Bank for Cellular and Molecular Immunology 7th Edition Abul K Abbas Download

Test Bank for Cellular and Molecular Immunology 7th

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Diseases Caused by Immune Responses: Hypersensitivity and Autoimmunity

Test Bank

Multiple Choice

1. All of the following are effector mechanisms of antibody-mediated disease EXCEPT:

A. Opsonization and phagocytosis of cells
B. Fas-dependent apoptosis of cells
C. Complement- and Fc receptor–mediated inflammation and tissue injury
D. Antibody stimulation of cell surface receptors in the absence of the physiologic
ligands
E. FcR crosslinking

ANS: B. Fas-dependent apoptosis is a regulatory mechanism in T cell–mediated

responses and may be involved in T cell–mediated damage to other cells, but the Fas
pathway is not stimulated by antibodies. Antibody-mediated (types I to III)
hypersensitivity diseases involve four main effector mechanisms: (1) IgE coats mast cells
and links the presence of allergens with mast cell activation and release of inflammatory
mediators; (2) antibody-mediated opsonization of cells and activation of complement
promotes phagocytosis of cells through phagocyte Fc or C3 receptors; (3) antibody
binding to tissues can promote recruitment of leukocytes via binding to Fc receptors on
leukocytes or by activation of complement with release of chemotactic byproducts; and
(4) autoantibodies specific for cell surface receptors either stimulate receptor activity in
the absence of the physiologic ligand or inhibit binding of physiologic ligands to their
receptors.

2. The figure shows routine histologic and immunofluorescence images of a kidney

biopsy specimen taken from a 53-year-old man with acute-onset renal failure and
hemoptysis (coughing up blood). The histologic section is notable for glomerular
inflammation in a crescentic distribution. Staining, using fluorescently tagged anti-
IgG antibody, shows linear deposits of IgG along the glomerular basement
membrane. Urinalysis is positive for moderate proteinuria and red cell casts. A chest
radiograph shows pulmonary infiltrates. Which of the following is the most likely
diagnosis?

A. Systemic lupus erythematosus

B. Graves’ disease
C. Chronic allograft rejection

Copyright © 2015 by Saunders, an imprint of Elsevier Inc.

Test Bank 2

D. Goodpasture’s syndrome
E. Poststreptococcal glomerulonephritis

ANS: D. Goodpasture’s syndrome is a type II hypersensitivity disease in which IgG

antibodies against the glomerular basement membrane (GBM) of the kidney deposit in a
linear distribution, causing complement- and Fc receptor–mediated inflammation and
subsequent nephritis. These anti-GBM antibodies cross-react with pulmonary alveolar
basement membranes to produce the typical clinical scenario of pulmonary hemorrhages
associated with renal failure. Note that the pathology here contrasts to that seen in
glomerulonephritis caused by type III hypersensitivity diseases (e.g., systemic lupus
erythematosus, poststreptococcal glomerulonephritis) in that deposits are linear and
smooth (antibody) versus granular and coarse (antigen-antibody immune complex).
Chronic allograft rejection more closely resembles a type IV hypersensitivity reaction.
Graves’ disease does not directly involve the kidney.

3. Which type of hypersensitivity disease is caused by deposition of antigen-antibody

complexes in blood vessel walls?
A. Type I
B. Type II
C. Type III
D. Type IV
E. Type V

ANS: C. Hypersensitivity diseases are often categorized by numerical designation. Type

III is immune complex disease. Type I is immediate hypersensitivity (allergic) disease.
Type II is disease caused by antibodies binding to antigens in tissues. Type IV is T cell–
mediated disease. There is no type V hypersensitivity.

4. Which of the following statements about immune complex–mediated diseases is NOT

true?
A. Immune complexes may contain antibodies bound to either self or foreign
antigens.
B. Immune complex–mediated diseases generally show systemic manifestations.
C. Pathologic features of immune complex diseases are determined by the cellular
source of the antigen.
D. Small complexes are deposited in vessels more than large complexes, which are
usually efficiently phagocytosed.
E. Complexes containing cationic antigens are more likely to produce severe, long-
lasting injury by depositing in blood vessels and renal glomeruli.

ANS: C. A hallmark of immune complex–mediated disease is that pathologic features

reflect the site of immune complex deposition and are not determined by the cellular
source of the antigen. As such, immune complex–mediated diseases tend to be systemic,
with little or no specificity for particular tissues. Immune complexes that cause disease
may be composed of either self antigens or foreign antigens with bound antibodies. These
complexes are produced during normal immune responses, but they cause disease only
when they are produced in excessive amounts or are not efficiently cleared so that they
become deposited in tissues. Small complexes are often not phagocytosed and tend to be

Copyright © 2015 by Saunders, an imprint of Elsevier Inc.

Test Bank 3

deposited in vessels more readily than large complexes, which are usually cleared by
phagocytes. Complexes containing cationic antigens bind tightly to negatively charged
components of basement membranes of blood vessels and kidney glomeruli, typically
producing long-lasting injury.

5. In which of the following disorders is the underlying pathogenic mechanism NOT

due to antibody-mediated damage to cells or tissues?
A. Pernicious anemia
B. Autoimmune hemolytic anemia
C. Pemphigus vulgaris
D. Acute rheumatic fever
E. Hyperacute allograft rejection

ANS: A. Pernicious anemia is caused by neutralizing autoantibodies specific for intrinsic

factor, which is a secreted protein required for absorption of vitamin B12 in the
gastrointestinal tract. The lack of vitamin B12 absorption leads to decreased
erythropoiesis, with subsequent anemia. Autoimmune hemolytic anemia is caused by
opsonizing antibodies specific for erythrocyte membrane antigens, leading to their
destruction by phagocytes. Pemphigus vulgaris occurs when autoantibodies specific for
epidermal cell intracellular junctions cause inflammatory disruption of the skin, leading
to formation of skin vesicles. Acute rheumatic fever is caused by antistreptococcal cell
wall antibodies that cross-react with myocardial antigens, leading to inflammation and
damage to myocardium. Hyperacute allograft rejection is caused by antibodies specific
for alloantigens on graft endothelial cells, leading to blood vessel wall damage and
thrombosis.

6. Which of the following is NOT associated with increased relative risk of developing
systemic lupus erythematosus?
A. Female gender
B. Deficiency in complement protein C2
C. African-American ethnicity
D. Presence of HLA-DR3
E. Defect in B cell maturation

ANS: E. Systemic lupus erythematosus (SLE) is a chronic, remitting and relapsing,

multisystem disease that affects predominantly women, with an incidence of 1 in 700 in
women between the ages of 20 and 60 years. Incidence increases to about 1 in 250 in
African-American women. The female-to-male ratio is 10:1. Deficiencies of classical
complement proteins, especially C2 or C4, are seen in about 10% of patients with SLE;
abnormal complement levels may result in defective clearance of immune complexes.
Individuals with the class II DR2 or DR3 HLA allele have a five-fold higher probability
of developing SLE. In contrast, patients with defects in B cell maturation would typically
have impaired antibody synthesis; thus it is unlikely that these patients would develop an
autoimmune disease characterized by the production of autoantibodies.
Matching

Questions 7-10

Copyright © 2015 by Saunders, an imprint of Elsevier Inc.

Test Bank 4

For each of the clinical scenarios in questions 7-10, choose the hypersensitivity type (A-
D) that best matches the associated immunologic disease. (Answers may be used more
than once.)
A. Type I hypersensitivity
B. Type II hypersensitivity
C. Type III hypersensitivity
D. Type IV hypersensitivity

7. A 5-year-old girl is taken to the emergency department with lethargy, confusion,

vomiting, abdominal pain, and flushed skin that is warm to the touch. Respirations are
fast and shallow (Kussmaul) and emanate a strong, fruity odor. The mother notes that
the child has been excessively thirsty over the past week and that she began wetting
her bed during naps. Urine dipstick testing reveals markedly elevated levels of
glucose and ketones.

ANS: D. This patient is in diabetic ketoacidosis, a serious complication of her previously

undiagnosed insulin-dependent diabetes mellitus (type 1). Her insulin deficiency results
from destruction of the insulin-producing beta cells of the islets of Langerhans in the
pancreas. Several mechanisms may contribute to beta cell destruction. Prominent among
these mechanisms are type IV (delayed-type) hypersensitivity reactions mediated by
CD4+ TH1 cells reactive with islet antigens, and cytotoxic T-lymphocyte (CTL)-
mediated lysis of islet cells.

8. A 60-year-old man is evaluated for shortness of breath, lightheadedness, diarrhea,

abdominal pain, and tingling in his fingers and toes. A blood smear from the patient is
shown in the figure. Antibodies to intrinsic factor are detected in his serum.

ANS: B. This patient has pernicious anemia, a type II hypersensitivity disease in which
autoantibodies against intrinsic factor of gastric parietal cells lead to neutralization of
intrinsic factor, which is required for intestinal absorption of vitamin B12. Deficiency in
vitamin B12 leads to abnormal erythropoiesis with macrocytic anemia and
hypersegmented neutrophils (as shown in the figure).

9. A 29-year-old woman gives birth to an infant who is lethargic, jaundiced, and

severely anemic and has an enlarged liver and spleen. The mother is RhD negative
and the father is homozygous RhD positive. This is their second child.
ANS: B. This condition, called erythroblastosis fetalis, is a severe form of hemolytic
disease of the newborn that occurs when an Rh-negative mother gives birth to an infant
who is Rh positive (since the father is homozygous Rh positive). In this disease, the
mother produces IgG antibodies against Rh-positive cells to which she has been

Copyright © 2015 by Saunders, an imprint of Elsevier Inc.

Test Bank for Cellular and Molecular Immunology 7th Edition Abul K Abbas Download

Test Bank 5

previously exposed (i.e., during the delivery of her first Rh-positive child). Because the
mother’s immune system recognizes Rh antigen as “foreign,” she produced large
amounts of anti-Rh antibody when she encountered the antigen during the second
pregnancy. This antibody crossed the placenta and mediated cellular injury in the second
infant. Therefore, this is an example of type II hypersensitivity. Note that the most
commonly involved antigen in erythroblastosis fetalis is RhD.

10. A 23-year-old medical student is taken to the emergency department because of

diffuse facial erythema (redness), tightness of the chest, and difficulty breathing. He
reports that the symptoms began shortly after he ate a shellfish dinner at a nearby
Thai restaurant. On physical examination, he appears to be in acute distress with
elevated heart rate and respiratory rate and a dangerously low blood pressure. He is
treated with epinephrine.

ANS: A. This young man is in anaphylactic shock, secondary to systemic exposure to

shellfish antigens, to which he produced IgE antibodies when he was previously exposed.
This is a classic example of type I (immediate) hypersensitivity.

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