Pathophysiology, 5th Edition By Lee-Ellen C. Copstead
Pathophysiology, 5th Edition By Lee-Ellen C. Copstead
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Chapter 10: Alterations in Immune Function
Complete Chapter Questions With Answers
Sample Questions Are Posted Below
MULTIPLE CHOICE
| a. | massive histamine release from mast cells leads to vasodilation. |
| b. | toxins released into the blood interfere with cardiac function. |
| c. | anaphylaxis results in large volume losses secondary to sweating. |
| d. | hypoxia due to bronchoconstriction impairs cardiac function. |
ANS: A
Hypotension can occur in type I hypersensitivity due to massive histamine release leading to vasodilation. Toxins are not released during type I hypersensitivity reactions. Sweating occurs as a reaction to shock from severe hypotension; the hypotension occurs first and is due to histamine release. Hypoxia occurs in anaphylaxis due to shock from severe hypotension; the hypotension occurs first and is due to histamine release.
REF: Pgs. 199-200
| a. | Systemic lupus erythematosus |
| b. | Graves disease |
| c. | Erythroblastosis fetalis |
| d. | Seasonal allergic rhinitis |
ANS: A
Systemic lupus erythematosus is a type III hypersensitivity disorder. Type III hypersensitivity is characterized by antigen-antibody complex deposition into tissues, with consequent activation of complement and a subsequent self-sustaining inflammatory reaction. Graves disease and erythroblastosis fetalis are type II hypersensitivity reactions. Seasonal allergic rhinitis is a type I hypersensitivity reaction.
REF: Pgs. 204-206
| a. | I |
| b. | II |
| c. | III |
| d. | IV |
ANS: C
Immune complex glomerulonephritis (an inflammatory renal disorder) is an example of a type III hypersensitivity reaction. The circulating immune complex is then deposited in the glomerular capillary wall and mesangium. Glomerulonephritis secondary to strep throat is not a type I, II, or IV sensitivity reaction.
REF: Pg. 206
| a. | negative; positive; positive |
| b. | positive; negative; negative |
| c. | negative; negative; positive |
| d. | negative; negative; negative |
ANS: C
If a woman is Rh-negative, RhoGAM is administered for prevention of Rh-positive antibodies. Erythroblastosis fetalis develops during pregnancy when an Rh-negative mother is sensitized to her fetus’s Rh-positive red cell group antigens because of exposure during her current or a previous pregnancy. RhoGAM contains antibodies against Rh antigens on fetal blood cells and is given to the mother to destroy fetal cells that may be present in her circulation before her immune system becomes activated and begins to produce anti-Rh antibodies. RhoGAM is not effective if the mother already has a positive antibody titer for fetal Rh antigens. An Rh-positive woman with negative Rh antibody titer carrying Rh-negative fetus does not require RhoGAM because the mother is Rh-positive and the fetus is Rh-negative.
REF: Pg. 203
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