NURS 611 ADVANCED PATHOPHYSIOLOGY EXAM 1
2026 LATEST UPDATE QUESTIONS AND CORRECT
VERIFIED ANSWERS ALREADY GRADED A+
Type IV (Delayed-Type Hypersensitivity) - ANS-Mediated by T cells
Delayed hypersensitivity
-Tissue damage resulting from a delayed cellular reaction to antigen
No primary antibody involvement
Principal mediators- lymphocytes
Principal effector cells- lymphocytes & macrophages
Sensitized T cells react with altered or foreign cells initiate inflammation ,cell destruction
Sensitized TH1 cells activated t release cytokines upon binding to antigen, resulting in
macrophages and cytotoxic T cell accumulation
Disease examples include: contact dermatitis, chronic transplant rejection
HIstamine - ANS-Increased vascular permeability, vasodilation, urticaria smooth muscle
constriction, mucus secretion, pruritus (H1 receptor stimulated)
Immunoglobulins involved in Hypersensitivity Reactions - ANS-Cutaneous basophil
hypersensitivity
-Most rapid, skin swelling
Contact hypersensitivity
,-Most familiar type, epidermal phenomenon
-Peaks 48 -72 hrs
Tuberculin-type hypersensitivity
-Individual (previously infected by TB) exposed to tuberculin antigen in TB test
-Dermal phenomenon peaks 48 -72 hrs
Granulomatous hypersensitivity
-Chronic
-Tissue destruction
-Antigen not destroyed within the macrophages
-Failure of lysosome-phagosome fusion
-Forms a granulomascar tissue or necrosis (caseous /cheesy )
Immunoglobulins - ANS-IgG, IgM, IgA, IgD and IgE
IgA - ANS-Found in gastrointestinal, respiratory and urogenital tract muscosa
Prevents the colonization by pathogen
Also present in saliva, tears, and milk
Protects against pathogens in these areas
IgD - ANS-Membrane immunoglobulin
It is part of the membrane receptor of naive B lymphocytes (BCR)
Part of the B cell receptor
,Activates basophils and mast cells
IgE - ANS-Involved in allergic and parasitic processes
Its interaction with basophils and mastocytes causes histamine release
Protects against parasitic worms
Responsible for allergic reactions
IgG - ANS-Main immunoglobulin of acquired immunity
It has the capacity to cross the placental barrier
Secreted by plasma cells in the blood
Able to process the placenta to the fetus
IgM - ANS-It is part of the membrane receptor of naive B lymphocytes (BCR)
Form found in the serum, secreted early in acquired immune response
May be attached to the surface of a B cell of secreted into the blood
Responsible for the early stages of immunity
First responder:)
Only one that is not a monomer
*Chapter 11: Malignant Disorders of White Blood Cells* - ANS-
Typical Signs and Symptoms of Malignant Disorders of WBCs - ANS-Malaise, weakness
Unexplained fever, night sweats
, Recurrent infections
Enlarged, nontender lymph nodes (lymphadenopathy) with lymphoma and some leukemias
Very high total white blood cell count or the presence of abnormal cell types
*related to leukopenia, anemia, and thrombocytopenia
Anemia Common Clinical Manifestations - ANS-Pallor
Fatigue
Malaise
Shortness of breath
Decreased activity tolerance
Acute Leukemia - ANS-Typically present with pancytopenia, or a decrease in the counts of all of
the normal blood cells, including the normal white cells (the leukemic cells accounting for
almost all of the high total WBCs), red blood cells, and platelets.
This is caused by the crowding out of normal precursors in the bone marrow by the abnormally
dividing blast cells, and by the inhibition of normal hematopoiesis due to secretion of cytokines
and inhibitory substances.
The patient's presenting symptoms are directly related to the blood abnormalities.
The fatigue and pallor are due to the anemia (lack of red blood cells) and the resulting reduced
oxygen-carrying capacity.
The petechiae and bleeding are from the lack of platelets, inhibiting the ability of the blood to
clot.
Patients with leukemia are susceptible to serious infections due to the lack of normal WBCs.
Finally, the markedly elevated numbers of leukemic cells can clog small blood vessels and result
in strokes, retinal vein occlusion, and pulmonary infarction.
Non-Hodgkin's Lymphoma - ANS-Do not have Reed-Sternberg cells
2026 LATEST UPDATE QUESTIONS AND CORRECT
VERIFIED ANSWERS ALREADY GRADED A+
Type IV (Delayed-Type Hypersensitivity) - ANS-Mediated by T cells
Delayed hypersensitivity
-Tissue damage resulting from a delayed cellular reaction to antigen
No primary antibody involvement
Principal mediators- lymphocytes
Principal effector cells- lymphocytes & macrophages
Sensitized T cells react with altered or foreign cells initiate inflammation ,cell destruction
Sensitized TH1 cells activated t release cytokines upon binding to antigen, resulting in
macrophages and cytotoxic T cell accumulation
Disease examples include: contact dermatitis, chronic transplant rejection
HIstamine - ANS-Increased vascular permeability, vasodilation, urticaria smooth muscle
constriction, mucus secretion, pruritus (H1 receptor stimulated)
Immunoglobulins involved in Hypersensitivity Reactions - ANS-Cutaneous basophil
hypersensitivity
-Most rapid, skin swelling
Contact hypersensitivity
,-Most familiar type, epidermal phenomenon
-Peaks 48 -72 hrs
Tuberculin-type hypersensitivity
-Individual (previously infected by TB) exposed to tuberculin antigen in TB test
-Dermal phenomenon peaks 48 -72 hrs
Granulomatous hypersensitivity
-Chronic
-Tissue destruction
-Antigen not destroyed within the macrophages
-Failure of lysosome-phagosome fusion
-Forms a granulomascar tissue or necrosis (caseous /cheesy )
Immunoglobulins - ANS-IgG, IgM, IgA, IgD and IgE
IgA - ANS-Found in gastrointestinal, respiratory and urogenital tract muscosa
Prevents the colonization by pathogen
Also present in saliva, tears, and milk
Protects against pathogens in these areas
IgD - ANS-Membrane immunoglobulin
It is part of the membrane receptor of naive B lymphocytes (BCR)
Part of the B cell receptor
,Activates basophils and mast cells
IgE - ANS-Involved in allergic and parasitic processes
Its interaction with basophils and mastocytes causes histamine release
Protects against parasitic worms
Responsible for allergic reactions
IgG - ANS-Main immunoglobulin of acquired immunity
It has the capacity to cross the placental barrier
Secreted by plasma cells in the blood
Able to process the placenta to the fetus
IgM - ANS-It is part of the membrane receptor of naive B lymphocytes (BCR)
Form found in the serum, secreted early in acquired immune response
May be attached to the surface of a B cell of secreted into the blood
Responsible for the early stages of immunity
First responder:)
Only one that is not a monomer
*Chapter 11: Malignant Disorders of White Blood Cells* - ANS-
Typical Signs and Symptoms of Malignant Disorders of WBCs - ANS-Malaise, weakness
Unexplained fever, night sweats
, Recurrent infections
Enlarged, nontender lymph nodes (lymphadenopathy) with lymphoma and some leukemias
Very high total white blood cell count or the presence of abnormal cell types
*related to leukopenia, anemia, and thrombocytopenia
Anemia Common Clinical Manifestations - ANS-Pallor
Fatigue
Malaise
Shortness of breath
Decreased activity tolerance
Acute Leukemia - ANS-Typically present with pancytopenia, or a decrease in the counts of all of
the normal blood cells, including the normal white cells (the leukemic cells accounting for
almost all of the high total WBCs), red blood cells, and platelets.
This is caused by the crowding out of normal precursors in the bone marrow by the abnormally
dividing blast cells, and by the inhibition of normal hematopoiesis due to secretion of cytokines
and inhibitory substances.
The patient's presenting symptoms are directly related to the blood abnormalities.
The fatigue and pallor are due to the anemia (lack of red blood cells) and the resulting reduced
oxygen-carrying capacity.
The petechiae and bleeding are from the lack of platelets, inhibiting the ability of the blood to
clot.
Patients with leukemia are susceptible to serious infections due to the lack of normal WBCs.
Finally, the markedly elevated numbers of leukemic cells can clog small blood vessels and result
in strokes, retinal vein occlusion, and pulmonary infarction.
Non-Hodgkin's Lymphoma - ANS-Do not have Reed-Sternberg cells
