exam 1.Exam 2 & Exam 3: NSG530/ NSG 530 (Latest 2023/ 2024 UPDATES STUDY BUNDLE WITH COMPLETE SOLUTIONS) – Advanced Pathophysiology Exams | Questions and Verified Answers| 100% Correct| Grade A
Exam 2: NSG530/ NSG 530 (Latest 2023/
2024) – Advanced Pathophysiology Exam
Review| Complete Guide with Verified
Answers| 100% Correct
Q: Oncogenes
Answer:
genes that cause cancer by blocking the normal controls on cell reproduction
Q: Proto-oncogenes
Answer:
the corresponding normal cellular genes that are responsi- ble for normal cell growth and
division
Q: Oncogene activation
Answer:
point mutation in RAS gene converts from regulated to unregulated
Q: tumor suppressor genes
Answer:
A gene whose protein product inhibits cell division, thereby preventing the uncontrolled cell
growth that contributes to cancer.
Q: replicative immortality
Answer:
normal body cells are not immortal and can only divide a limited number of times, CA cells can
live forever, unlimited lifespan
Q: Telomeres
Answer:
ends of chromosomes, protective caps on each chromosome
Q: genomic instability
Answer:
-increased tendency for genomic mutations during life cycle of the cell
-risk for cancer increases
-chromosome instability
Q: Angiogenesis
Answer:
cancer has the ability to from and grow new and own blood vessels, giving CA cells direct
access to blood vessels
Q: metastasis
Answer:
The spread of cancer cells to locations distant from their original site.
Q: what are changes in tumor microenvironment that initiate mets?
Answer:
-transition into mesenchymal like loss of polarity, increase migratory capacity, increase resistance to apoptosis, ability to re-differential into other cells
Q: cellular dedifferentiation
Answer:
regeneration, cells revert to an earlier stage of de- velopment
they can now separate from primary tumor and flourish in a secondary potential hostile
secondary site.
Q: Skin cancer types
Answer:
basal cell carcinoma, squamous cell carcinoma, melanoma
Q: skin cancer risk factors
Answer:
- Fair skin
- Too much exposure to UV rays.
Q: basal cell carcinoma
Answer:
Most common and least severe type of skin cancer; often characterized by light or pearly flesh
colored nodules.
Q: squamous cell carcinoma
Answer:
malignant tumor of the squamous epithelial cells in the epidermis; appears on ear, face, nose,
neck, back- appears to be a scab that will not heal
Q: Melanoma
Answer:
The most serious form of skin cancer; can develop from an existing mole. ABCDE warnings
Q: most common type of cancer
Answer:
skin cancer
Q: Breast cancer staging
Answer:
T: is) in situ, 1) <2cm, 2) 2-5cm, 3) >5cm, 4) extension into chest wall / skin or inflammatory
carcinoma
N: 1) movable ipsilateral axillary LN, 2) fixed ipsilateral axillary LN or clinically apparent
ipsilateral internal mammary node, 3) axillary and internal mammary nodes
M: 1) metastasis
Q: cervical cancer
Answer:
Malignant cell growth in the cervix; can be caused by HPV
virus
Q: HPV (human papilloma virus) causing CA
Answer:
HPV 16 or HPV 18
Q: cervical dysplasia
Answer:
the presence of precancerous changes in the cells that make up the inner lining of the cervix
Exam 1: NSG530/ NSG 530 (Latest 2023/ 2024) – Advanced Pathophysiology Exam | Questions and Verified Answers| 100% Correct| Grade A
Exam 1: NSG530/ NSG 530 (Latest 2023/
2024) – Advanced Pathophysiology Exam |
Questions and Verified Answers| 100%
Correct| Grade A
Q: When antibodies are formed against red blood cell antigens of the Rh system, how are the
blood cells destroyed?
a. Complement-mediated cell lysis b. Phagocytosis by macrophages c. Phagocytosis in the spleen
d. Neutrophil granules and toxic oxygen products
Answer:
C
Antibodies against platelet-specific antigens or against red blood cell antigens of the Rh system
coat those cells at low density, resulting in their preferential removal by phagocytosis in the
spleen, rather than by complement-mediated lysis. These blood cells are not destroyed by
complement-mediated cell lysis, phagocytosis by macrophages, neutrophil granules, or toxic
oxygen products.
Q: When soluble antigens from infectious agents enter circulation, what is tissue damage a
result of?
a. Complement-mediated cell lysis b. Phagocytosis by macrophages c. Phagocytosis in the spleen
d. Neutrophil granules and toxic oxygen products
Answer:
D
Of the options available, only the components of neutrophil granules as well as the several toxic
oxygen products produced by these cells, damage the tissue.
Q: How are target cells destroyed in a type II hypersensitivity reaction?
a. Complement-mediated cell lysis b. Phagocytosis by macrophages
c. Neutrophil granules and toxic oxygen products d. Natural killer cells
Answer:
D
The mechanism that results in a type II hypersensitivity reaction involves a sub- population of
cytotoxic cells that are not antigen specific (natural killer [NK] cells). Antibody on the target cell
is recognized by Fc receptors on the NK cells, which releases toxic substances that destroy the
target cell. The other options do not cause the destruction of target cells related to a type II
hypersensitivity reaction.
Q: Graves disease (hyperthyroidism) is an example of which type II hyper- sensitivity reaction?
a. Modulation
b. Antibody-dependent cell-mediated cytotoxicity c. Neutrophil-mediated damage
d. Complement-mediated lysis
Answer:
A
The antibody reacts with the receptors on the target cell surface and modulates the function of
the receptor by preventing interactions with their normal ligands, replacing the ligand and
inappropriately stimulating the receptor or destroying the receptor. For example, in the
hyperthyroidism (excessive thyroid activity) of Graves disease, autoantibody binds to and
activates receptors for thyroid-stimulating hor- mone (TSH) (a pituitary hormone that controls
the production of the hormone thyroxine by the thyroid). Graves disease is not a result of cellmediated cytotoxicity, neutrophil-mediated damage, or complement-mediated lysis.
Q: Type III hypersensitivity reactions are a result of which of these?
a. Antibodies coating mast cells by binding to receptors that signal its degran- ulation,
followed by the discharge of preformed mediators
b. Antibodies binding to soluble antigens that were released into body fluids and the
immune complexes being deposited in the tissues
c. Tc cells or lymphokine-producing Th1 cells directly attacking and destroying cellular targets
d. Antibodies binding to the antigen on the cell surface
Answer:
B
Antigen-antibody (immune) complexes that are formed in the circulation and then deposited later
in vessel walls or extravascular tissues cause most type III hypersen- sitivity diseases. Type III
hypersensitivity reactions are not the result of antibodies coating mast cells to signal their
degranulation, immune cells directly attacking and destroying targets, or antibodies binding to
the antigen on the cell surface.
Q: A type IV hypersensitivity reaction causes which result?
a. Antibodies coating mast cells by binding to receptors that signal its degran- ulation,
followed by the discharge of preformed mediators
b. Antibodies binding to soluble antigens that were released into body fluids and the
immune complexes being deposited in the tissues
c. Lymphokine-producing Th1 cells directly attacking and destroying cellular targets
d. Antibodies binding to the antigen on the cell surface
Answer:
C
Type I, II, and III hypersensitivity reactions are mediated by antibody, type IV
reactions are mediated by T lymphocytes and do not involve antibody. Type IV
mechanisms occur through either Tc cells or lymphokine-producing Th1 cells. Tc cells directly
attack and destroy cellular targets.
Q: In a type III hypersensitivity reaction, the harmful effects after the immune complexes that
are deposited in tissues are a result of what?
a. Cytotoxic T cells
b. Natural killer cells
c. Complement activation
d. Degranulation of mast cells
Answer:
C
Complement activation, particularly through the generation of chemotactic factors for
neutrophils, causes the harmful effects of immune complex deposition. The neutrophils bind to
antibody and C3b contained in the complexes and attempt to ingest the immune complexes. Type
III hypersensitivity reactions as described are not the result of cytotoxic T cells, natural killer
cells, or degranulation of mast cells.
Q: Raynaud phenomenon is classified as a type III hypersensitivity reaction and is due to:
a. Immune complexes that are deposited in capillary beds, blocking circulation b. Mast cells that
are bound to specific endothelial receptors, causing them to degranulate and creating a localized
inflammatory reaction that occludes capillary
circulation
c. Cytotoxic T cells that attack and destroy the capillaries so that they are unable to
perfuse local tissues
d. Antibodies that detect the capillaries as foreign protein and destroy them using
lysosomal enzymes and toxic oxygen species
Exam 2: NSG530/ NSG 530 (Latest 2023/ 2024) – Advanced Pathophysiology Exam | Questions and Verified Answers| 100% Correct| Grade A
Exam 2: NSG530/ NSG 530 (Latest 2023/
2024) – Advanced Pathophysiology Exam |
Questions and Verified Answers| 100%
Correct| Grade A
Q: A patient was diagnosed as HIV positive several years ago. Which of the following blood
tests is most clinically useful for determining the stage and severity of her disease?
Answer:
CD4+ cell counts
Q: When the maternal immune system becomes sensitized against antigens expressed by the
fetus, what type of immune reaction occurs? (transfusions, transplant tissues, pregnancy)
Answer:
Alloimmune
Q: A 10-year-old male is stung by a bee while playing in the yard. He begins itching and
develops pains, swelling, redness and respiratory difficulties. He is suffering from
Answer:
: anaphylaxis
Q: When a patient presents at the ED for an allergic reaction, the nurse rec- ognized the most
severe consequences of a type I hypersensitivity reaction is
Answer:
: anaphylaxis
Q: A nurse recalls that an example of an immune-complex-mediated disease is
Answer:
: serum sickness
Q: When a nurse cares for a patient with systemic lupus erythematosus (SLE), the nurse
remembers this disease is an example of
Answer:
: autoimmunity (disturbance in immunologic tolerance of self-antigens)
Q: A 30-year-old female c/o fatigue, arthritis, rash and changes in urine color. Laboratory
testing reveals anemia, lymphopenia and kidney inflammation. Assuming a diagnosis of SLE,
which of the following is also likely to be present?
Answer:
Autoantibodies
Q: A 40-year-old is diagnosed with SLE. Which of the following findings would be considered
a symptom of this disease?
Answer:
Photosensitivity + facial rash con- fined to cheeks (malar rash)
Q: A person is given an attenuated antigen as a vaccine. When the person asks what was given
in the vaccine, how should the nurse respond? The antigen is
Answer:
: alive, but less infectious.
Q: An immunologist is discussing endotoxin production. Which information should the
immunologist include? Endotoxins are produced by
Answer:
: gram-nega- tive bacteria.
Q: A 50-year-old female experiences decreased blood pressure, decreased oxygen delivery,
cardiovascular shock and subsequent death. A complication of endotoxic shock is suspected.
Which of the following is the most likely cause?
Answer:
Gram-negative bacteria
Q: Which information indicates a correct understanding of viral vaccines? Most viral vaccines
contain
Answer:
: attenuated viruses.
Q: A 22-year-old was recently diagnosed with acquired immunodeficiency syndrome (AIDS).
Which decreased lab finding would be expect to accompany this virus?
Answer:
CD4+ T-helper
Q: A 30-year-old male was diagnosed with HIV. Which of the following treat- ments would be
most effective?
Answer:
Antiretroviral therapy (ART)
Q: When the immunologist says that pathogens possess virulence, what does virulence mean?
Answer:
Causes disease.
Exam 3: NSG530/ NSG 530 (Latest 2023/
2024) – Advanced Pathophysiology Exam
Review| Guide with Questions and Verified
Answers| 100% Correct
Q: the stomach is impermeable to what?
Answer:
water, but can absorb alcohol and aspirin as they are lipid soluble.
Q: blood to stomach is supplied by ?
Answer:
celiac artery- abundant!
Q: Three phases of gastric secretion
Answer:
1.cephalic phase
2.gastric phase
3.intestinal phase
Q: Motilin
Answer:
increases peristalsis
Q: Secretin
Answer:
decreases peristalsis
Q: Gastric mixing and emptying
Answer:
- Retropulsion
- Rate dependent on volume, osmotic pressure, and chemical composition
Q: Stimulation of gastric secretion
Answer:
-Eating
-Gastrin
-Paracrine pathways
-Acetylcholine
-Chemicals
–Ethanol, coffee, protein
Q: intrinsic factor
Answer:
makes the absorption of vitamin B12 happen
Q: gastroferritin
Answer:
binds Fe2+ and transports it to small intestine
Q: phases of gastric secretion
Answer:
1.cephalic phase
2.gastric phase
3.intestinal phase
Q: Gastric juices include
Answer:
- Pepsin, an enzyme that digests protein
- Other Enzymes
- Hydrochloric Acid
- Mucus
- Salts
- Water
Q: acid plays what role in gastric secretion?
Answer:
dissolves food fibers, act as bac- tericide, convert pepsinogen to pepsin
Q: Pepsin
Answer:
Enzyme that breaks down proteins in the stomach secreted by chief cells
Q: Mucous in stomach
Answer:
Protects stomach cells from gastric juices
Q: small intestine
Answer:
Digestive organ where most chemical digestion and absorption of food takes place
Q: Three sections of the small intestine
Answer:
1.Duodenum
2.Jejunum
3.Ileum
Q: ileocecal valve
Answer:
valve between the ileum of the small intestine and the cecum of the large intestine
Q: peritoneum
Answer:
Double-layered membrane surrounding the abdominal organs
Q: mesentery
Answer:
a fused double layer of the parietal peritoneum that attaches parts of the intestine to the interior
abdominal wall
Q: duodenum
Answer:
first part of the small intestine- supplied by the gastroduodenal artery
Q: jejunum
Answer: