NUR 376 FINAL MODULES EXAM QUESTIONS WITH COMPLETE
SOLUTION
Compare malignant (including angiogenesis) and benign conditions.
Malignant: Poorly differentiated, invasive and penetrative. Lack adhesion to the tumor
mass and easily break free to metastasize from a primary site to a distant site through
lymph or blood.
Benign: well-differentiated and remain localized, cohesive, and well-demarcated from
surrounding tissue. Not invasive, do not destroy surrounding tissue, and do not break
away or travel from the tumor cell mass.
What are the stages of carcinoma?
Initiation: alteration of genes arising spontaneously or induced by carcinogenic agent.
Promotion: actively proliferating pre-neoplastic cells accumulate. Within this period, the
process can be altered by chemopreventive agents that affect growth rates.
Progression: phase between a premalignant lesion and the development of invasive
cancer.
Metastasis: where genetic and phenotypic changes and cell proliferation occur. Rapid
increase in tumor size.
Interpret TNM staging
T: Tumor Size
N: Lymph node involvement
M: Metastasis to distinct organs
Example: If a patient has a 2.5-cm tumor in the right breast, palpable lymph nodes, and
a computerized tomography (CT) scan indicative of a metastatic lesion in the liver, it
would be staged as T2N1M1 breast cancer
T (TUMOR)
TX: Main tumor cannot be measured
TO: Main tumor cannot be found
Tis: Carcinoma in situ
T1−4: Progressive increase in tumor size or involvement
N (NODES)
NX: Cancer in nearby lymph nodes cannot be measured
NO: No cancer in nearby lymph nodes
N1−3: Increasing involvement of regional lymph nodes
M (METASTASIS)
MX: Metastasis cannot be measured
, MO: Cancer has not spread to other parts of the body
M1: Cancer has spread to other parts of the body
Interpret cancer grading
Grade I: Cells well differentiated
Grade II: moderately differentiated
Grade III: poorly differentiated or anaplastic
Prostate cancer: pathophysiology, prevention and clinical manifestations
Pathophysiology: Carcinogenic mutations, spurred on by testosterone, proliferate
glandular cells. Mutates Tp53 and Rb gene, leading to tumor progression and
metastasis.
S/S: Decrease force of urine strea, urine hesitancy, incomplete emptying of bladder, e
hematuria, azotemia, anemia, anorexia, and back pain (vertebral bone metastasis).
Prevention: Prostate exams, screen family history, BRCA 1 and 2 genes, age, ethnicity
(African American), HPC1 and HPC2. Eat plant based.
Colon cancer: pathophysiology, prevention and clinical manifestations
Pathophysiology: Usually a polyp that becomes cancerous. Likely due to defective
tumor suppressor genes, activated oncogenes, or mismatched gene repair.
S/S: fatigue, weakness, abdominal cramping, weight loss, iron-deficiency anemia,
changes in bowel habits, blood in the stool (iron-deficiency anemia is frequently a sign
of slow GI blood loss that occurs in colon cancer), diarrhea, and constipation.
Prevention: Likely due to genetic factors. Familial adenomatous polyposis (FAP) can
lead to it. The APC (adenomatous polyposis coli) gene is a defective tumor suppressor
gene, and it confers an almost 100% likelihood of colon cancer development. Eat plant
based.
Breast cancer: pathophysiology, prevention and clinical manifestations
Pathophysiology: Usually epithelial cell tumors that develop from cells lining the ducts or
lobules of the breast. An unknown triggering factor starts causing cells to replicate and
proliferate, and invade surrounding tissue. Estrogen and progesterone stimulate the
growth typically.
S/S: Mass in breast tissue with irregular borders. Firm and connected to skin or chest
wall. Nipple discharge, swelling in one breast, nipple or skin retraction, and peau
d'orange—thickening of skin. Paget's disease of the breast, which involves redness,
crusting, pruritus, and tenderness of the nipple, is also characteristic of a cancerous
change.
Prevention: BRCA 1 and BRCA 2 screening (preventative mastectomy), regular breast
exams, mammograms
Normal lab values for PTT/aPTT/INR and what pathway are they involved with?
Intrinsic: activated with injury to endothelial lining (inside the vessel). PTT (25-35
seconds)
SOLUTION
Compare malignant (including angiogenesis) and benign conditions.
Malignant: Poorly differentiated, invasive and penetrative. Lack adhesion to the tumor
mass and easily break free to metastasize from a primary site to a distant site through
lymph or blood.
Benign: well-differentiated and remain localized, cohesive, and well-demarcated from
surrounding tissue. Not invasive, do not destroy surrounding tissue, and do not break
away or travel from the tumor cell mass.
What are the stages of carcinoma?
Initiation: alteration of genes arising spontaneously or induced by carcinogenic agent.
Promotion: actively proliferating pre-neoplastic cells accumulate. Within this period, the
process can be altered by chemopreventive agents that affect growth rates.
Progression: phase between a premalignant lesion and the development of invasive
cancer.
Metastasis: where genetic and phenotypic changes and cell proliferation occur. Rapid
increase in tumor size.
Interpret TNM staging
T: Tumor Size
N: Lymph node involvement
M: Metastasis to distinct organs
Example: If a patient has a 2.5-cm tumor in the right breast, palpable lymph nodes, and
a computerized tomography (CT) scan indicative of a metastatic lesion in the liver, it
would be staged as T2N1M1 breast cancer
T (TUMOR)
TX: Main tumor cannot be measured
TO: Main tumor cannot be found
Tis: Carcinoma in situ
T1−4: Progressive increase in tumor size or involvement
N (NODES)
NX: Cancer in nearby lymph nodes cannot be measured
NO: No cancer in nearby lymph nodes
N1−3: Increasing involvement of regional lymph nodes
M (METASTASIS)
MX: Metastasis cannot be measured
, MO: Cancer has not spread to other parts of the body
M1: Cancer has spread to other parts of the body
Interpret cancer grading
Grade I: Cells well differentiated
Grade II: moderately differentiated
Grade III: poorly differentiated or anaplastic
Prostate cancer: pathophysiology, prevention and clinical manifestations
Pathophysiology: Carcinogenic mutations, spurred on by testosterone, proliferate
glandular cells. Mutates Tp53 and Rb gene, leading to tumor progression and
metastasis.
S/S: Decrease force of urine strea, urine hesitancy, incomplete emptying of bladder, e
hematuria, azotemia, anemia, anorexia, and back pain (vertebral bone metastasis).
Prevention: Prostate exams, screen family history, BRCA 1 and 2 genes, age, ethnicity
(African American), HPC1 and HPC2. Eat plant based.
Colon cancer: pathophysiology, prevention and clinical manifestations
Pathophysiology: Usually a polyp that becomes cancerous. Likely due to defective
tumor suppressor genes, activated oncogenes, or mismatched gene repair.
S/S: fatigue, weakness, abdominal cramping, weight loss, iron-deficiency anemia,
changes in bowel habits, blood in the stool (iron-deficiency anemia is frequently a sign
of slow GI blood loss that occurs in colon cancer), diarrhea, and constipation.
Prevention: Likely due to genetic factors. Familial adenomatous polyposis (FAP) can
lead to it. The APC (adenomatous polyposis coli) gene is a defective tumor suppressor
gene, and it confers an almost 100% likelihood of colon cancer development. Eat plant
based.
Breast cancer: pathophysiology, prevention and clinical manifestations
Pathophysiology: Usually epithelial cell tumors that develop from cells lining the ducts or
lobules of the breast. An unknown triggering factor starts causing cells to replicate and
proliferate, and invade surrounding tissue. Estrogen and progesterone stimulate the
growth typically.
S/S: Mass in breast tissue with irregular borders. Firm and connected to skin or chest
wall. Nipple discharge, swelling in one breast, nipple or skin retraction, and peau
d'orange—thickening of skin. Paget's disease of the breast, which involves redness,
crusting, pruritus, and tenderness of the nipple, is also characteristic of a cancerous
change.
Prevention: BRCA 1 and BRCA 2 screening (preventative mastectomy), regular breast
exams, mammograms
Normal lab values for PTT/aPTT/INR and what pathway are they involved with?
Intrinsic: activated with injury to endothelial lining (inside the vessel). PTT (25-35
seconds)
