Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Advanced Patho Test 1 > TEST 1: Cancer > Flashcards

TEST 1: Cancer Flashcards

1
Q

Neoplasm

A

Global term for mass. Refers to any new and abnormal growth of tissue in the body that can be benign or malignant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Benign tumors characteristics (5)

A
  1. Usually grow slowly: allows for more manageable treatment (low mitotic index)
  2. non-invasive
  3. non-metastatic
  4. generally have well defined boundaries surrounded by fibrous capsule: decreases ability to invade surrounding tissues (easy surgery)
  5. Well differentiated: closely resemble normal cells in both structure and function decreasing risk of aggressive behavior

Ex: Uterine fibroids, lipomas, adenomas (glandular growths)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Malignant tumor characteristics (6)

A
  1. Invasive to nearby tissues: do not respond to normal regulatory mechanisms, aggressive invasion
  2. Metastatic through blood stream or lymphatic system to local or distant parts of the body
  3. Often grow rapidly (high mitotic index)
  4. Have irregular and poorly defined boundaries no capsule, easy to invade neighbors
  5. typically arises due to genetic mutations that affect cell growth and division
  6. poorly differentiated (anaplastic)

Ex: carcinomas, sarcomas, leukemias

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Carcinomas

A

Cancer arising from epithelial cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Sarcomas

A

Cancer arising from connective tissues

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Leukemias

A

Cancer arising from blood-forming tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Anaplastic

A

-lack of differentiation
-do not resemble normal cells in structure or function
-lack of differentiation correlates with increased malignancy and aggressive behavior

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Contact inhibition

A

normal cells will stop dividing when they come into contact with another cell

Cancer cells lose this ability and continue to divide leading to uncontrolled growth and tumor formation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Suspension (cellular)

A

Normal cells require solid surface to grow

Cancer cells can grow in suspension and survive without attaching to any surface. Allowing them to potentially spread though the body fluids or metastasize to distant sites.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Cancer cellular life span vs. normal cells

A

normal cells have finite life span and enter apoptosis when old or damaged

cancer cells have extended lifespan. Evade apoptosis, accumulate genetic mutations over time and persist, contributing to tumor growth and cancer progression.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Pleomorphic cells

A

Cancer: pleomorphic: exhibit variability in size and shape. Reflects their abnormal growth and lack of organized structure.

Normal: uniform in size and shape within a specific tissue type

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Cellular division: normal cells vs cancer cells

A

Normal cells: divide at controlled rate, require optimal conditions for survival

Cancer cells: rapid division, survive in suboptimal conditions (low O2 or acidic environments). Therefore thrive in harsh microenvironments that typically inhibit cell growth.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Utilization of Nutrients: normal cells vs cancer cells

A

Normal cells: require nutrients to support growth and function

Cancer: utilize nutrients from their environment aggressively, often at the expense of surrounding normal cells. Enhanced nutrient uptake supports rapid proliferation and survival

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Metabolic pathways: normal vs cancer

A

Normal: primarily generate energy though oxidative phosphorylation in mitochondria producing ATP efficiently.

Cancer: often rely on glycolysis even in the presence of O2. Allows them to meet energy needs quickly but less efficiently. Can still synthesize lipids and other essential cellular components despite glycolysis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Warburg Effect

A

Aerobic glycolysis or the use of glycolysis (anaerobic metabolism) despite O2 presence. Used by cancer cells.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Stem cell regeneration: normal vs cancer

A

Normal: tissue regeneration facilitated by adult stem cells, multipotent or pluripotent.

Cancer: exhibit heterogeneity and can contain “cancer stem cells” (CSCs) that drive tumor growth and heterogeneity. CSCs share characteristics with normal stem cells but contribute to the persistence and progression of cancer by promoting tumor initiation, maintenance, and resistance to therapy.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Definition of Heterogeneity of cancer cells

A

The state of having more than one cell type in a given tissue or tumor. Aka cellular diversity within a single tumor. Including genetic, phenotypic, function and spatial.

Ex: Normal cell becomes cancer cell type 1, after growth mutation makes cell type 2. Now tumor is comprised of normal cells, cancer cell 1, AND cancer cell 2 at the same time.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Angiogenesis

A

Cancer cells promote the formation of new blood vessels to ensure a blood supply for growth.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Two genetic alterations that contribute to unregulated cell proliferation in cancer

A
  1. Activation of Oncogenes- promotes cell growth and division
  2. Tumor suppressor gene INactivation- turning off genes that would inhibit cell proliferation and promote apoptosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is genetic heterogeneity

A

INTRATUMORAL genetic variability: cancer cells in the same tumor can harbor different genetic mutations. Diversity arises due to ongoing mutation and and genomic instability, resulting in subclonal populations with distinct genetic profiles.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is Phenotypic Heterogeneity

A

Cellular morphology and behavior: exhibit variability in morphology (size/shape) and behavior (proliferation/metabolism).

This phenotypic diversity can influence how cells respond to treatment and their ability to invade surrounding tissues

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is Functional Heterogeneity

A

Metabolic Activity and response to stimuli: cancer cells may display different metabolic pathways (glycolysis vs. oxy. phos.)

Can affect how cells adapt to the tumor microenvironment and survive therapeutic interventions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is spatial heterogeneity

A

Spatial distribution within tumor: different regions of a tumor may have distinct microenvironments with variation in nutrient availability, O2, and immune cell infiltration.

Can impact treatment efficacy and the likelihood of metastasis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

5 reasons to pay attention to heterogeneity

A
  1. Treatment Resistance: subpopulations could be resistant to chemo, radiation, or targeted therapy.
  2. Metastatic potential: with increased diversity it may acquire mutations that confer enhanced invasive and metastatic capabilities.
  3. Prognosis and Clinical Outcome: high genetic and phenotypic diversity is associated with poorer clinical outcomes due to treatment resistance
  4. Personalized Medicine: Understanding of diversity is critical for development of personalized treatment strategy. Use of genomic profiling and single-cell sequencing allow for targeting of vulnerabilities in different subclones within a tumor
  5. Tumor Evolution and Adaptation: diversity contributes to evolution over time. Subclones can develop beneficial mutation and outgrow others in response to microenvironmental pressures or treatment pressure.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

-OMA suffix

A

Used to denote a tumor or neoplasm.

Denotes it arises from a specific tissue.

Ex: melanOMA from melanocytes
fibrOMA from fibrous tissue
chondrOMA benign tumor of cartilage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What is carcinoma

A

cancers arising from epithelial cells (line the surfaces and cavities of organs and glands)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Adenocarcinoma

A

Cancer arising from glandular or ductal tissue such as breasts, prostate, or colon

(adeno: glandular or ductal…
WITHIN epithelial therefore carcinoma)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Squamous cell carcinoma

A

cancer of squamous epithelial cells that are found in the lungs, skin, and other organs

(epithelial therefore carcinoma)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

-sarcoma suffix

A

sarcomas are cancers arising from mesenchymal tissue, including connective tissue, muscle and bone.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Osteosarcoma

A

Bone cancer originating from osteoblasts (form bone cells)

(mesenchymal therefore sarcoma)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Fibrosarcoma

A

cancer of fibrous connective tissue

(mesenchymal therefore sarcoma)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Lung adenocarcinoma

A

Arise from glandular cells of lung tissue

(adeno: glandular or ductal…
WITHIN epithelial therefore carcinoma)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Pancreatic Adenocarcinoma

A

arise from glandular cells in pancreas

(adeno: glandular or ductal…
WITHIN epithelial therefore carcinoma)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Leukemia

A

Cancers of blood forming cells specifically affecting the bone marrow and blood cells including leukocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Acute meyloid leukemia (AML)

A

fast growing cancer of myeloid line of blood cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Chronic lymphocytic leukemia (CLL)

A

slow growing cancer of the lymphocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Lymphoma

A

cancer of the lymphatic tissue including lymph nodes, spleen, and lymphatic vessels

(lymph- from lymphocyte or lymphoid tissues; -oma - tumor or neoplasm)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Hodgkin Lymphoma

A

type of lymphoma with the presence of Reed-Sternberg cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Non-hodgkin lymphoma

A

Diverse group of Lymphomas WITHOUT Reed-Sternberg cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

-blastoma

A

refers to malignancies derived from precursor cells or blasts often found in embryonic or fetal tissues.
Indicates they originate from undifferentiated cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Retinoblastoma

A

cancer of the retina that typically affects young children

(-blastoma therefore from undifferentiated cells)

42
Q

Nephroblastoma (Wilms tumor)

A

kidney cancer primarily affecting children
(-blastoma therefore from undifferentiated cells)

43
Q

what is Carcinoma in Situ

A

group of abnormal cells that have the potential to become cancer. they are in their ORIGINAL location.

May or may not become cancer

44
Q

Three possible paths for carcinoma in Situ

A
  1. Remain dormant: stay in original location and don’t progress further
  2. Regression: abnormal cells revert back to normal
  3. progression: abnormal cells break through the basement membrane and become invasive cancer with the potential to metastasize
45
Q

Characteristics of Carcinoma in Situ

A
  1. In original location
  2. may or may not become cancer
  3. pre-invasive: have NOT breached the basement membrane that separates the lining of an organ from the underlying tissue.
  4. Atypical cells: show signs of uncontrolled growth with some signs of dysplasia. More dysplastic the cells appear the more likely they will become invasive cancer
46
Q

Normal role of proto-oncogenes

A

essential for normal cell growth, division and differentiation

-encode proteins that act as signaling molecules in pathways that control cell division

47
Q

How does a proto-oncogene become an oncogene? (2)

A

mutation or over-expression.

Proto-oncogenes MUTATION oncogenes that cause the cell to divide uncontrollably

OVER EXPRESSION: “like having too many gas pedals in the car increasing the chance of uncontrolled cell division

48
Q

Function of ONCOgenes

A
  1. promote cell division: increase activity of proteins in division pathways leading to rapid uncontrolled cell growth
  2. Inhibit cell death: some oncogenes can interfere with mechanisms that trigger apoptosis allowing damaged cells to survive and potentially become cancerous
  3. Disrupt cell differentiation: prevent cells from maturing into specialized cell types, leading to a more immature and potentially cancerous state.
49
Q

what is Amplification

A

the duplication of oncogenes within a cells DNA creating multiple copies of the mutated gene accelerating the uncontrolled cell growth.

50
Q

Immune surveillance

A

immune system will normally recognize and eliminate cancer via cytotoxic T cells and natural killer cells. Inflammation enhances surveillance promoting recognition of cancer cell antigens

51
Q

Tumor suppressor genes

A

Inflammatory responses can activate tumor suppressor genes (anti-oncogenes) that inhibit or slow proliferation.

52
Q

What is the natural defense against cancer

A

Inflammatory cytokines and immune cells can induce apoptosis in cancer cells eliminating them before they proliferate or metastasize

53
Q

Effects of chronic inflammation (4)

A
  1. pro-tumorigenic environment: where cancer cells exploit the inflammatory response to promote their survival and growth
  2. Promotion of angiogenesis: inflammation induces the production of growth factors and cytokines that stimulate angiogenesis. Facilitating growth and metabolism
  3. Immune suppression: chronic inflammation can lead to immune suppression. Ex: tumor associated macrophages recruited to the tumor site may switch to a phenotype that supports tumor growth by promoting tissue remodeling and suppressing cytotoxic immune cells
  4. Altered T regulatory cells: inflammatory signals can alter the function of regulatory t-cells (Tregs) that normally help maintain immune tolerance. Dysfunctional tregs may fail to suppress caner-promoting inflammation leading to enhanced tumor growth and evasion of immune surveillance
54
Q

What is therapeutic targeting

A

targeting inflammatory pathways or molecules (cytokines, chemokines etc.) that promote tumor growth and immune suppression. It’s a promising approach for cancer treatment.

55
Q

What are anti-inflammatory therapies

A

some cancers associated with chronic inflammation (ex: colorectal or liver) may benefit from anti-inflammatory therapies to reduce the tumor-promoting effects of inflammation

56
Q

What is Immunotherapy

A

a treatment enhancing anti-tumor immune responses such as immune checkpoint inhibitors, that can counteract the immune suppressive effects of inflammation and boost immune surveillance against cancer cells

57
Q

What are paraneoplastic syndromes

A

group of rare disorders that occur in some people with cancer, caused by substances produced by the tumor cells or by an immune response triggered by the body’s attempt to fight the cancer. Can affect various organ systems but are not caused by the local presence of the tumor

58
Q

What are examples of hormonal imbalances caused by paraneoplastic syndromes (4)

A
  1. Cushing’s (excess cortisol)
  2. SAIDH (excessive H2O retention)
  3. Hypercalcemia
  4. Hypoglycemia
59
Q

What are 2 examples of neurologic disorders caused by paraneoplastic syndromes

A
  1. Myasthenia gravis
  2. CNS or PNS disorders
60
Q

What are 2 examples of skin changes caused by paraneoplastic syndromes

A
  1. Acanthosis nigricans (dark velvety patches on skin)
  2. Dermatomyositis (muscle inflammation and skin rash)
61
Q

What are examples of systemic changes caused by paraneoplastic syndromes

A
  1. Hypertrophic osteoarthropathy
  2. Clubbing of fingers
  3. Increased risk of blood clots
  4. DIC
  5. Nonbacterial thrombotic endocarditis
  6. Red cell aplasia (blood marrow failure leading to low RBCs)
  7. Nephrotic syndrome
62
Q

What are the 4 effects of the metabolic syndrome Cachexia

A
  1. Muscle wasting: can be with or without fat loss
  2. Systemic inflammation: ongoing inflammatory response to cancer contributes to this problem
  3. Negative protein and energy balance: body burning more calories that is taking in leading to increased muscle breakdown
  4. Loss of lean muscle mass: significantly affect strength and function
63
Q

Cachexia clinical symptoms and prevalence

A

50-80% of patients with advanced cancer

Sx: Extreme fatigue, weakness, loss of appetite, weight loss, muscle wasting with or without fat loss.

64
Q

What 5 ways are cancer (tumor or bio) markers used in clinical practice?

A
  1. Diagnosis: can indicate the likelihood of cancer and prompt further testing
  2. Prognosis: provide info about the likely course of the disease. (Ex: some higher levels of markers may indicate a more aggressive cancer etc.)
  3. Monitoring treatment: monitor efficacy of treatment like chemo or radiation. aka trending
  4. Detecting recurrence: after tx levels can be monitored to detect signs of recurrence
  5. Screening: used to detect cancer in early stages before symptoms develop. Most markers are not sensitive or specific enough to be used as a standalone screening test.
65
Q

What is Alpha Fetoprotein (AFP)

A

produced by the fetal live and yolk sac during fetal development. In adults is a tumor marker, elevated AFP can indicate some cancers, primarily hepatocellular carcinoma and non-seminomatous germ cell tumors.
-NOT specific to cancer, will be elevated in cirrhosis and hepatitis as well.

66
Q

What is AFP used for

A

-Aids in diagnosis and monitoring of hepatocellular carcinoma
-monitor treatment response
-Detect recurrence with germ cell tumors
-not specific to Cancer (use with caution)

67
Q

What is Prostate Specific Antigen (PSA)

A

protein produced by the prostate. Elevated levels can indicate prostate can OR other prostate related conditions such as BPH

68
Q

What is PSA used for?

A

-Screening for prostate Ca
-Monitoring disease progression
-Monitoring response to prostate cancer treatment.
-CAN create false positives resulting in unnecessary biopsy or overdiagnosis. Must be interpreted in clinical context

69
Q

Importance of cancer staging

A
  1. Treatment planning (staging helps determine appropriate treatment)
  2. Prognosis prediction
  3. Clinical trial availability
  4. Monitoring response for how well/ not treatment is working
70
Q

Risk of cancer in children

A

-Uncommon, however remains a leading cause of death in children
-most childhood cancers originate from the mesoderm germ layer (the embryonic layer that forms muscle, bone, tissue, blood, connective tissue)
-often fast growing and aggressive in kids
-Around 80% of cancers in kids have metastasized by time of diagnosis
-Despite aggressive nature, have a high cure rate (85%)
-Common types: Leukemia and brain/ CNS cancers (under age 14)
-Common types >14: Hodgkin and non-Hodgkin lymphoma, leukemia, germ cell (reproductive), thyroid and sarcoma

71
Q

Cancer risk in adults

A

-Risk of developing increases with age (accumulation of genetic mutations over time)
-Thought to be due to chronic inflammation over time
-Lifestyle choices: smoking, etoh, unhealthy diet
-early detection remains critical for good outcomes

72
Q

Cancer Overview
(Etiology, Risk factors, manifestations, patho, metastasis)

A
  1. Etiology: often involves genetic mutations/ exposure to carcinogens
  2. Risk factors: genetics, lifestyle, environmental exposure, hormonal imbalance, infections (HPV)
  3. Manifestations seen: abnormal lumps, bleeding, weight loss, pain, changes in bodily functions (bowel in colon CA)
  4. Pathophysiology: abnormal cell growth, tissue invasion, spread to organs
  5. Common sites of metastasis: liver, lungs, bones, brain, lymph nodes.
73
Q

Metastatic Organotropism

A

-Refers to the tendency of cancer cells to preferentially spread to specific organs
-Influenced by blood flow patterns, micro environment of potential metastatic sites, and molecular interactions between cancer cells and target tissue

74
Q

Lung Cancer

A

-Etiology: genetic mutations, carcinogens
-Risk factor: smoking, environment, chronic inflammation
-Manifestations: persistent cough, hemoptysis, chest pain, recurrent infections
-Pathophysiology: abnormal cell growth in lung tissues leading to tumor forming
-Sites of Metastasis: brain, bones, liver, adrenal glands

75
Q

Squamous Cell Carcinoma (Lung)
Etiology, risk, sx, patho, mets

A

-Etiology: smoking
-Risk factors: ionizing radiation, genetics
-Manifestation: persistent cough, hemoptysis, chest pain
-Pathophysiology: central lung tumors that may cause airway obstruction
-Site of metastasis: lymph nodes, bones, liver, adrenal glands

76
Q

Adenocarcinoma (Lung)

A

-Etiology: non-smokers/ women
-Risk factors: smoking, genetics, chronic lung diseases
-Manifestations: persistent cough, chest pain, weight loss
-Pathophysiology: peripheral lung tumors that metastasize early
-Site of metastasis: lymph nodes, bone, liver, adrenal glands

77
Q

Large cell carcinoma (lung)

A

-Etiology: genetic mutation
-Risk factors: smoking, carcinogens
-Manifestations: persistent cough, chest pain, weight loss
-Pathophysiology: large, undifferentiated cells in any part of the lung
-sites of metastasis; lymph nodes, bone, liver, adrenal glands

78
Q

Small cell carcinoma (lung)

A

-Etiology: neuroendocrine origin
-Risk factors: heavy smoking, radon, asbestos
-Manifestations: persistent cough, hemoptysis, chest pain, paraneoplastic syndromes
-Pathophysiology: highly aggressive, rapid growth and spread
-Site of metastasis: brain, liver, bones, adrenal glands

79
Q

Esophageal cancer

A

-Etiology: Barrett’s esophagus, GERD, lifestyle factors
-Risk factors: low fruit/ veggie intake, hot beverages, smoking, obesity
-Manifestations: dysphagia, weight loss, chest pain
-Pathophysiology: ESCC/ EAC forms and invades local tissues
-Sites of metastasis: lymph nodes, liver, lungs, bones, brain, adrenal glands

80
Q

What is Carcinoembryonic Antigen (CEA)

A

glycoprotein normally produced during fetal development. Elevation in adults can indicate various cancers including colorectal, lung, breast, and pancreatic.

81
Q

What is CEA used for?

A

-monitoring response to treatment in colorectal cancer
-assessing disease activity and prognosis in other cancers
-MAY be elevated in NON cancerous conditions suck as inflammatory bowel or liver disease.
-Assess trend rather than single value

82
Q

What is Bence Jones Protein?

A

-abnormal immunoglobulin light chains found in urine.

-Associated with multiple myeloma, cancer of plasma cells or bone marrow.

83
Q

What are Bence Jones proteins used for

A

-diagnosis of multiple myeloma
-assess response to treatment or evaluation of disease recurrence
-Serial values needed as monitoring for progression

84
Q

Colon Cancer

A

-Etiology: polyps, genetic mutations (APC gene)
-Risk factors: high fat diet, low fiber, family history, smoking, irritable bowel
-Manifestations: changes in bowel habits, blood in stool, abdominal pain
-Pathophysiology: tumor invasion of colonic wall
-Sites of metastasis: liver, lungs, peritoneum

85
Q

What is Neuron-specific Enolase (NSE)?

A

enzyme found in neurons and neuroendocrine cells.
-elevated levels CAN indicate small cell lung cancer (neuroendocrine) and neuroblastoma.

86
Q

What is NSE used for?

A

-diagnosis and monitoring of small cell lung ca
-assessing tx response and disease progression for neuroblastoma
-CAN be elevated in other conditions like stroke and neurologic disorders. Interpret carefully!

87
Q

What are BRCA1 & BRCA2

A

-genes involved in DNA repair. Mutations in these genes increase the risk of breast, ovarian, and other cancers
-RISK

88
Q

Pancreatic Cancer

A

-Etiology: genetic mutations (BRCA2, k-ras)
-Risk factors: smoking, chronic pancreatitis, DM, family history
-Manifestations: jaundice, weight loss, abdominal pain
-Pathophysiology: tumors in exocrine pancreas, rapid spread
-Sites of metastasis: liver, lungs, peritoneum

89
Q

What are BRCA1 & BRCA2 used for?

A

-assessing hereditary risk of breast and ovarian ca
-guiding personalized prevention strategies and treatment decisions (risk reducing surgery)
-Targeted therapy (PARP inhibitors) for those with increased genetic risk

90
Q

Ovarian Cancer

A

-Etiology: genetic mutation
-Risk factors: age >63, BRCA 1/2 mutations, family history
-Manifestations: abdominal bloating, pelvic pain, changes in bowel habits (often diagnosed at advanced stage; asymptomatic early on)
-Pathophysiology: epithelium origin, spread within the abdominal cavity
-Sites of metastasis: peritoneum, diaphragm, omentum, liver

91
Q

What are the goals (5) for personalized medicine

A
  1. Predict treatment response: markers can indicate likely response. Some genetic mutations or expression patterns may suggest sensitivity or resistance to targeted therapy
  2. Select Targeted Therapy: molecular profiling tumors can identify specific targets or pathways that drive growth and treatment can target those. Hopefully to be more effective
  3. Monitor Treatment Efficacy: monitor changes for resistance can allow for an adjustment in treatment
  4. Identify Risk of Recurrence: some markers can indicate risk of recurrence after treatment. Can help guide decisions of duration and intensity of therapy and surveillance.
  5. Screen for early detection: some markers are used for screening those at high risk from family or genetic predisposition.
92
Q

Endometrial (uterine) cancer

A

-Etiology: hormonal imbalances
-Risk factors: prolonged estrogen exposure, obesity, DM, HTN
-Manifestations: post menopausal vaginal bleeding, weight loss
-Pathophysiology: glandular epithelium origin (lining of the uterus) local invasion
-Sites of metastasis: lymph nodes, liver, lungs, bones

93
Q

Cervical cancer

A

-Etiology: persistent high risk HPV strains
-Risk factors: HPV infection, smoking, immunosuppression
-Manifestations: abnormal vaginal bleeding and discharge, abnormal PAP smear
-Pathophysiology: cervical transformation zone, local and distant spread
-Sites of metastasis: lymph nodes, lung, liver, bones

94
Q

What is Next-generation sequencing (NGS)

A

comprehensive profiling of tumor genomes, transcriptomes and proteomes to inform personalized treatment strategies.

95
Q

What is the T in TNM staging, and what does it mean?

A

T = Tumor, T0 = no tumor

Meaning: describes the primary tumor and its size, location, and extent of invasion into nearby tissues.

96
Q

Testicular cancer

A

-Etiology: germ cell origin
-Risk factors: cryptorchidism, family history, HIV/ AIDS
-Manifestations: painless testicular mass, lumbar pain with metastasis
-Pathophysiology: germ cell tumors, rapid lymphatic and blood spread
-sites of metastasis: retroperitoneal lymph nodes, lungs, liver, bones

97
Q

How do you score the T in TNM staging

A

T0= no tumor
Tis=carcinoma in situ (early localized, NO invasion of other tissue)
T1-T4= increasing size and or local extent of tumor

98
Q

Prostate cancer

A

-Etiology: hormones, genetic mutations (BRCA 1/2)
-Risk factors: age, African American race, high fat diet, family history
-Manifestations: urinary obstruction, blood in urine, pelvic pain
-Pathophysiology: imbalance in androgen and estrogen, slow growth, local invasion
-Sites of metastasis: bones (esp spine), liver, lungs

99
Q

How do you score the N in TNM staging

A

N0= no node involvement
N1-N3= increasing involvement of regional lymph nodes, often categorized by the number of nodes affected and their location relative to the primary tumor

100
Q

Breast cancer

A

-Etiology: genetic mutations, hormonal Influence
-Risk factors: age > 55, BRCA 1/2 mutations, family history, hormone use, obesity
-Manifestations: breast lump, nipple/ skin changes, nipple discharge
-Pathophysiology: originates in milk ducts lobules, lymphatic spread
-Sites of metastasis: bones, liver, lungs, brain

101
Q

How do you score the M in TNM staging

A

M0= no distant metastasis
M1=Presence of distant metastasis

102
Q

Polycystic ovary syndrome (PCOS)

A

-Disrupts ovulation and hormone levels
-Doesn’t directly cause cancer, but can create conditions that increase the risk of developing cancer endometrial cancer
-Without regular ovulation, lining of the uterus is exposed to estrogen for long periods of time without balancing the effect of progesterone. Can lead to thickening of endometrium which increases cancer risk
-Risk factors: family history, Insulin resistance, obesity, hormonal imbalance
-Characteristics: irregular or no periods, polycystic ovaries on ultrasound, excess male hormones, difficult conceiving, hirsutism, hair loss
-Pathophysiology: not well understood, likely a combo of environment and genetic factors (as well as insulin resistant and elevated androgen levels)

Advanced Patho Test 1 (20 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions