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General Pathology -- Roecker > Gen Path Exam 3 Section 5: Neoplasia > Flashcards

Gen Path Exam 3 Section 5: Neoplasia Flashcards

1
Q

Top three estimated cancer incidences in males and females

A

Males:

  1. Prostate
  2. Lung and Bronchi
  3. Colon and Rectum

Females:

  1. Breast
  2. Lung and Bronchi
  3. Colon and Rectum
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2
Q

Top three estimated cancer deaths in males and females

A

Males:

  1. Lung and Bronchus
  2. Prostate
  3. Colon and Rectum

Females

  1. Lung and Bronchus
  2. Breast
  3. Colon and Rectum
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3
Q

Neoplasm

A

= “new growth”; refers to tissue masses called tumors; all have dysregulated growth; can be benign or malignant, which will determine prognosis

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4
Q

Benign Tumors

A

= neoplasms that have “relatively innocent” cellular characteristics

  • localized to single area; will NOT metastasize
  • most cause no harm; but some can b/c they do take up space
  • most likely to be excised due to lack of invasivness
  • slow growing, encapsulated or surrounded by CT, fairly mobile when palpated
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5
Q

What determines the dysfunction caused by Benign Tumor’s pressure?

A
  1. which tissues being compressed

2. how much compression is occurring

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6
Q

Naming of a benign tumor

A

tissue type involved, plus the suffix “-oma”
Ex: Hemangioma
Exception: melanocytic Nevus

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7
Q
  1. Fibrotic tissue
  2. Fat tissue
  3. Cartilaginous tissue
  4. Glandular Tissue
    What are the benign tumor names?
A
  1. fibroma
  2. lipoma
  3. chondroma
  4. adenoma
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8
Q

Hemangioma

A

benign tumor of capillary endothelia

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9
Q

Leiomyoma

A

benign smooth muscle tissue tumor, AKA “uterine fibroid”

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10
Q

Fibroadenoma

A

MC benign tumor of breast; benign; multiple tissues, “mixed” tumor, contain fibrotic component and a glandular component

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11
Q

Polyp

A

mass of tissue that projects above a mucosal surface; a gross structure; and must be biopsied to know cellular nature
Ex: colon polyp

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12
Q

Papilloma

A

a benign epithelia neoplasm that produces microscopic “finger-like fronds”; very small extensions/outgrowths away from the surface

  • macroscopically = a wart (verruca)
  • stimulated by HPV infections
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13
Q

Hamartoma

A

mass of overgrowing tissues that are native to site/tissues of the area; very similar to normal cells (therefore usually always benign)
Ex: pulmonary hamartoma

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14
Q

What two things are all tumors composed of?

A
  1. parenchyma

2. stroma

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15
Q

Parnechyma

A

the genetically altered component of a tumor; determines biological nature (aggressiveness) of tumor; also determines name given to tumor

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16
Q

Stroma

A

composed of tissues that support and surround parenchyma mass; provides blood supply and supportive structures to tumor

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17
Q

Mixed tumors

A

when tumor performs “divergent differentiation” and multiple tissue types are found within a tumor
- more likely to be benign and less aggressive

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18
Q

Differentiation

A

degree to which tumor cells resemble their cell of origin

  • well-differentiated tumors = very similar to progenitor cells
  • poorly differentiated tumors = do NOT resemble their progenitor cells
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19
Q

Anaplasia

A

a lack of differentiation in neoplastic cells; cells that lack specialization; more “immature” and DO NOT contain cellular features expected in more “mature”/differentiated cells

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20
Q

Pleomorphic Adenoma

A

of salivary galnds; benign mixed tumor, contain glandular tissue, osseous tissue, and cartilaginous tissue

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21
Q

Teratomas

A

mixed tumor; involves at least two of the three embryonic germ layers; frequently all three

  • Commonly involves: bone, cartilage, epithelia, muscle, fat, hair, teeth, or nerves
  • may be benign OR malignant
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22
Q

Malignant tumors (malignancies)

A

= cancers; sarcomas and carcinomas

Naming: prefix = tissue type and “carcinoma” or “sarcoma” is the suffix

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23
Q

Sarcomas

A

malignant neoplasms that originate from solid mesenchymal (CT)

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24
Q

What are cancers that arise from mesenchymal cells in the blood?

A
  1. leukemia - WBC cancer in circulating blood or in bone marrow
  2. lymphoma - WBC cancer in lymphatic system
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25
Q

What type of individuals do sarcomas usually affect?

A

young (pediatric) and those in adulthood and older adulthood (geriatrics)

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26
Q

What are the MC pediatric tumors?

A

leukemia and bone cancer (osteosarcoma)

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27
Q

Carcinomas

A

cancers that originate from epithelial cells (from endoderm or ectoderm)

  • MC form of cancer in humans
  • develop in a pattern: dysplasia –> carcinoma in situ –> invasive carcinoma
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28
Q

What type of individuals are affected by carcinomas?

A

more likely age-related cancers; very unlikely in first 1/2 of life

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29
Q

What are adenocarcinomas and squamous cell carcinomas examples of?

A

carcinomas
adenocarcinoma = develop in glandular pattern
squamous cell carcinomas = develop in squamous pattern

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30
Q

Dysplasia

A

disorderly proliferation of cells and is risk for further cellular irregularities

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31
Q

Carcinoma In Situ

A

earliest form of cancer; referred to as “pre-invasive” cancer

  • Stage 0 b/c yet to penetrate tissues
  • lies at division b/w pre-neoplastic (pre-cancerous) lesions and invasive carcinomas
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32
Q

What is Ductal Carcinoma In Situ an example of?

A

a carcinoma in situ

- a very common form of “Stage 0” breast cancer; frequently discovered upon mammography

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33
Q

What are the four main characteristics talked about for tumors?

A
  1. if benign or malignant
  2. Rate of Growth
  3. Local Invasion
  4. Metastasis
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34
Q

Benign vs malignant tumors and cell types

A

benign tumors = more likely to have cells with greater degrees of differentiation
malignant = more likely to contain anaplasia

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35
Q

Rate of Growth and association with Benign and Malignant tumors

A

in general:

  • malignant tumors have more rapid growth
  • BUT slow growing cancers are fairly common (Ex: prostate cancer, Hodgkin Lymphoma)
  • AND some benign tumors may grow rapidly (Ex: giant cell tumor of bone with distal radius)
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36
Q

Local Invasion and association with tumors

A

= infiltration or local destruction

  • represents a tumor invading surrounding tissues as it grows
  • Benign tumors – tend to grow slowly and be encapsulated
  • NOT all benign tumors are encapsulated
  • rare cases some malignant tumors are encapsulated and some benign tumors are uncapsulated (Ex: hemangioma)
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37
Q

Metastasis and association with tumors

A

= “mets” for short; the spread of tumor to distant sites within body that are no longer continuous with primary tumor
*characteristic of malignant tumors (no benign tumor performs mets)
~30% all tumors are diagnosed at point where have metastasized

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38
Q

Where may a tumor invade (metastasis)?

A

tissue cavities, lymphatics, or hematopoietic (blood) system
- in general, larger the tumor and more anaplastic cells = more likely to metastasize

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39
Q

Why are blood cell cancers a special exception to metastasis?

A

leukemias and lymphomas are already throughout blood stream and lymphatic system, therefore virtually all are metastatic and time of diagnosis

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40
Q

What are the 3 routs of Metastasis?

A
  1. Seeding within Body Cavities
  2. Lymphatic Spread
  3. Hematopoietic Spread
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41
Q

Seeding within Body Cavities (metastasis)

A

(transcoelomic spread)

  • rare compared to other types
  • characteristic of ovarian cancers and cancers of CNS that spread within preexisting cavities where located
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42
Q

Lymphatic Spread (metastasis)

A
  • characteristic of metastasis for carcinomas
  • location of primary cancer and proximity to local lymphatics
  • “sentinel lymph node”
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43
Q

Sentinel Lymph node

A

first lymph node that receives lymphatic drainage from area where primary tumor located
- enlargemnt of this node = lymphadenopathy

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44
Q

Hematopoietic Spread (metastasis)

A
  • characteristic spread for sarcomas (CT)
  • frequently spread to 1st capillary bed encountered
    Ex:
  • colorectal and GI cancers —> liver
  • bone cancer/other organ system cancers –> lungs
  • vert. mets = common site for cancer to mets to
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45
Q

Epidemiology

A

the study of death and disease in groups of people (populations)
- provides info on pathogenesis of tumors and info on risk factors ass. with diff cancers

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46
Q

What are the common cancers in these geographic locations?

  1. US
  2. Africa
  3. Japan
A
  1. breast, colorectal, and esophageal cancer
  2. liver cancer
  3. stomach cancer
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47
Q

What ages have the highest rates of cancer related deaths?

A

ages 55-75
Due to:
- somatic mutations with exposure to env. carcinogens
- less active immune system
- cell activities less active and efficient

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48
Q

Is cancer diagnosis increasing or decreasing?
Are cancer rates stable or not stable?
Are rates of cancer related deaths in US increasing or decreasing?

A
  • cancer diagnosis is increasing, mainly due to increasing population
  • cancer rates are stable
  • rates of cancer-related deaths in US is decreasing (~20% reduction for men; ~10% reduction for women)
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49
Q

What are sporadic cancers?

A

develop with NO family history of cancer; due to harmful env. exposure and damage to individuals genetic material

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50
Q

What are common characteristics for preneoplastic lesions?

A

cellular metaplasia and dysplasia

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51
Q

Where do most tumors/ preneoplastic lesions develop?

A

at sites of chronic inflammation

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52
Q

What do sites for preneoplastic changes tell us about risk of cancer?

A

increase risk of cancer, BUT in most cases cancer does NOT develop

  • most benign tumors = NOT precancerous lesions
  • —-Exception: adenoma in lumen of colon –> they have a high rate of malignant transformation and ARE preneoplastic lesions
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53
Q

What are Cancer Genes?

A

= cancer developing following genetic alterations

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54
Q

What are germ line mutations?

A

gene mutations that are inherited

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55
Q

What three things can alter genes that regulate cellular growth?

A
  1. carcinogenic chemicals
  2. ionizing radiation
  3. viral infections
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56
Q

What are proto-oncogenes?

A

normal genes that promote cellular growth; can be altered/ mutated into cancer-promoting “oncogenes”

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57
Q

What are oncogenes?

A

when an proto-oncogene is altered

- only need a single allele to alter proto-oncogene = Dominant Change of Gene Expression

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58
Q

What are Tumor Suppressor Genes?

A

(TSGs)
= normal genes that slow down cellular growth
- if altered they lose ability to slow down growth
- BOTH TSGs alleles need to be altered = Recessive Change of Gene Expression

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59
Q

What are Apoptosis Genes?

A

kill off cells defected with genetic alterations
- successful cancers deactivate this pathway and therefore increase chance cells with dangerous cancer promoting mutations survive and lead to carcinogenesis

60
Q

What are DNA repair Genes?

A

contribute to DNA repair mechanisms

- can be altered and gene abnormalities go uncorrected and lead to carcinogenesis

61
Q

What are the two categories we are classifying genetic alteration into?

A
  1. Mutations

2. Epigenetic Modifications

62
Q

What are Driver Mutations?

A

mutations that directly contribute to development and progession of specific cancer

  • most likely from env. (Ex: UV light/cigarette smoke)
  • occur in characteristic “cancer genes”
63
Q

What are Passenger Mutations?

A

are neutral in terms of driving cancer progression

  • occur more randomly throughout genome
  • known to produce growth variants (subclones) that give a tumor advance against therapy
64
Q

What are Germline Mutations?

A

inherit via germ line (egg or sperm)

- more likely to affect entire body

65
Q

What are Point Mutations?

A

well known to activate proto-oncogenes causing oncogenes

  • can activate or deactivate proteins
  • known to deactivate TP53 alleles (TSGs)
66
Q

What gene are Single Point Mutations known at activate?

A

RAS gene

67
Q

What are Gene Rearrangements (ass. with mutations)?

A

occur at level of chromosomes; include balanced translocations

68
Q

What type of cancer is frequently associated with specific Balanced Translocations between chromosomes?

A

Hematopoietic cell cancers (leukemia and lymphomas)
Ex: Chronic Myelogenous Leukemia (CML); in 95% cases
Ex: Burkitt Lymphomas

69
Q

What are Deletions (ass. with mutations)?

A

loss of section of genetic material; may alter one (or two) of alleles needed to alter to deactivate TSG

70
Q

What are Gene Amplifications (ass. with mutations)?

A

segment of genetic material multiplied many times; may over express proto-oncogene and activate an oncogene
Ex: HER2 gene

71
Q

What technique is used to look for Gene Amplifications?

A

G banding Staining Technique

- see “homogenously stained region”

72
Q

Epigenetic Modifications

A

involves reversible changes to gene expression, may be transmitted down the germ line (heritable)

73
Q

Two Mechanisms for Epigenetic change:

A
  1. DNA methylation
  2. Histone Modification
    - both deactivate or “silence” involved genes and therefore change gene activity and change observable phenotype of involved genes
74
Q

Is carcinogenesis a single step or a multi-step progression?

A

multi-step process and involves accumulation of multiple genetic alterations over time

75
Q

What are subclones?

A

they develop as cancer accumulates greater gene alterations

76
Q

Does cancer develop from a single transformed cell?

A

yes; will develop different gene alterations in clonal cells and result in genetic and cellular HETERogenicity

77
Q

What are Hallmarks of Cancer?

A

unique characteristics that contribute to dysregulation of cellular growth of cancer cells; describe fundamental properties in cancer cells that DO NOT occur in normal cells

78
Q

What are “Enabling Hallmarks” of cancer?

A

when cancers involve tumor-promoting inflammation and genomic instability

79
Q

What are some of the Hallmarks for cancer?

A
  • self-sufficiency in growth signaling
  • evasion of immune detection
  • insensitivity to anti-growth signaling
  • cellular immortality (limitless growth potential)
  • altered cellular metabolism
  • sustained angiogensis
  • evasion of apoptosis
  • invasion and metastasis
80
Q

What two genes are the most characteristic TSGs associated with carcinogenesis?

A
  1. RB Gene

2. TP53 Gene

81
Q

What is RB Gene’s function?

A

(is a TSG)
mediates cell cycle by producing RB protein that regulates G1 to S phase of cell cycle (final checkpoint before genetic material is copied)
- if altered, then can enter S-phase and pass on altered genetic material to daughter cells

82
Q

What types of cancer is an altered RB gene usually found in?

A

osteosarcoma, breast cancer, small cell lung cancers, and bladder cancer

83
Q

What is the TP53 gene sometimes called?

A

“Gaurdian of the Genome” b/c becomes activated when cellular stress associated and carcinogenesis occurs
- classic TSG, produces protine P53

84
Q

What are the 3 primary stimuli for activating p53 Response?

A
  1. cellular anoxia
  2. inappropriate pro-growth signaling
  3. genetic damage
85
Q

What are the pathway control mechanisms for an activated p53?

A
  1. Quiescence
  2. Senesence
  3. Apoptosis
86
Q

Quiescence

A

temporary pause in affected cell’s cycle
- p53 will attempt to fix in this stage and if it can’t it will initiate senescence or apoptosis; if it can it will release into normal cell cycle activity

87
Q

Senescence

A

permanent arresting of affected cell’s cell cycle

88
Q

Apoptosis

A

controlled or programmed cellular death

89
Q

What occurs when TP53 gene is mutated or has loss of normal function?

A

results in DNA damage remaining unrepaired and mutations being copied into daughter cells
- TP53 mutations are present in ~70% all human cancers

90
Q

What types of lethal cancers are TP53 gene alteratiosn found in?

A

lung cancers, colorectal cancers, and breast cancers

91
Q

What viral infections may alter p53?

A

HPV or hepatitis B virus (HBV) may deactivate p53 protein = a “functional mutation”–when protein product of a TSG is deactivated

92
Q

Li-Fraumeni Syndrome

A

when altered TP53 gene is inherited

  • develop multiple tumors at younge age
  • increase risk of developing cancer by 250fold
  • “SBLA” for main forms cancer may develop
93
Q

What are the four main form forms of cancner Li-Fraumeni Syndrome increase risk of?

A 
(recall: altered TP53 gene is inherited)
"SBLA"
S - Sacrcomes
B - Breast cancer
L - Leukemias
A - Adrenal Cortex adenocarcinomas

also brain tumors

94
Q

What is it called when cancer cells shift their metabolism and what type of metabolism do they switch to?

A

= Warburg Effect

  • switch to aerobic glycolysis; even in presence of oxygen
  • this path produces many byproducts needed from rapidly-growing cells
  • more efficient than oxidative phosphorylation when it comes to successful tumor growth and survival
95
Q

What is the Hayflick Limit?

A

a normal number of cellular divisions; which normal cells have, BUT cancer cells do not

96
Q

What can the disabling of TSG’s lead to?

A

older cell with short telomers that may not enter cellular senescence–> leading to “nonhomologous end-joining” of chromosomes

97
Q

What does “nonhomologous end-joining” of chromosomes create?

A

“dicentric chromosomes” = irregular chromosomes with two centromeres
- when this is occuring telomerase is reactivated in tumor cells (~90% all cancers)

98
Q

Why do tumors need sustained angiogenesis?

A

1-2mm = maximum distance oxygen, nutrients, and wastes can diffuse
- therefore tumors must stimulate angiogenesis to grow larger

99
Q

What is neoangiogensis?

A

new blood vessles; sproud via existing vessels in tumor; secrete growth factors; allows for tumor mets to enter systemic circulation
- are NOT well constructed; more likely to dilate, tortous, and leak
= common mechanism for edema

100
Q

What are the four steps in the Invasion-Metastasis Cascade?

A
  1. Invasion into Surrounding ECM
  2. Spreading into the Vasculature (intravasation)
  3. Spreading out of the Circulation and Invading a Distant Tissue (Extravasation)
  4. Survival and Proliferation of Micrometastasis
101
Q
  1. Invasion into the Surrounding ECM
A
  • cancer cells deactivate E-cadherin genes around them to loosen intracellular connections
  • secrete proteolytic enzymes to degrade ECM
  • once penerates basement membrane it goes from “in situ / stage 0” to —> stage 1 or “invasive cancer”
102
Q
  1. Spreading into the Vasculature (Intravasation)
A
  • once gets into lymphatic or hematopoietic (blood) vessels –> now cancer has ability to spread
  • Cancer Embolus = cancer cells w/in circulation
  • once cancer cells are in circulation they are vulnerable to immune system
103
Q
  1. Spreading out of Circulation and Invading a distant tissue (extravasation)
A
  • in cancer embolus avoids being killed it will find a site to survive
  • predicted y anatomical location and vascular drainage and first capillary bed cancer embolus encoutners
104
Q
  1. Survival and Proliferation of Micrometastasis
A

Certain areas are more prone to mets, like:
- stasis (slow blood flow)
- abundant capillaries
- physical protection/protection from immune system
These tissues include–> lungs, liver, and bone marrow

105
Q

What results if altered/mutations go unchecked/uncorrected?

A

genetic microsatellite instabilities (can be detected on genetic analysis)
- increases risk of future genetic alterations that occur in mass of cancer cells

106
Q

What are the 3 Inherited DNA Repair Defects?

A
  1. DNA Mismatch Repair
  2. Nucleotide Excision Repair
  3. Homologous Recombination
107
Q

What cancer is DNA Mismatch Repair most commonly associated with?

A

Hereditary nonpolyposis colon cancer (HNPCC or lynch syndrome)

  • inherit 1 altered allele
  • acquire a second altered allele in colonic epithelial cells from env. carcinogens
  • increased risk of colon cancer (proximal colon or cecum)
  • increased risk of developing tumors; endometrial cancer or ovarian cancer
108
Q

What cancer is Nucleotide Excision Repair most commonly associated with?

A 
Xeroderma pigmentosum (XP)
- children with is = "moon children" b/c must avoid all UV light
109
Q

What is Homologous Recombination most commonly associated with?

A

BRCA1 and BRCA2 gene mutations (they regulate body’s homologous recombination repair system)
- ind. more sensitive to env. carcinogens (Ex: ionizing radiation)

110
Q

Individuals with mutated BRCA1 or BRCA2 genes have an increased risk of developing what kinds of cancer?

A
  • breast cancer
  • ovarian cancer
  • Fallopian (uterine) tube cancer
  • prostate cancer
  • pancreatic cancer
  • stomach cancer
  • melanoma
111
Q

What adds to cancer’s ability to invade and destroy tissues?

A
  1. release of growth factors
  2. angiogenesis
  3. local invasion
112
Q

What are the most common types of skin cancer?

A
  1. basal cell carcinoma
  2. squamouns cell carcinoma
  3. melanoma (most deadly skin cancer)
113
Q

Ionizing radiation has what risk?

A
  • Exposure to UV light and sunburn, increase risk of skin cancer
  • Miners have a 10-fold increase of lung cancer
  • Inds. surviving atomic blast at end of WWII
  • it is known to cause chromosomal breaks
114
Q

What are the 5 Microbial Infections Known to Contribute to Cancer?

A
  1. HTLV-1 (Human T-cell lymphotrophic virus Type 1)
  2. HPV (Human Papillomavirus)
  3. EBV (Epstein-Barr Virus)
  4. HBV and HCV (Hepatitis B and C virus)
  5. Helicobacter pylori (H. Pylori)
115
Q

What does HTLV-1 do to infect?

A

it is an oncogenic RNA virus that infects CD4+ T-cells by injecting RNA genes (spec. TAX gene) into cell and activates cyclins to accelerated cellular growth

116
Q

How does infection of HTLV-1 occur?

A

after sexual contact, direct contact with infected blood, or breastfeeding

117
Q

What does HTLV-1 increase your risk of getting?

A

increase risk of T cell leukemia or lymphoma

- ass. with developing T-cell cancers ~50 years after initial infection (meaning env. carcinogens involved too)

118
Q

What type of HPV promotes warts?

A

HPV -6 and HPV -11

119
Q

What type of HPV is more aggressive and increases risk of cancerous transformation?

A

HPV -16 and HPV - 18

120
Q

Whats it HPV’s tactic to infect?

A

injects genetic material into cells and…
- E6 gene binds to p53 protein
- E7 gene binds to RB protein
~~cause “functional mutations” in 2 classic TSG’s

121
Q

What type of cancer is HPV most commonly associated with?

A

squamous cell carcinomas of cervix or anogenital region

- considered a sexually transmitted infection

122
Q

What is EBV cause?

A

EBV = Epstein-Barr Virus

- causes “mono” (infectious mononucleosis)

123
Q

What type of cancer does EBV increase the risk of?

A

Increase risk of:

  • B-cell lymphomas (Burkitt Lymphoma in inds. with immunosuppression)
  • nasopharyngeal carcinomas
124
Q

What types of cancer is HBV and HCV most commonly associated with?

A

(= hepatitis B and C virus)

  • causes inflammation in liver
  • ~770-85% all cases of liver cancer result of chronic HBV or HCV infections
  • (most likely to occur in Africa and Asia)
125
Q

What disease is Heliobacter pylori most commonly associated with?

A

= an BACTERIAL infection in distal stomach/proximal SI

  • contribute to ~90% peptic ulcer disease
  • causes inflammation contributing to increase in reactive oxidative species (ROS) exposure and increase in growth factor supply
126
Q

What cancers are Helicobacter pylori most commonly associated with?

A
  • gastric (stomach) adencocarcinomas

- mucosa ass. lymphoid tumors (MALT lymphomas)

127
Q

What three things does the impact of tumor growth depend on?

A
  1. location of tumor
  2. fucntional activity of tumor
  3. destruction caused by tumor’s growth/invasion
128
Q

What is Cachexia?

A

wasting away of body fat and lean muscle mass

129
Q

What is Cancer Cachexia?

A

when wasting away of body fat and lean muscle mass occurs b/c of advanced cancer

  • is the effect o widespread cancer having hypermetabolic state on body
  • present in ~1/2 all patients with advanced (mets) cancer
130
Q

What is TNF (Tumor Necrosis Factor)?

A

a cytokine

  • commonly increased in advanced cancer states when cancer cachexia is present
  • suppresses appetite
131
Q

What are Paraneoplastic Syndromes?

A

collection of sign and symptoms taht occur in someone with a neoplasia

  • MC in advanced cancer
  • NOT due to tumor putting pressure on tissues or local destructive tumor
  • occur in ~15% all cancer cases
  • widely variable and ass. with various cancers
132
Q

What are Paraneoplastic syndromes most like to manifest after?

A
  • most likely manifests following hormonal abnormalities or immune dysregulation that occurs in advanced stages of cancers
133
Q

What are examples of Paraneoplastic Syndromes manifestations?

A
  • cushing syndrome (lung cancer)
  • hypercalcemia (lung, breast, renal cancer, leukemia/ lymphoma)
  • polycythemia (renal and liver cancer)
  • acanthosi nigricans (stomach, lung, and uterine cancer)
  • hypertrophic osteoarthropathy (lung cancer)
134
Q

What is Cushing Syndrome?

A

an endocrine disorder involving elevated glucocorticoid levels (hypercortisolism)
- MC reason for elevated glucocorticoid levels = receiving exogenous glucocorticoid medications

135
Q

What is Cushing disease?

A

describes when hypercortosolism results from pituitary adenoma

136
Q

What are some clinical features of Cushing Syndrome?

A
  • weight gain
  • purple striae (stretch marks)
  • hypertension
  • muscle atrophy and weakness
  • osteoporosis
  • hirsutism
  • menstrual abnormalities
  • psychological irregularities (mood swings or depression)
137
Q

Grading of Cancer

A
  • quantifying tumors level of cellular differentiation

Grade of I -IV (higher # = increase anaplasia and increase worse prognosis)

138
Q

Staging of Cancer

A
  • quantify tumors extent to spread
    Stage 0 -IV (higher # = greater extent to spread and worst prognosis)
    **greater clinical value compared to Grading of Cancer
139
Q

What information is used to determine Cancer’s Stage? (Staging of Cancer)

A
  1. size of primary tumor
  2. whether cancer has spread to lymph nodes
  3. presence of hematopoietic metastasis
  4. info obtained during clinical exam
  5. info obtained from imaging studies (MRI, CT, radiography)
140
Q

Excision

A

partial removal of an organ or tissue from body
Named:
- name of organ followed by “-ectomy”
EXCEPT: “lumpectomy” = removal of lump

141
Q

Biopsy

A

removal of a smaller sample of cells, compared to an excision
Ex: cone biopsy–commonly used during a colposcophy

142
Q

Colposcopy

A

an imaging procedure used to view an illuminated and magnified image of cervix

143
Q

Fine - Needle Aspiration

A

removal of cells via aspiration with a needle
- MC used with superficial tumors, easily palpated
Example of Organs used:
- breast, thyroid, lymph nodes, salivary glands
- liver and pancreas more recently

144
Q

Cytological (Papanicolaou) Smear

A

“pap smear”; MC ass. with sampling shed cells of cervix
- cells on surface of organ or cells sloughed off from a tumor = ideal sampling via this way
Tissues used:
- cervix, endometrium, meninges (CSF), bronchi, urinary bladder, prostate, and stomach

145
Q

What are Tumor Markers?

A

types of techniques used to sample body’s fluids for biochemical abnormalities or irregular enzyme levels
- may indicate presence of cancers
-best used for SCREENING purposes
- are NONdiagnosic and CANNOT indicate presence of cancer or their own
Ex: PSA Test

146
Q

What is the PSA (Prostate-Specific Antigen) Test?

A

evaluates for a specific prostate enzyme

- PSA is secreted by prostate gland and increased levels indicates increased levels of prostate activity

147
Q

What conditions increase Prostate Gland activity?

A
  • benign prostatic hyperplasia (BPH)
  • recent ejaculation
  • prostate cancer
    ~~therefore NOT specific to prostate cancer

General Pathology -- Roecker (7 decks)

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