NUR 213 Final Exam V2
• Describe the role of immunosuppression in cancer.: Immunosuppression
-> release immunosuppression factors into the tumor environment to increaseresistance to
chemo/radiation.
• Describe the role of viruses in cancer.: Viruses -> insert their genes into thehost cell's
genome so the host becomes the manufacturer of the virus.
• Describe the classification/grading system for staging of neoplasms.: I =well
differentiated
II = moderately differentiatedIII: poorly differentiated
IV= undifferentiated
• Identify the factors affecting blood flow in the systemic circulation.: Pres-sure, resistance,
velocity, viscosity, laminar vs. turbulent, and vascular compliance.
• Describe the mechanisms involved in the regulation of blood pressure.: -
Neural regulatory system, RAAS, and posterior pituitary gland.
• Characterize primary hypertension: no identifiable causes, develops over time from a
combination of genetics, environment, and lifestyle. Risk factors includefamily history, age,
obesity, stress, smoking, and physical inactivity.
• Characterize secondary hypertension.: known and treatable causes like kid-ney disease,
hormone disorders, and some drugs. Risk factors include underlying medical conditions and
medications.
• Describe the vessel changes occurring with atherosclerosis.: 1. endothelialinjury
2. inflammation and lipid accumulation
3. plaque formation
4. vessel narrowing
5. Plaque rupture and clot formation
• Endothelial injury: the endothelium becomes damaged because of hyperten-sion,
smoking, high LDL, or diabetes.
• Inflammation and lipid accumulation: damaged endothelium attracts white blood cells
and allows LDL cholesterol to enter the vessel wall. Monocytes becomemacrophages, which
engulf the LDL and turn into foam cells, forming fatty streaks.
• Plaque formation: foam cells and other immune cells accumulate.
• Vessel narrowing: The plaque narrows the arterial lumen, reducing blood flow.Over time,
,the vessel becomes less elastic and prone to rupture.
• Plaque rupture and clot formation: if the fibrous cap ruptures, the contents are exposed to
blood. This triggers platelet activation and clot formation, which canblock the artery, causing
MI or CVA.
• Identify coronary arterial diseases and peripheral arterial diseases that areusually associated
with atherosclerosis.: 1. Stable angina
2. Unstable angina
3. Myocardial infarction
4. Sudden cardiac death
5. Heart failure
• Stable angina: chest pain during exertion due to reduced blood flow
• Unstable angina: chest pain at rest, more serious and unpredictable
• Myocardial infarction: complete blockage of the coronary artery due to plaquerupture and
clot formation.
• Sudden cardiac death: often fatal arrhythmias following ischemia or MI.
• Heart failure: weakened heart muscle from chronic poor blood supply.
• Describe the pathophysiology of deep venous thrombosis (DVT) and iden-tify key risk
factors: Pathophysiology of DVT: venous stasis, arterial blood flow in
the lower extremity, because venous return is occluded.
Risk factors: venous stasis, endothelial injury, and hypercoagulability.
• Which of the following characteristics are associated with the development of a cancerous
cell? (Select all that apply): 1. The cancer cell is independent fromnormal cellular controls
2. Cancer cells show defects or variations in differentiation
• Differentiate five cellular adaptive processes.:
Atrophy
Hypertrophy
Metaplasia
Hyperplasia
Dysplasia
• major cause of cellular injury: Free radicals and hypoxia
, • differences between apoptosis and necrosis: Apoptosis is regulated and doesnot cause
inflammation.
Necrosis causes inflammation
• A nurse describes atrophy to a patient experiencing decreased mobility. Which
characteristic does the nurse include in the teaching session?: De-creased cell size
• A healthcare provider identifies abnormal cell growth in a patient's cervicaltissue during a
routine Pap smear. The provider explains to the patient that the changes in the cells are
potentially pre-cancerous. What type of cellular adaptation is most likely occurring?:
Dysplasia
• Describe the basic characteristics of the vascular acute inflammatory re- sponse.:
Vasodilation, increased permeability, leakage, WBC adherence to inner walls, and migration
through vessels.
• Identify the role of mast cells, neutrophils, and macrophages in the inflam-matory
response.: Mast cells: release inflammatory mediators
Neutrophils: arrive first to remove debris and phagocytose bacteria
Macrophages: prolonged phagocytosis at the site because they divide and releasecytokines.
• Identify the local and systemic manifestations of acute inflammation.: Local:redness, heat,
swelling, pain, loss of function
Systemic: fever, leukocytosis, increases acute-phase proteins, malaise, fatigue,anorexia,
elevated HR
• Identify the local and systemic manifestations of chronic inflammation.: Lo-cal: redness,
heat, swelling, pain, loss of function
Systemic: low-grade fever, weight loss, fatigue, anemia , elevated inflammatorymarkers,
persistence leukocytosis or lymphocytosis
• Explain the phases of wound healing:1st: Inflammation phase
- stop bleeding and prepare the wound for healing
- neutrophils, macrophages clean would
- cytokines and growth factors signal next phase
• Explain the phases of wound healing:
2nd reconstruction phase: reconstruction phase
- aka proliferative phase
- build new tissue
• Explain the phases of wound healing:
• Describe the role of immunosuppression in cancer.: Immunosuppression
-> release immunosuppression factors into the tumor environment to increaseresistance to
chemo/radiation.
• Describe the role of viruses in cancer.: Viruses -> insert their genes into thehost cell's
genome so the host becomes the manufacturer of the virus.
• Describe the classification/grading system for staging of neoplasms.: I =well
differentiated
II = moderately differentiatedIII: poorly differentiated
IV= undifferentiated
• Identify the factors affecting blood flow in the systemic circulation.: Pres-sure, resistance,
velocity, viscosity, laminar vs. turbulent, and vascular compliance.
• Describe the mechanisms involved in the regulation of blood pressure.: -
Neural regulatory system, RAAS, and posterior pituitary gland.
• Characterize primary hypertension: no identifiable causes, develops over time from a
combination of genetics, environment, and lifestyle. Risk factors includefamily history, age,
obesity, stress, smoking, and physical inactivity.
• Characterize secondary hypertension.: known and treatable causes like kid-ney disease,
hormone disorders, and some drugs. Risk factors include underlying medical conditions and
medications.
• Describe the vessel changes occurring with atherosclerosis.: 1. endothelialinjury
2. inflammation and lipid accumulation
3. plaque formation
4. vessel narrowing
5. Plaque rupture and clot formation
• Endothelial injury: the endothelium becomes damaged because of hyperten-sion,
smoking, high LDL, or diabetes.
• Inflammation and lipid accumulation: damaged endothelium attracts white blood cells
and allows LDL cholesterol to enter the vessel wall. Monocytes becomemacrophages, which
engulf the LDL and turn into foam cells, forming fatty streaks.
• Plaque formation: foam cells and other immune cells accumulate.
• Vessel narrowing: The plaque narrows the arterial lumen, reducing blood flow.Over time,
,the vessel becomes less elastic and prone to rupture.
• Plaque rupture and clot formation: if the fibrous cap ruptures, the contents are exposed to
blood. This triggers platelet activation and clot formation, which canblock the artery, causing
MI or CVA.
• Identify coronary arterial diseases and peripheral arterial diseases that areusually associated
with atherosclerosis.: 1. Stable angina
2. Unstable angina
3. Myocardial infarction
4. Sudden cardiac death
5. Heart failure
• Stable angina: chest pain during exertion due to reduced blood flow
• Unstable angina: chest pain at rest, more serious and unpredictable
• Myocardial infarction: complete blockage of the coronary artery due to plaquerupture and
clot formation.
• Sudden cardiac death: often fatal arrhythmias following ischemia or MI.
• Heart failure: weakened heart muscle from chronic poor blood supply.
• Describe the pathophysiology of deep venous thrombosis (DVT) and iden-tify key risk
factors: Pathophysiology of DVT: venous stasis, arterial blood flow in
the lower extremity, because venous return is occluded.
Risk factors: venous stasis, endothelial injury, and hypercoagulability.
• Which of the following characteristics are associated with the development of a cancerous
cell? (Select all that apply): 1. The cancer cell is independent fromnormal cellular controls
2. Cancer cells show defects or variations in differentiation
• Differentiate five cellular adaptive processes.:
Atrophy
Hypertrophy
Metaplasia
Hyperplasia
Dysplasia
• major cause of cellular injury: Free radicals and hypoxia
, • differences between apoptosis and necrosis: Apoptosis is regulated and doesnot cause
inflammation.
Necrosis causes inflammation
• A nurse describes atrophy to a patient experiencing decreased mobility. Which
characteristic does the nurse include in the teaching session?: De-creased cell size
• A healthcare provider identifies abnormal cell growth in a patient's cervicaltissue during a
routine Pap smear. The provider explains to the patient that the changes in the cells are
potentially pre-cancerous. What type of cellular adaptation is most likely occurring?:
Dysplasia
• Describe the basic characteristics of the vascular acute inflammatory re- sponse.:
Vasodilation, increased permeability, leakage, WBC adherence to inner walls, and migration
through vessels.
• Identify the role of mast cells, neutrophils, and macrophages in the inflam-matory
response.: Mast cells: release inflammatory mediators
Neutrophils: arrive first to remove debris and phagocytose bacteria
Macrophages: prolonged phagocytosis at the site because they divide and releasecytokines.
• Identify the local and systemic manifestations of acute inflammation.: Local:redness, heat,
swelling, pain, loss of function
Systemic: fever, leukocytosis, increases acute-phase proteins, malaise, fatigue,anorexia,
elevated HR
• Identify the local and systemic manifestations of chronic inflammation.: Lo-cal: redness,
heat, swelling, pain, loss of function
Systemic: low-grade fever, weight loss, fatigue, anemia , elevated inflammatorymarkers,
persistence leukocytosis or lymphocytosis
• Explain the phases of wound healing:1st: Inflammation phase
- stop bleeding and prepare the wound for healing
- neutrophils, macrophages clean would
- cytokines and growth factors signal next phase
• Explain the phases of wound healing:
2nd reconstruction phase: reconstruction phase
- aka proliferative phase
- build new tissue
• Explain the phases of wound healing:
