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COM: MOD II - Midterm COPY > Chapter 7 > Flashcards

Chapter 7 Flashcards

1
Q

Where does carcinoma in situ commonly occur?

A
  • skin, breast and certain other sites

- best illustrated by carcinoma of the uterine cervix

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2
Q

List the oncogenic DNA viruses

A 
HPV
EBV (and Burkitt lymphoma)
HBV (and HCV)
Merkel cell polyomavirus 
HHV-8
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3
Q

T/F: Rapidly growing tumors develop large central areas of ischemic necrosis

A

True -> growing tumor cells obviously require a blood supply, but the vascular stroma is insufficient leading to ischemia

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4
Q

What are hamartomas?

A

Disorganized but benign masses composed of cells indigenous to the involved site

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5
Q

__________ is a complex locus that encodes 2 tumor suppressive proteins, p16/INK4a, a cyclin-dependent kinase inhibitor that augments RB functions, and ARF which stabilizes p53

A

CDKN2A

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6
Q

Explain the pathway of malignant tumor spread: seeding of body cavities and surfaces

A
  • may occur whenever a malignant neoplasm penetrates into a natural open field lacking physical barriers
  • most often involved is the peritoneal cavity, but any cavity may be involved
  • particularly characteristic of carcinomas arising in the ovaries
  • sometimes mucus secreting appendiceal carcinomas or ovarian carcinomas fill the peritoneal cavity with a gelatinous neoplastic mass -> pseudomyxoma peritonei
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7
Q

List the paraneoplastic syndromes that fall under the category of nerve and muscle syndromes

A

Myasthenia

Disorders of the CNS and PNS

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8
Q

Differentiate between normal cells and cancer cells

A
  • normal cells have a large cytoplasm and cancer cells have a small cytoplasm
  • Normal cells have a single nucleus and nucleolus whereas cancer cells have multiple nuclei and nucleoli
  • normal cells have fine chromatin and cancer cells have coarse chromatin
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9
Q

What tumor types is catecholamines and metabolites good markers for?

A

Pheochromocytoma and related tumors

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10
Q

________ pathway is a potent inhibitor of cellular proliferation in normal tissues

A

TGF-beta

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11
Q

What 2 organs are most frequently involved in hematogenous dissemination?

A
  • liver and lungs
  • all portal area drainage flows to the liver and all caval blood flows into the lungs
  • cancers arising in close proximity to the vertebral column often embolism thorugh the paravertebral plexus and this pathway is involved in the frequent vertebral metastases of carcinomas of the thyroid and prostate
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12
Q

Explain dysplasia

A
  • disordered growth
  • encountered principally in epithelia
  • Characterized by a constellation of changes that include a loss in the uniformity of the individual cells as well as a loss in their architectural orientation
  • dysplastic cells may exhibit considerable pleomorphism and often contain large hyperchromatic nuclei with a high nuclear-to-cytoplasm ratio
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13
Q

What tumor types is neuron-specific enolase a good marker for?

A

Small cell cancer of lung, neuroblastoma

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14
Q

What protein is related to certain CNS tumors, renal cysts, neuroendocrine tumors, and renal cell carcinoma?

A

VHL

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15
Q

What tumor types is CA-125 a good marker for?

A

Ovarian cancer

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16
Q

Define a polyp

A
  • when a neoplasm (benign or malignant) produces a microscopically visible projection above a mucosal surface and projects into the gastric or colonic lumen (example)
  • if the polyp has glandular tissue its called an adenomatous polyp
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17
Q

What is the epigenetic gene mutation in 90% of pts with follicular lymphoma?

A

MLL2

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18
Q

What tumors are associated with HRAS?

A

Bladder and kidney tumors

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19
Q

What tumor types is carcinoembryonic Ag a good marker for?

A

Carcinomas of the colon, pancreas, lung, stomach and heart

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20
Q

What chromosomal translocation is associated with chronic myelogenous leukemia (CML)?

A

9 (ABL);22 (BCR)

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21
Q

What is Xeroderma pigmentosa?

A
  • defect in the nucleotide excision repair pathway

- increased risk to get skin cancer from UV light due to inability to repair pyrimidine dimers

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22
Q

T/F: Dysplasia often occurs in metaplastic epithelium, not all metaplastic epithelium is dysplastic

A

True

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23
Q

Explain the pathway of malignant tumor spread: hematogenous spread

A
  • typical of sarcomas but also seen with carcinomas
  • arteries (thicker walls) are less readily penetrated than veins
  • arterial spread may occur when tumor cells pass through the pulmonary capillary beds or pulmonary arteriovenous shunts or when pulmonary metastases themselves give rise to additional tumor emboli
  • With venous invasion, bloodborne cells follow the venous flow draining the site and tumor cells often come to rest in the first capillary bed they encounter
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24
Q

What protein is considered the “gatekeeper of colonic neoplasia”?

A

APC

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25
Q

What type of cancer is associated with a tumor caused by a point mutation of ABL?

A

Acute lymphoblastic leukemia

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26
Q

Define anaplasia

A

Lack of differentiation -> considered a hallmark of malignancy

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27
Q

Differentiate eukaryotes and prokaryotes

A

Eukaryotes = any organism whose cells contain a nucleus and other organelles enclosed within membranes

Prokaryotes = single-celled organism that lacks a membrane-bound nucleus, mito or any other membrane-bound organelle

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28
Q

What is a major proto-oncogene associated with nonreceptor tyrosine kinase?

A

ABL

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29
Q

Explain encapsulation of malignant tumors

A
  • poorly demarcated from the surrounding normal tissue and a well-defined cleavage plane is lacking
  • slowly expanding malignant tumors may develop an apparently enclosing fibrous capsule and may push along a broad front into adjacent normal tissues -> pseudoencapsulated masses
  • on histology, the pseudoencapsulated masses show rows of cells penetrating the margin and infiltrating the adjacent structures -> a crablike pattern of growth that constitutes the popular image of cancer
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30
Q

Dissemination of cancers may occur through one of 3 pathways, what are they?

A
  1. Direct seeding of body cavities or surfaces
  2. Lymphatic spread
  3. Hematogenous spread
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31
Q

What is a leiomyoma?

A

Benign, well-differentiated tumor contains interlacing bundles of neoplastic SM cells virtually identical to normal SM cells

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32
Q

Explain the pathway of malignant tumor spread: lymphatic spread

A
  • transport through lymphatics is the most common pathway for the initial dissemination of carcinomas
  • sarcomas may use this route too
    — tumors dont contain functional lymphatics but lymphatic vessels located at the tumor margins are sufficient for the lymphatic spread
  • pattern of LN involvement follows the natural routes of lymphatic drainage
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33
Q

What are cystadenomas?

A
  • benign epithelial neoplasms that form large cystic masses such as in the ovary
  • some produce papillary patterns that protrude into cystic spaces and are called papillary cystadenomas
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34
Q

T/F: nodal enlargement in proximity to a cancer does not necessarily equate with dissemination of the primary lesion

A

True -> drainage of tumor cell debris or tumor Ags, or oth, induces reactive changes within in the nodes so enlargement of nodes may be caused by the spread and growth of cancer cells or reactive hyperplasia

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35
Q

Malignant neoplasms of epithelial cell origin, derived from any of the 3 germ layers are called __________

A

Carcinomas

  • may be further classified…. squamous cell carcinoma, adenocarcinoma (lesion in which the neoplastic epithelial cells grow in a glandular pattern)
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36
Q

Mutations in BRAF have been detected in close to 100% of _______ Cell leukemias

A

Hairy

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37
Q

What is the function of VHL and what are the familial syndromes and sporadic cancers it causes?

A
  • functions = inhibitor of hypoxia-induced transcription factors
  • familial syndromes = Von Hippel Lindau syndrome
  • sporadic cancers = renal cell carcinoma
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38
Q

Explain the abnormal nuclear morphology of neoplasms

A
  • nuclei are disproportionately large for the cell
  • nuclear-to-cytoplasm ratio is 1:1 where normal is 1:4 or 6
  • nuclear shape is variable and often irregular
  • chromatin is often coarsely clumped and distributed along the nuclear membrane or more darky stained than normal (hyperchromatic)
  • abnormally large nucleoli are commonly seen
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39
Q

__________ encodes membrane receptor that is a negative regulator of the Hedgehog signaling pathway

A

PTCH1

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40
Q

What 3 characteristics make a tumor benign?

A
  • it will remain localized
  • it will not spread to other sites
  • amenable to local surgical removal

Pt generally survives

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41
Q

What 4 characteristics distinguish benign and malignant tumors from each other?

A
  • degree of differentiation
  • rate of growth
  • local invasiveness
  • distant spread
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42
Q

Carcinomas of the breast usually arise in the upper outer quadrants and generally disseminate first to the __________ LNs. Cancers of the inner quadrants drain to the nodes along the _________________. Thereafter, the _____________ and ___________ nodes may be involved. Carcinomas of the lung arising in the major respiratory passages metastasize first to the ______________ and ___________ nodes

A

Axillary; internal mammmary arteries; infraclavicular and supraclavicular; perihilar tracheobronchial and mediastinal nodes

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43
Q

What types of tumors are associated with KRAS?

A

Colon, lung and pancreatic tumors

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44
Q

What is an adenoma?

A
  • benign epithelial neoplasms derived from glands; they may or may not form glandular structures
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45
Q

What are paraneoplastic syndromes?

A

Symptom complexes in individuals with cancer that cant be explained by tumor spread or release of hormones that are indigenous to the tumor cell of origin

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46
Q

What tumor types is calcitonin a good marker for?

A

Medullary carcinoma of thyroid

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47
Q

List the cell and molecular hallmarks of cancer

A
  • self-sufficiency in growth signals
  • insensitivity to growth—inhibitory signals
  • altered cellular metabolism
  • evasion of apoptosis
  • limitless replicative potential
  • sustained angiogenesis
  • ability to invade and metastasize
  • ability to evade host immune response
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48
Q

What is the function of NF2 and what familial syndromes and sporadic cancers does it cause?

A
  • functions = cytoskeletal stability, hippo signaling pathway
  • familial syndromes = neurofibromatosis type 2
  • sporadic cancers = schwannoma, meningitis
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49
Q

What are tumor giant cells?

A

Tumor cells that are many times larger than their neighbors. Some possess only a single huge polymorphic nucleus while others may have 2 or more large, hyperchromatic nuclei.

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50
Q

_____________ is a cell adhesion molecule that plays an important role in contact-mediated growth inhibition of epithelial cells; it also binds and sequesters beta-catenin, a signaling protein that functions in the WNT pathway

A

E-cadherin

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51
Q

What tumor types is TP53, and RAS mutants in stool and serum a good marker for?

A

Pancreatic cancer

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52
Q

What tumor types is CA-19-9 a good marker for?

A

Colon cancer and pancreatic cancer

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53
Q

What is the function of APC and what familial syndromes and sporadic cancers does it cause?

A
  • function = inhibitor of WNT signaling
  • familial syndromes = familial colonic polyps and carcinomas
  • sporadic cancers = carcinomas of stomach, colon, pancreas; melanoma
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54
Q

_____ encodes a GTPase that acts as a negative regulator of RAS

A

NF1 -> encodes neurofibromin 1

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55
Q

Differentiate between proto-oncogenes, Oncogenes and oncoproteins

A
  • proto-oncogenes = normal cellular genes whose products promote cell proliferation
  • oncogenes = matted or overexpressed versions of proto-oncogenes that function autonomously, having lost dependence on normal growth promoting signals
  • oncoprotein = a protein encoded y an oncogene that drives increased cell proliferation through one of several mechanisms
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56
Q

Explain mitoses seen in neoplasms

A
  • in undifferentiated tumors, many cells are seen in mitosis
  • the presence of mitoses however doesnt necessarily indicate that a tumor is malignant or that the tissue is neoplastic
  • important as a morphologic feature of malignancy are atypical, bizarre mitotic figures, sometimes with tripolar, quadripolar, or multipolar spindles
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57
Q

What tumor types is CA-15-3 a good marker for?

A

Breast cancer

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58
Q

What cancers have a propensity for invasion of the veins?

A
  • renal cell carcinoma often invades the branches of the renal vein then the renal vein itself and may grow in a snakelike fashion up the IVC sometimes reaching the right side of the heart
  • hepatocellular carcinomas often penetrate portal and hepatic radicle to grow within them into the main venous channels
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59
Q

T/F: Dysplasia indicates cancer

A

False! Although dysplasia may be a precursor to malignant transformation, it doesnt always progress to cancer

**With removal of the inciting causes, mild to moderate dysplasia that dont involve entire thickness of epithelium may be completely reversible

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60
Q

What protein is considered “the governor of proliferation”?

A

RB

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61
Q

In greater than 85% of follicular Bcell lymphomas, the anti-apoptotic gene ______ is overexpressed due to a 14;18 translocation

A

BCL2

**Overexpression of other BCL2 family members such as MCL-1 is also linked to cancer cell survival and drug resistance

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62
Q

What is HNPCC syndrome?

A
  • defects in the mismatch repair system
  • leads to carcinomas of the colon
  • show microsatellite instability that is characterized by changes in the short repeats throughout the genome
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63
Q

What is the epigenetic gene mutation in 90% of infants with acute leukemia?

A

MLL1

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64
Q

Teratomas originate from totipotent stem cells that are normally present where?

A

In the ovary and testis and sometimes found in abnormal midline embryonic rests

  • Ex. Ovarian cyst teratoma (dermoid cyst) differentiates principally along ectodermal lines to create a cystic tumor lined by skin replete with hair, sebaceous glands and tooth structures
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65
Q

What is the function of Rb protein and what are the familial syndromes and sporadic cancers that it causes?

A
  • function = inhibitor of G1/S transition during the cell cycle
  • familial syndromes = familial retinoblastoma
  • sporadic cancers = retinoblastoma, osteosarcoma, carcinomas of the breast, lung and colon
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66
Q

What tumor type is TP53 and RAS mutants in sputum and serum a good marker for?

A

Lung cancer

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67
Q

Differentiate between tumors grading and staging

A
  • grading: determined by cytologic appearance; based on the idea that behavior and differentiation are related, with poorly differentiated tumors having more progressive behavior
  • staging determined by surgical exploration or imaging, is based on size, local and regional LNs spread and distant metastasis

**Staging has a greater clinical value

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68
Q

Benign tumors create a capsule that creates a tissue plane that makes the tumor discrete, readily palpable, moveable, and easily excisable. What is the exception to this?

A
  • Hemangiomas (neoplasms composed of tangled BVs) are often unencapsulated and permeate the site in which they arise (dermis of skin and liver)
  • when these are extensive, they may be unresectable
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69
Q

List the paraneoplastic syndromes that fall under the category of vascular and hematologic changes

A 
Venous thrombosis (Trousseau phenomenon)
Disseminated intravascular coagulation 
Nonbacterial thrombotic endocarditis 
Red cell aplasia
70
Q

Explain how malignant neoplasms are graded by degree of cell differentiation and tissue organization

A
  • well differentiated = closely resembles parent tissue
  • moderately differentiated = features of the original tissue type identifiable, but its not the dominant pattern, with additional atypia
  • poorly differentiated = a small minority of cellular constituents allow identification of the parent tissue; associated with cellular anaplasia
  • undifferentiated = tissue of origin cant be discerned by histopathologic appearance of the neoplasm; always associated with anaplasia
71
Q

What is it called when malignant tumors metastasize by bypassing local LNs and why might this occur?

A
  • Skip metastasis

- because of venous-lymphatic anastomoses or because inflammation or radiation has obliterated lymphatic channels

72
Q

When do you add the -oma suffix to a tumor name?

A

When a tumor is benign you attach the -oma suffix to the name of the cell type from which the tumor originates; tumors of mesenchymal cells generally follow this rule
- Ex. Benign tumor arising from fibrous tissue = fibroma

73
Q

Malignant tumors arising in solid mesenchymal tissues are usually called ___________

A

Sarcomas

  • Sar = fleshy; fibrosarcoma, chondrosarcoma, leiomyosarcoma, rhadomyosarcoma
74
Q

What tumor types is alpha-fetoprotein a good marker for?

A

Liver cell cancer, nonseminomatous germ cell tumors of testis

75
Q

An oncoprotein is a protein encoded by an oncogene that drives increreased cell proliferation through one of several mechanisms. What are they?

A
  • constitutive expression of growth factors and their cognate growth receptors set up autocrine signaling
  • mutations in growth factor receptors, non-receptor tyrosine kinases or downstream signaling molecules that leads to constitutive signaling
  • increased expression of MYC
  • mutations that increase the activity of CDK4/D cyclin complexes which promote cell cycle progression
76
Q

What tumor types if human chorionic gonadotropin a good marker for?

A

Trophoblastic tumors

Nonseminomatous testicular tumors

77
Q

Explain differentiation of neoplasms

A
  • differentiation refers to the extent to which neoplastic parenchymal cells resemble the corresponding normal parenchymal cells, both morphologically and functionally
  • benign tumors are well differentiated
78
Q

______ encodes a cytoskeletal protein involved in contact inhibition

A

NF2 -> encodes neurofibromin 2 (merlin)

79
Q

What is the epigenetic mutation found in all pts with malignant rhabdoid tumor?

A

SNF5

80
Q

T/F: Once a cell enters the S phase it is obligated to complete mitosis

A

True

81
Q

What type of tumor is associated with NMYC?

A

Neuroblastoma

82
Q

List the oncogenic RNA viruses

A

HTLV-1

83
Q

Cells that lose APC behave as if they are being continuously stimulated by _______

A

Wnt -> unregulated growth and proliferation

84
Q

What is characteristic of a desmoplasia and what is an example of this?

A
  • desmoplasia = tumors containing parenchymal cells that stimulate the formation of an abundant collagenous stroma
  • Ex. Some cancers of the female breast are stony hard or scirrhous
85
Q

What chromosomal translocations are associated with Burkitt lymphoma?

A

8;14

86
Q

Explain the function of VHL

A
  • VHL protein complex is a component of a ubiquitin ligase
  • Substrate for the VHL ubiquitin ligase is HIF
  • Mutated copies of VHL cancer bind to, sequester and degrade HIF leading to HIF accumulation under normoxic conditions -> associated with increased levels of angiogenic growth factors and alterations in cellular metabolism that favor growth
87
Q

What proto-oncogenes are associated with transcriptional activators?

A
  • Myc (translocation)

- NMYC (amplification)

88
Q

Wat chromosomal translocations are associated with follicular lymphoma?

A

14;18

89
Q

What is the function of CDH1 and what are the familial syndromes and sporadic cancers it causes?

A
  • CDH1 = E-cadherin
  • functions = cell adhesion, inhibition of cell motility
  • familial syndromes = familial gastric cancer
  • sporadic cancers = gastric carcinoma, lobular breast carcinoma
90
Q

Define cachexia

A

Progressive loss of body fat and lean body mass, accompanied by profound weakness, anorexia, and anemia, that is caused by release of factors by the tumor or host immune cells

91
Q

What 2 cancers are often disseminated at diagnosis and are always taken to be malignant?

A

Leukemias and lymphomas

92
Q

What is the function of PTCH and what familial syndromes and sporadic cancers does it cause?

A
  • functions = inhibitor of hedgehog signaling
  • familial syndromes = Gorlin syndrome
  • sporadic cancers = basal cell carcinoma, medulloblastoma
93
Q

What is a mixed tumor?

A
  • Ex. Tumor of salivary gland: contains epithelial components scattered within a myxoid stroma that may contain islands of cartilage or bone. All of these elements arise from a single clone capable of producing both epithelial and myoepithelial cells -> called pleomorphic adenoma
  • *Usually contain cells from a single germ layer
94
Q

All malignant tumors can metastasize, but some do very infrequently, what is a prime example of this?

A

Gliomas (malignant neoplasms of the glial cells) and basal cell carcinomas of the skin

  • Both of these cancers invade early in their course but rarely metastasize -> properties of invasion and metastasis are separable
95
Q

Breast carcinoma preferentially spreads to _________, bronchogenic carcinomas tend to involve the ___________ and __________, and neuroblastomas spread to the _________ and _______. Conversely, ___________ and __________ are rarely the site of secondary deposits.

A

Breast carcinoma = bone
Bronchogenic carcinomas = adrenals and brain
Neuroblastomas = liver and bones
Skeletal muscle and spleen = rare site of secondary deposits

96
Q

______ encodes a component of a ubiquitin ligase that is responsible for degradation of HIF’s, transcription factors that alter gene expression in response to hypoxia

A

VHL

97
Q

What tumors are associated with NRAS?

A

Melanomas and hematologic malignancies

98
Q

Explain pleomorphism in regards to neoplasms

A
  • variation in size and shape
  • cells wihtin the same tumor are not uniform and may range from small cells to tumor giant cells many times larger than their neighbors
99
Q

Explain the function of MSH2, MLH1 and MSH6 proteins and the familial syndromes and sporadic cancers they cause

A
  • functions = DNA mismatch repair
  • familial syndromes = hereditary nonpolyposis colon carcinoma
  • sporadic cancers = colonic and endometrial carcinoma
100
Q

Classification of tumors and their biologic behavior are based primarily on the ____________ component, but their growth and spread are critically dependent on their ____________.

A

Parenchymal component; stroma

101
Q

Explain the localization of benign tumors and capsule formation

A
  • nearly all benign tumors grow as cohesive expansile masses that remain localized and lack capacity to infiltrate, invade or metastasize to distant sites
  • benign tumors usually develop a rim of compressed fibrous tissue called a capsule that separates them from the host tissue
  • Capsule consists largely of ECM deposited by stromal cells which are activated by hypoxic damage resulting from the pressure of the expanding tumor
  • *doesnt prevent tumor growth but creates a tissue plant that makes the rumore discreate, moveable, and easily excisable
102
Q

What is the function of E7 protein of HPV on Rb protein?

A

The viral protein E7 from HPV binds to the hypophosphorylated form of Rb in the same binding site that the E2F fits into thereby inhibiting it

Through this mechanism, HPV viruses confer a high risk of cervical carcinoma if it expresses the E7 protein

103
Q

What effect does HPV have on p53?

A

HPV E6 of high risk HPV subtypes binds to p53 and degrades it

104
Q

What are sentinel LNs and why would you biopsy them?

A
  • They are the first node in a regional lymphatic basin that receives lymph flow from the primary tumor
  • Biopsy is often used to assess the presence or absence of metastatic lesions in the LNs -> sentinel node mapping can be done y infection of radiolabbeled tracers or dyes
  • sentinel node examination is used for detecting spread of melanomas, colon cancers, breast cancer
105
Q

How do mitotic figures differ in dysplastic cells?

A
  • they are more abundant than in normal tissue and rather than being confined to the basal layer may instead be seen at all levels, including surface cells
106
Q

____ renders Rb protein unable to bind the E2F transcription factor (loss of function)

A

E7

107
Q

What is the function of NF1 and what familial syndromes and sporadic cancers does it cause?

A
  • function = inhibitor of RAS/MAPK signaling
  • familial syndromes = neurofibromatosis type 1
  • sporadic cancers = neuroblastoma, juvenile myeloid leukemia
108
Q

What chromosomal translocations are associated with acute myeloid leukemia (AML)?

A

8;21 -> better prognosis

15;17 -> associated with bleeding consequences

109
Q

What is the function of TP53 and what are the familial syndromes and sporadic cancers that it causes?

A
  • Functions = cell cycle arrest and apoptosis in response to DNA damage
  • familial syndrome = Li-Fraumeni syndrome (diverse cancers)
  • sporadic cancers = most human cancers
110
Q

Explain the functions of WT1 and the familial syndromes and sporadic cancers that it causes

A
  • functions = transcription factors
  • familial syndromes = familial wilms tumor
  • sporadic cancers = wilms tumor, certain leukemia’s
111
Q

What are the functions of BRCA1 and BRCA2 and what familial syndromes and sporadic cancers do they cause?

A
  • functions = repair of double stranded breaks in DNA
  • familial syndromes = familial breast and ovarian carcinoma, carcinomas of male breast, chronic lymphocytic leukemia
  • sporadic cancers = rare
112
Q

What is the only absolute criterion of malignancy?

A

Metastasis

113
Q

What tumor types is TP53, APC, and RAS mutants in stool and serum a good marker for?

A

Colon cancer

114
Q

What are papillomas?

A
  • benign epithelial neoplasms producing microscopically or microscopically visible fingerlike warty projections from epithelial surfaces
115
Q

________ encodes a transcription factor that is required for normal development of genitourinary tissues

A

WT1

116
Q

What chromosomal translocations are associated with Mantle cell lymphoma?

A

11;14

117
Q

List the paraneoplastic syndromes that fall under the category of endocrinopathies

A 
Cushing syndrome
Syndrome of inappropriate ADH secretion 
Hypercalcemia 
Hypoglycemia 
Polycythemia
118
Q

What are the 2 basic components of tumors?

A
  1. Neoplasticism cells that constitute the tumor parenchyma
  2. Reactive stroma made up of connective tissue, blood vessels, and variable numbers of cells of the adaptive and innate immune system
119
Q

Differentiate between “carcinoma in situ” and invasive

A
  • Carcinoma in situ = dysplastic changes are marked and involve the full thickness of the epithelium but the lesion doesnt penetrate the basement membrane
  • invasive = once the tumors cells breach the basement membrane
120
Q

In 2011, the 2 drugs that most frequently caused adverse reactions reported to the Food and Drug Administration were the oral anticoagulants ___________ and ___________

A

Warfarin and dabigatran

121
Q

The most common type of menopausal hormone therapy consists of what kind of hormone combination?

A

Administration of estrogens together with progestogen

**Because of the risk of uterine cancer, estrogen therapy alone is used only in hysterectomized women

122
Q

What effect do oral contraceptives have on the risk of developing breast carcinoma, endometrial cancer, ovarian cancers and cervical cancer?

A
  • do not increase risk of breast cancer
  • have protective affect against endometrial and ovarian cancers
  • may increase risk of cervical cancer in women infected with human papilloma virus
123
Q

How do oral contraceptives affect the risk of thromboembolism?

A

They are associated with a 3-6 fold increased risk of venous thrombosis and pulmonary thromboembolism due to a hypercoagulable state; risk may be even higher with newer OC’s that contain synthetic progestin

**risk associated with OC use is 2-6 times lower than the risk of thromboembolism associated with pregnancy

124
Q

How do oral contraceptives affect the risk of cardiovascular disease?

A
  • do not increase the risk of coronary artery disease in women younger than 30 or in older women who are nonsmokers
  • risk does approximately double in women older than 35 who smoke
125
Q

What rare tumor is associated with oral contraceptives especially in older women who have used OC’s for prolonged periods?

A

Hepatic adenoma -> rare benign hepatic tumor that appears as a large, solitary, and well-encapsulated mass

126
Q

What are the adverse effects associated with anabolic steroid use?

A

Stunted growth in adolescents
Acne
Gynecomastia
Testicular atrophy in males
Growth of facial hair and menstrual changes in women
Psychiatric disturbances and increased risk of MI
Hepatic cholestasis may develop in pts receiving orally administered anabolic steroids

127
Q

What is the most commonly used analgesic in the US?

A

Acetaminophen

128
Q

Explain how acetaminophen is detoxified in the body

A
  • 95% undergoes detoxification in the liver by phase II enzymes and is excreted in the urine as glucuronate or sulfate conjugates
  • 5% is metabolized Through the activity of CYPs, primarily CYP2E, to NAPQI which is normally conjugated with GSH
129
Q

Explain the pathogenesis behind acetaminophen toxicity

A
  • when taken in large doses NAPQI accumulates and causes hepatocellular injury, leading to centrilobular necrosis that may progress to liver failure
  • involves 2 mechanisms: covalent binding to hepatic proteins causing damage to cellular membranes & mito dysfunction; depletion of GSH making hepatocyte more susceptible to ROS injury
130
Q

How are chronic alcoholics affected by acetaminophen toxicity?

A

Alcohol induces CYP2W in the liver so acetaminophen toxicity can occur at lower doses in chronic alcoholics

131
Q

What are the symptoms of acetaminophen toxicity?

A
  • begins with nausea, vomiting, diarrhea, and sometimes shock
  • followed in a few days by evidence of jaundice
  • in serious overdose liver failure ensues starting with centrilobular necrosis that may extend to entire lobules
132
Q

How is acetaminophen toxicity treated?

A

Early stages (within 12 hours) can be treated by administration of N-acetylcysteine which restores GSH levels

133
Q

Explain chronic aspirin toxicity (salicylism)

A
  • may develop in a person who takes 3g or more daily for long periods of time
  • manifested by headaches, dizziness, tinnitus, hearing impairment, mental confusion, drowsiness, nausea, vomiting and diarrhea
  • CNS changes may progress to convulsions and coma
  • acute erosive gastritis can occur which produces GI bleeding and leads to gastric ulceration
  • petechial hemorrhage’s may appear in the skin and internal viscera and bleeding from gastric ulceration may be exaggerated
134
Q

Why might a bleeding tendency appear concurrently with chronic aspirin toxicity?

A

Aspirin acetylation platelet cyclooxygenase and irreversibly blocks production of thromboxane A2

135
Q

_____________ and _____________ are important complications of large doses of aspirin

A

Gastric ulceration and bleeding

136
Q

What is analgesic nephropathy?

A

Tubulointerstitial nephritis with renal papillary necrosis that develops from analgesic mixtures of aspirin and phenacetin or acetaminophen taken over several years

137
Q

What is the difference between cocaine and crack and which is more potent?

A
  • cocaine = extract from leaves of the coca plant that is prepared as a water-soluble powder, cocaine hydrochloride
  • crack = crystallization of the pure alkaloid -> far more potent
138
Q

The most serious physical effects of cocaine relate to its acute action on the ___________ system

A

Cardiovascular system

139
Q

Explain the pathogenesis and sx of cocaine use

A
  • facilitates neurotransmission both in CNS where it blocks reuptake of dopamine and at adrenergic nerve endings where it blocks reuptake of epi and NE stimulating presynaptic release of NE
  • Net effect = accumulation of these 2 NTs in synapses resulting in excess stimulation manifested by tachycardia, HTN, and peripheral vasoconstriction
  • may also cause myocardial ischemia by causing coronary artery vasoconstriction and y enhancing platelet aggregation and thrombus formation
140
Q

How does cigarette use influence the effects of cocaine?

A
  • potentiates cocain-induced coronary vasospasm setting the stage for myocardial ischemia that may lead to MI
141
Q

How can cocain produce lethal arrhythmias?

A
  • y enhanced sympathetic activity as well as by disrupting normal ion transport in the myocardium
142
Q

What are the most common acute affects on the CNS caused by cocaine use?

A
  • hyperpyrexia thought to be caused by aberrations of dopaminergic pathways that control body temp
  • seizures
143
Q

What effects does cocaine have on pregnancy?

A
  • May cause acute decreases in blood flow to the placenta resulting in fetal hypoxia and spontaneous abortion
  • neurologic development may be impaired in the fetus
144
Q

Explain the pulmonary injury caused by opiates

A 
Severe to moderate edema 
Septic embolism from endocarditis 
Lung abscess 
Opportunistic infections 
Foreign body granulomas from talc occur principally in the lung and sometimes found in the mononuclear phagocyte system particularly in the spleen, liver and LNs that drain the UEs
145
Q

Infectious complications of opiates are common, what are the 4 sites most commonly affected?

A

Skin and subcutaneous tissue
Heart valves
Liver
Lungs

146
Q

What is the most common infection among individuals addicted to opiates?

A

Viral hepatitis, acquired from sharing dirty needles

147
Q

What is the most frequent telltale sign of heroin addiction?

A

Cutaneous lesions

148
Q

What acute changes are seen in the skin of opiate users?

A

Abscesses
Cellulitis
Ulceration
Scarring at injection sites, hyperpigmentation over commonly used veins and thrombosis veins

149
Q

Kidney disease is a relatively common hazard associated with opiate use, what are the 2 forms most frequently encountered?

A
  1. Amyloidosis generally secondary to skin infections
  2. Focal and segmental glomerulosclerosis

**both induce proteinuria and the nephrotic syndrome

150
Q

What is the leading cause of opiate related death in the US?

A

Use of oxycodone, a potent respiratory suppressant

151
Q

Explain the MOA of methamphetamine

A
  • closely related to amphetamine but has stronger effects in the CNS
  • acts by releasing dopamine in the brain, which inhibits presynaptic neurotransmission at corticostriatal synapses, slowing glutamate release
  • produces a feeling of euphoria which is followed by a crash
  • long-term use leads to violent behaviors, confusion and psychotic features that include paranoia and hallucinations
152
Q

Explain the MOA of MDMA

A
  • generally taken orally and induces euphoria and hallucinogen-like feelings that last 4-6 hours
  • increase in serotonin release in the CNS
  • as the drug wears off, this increased release coupled with its ability to interfere with serotonin synthesis causes subsequent, post-use drop in serotonin that is only slowly replenished
  • also reduces number of serotonergic axon terminals in the striatum and cortex and may increase the peripheral effects of dopamine and adrenergic agents
153
Q

What is the most widely used illicit drug globally?

A

Marijuana

154
Q

What are the potential benefits of marijuana use?

A
  • treat nausea secondary to cancer chemotherapy and as an agent capable of decreasing pain in some chronic conditions
155
Q

What are the effects of marijuana use?

A
  • distorts sensory perception and impairs motor coordination; these effects clear in 4-5 hrs
  • continued use progresses to cognitive and psychomotor impairments such as inability to judge time, speed and distance
  • increases HR and sometimes BP and it may cause angina in a pt with coronary artery disease
156
Q

How is the respiratory system affected by chronic marijuana use?

A
  • laryngitis, pharyngitis, bronchitis, cough and hoarseness
  • also mild but significant airway obstruction

**Smoking a marijuana cigarette is associated with a 3 fold increase in the amount of tar inhaled in retained in the lungs versus a tobacco cigarette

157
Q

How are burns classified?

A
  • superficial burns (formerly 1st degree) = confined to epidermis
  • partial thickness burns (formerly 2nd degree) = involve injury to dermis
  • full-thickness burns (formerly 3rd degree) = extend to subcutaneous tissue; may also involve damage to muscle tissue underneath the subcutaneous tissue (formerly 4th degree)
158
Q

________, __________, and _________ are the greatest threats to life in burn patients

A

Shock, sepsis and respiratory insufficiency

159
Q

Explain what occurs in pts with burns of more than 0% of the body surface

A
  • There is a rapid (within hrs) shift of ody fluids into the interstitial compartments both at the burn site and systemically due to the systemic inflammatory response syndrome, leading to shock
  • there’s generalized edema, including pulmonary edema
  • development of a hypermetabolic state associated with excess heat loss and an increased need for nutritional support -> when more than 40% of the body surface is burned the resting metabolic rate doubles
160
Q

Why do virtually all burns become colonized with bacteria?

A
  • burn site is ideal for the growth of microorganisms
  • the serum and debris provide nutrients and the. Burn injury compromises blood flow, blocking effective inflammatory responses
  • cellular and humoral defenses against infections are compromised and both lymphocyte and phagocyte functions are impaired
161
Q

What is the most common bacteria to infect burn sites?

A

Pseudomonas aeruginosa

162
Q

What are the most serious sequelae associated with bacterial colonization of a burn site?

A

Pneumonia or septic shock with renal failure and/or the acute respiratory distress syndrome

163
Q

How are the airways and lungs affected by burns?

A
  • injury to airways and lungs may develop within 24-48 hrs after the burn
  • may result Fromm direct effect of heat on the mouth, nose, and upper airways or from the inhalation of heated air and noxious gases in the smoke
  • water soluble gases may react with water to form acids or alkalis particularly in the upper airways producing inflammation and swelling which may lead to airway obstruction
  • lipid soluble gases are more likely to reach deeper airways producing pneumonitis
164
Q

What is a common complication of burn injury?

A

Hypertrophic scarring -> marked by excessive deposition of collagen in th healing wound bed

165
Q

Explain the morphology of the varying degrees of burns

A
  • full thickness burns are white or charred, dry and painless
  • partial thickness burns are pink or mottled with blisters and painful
  • devitalized tissue reveals coagulative necrosis adjacent to vital tissue that quickly accumulates inflammatory cells and marked exudation
166
Q

Explain heat cramps

A
  • result from loss of electrolytes via sweating
  • cramping of voluntary muscles usually in association with vigorous exercise
  • heat-dissipating mechanisms are able to maintain normal core body temp
167
Q

WHat is the most common hyperthermia syndrome? Explain it

A
  • heat exhaustion
  • onset is sudden, results from failure of the CV system to compensate for hypovolemia caused by dehydration
  • after a period of collapse, which is brief, equilibrium is spontaneously re-established if the victim is able to rehydrate
168
Q

What are symptoms of heat stroke?

A
  • there is marked generalized vasodilation with peripheral pooling of blood and decreased effective circulating blood volume
  • hyperkalemia, tachycardia, Arrhythmias all common
  • sustained contractions of skeletal muscle that can exacerbate the hyperthermia and lead to muscle necrosis (rhabdomyolysis)
169
Q

Explain the pathogenesis of heat stroke as it relates to skeletal muscle symptoms

A
  • nitrosylation of ryanodine receptor 1 (RYR1) which is located in the SR of skeletal muscle
  • RYR1 regulates release of calcium from the sarcoplasm
  • heat stroke deranged RYRR1 function and allows calcium to leak into the cytoplasm where it stimulates muscle contraction and heat production
170
Q

Explain the general conditions causing hypothermia and associated symptoms

A
  • high humidity, wet clothing, and dilation of superficial blood vessels resulting from the ingestion of alcohol hasten the lowering of body temp
  • at a body temp of about 90, loss of consciosness occurs followed by bradycardia and Afib

COM: MOD II - Midterm COPY (4 decks)

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