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*First Aid in Brainscape* > Steve Perry's Pathology Journey > Flashcards

Steve Perry's Pathology Journey Flashcards

1
Q

Apoptosis

A

Programmed cell death;ATP required; intrinsic and extrinsic pathways both cause activation of cytosolic capsases that mediate cellular breakdown; no inflammation (unlike necrosis).
Appearance: eosinophilic cytoplasm, cell shrinkage, nuclear shrinkage (pyknosis), basophilia, membrane blebbing, nuclear fragmentation (karyorrhexiz), formation of apoptotic bodies.

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2
Q

What is a test to check if a cell is undergoing apoptosis

A

DNA laddering is indicator of apoptosis: during karyorrhexis, endocucleases cleave at internucleosomal regions, yielding 180bp fragments.

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3
Q

Radiation therapy causes apoptosis of tumors and surrounding tissue via

A

free radical formation and dsDNA breakage. Rapidly dividing cells (e.g. skin and GI mucosa) are very susceptible to radiation therapy-induced apoptosis

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4
Q

Intrinsic pathway of apoptosis

A

Involved in tissue remodeling in embryogenesis. Occurs when a regulating factor is withdrawn from a proliferating cell population (e.g. decreased IL-2 after a completed immunological reaction leading to apoptosis of proliferating effector cells). Also occurs after exposure to injurious stimuli. Changes in proportions of anti- and pro- apoptotic factors lead to increase mitochondrial permeability and cytochrome c release. BAX and BAK are pro-apoptotic and BCL-2 is anti apoptotic.

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5
Q

BCL-2

A

prevents cytochrome C release by binding to and inhibiting Apaf-1. Apaf-1 normally induces the activation of caspases. If Bcl-2 is overexpressed (e.g. follicular lymphoma), then Apaf-1 is overly inhibited, leading to decrease caspase activation and tumorigenesis.

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6
Q

Extrinsic pathway of apoptosis

A

2 pathways: 1. Ligand receptor interactions (FasL binding to Fas (CD95)). Fas-FasL interaction is necessary in thymic medullary negative selection. Mutation in Fas increase numbers of circulating self-reacting lymphocytes (auto-immune disorders). Fas molecules coalesce and form death-domain containing adapter protein FADD which binds and activates caspases.
2. Immune cell (cytotoxic T cell release of perforin and granzyme B). Perforin and granzymes pathway

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7
Q

Necrosis: define it

A

Enzymatic degradation and protein denaturation of a cell resulting from exogenous injury. Intracellular components leak; inflammatory process (unlike apoptosis)

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8
Q

Coagulative necrosis

A

heart, liver, kidney; occurs in tissues supplied by end-arteries; increase cytoplasmic binding of acidophilic dye. Proteins denature first, followed by enzymatic degradation.

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9
Q

Liquefactive necrosis

A

brain, bacterial abscess; occurs in CNS due to high fat content. In contrast to coagulative necrosis, enzymatic degradation due to the release of lysosomal enzymes occurs first.

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10
Q

Caseous necrosis

A

TB, systemic fungi, Nocardia

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11
Q

Fatty necrosis

A

Enzymatic (pancreatitis [saponification]). and nonezymatic (e.g. breast trauma); calcium deposits appear dark blue on staining

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12
Q

Fibrinoid necrosis

A

Vasculitides (e.g. HSP, churg-strauss), malignant HTN; amorphous and pink on H&E.

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13
Q

Gangrenous necrosis

A

Dry (ischemic coagulative) and wet (infection); common in limbs and GI tract.

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14
Q

Cell injury: Type that is reversible with O2

A

Caused by ATP depletion; cellular/mitochondrial swelling (decrease ATP leads to decreased Na/K pump); Nuclear chromatin clumping; decreased glycogen; fatty change; ribosomal/polysomal detachment (decreased protein synthesis); membrane blebbing

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15
Q

Cell injury: type that is irreversible with O2

A

See nuclear pyknosis, karyorrhexis, karyolysis; plasma membrane damage (degradation of membrane phospholipids); lysosomal rupture; mitochondrial permeability/vacuolization; phospholipid- containing amorphous densities within mitochondria (swelling alone is reversible)

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16
Q

Ischemia: susceptible areas in the brain

A

ACA/MCA/PCA boundary areas (watershed areas where the blood supply is from distal branches of 2 arteries leave that area open to hypoperfusion if low BP, but do protect if one artery is cut off)

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17
Q

Ischemia: susceptible areas in the Heart

A

Subendocardium (especially LV)

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18
Q

Ischemia: susceptible areas in the Kidney

A

Straight segment of proximal tubule (medulla); thick ascending limb (medulla)

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19
Q

Ischemia: susceptible areas in the Liver

A

Area around central vein (zone III, which is where you gind cytochrome p450)

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20
Q

Ischemia: susceptible areas in the Colon

A

splenic flexure (watershed), rectum (watershed)

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21
Q

Red infarct

A

Red=hemorrhagic infarct; occur in loose tissue with multiple blood supplies, such as liver, lungs. and intestine

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22
Q

reperfusion injury is due to

A

damage by free radicals

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23
Q

Pale infarct

A

occur in solid tissue with a single blood supply, such as heart or kidney or spleen

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24
Q

Shock: what do you see

A

First sign of shock is tachycardia. shock in the setting of DIC secondary to trauma is likely due to sepsis. Distributive shock includes septic, neurogenic, and anaphylactic shock.

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25
Q

Distributive shock

A

High-output failure (decreased TPR, Increased CO, Increased venous return); Decreased PCWP (wedge pressure); vasodilation (warm, dry skin); failure to increase blood pressure with IV fluids

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26
Q

Hypovolemic/cardiogenic shock

A

low-ouput failure (Increased TPR, decreased CO, decreased venous return); increased PCWP in cardiogenic shock, decreased PCWP in hypovolemic shock; vasoconstriction (cold, clammy patient); blood pressure restored with IV fluids.

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27
Q

Atrophy

A

Reduction in the size and/or number of cells; causes include: decreased endogenous hormones (e.g. postmenopausal ovaries), increased exogenous hormones (ball shrinkage due to steroids), decreased innervation, decreased blood flow and nutrients, Decreased metabolic demand (don’t use it, ya lose it), Increased pressure (nephorlithiasis), Occlusion of secretory ducts (Cystic fibrosis)

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28
Q

Inflammation is characterized by

A

rubor-redness, Dolor-pain, calor-heat, tumor-swelling, functio laesa-loss of function

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29
Q

Inflammation: vascular component is doing what

A

increased vascular permeability, vasodilation, endothelial injury

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30
Q

Inflammation: the cellular component is doing what

A

Neutrophils extravasate from circulation to injured tissue to participate in inflammation through phagocytosis, degranulation, and inflammatory mediator release.

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31
Q

Acute inflammation

A

Neutrophil, eosinophil, and antibody mediated; Acute inflammation is rapid onset (seconds to minutes), last minutes to days; outcomes include complete resolution, abscess formation, and progression to chronic inflammation

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32
Q

Chronic inflammation

A

Mononuclear cell and fibroblast mediated; characterized by persistent destruction and repair; associated with blood vessel proliferation, fibrosis; Granuloma: nodular collections of epitheliod macrophages and giant cells. Outcomes include scarring and amyloidosis

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33
Q

Chromatolysis

A

Process involving the cell body following axonal injury; Changes reflect increased protein synthesis in effort to repair the damaged axon. Characterized by: round cellular swelling, displacement of the nucleus to the periphery, dispersion of Nissl substance throughout cytoplasm

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34
Q

Dystrophic calcification

A

Calcium deposits in tissues secondary to necrosis: tends to be localized (e.g. on heart valve); seen in TB, liquefactive necrosis of chronic abscesses, fat necrosis, infarcts, thrombi, schistosomiasis, Monckeberg arteriolosclerosis, congenital CMV + toxoplasmosis, psammoma bodies; is not directly associated with hypercalcemia (patients usually have normal ca levels)

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35
Q

Metastatic Calcification

A

Widespread deposition of calcium in normal tissue secondary to hypercalcemia (e.g. primary hyperthyroidism, hypervitaminosis D, sarcoidosis) or high calcium-phosphate product (e.g. chronic renal failure + secondary hyperparathyroidism, long term dialysis, calciphylaxis, warfarin); calcium deposits predominantly in interstitial tissues of kidney, lungs, and gastric mucosa (these tissues lose acid quickly; increase pH favors deposition). patients are not normocalcemic.

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36
Q

Leukocyte extravasation: what is it, name 4 steps

A

Extravasation predominantly occurs at post capillary venules. Leukocytes exit from blood vessels at sites of tissue injury and inflammation in 4 steps: 1. margination and rolling; 2. tight-binding; 3. Diapedesis-leukocytes travel between endothelial cells and exit blood vessel; 4. Migration- leukocytes travel through interstitium to site of injury or infection guided by chemotactic signals.

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37
Q

Leukocyte extravasation: what mediates margination and rolling

A

Vasculature/stroma contains: E-selection, P-selection, GlyCAM-1, CD34;
Leukocyte has Sialyl-lewisX and L-selectin;
Sialyl-lewisX bind E and P selectin; glyCAM-1 binds L-selectin

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38
Q

Leukocyte extravasation: what mediates Tight-binding

A

Vasculature/stroma contains ICAM-1 (CD54) and VCAM-1 (CD106);
Leukocyte contains CD11/18 integrins (LFA-1, Mac-1), VLA-4 integrin;
LFA-1 binds ICAM-1, brings it in close

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39
Q

Leukocyte extravasation: what mediates Leukocyte Diapedisis

A

leukocyte PECAM-1 (CD31) binds PECAM-1 (CD31) on vasculature/stroma and guides it through

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40
Q

What chemotactic products released in response to bacteria guide leukocytes in migration

A

Chemotactic products are: C5a, IL-8, LTB4, kallikrein, platelet-activation factor

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41
Q

Free radicals damages cells via

A

membrane lipid peroxidation, protein modification, and DNA breakage

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42
Q

What initiates free radical injury

A

initiated via radiation exposure, metabolism of drugs (phase 1), redox reactions, Nitric oxide, transition metals, leukocyte oxidative burst.

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43
Q

How can you clear free radicals

A

Eliminated by enzymes (catalse, super-oxide dismutase, glutathione peroxidase), spontaneous decay, antioxidants (vitamins A,C,E)

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44
Q

Pathologies that are due to free radical damage

A

Retinopathy of prematurity, Bronchopulmonary dysplasia, carbon tetrachloride leading to liver necrosis (fatty change), Acetaminophen overdoes causing fulminant hepatitis and renal papillary necrosis, Iron overload (hemochromatosis), reperfusion injury (e.g. superoxide)

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45
Q

Inhalation injury

A

most common pulmonary complication after exposure to fire. Inhalation of products of combustion (carbon particles, toxic fumes) leads to chemical tracheobronchitis, edema, and pneumonia.

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46
Q

Scar formation: tensile strength and timeline

A

70-80% of tensile strength returns at 3 months following wound; little additional tensile strength will be regained.

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47
Q

Scar formation: hypertrophic scars

A

Get increased collagen synthesis; Parallel collagen arrangement; scar stays confined to borders of original wound; infrequently reocur following resection

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48
Q

Keloid scar formation

A

Greatly increased collagen synthesis; disorganized collagen arrangement; scar extends beyond the borders of original wound; frequently recur following resection. Also, it is scientifically proven to be huge and ugly

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49
Q

Wound healing tissue mediators: PDGF

A

platelet derived growth factor is secreted by activated platelets and macrophages; induces vascular remodeling and smooth muscle cell migration; stimulates fibroblast growth for collagen syntheses

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50
Q

Wound healing tissue mediators: FGF

A

Fibroblast growth factor stimulates all aspects of angiogenesis (growth of new blood vessels)

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51
Q

Wound healing tissue mediators: EGF

A

Epidermal growth factor stimulates cell growth via tyrosine kinase (e.g EGFR (EGF receptor) as expressed by ERBB2)

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52
Q

Wound healing tissue mediators: TGF-beta

A

Transforming growth factor beta stimulates angiogenesis, fibrosis, and cell cycle arrest

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53
Q

Wound healing tissue mediators: Metalloproteinases

A

stimulates tissue remodeling

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54
Q

Phase of wound healing (mediators and characteristics): Inflammatory (immediate)

A

Mediators: Platelets, neutrophils, macrophages
Characteristics: clot formation, increased vessel permeability and neutrophil migration into tissue; macrophages clear debris 2 days later.

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55
Q

Phase of wound healing (mediators and characteristics): Proliferative stage (2-3 days after wound

A

Mediators: Fibroblasts, myofibroblasts, endothelial cells, Keratinocytes, macrophages
Characteristics; Deposition of granulation tissue and collage, angiogenesis, epithelial cell proliferation, dissolution of clot, and wound contraction (mediated by myofibroblasts)

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56
Q

Phase of wound healing (mediators and characteristics): remodeling phase (1 week after wound)

A

mediators: Fibroblasts
Characteristics: Type III collagen replaced by type I collage, increased tensile strength of tissue

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57
Q

Granulomas and anti-TNF drugs: what is the big deal

A

Th1 cells secrete gamma-interferon, activating macrophages. TNF-alpha from macrophages induce and maintain granuloma formation. Anti-TNF drugs can, as a side effect, cause sequestering granulomas to break down, leading to disseminated disease. Always test for latent TB before starting anti-TNF therapy.

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58
Q

Exudate

A

Thick, cellular, protein rich, with a specific gravity > 1.020; Due to lymphatic obstruction, inflammation/infection, or malignancy

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59
Q

Transudate

A

thin, hypocellular, protein poor, specific gravity

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60
Q

Erythrocyte sedimentation rate is what

A

Products of inflammation (E.g. fibrinogen) coat RBCs and cause aggregation. When aggregated, RBCs fall at a faster rate within the test tube.

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61
Q

What can cause an increased ESR

A

most anemias, infections, inflammation, cancer, pregnancy, autoimmune disorders

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62
Q

What can cause a decreased ESR

A

Sickle cell (altered shape), Polycythemia (increased RBCs dilute aggregation factors), CHF (unknown)

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63
Q

Iron poisoning

A

One of the leading causes of fatality from toxicologic agents in children;
Mechanism- Cell death due to peroxidation of membrane lipids;
Acute symptoms- nausea, vomiting, gastric bleeding, lethargy;
Chronic symptoms- metabolic acidosis, scarring leading to GI obstructions;
Treatment- Chelation (e.g. IV deferoxamine, oral deferasirox), dialysis.

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64
Q

Amyloidosis

A

abnormal aggregation of proteins (or their fragments) into Beta pleated sheet structures leading to damage and apoptosis

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65
Q

AL (primary) amyloidosis

A

Due to deposition of proteins from Ig Light chains. Can occur as a plasma cell disorder or associated with multiple myeloma. Often affects multiple organ systems, including renal (nephrotic syndrome), Cardiac (restrictive cardiomyopathy, arrhythmia), hematologic (Easy bruising), GI (hepatomegaly), and neurologic (neuropathy)

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66
Q

AA (secondary) amyloidosis

A

Seen with chronic conditions, such as rheumatoid arthritis, IBD, spondyloarthropathy, protracted infection. Fibrils composed of serum Amyloid A. often multisystem like AL amyloidosis.

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67
Q

Dialysis related amyloidosis

A

Fibrils composed of beta2-microglobulin in patients with ESRD and/or on long-term dialysis. May present as carpal tunnel syndrome

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68
Q

Heritable Amyloidosis

A

Heterogenous group of disorders. Example is ATTR neurologic/cardiac amyloidosis due to transthyretin (TTR or prealbumin) gene mutation.

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69
Q

Age-related (senile) systemic amyloidosis

A

Due to deposition of normal (wild type) TTR in myocardium and other sites. Slower progression of cardiac dysfunction relative to AL amyloidosis

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70
Q

Organ specific amyloidosis

A

Amyloid deposition localized to a single organ. Most important form is amyloidosis in Alzheimer disease due to deposition of amyloid-Beta protein cleaved from amyloid precursor protein (APP)(in downs syndrome you get an extra copy of this gene). Islet amyloid polypeptide (IAPP) is commonly seen in diabetes mellitus type 2 and is caused by deposition of amylin in pancreatic islets

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71
Q

Lipofuscin

A

A yellow-brown “wear and tear” pigment associated with normal aging. Formed by oxidation and polymerization of autophagocytosed organellar membranes. Autopsy of elderly person will reveal deposits in heart, liver, eye, and other organs

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72
Q

P-glycoprotein

A

Also known as multidrug resistance protien 1 (MDR1). Expressed by some cancer cells (e.g. colon, liver) to pump out toxins, including chemotherapeutic agents (one mechanism of decreased responsiveness or resistance to chemotherapy over time).

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73
Q

Define: hyperplasia

A

Increase in number of cells: reversible

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74
Q

Define: metaplasia

A

one adult cell type is replaced by another. often secondary to irritation and/or environmental exposure: reversible

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75
Q

Define: dysplasia

A

Abnormal growth with loss of cellular orientation, shape, and size in comparison to normal tissue maturation; commonly preneoplastic: reversible

76
Q

Define: Anaplasia

A

Loss of structural differentiation and function of cells, resembling primitive cells of same tissue; often equated with undifferentiated malignant neoplasms. May see “giant cells” with single large nucleus or several nuclei: irreversible

77
Q

Define: neoplasia

A

A clonal proliferation of cells that is uncontrolled and excessive. Neoplasia may be benign or malignant: irreversible

78
Q

Define: Desmoplasia

A

Fibrous tissue formation in response to neoplasm (e.g. linitis plastica in diffuse stomach cancer): irreversible;
generally grows and surrounds the cancer tumor, can even make tumor chemo resistant

79
Q

Tumor grade

A

Determined by degree of cellular differentiation and mitotic activity on histology. Usually graded 1-4; 1= low grade, well differentiated; 4= high grade, poorly differentiated, anaplastic; stage is usually has more prognostic value than grade.

80
Q

Tumor stage

A

Degree of localization/spread based on site and size of primary lesion, spread to regional lymph nodes, presence of metastases. Based on clinical (c) or Pathology (p) findings. Example would be cT3N1M0; T=tumor size, N=node involvement, M=metastases, each having independent prognostic value

81
Q

Tumor nomenclature: define carcinoma

A

implies epithelial growth; most spread through lymphatics except for Renal cell carcinoma (renal vein spread), hepatocellular carcinoma (often invades hepatic vein), follicular carcinoma of the thyroid, and choriocarcinoma

82
Q

Tumor nomenclature: Sarcoma

A

denotes mesenchymal origin of malignancy; usually spreads hematogenously.

83
Q

Name for a benign and malignant epithelium tumor

A

benign: Adenoma, papilloma;
Malignant: adenocarcinoma, pappilary carcinoma

84
Q

Name for a benign and malignant: mesenchyme blood cell tumor

A

benign: no such thing;
Malignant: leukemia, lymphoma

85
Q

Name for a benign and malignant: mesenchyme blood vessel tumor

A

Benign is hemangioma;

Malignant is Angiosarcoma

86
Q

Name for a benign and malignant: mesenchyme smooth muscle tumor

A

benign is Leiomyoma;

Malignant is leiomyosarcoma

87
Q

Name for a benign and malignant: mesenchyme striated muscle tumor

A

benign is Rhabdomyoma;

malignant is Rhabdomyosarcoma

88
Q

Name for a benign and malignant: mesenchyme Connective tissue tumor

A

Benign is fibroma;

Malignant is fibrosarcoma

89
Q

Name for a benign and malignant: Mesenchyme bone tumor

A

benign is osteoma;

Malignant is Osteosarcoma

90
Q

Name for a benign and malignant: mesenchyme fat tumor

A

benign is lipoma; malignant is liposarcoma

91
Q

What is a benign tumor

A

Usually well differentiated, low mitotic activity, well demarcated, no metastasis, no necrosis.

92
Q

What is a malignant tumor

A

May be poorly differentiated, erratic growth, locally invasive/diffuse, may metastasize, decrease apoptosis (upregulation of telomerase prevents chromosome shortening and cell death)

93
Q

Cachexia

A

Weight loss, muscle atrophy, and fatigue that occur in chronic disease (e.g. cancer, AIDS, heart failure, TB). Mediated by TNF-alpha (nicknamed cachectin), IFN-gamma, and IL-6

94
Q

What neoplasm is associated with this disease: Acanthosis nigricans (hyperpigmentation and epidermal thickening)

A

Visceral malignancy (esp. stomach)

95
Q

What neoplasm is associated with this disease: Actinic keratosis

A

Squamous cell carcinoma of skin

96
Q

What neoplasm is associated with this disease: AIDS

A

Aggressive malignant lymphomas (non-hodgkin) and kaposi sarcoma

97
Q

What neoplasm is associated with this disease: Autoimmune diseases (Hashimoto, SLE, thyroiditis)

A

Lymphoma

98
Q

What neoplasm is associated with this disease: Barret esophagus

A

Esophageal adenocarcinoma

99
Q

What neoplasm is associated with this disease: Chronic atrophic gastritis, pernicious anemia, post-surgical gastric remnants

A

Gastic carcinoma

100
Q

What neoplasm is associated with this disease: Cirrhosis

A

Hepatocellular carcinoma

101
Q

What neoplasm is associated with this disease:Cushing syndome

A

Small cell lung cancer

102
Q

What neoplasm is associated with this disease: Dermatomyositis

A

Lung cancer

103
Q

What neoplasm is associated with this disease: Down syndrome

A

ALL and AML

104
Q

What neoplasm is associated with this disease: Dysplastic nevus

A

Malignant melanoma

105
Q

What neoplasm is associated with this disease: Hypercalcemia

A

Squamous cell lung cancer

106
Q

What neoplasm is associated with this disease: Immunodeficiency states

A

Malignant lymphomas

107
Q

What neoplasm is associated with this disease: Lambert-Eaton myasthenic syndrome

A

small cell lung cancer

108
Q

What neoplasm is associated with this disease: Paget disease of Bone

A

Secondary osteosarcoma and fibrosarcoma

109
Q

What neoplasm is associated with this disease:Plummer-Vinson syndrome (decreased iron)

A

Squamous cell carcinoma of esophagus

110
Q

What neoplasm is associated with this disease: Polycythemia

A

Renal cell carcinoma, hepatocellular carcinoma

111
Q

What neoplasm is associated with this disease: Radiation exposure

A

Leukemia, sarcoma, Papillary thyroid cancer, and breast cancer

112
Q

What neoplasm is associated with this disease: SIADH

A

small cell lung cancer

113
Q

What neoplasm is associated with this disease:Tuberous sclerosis

A

Giant cell astrocytoma, renal angiomyolipoma, and cardiac rhabdomyoma

114
Q

What neoplasm is associated with this disease: Ulcerative colitis

A

Colonic adenocarcinoma

115
Q

What neoplasm is associated with this disease: Xeroderma pigmentosum, albinism

A

Melanoma, basal cell carcinoma, and especially squamous cell carcinoma of skin

116
Q

Define oncogene

A

Gain of function mutations that lead to an increased risk of cancer. Need to damage only 1 allele

117
Q

What tumor is this oncogene associated with and what is its gene product: BRC-ABL

A

CML, ALL; codes for tyrosine kinase

118
Q

What tumor is this oncogene associated with and what is its gene product: bcl-2

A

Follicular and undifferentiated lymphomas; Anti-apoptotic molecules

119
Q

What tumor is this oncogene associated with and what is its gene product: BRAF

A

Melanoma; Serine/threonine kinase

120
Q

What tumor is this oncogene associated with and what is its gene product: c-kit

A

Gastrointestinal stromal tumor (GIST); codes for cytokine receptor (for stem cell factor)

121
Q

What tumor is this oncogene associated with and what is its gene product: c-myc

A

Burkitt lymphoma; transcription factor

122
Q

What tumor is this oncogene associated with and what is its gene product: HER2/neu (c-erbB2)

A

Breast, Ovarian and gastric carcinoma; codes for tyrosine kinase

123
Q

What tumor is this oncogene associated with and what is its gene product: L-myc

A

Lung tumor; codes for transcription factor

124
Q

What tumor is this oncogene associated with and what is its gene product: N-myc

A

Neuroblastoma; codes for transcription factor

125
Q

What tumor is this oncogene associated with and what is its gene product: ras

A

Colon cancer, lung cancer, pancreatic cancer; codes for GTPase

126
Q

What tumor is this oncogene associated with and what is its gene product: ret

A

MEN 2A and 2B; codes for tyrosine kinase

127
Q

define tumor suppressor gene

A

Loss of function of a gene that increases your risk of cancer; both alleles must be knocked out for expression of disease

128
Q

What tumor is this tumor suppressor gene associated with and what is its gene product: APC

A

colorectal cancer (associated with FAP);

129
Q

What tumor is this tumor suppressor gene associated with and what is its gene product: BRCA1

A

Breast and ovarian cancer; makes DNA repair protein

130
Q

What tumor is this tumor suppressor gene associated with and what is its gene product: BRCA2

A

Breast and ovarian cancer; makes DNA repair protein

131
Q

What tumor is this tumor suppressor gene associated with and what is its gene product: CPD4/SMAD4

A

Pancreatic cancer; DPC-deleted in pancreatic cancer

132
Q

What tumor is this tumor suppressor gene associated with and what is its gene product: DCC

A

Colon cancer; DCC-deleged in colon cancer

133
Q

What tumor is this tumor suppressor gene associated with and what is its gene product: MEN1

A

MEN type I;

134
Q

What tumor is this tumor suppressor gene associated with and what is its gene product: NF1

A

Neurofibromatosis type 1; RAS GTPase activating protein (neurofibromin)

135
Q

What tumor is this tumor suppressor gene associated with and what is its gene product: NF2

A

Neurofibromatosis type 2; Merlin (schwannomin) protein

136
Q

What tumor is this tumor suppressor gene associated with and what is its gene product: p16

A

Melanoma; produces cyclin-dependent kinase inhibitor 2A

137
Q

What tumor is this tumor suppressor gene associated with and what is its gene product: p53

A

Most human cancers; Li-Fraumeni syndrome; produces transcription factor for p21, blocks G1 going to S phase

138
Q

What tumor is this tumor suppressor gene associated with and what is its gene product: PTEN

A

Breast cancer, prostate, cancer, endometrial cancer

139
Q

What tumor is this tumor suppressor gene associated with and what is its gene product: Rb

A

Retinoblastoma, osteosarcoma; Inhibits E2F; blocks G1 going to S phase

140
Q

What tumor is this tumor suppressor gene associated with and what is its gene product: TSC1

A

Tuberous sclerosis; Hamartin protein

141
Q

What tumor is this tumor suppressor gene associated with and what is its gene product: TSC2

A

Tuberous sclerosis; Tuberin protein

142
Q

What tumor is this tumor suppressor gene associated with and what is its gene product: VHL

A

von Hippel-Lindau disease; inhibits hypoxia inducible factor 1a

143
Q

What tumor is this tumor suppressor gene associated with and what is its gene product: WT1

A

Wilms tumor (nephroblastoma);

144
Q

What tumor is this tumor suppressor gene associated with and what is its gene product: WT2

A

Wilms tumor (nephroblastoma);

145
Q

Tumor markers: what are their use

A

Tumor markers should not be used as the primary tool for cancer diagnosis. They may be used to monitor tumor recurrence and response to therapy, but definitive diagnosis can be made only via biopsy.

146
Q

Tumor marker that tells you what: Alkaline phosphatase

A

Metastases to bone, liver, Paget disease of bone, seminona (placental ALP)

147
Q

Tumor marker that tells you what: Alpha-fetoprotein

A

normally made by fetus. Hepatocellular carcinoma, hepatoblastoma, yolk sac (endodermal sinus) tumor, testicular cancer, mixed germ cell tumor (co-secreted with Beta-hCG)

148
Q

Tumor marker that tells you what: Beta-hCG

A

Hydratidiform moles and Choriocarcinomas (Gestational trophoblastic disease), testicular cancer. Commonly associated with pregnancy.

149
Q

Tumor marker that tells you what: CA-15-3/CA-27-29

A

Breast cancer

150
Q

Tumor marker that tells you what: CA-19-9

A

Pancreatic adenocarcinoma

151
Q

Tumor marker that tells you what: CA-125

A

Ovarian cancer

152
Q

Tumor marker that tells you what: Calcitonin

A

Medullary thyroid carcinoma

153
Q

Tumor marker that tells you what: CEA

A

CarcinoEmbryonic Antigen. Very nonspecific but produced by about 70% of colorectal and pancreatic cancers; also produced by gastric, breast, and medullary thyroid carcinomas

154
Q

Tumor marker that tells you what: PSA

A

Prostate specific antigen. Used to follow prostate adenocarcinoma. Can also be elevated in BPH and prostatitis. Questionable risk/benefit for screening

155
Q

Tumor marker that tells you what: S-100

A

Neural crest origin (e.g. melenomas, neural tumores, schwannomas, Langerhans cell histiocytosis)

156
Q

Tumor marker that tells you what: TRAP

A

Tartrate-Restistant Acid Phosphatase (TRAP). Hairy cell leukemia-a B-cell neoplasm.
TRAP the hairy animal. Largely replaced by flow cytrometry.

157
Q

Oncogenic microbe that causes what: EBV

A

Burkitt lymphoma, Hodgkin lymphoma, nasopharyngeal carcinoma, CNS lymphoma (in immunocompromised patients)

158
Q

Oncogenic microbes that causes what: HBV, HCV

A

Hepatocellular carcinoma

159
Q

Oncogenic microbe that causes what: HHV-8 (kaposi sarcoma-associated herpesvirus)

A

Kaposi sarcoma, body cavity fluid B-cell lymphoma

160
Q

Oncogenic microbe that causes what: HPV

A

Cervical and penile/anal carcinoma (16, 18), head and neck or throat cancer

161
Q

Oncogenic microbe that causes what: H pylori

A

Gastric adenocarcinoma and MALT lymphoma

162
Q

Oncogenic microbe that causes what: HTLV-1

A

Adult T-cell leukemia/lymphoma

163
Q

Oncogenic microbe that causes what: Liver fluke (clonorchis sinensis)

A

Cholangiocarcinoma

164
Q

Oncogenic microbe that causes what: Schistosoma haematobium

A

Bladder cancer (squamous cell)

165
Q

Carcinogens, their target and what they cause: Aflatoxins (aspergillus)

A

Liver; Hepatocellular carcinoma

166
Q

Carcinogens, their target and what they cause: Alkylating agents

A

Blood; Leukemia/lymphoma

167
Q

Carcinogens, their target and what they cause: Aromatic amines

A

Bladder; Transitional cell carcinoma

168
Q

Carcinogens, their target and what they cause: Arsenic

A

Liver, lung, skin; Angiosarcoma, lung cancer, squamous cell carcinoma

169
Q

Carcinogens, their target and what they cause: Carbon tetrachloride

A

Liver; centrilobular necrosis and fatty change

170
Q

Carcinogens, their target and what they cause: cigarette smoke

A

bladder-transitional cell carcinoma, esophagus-squamous and adenocarcinoma, kidney- renal cell carcinoma, larynx-squamous, lung-squamous and small cell carcinoma, pancreas-adenocarcinoma

171
Q

Carcinogens, their target and what they cause: Ethanol

A

liver-HCC

172
Q

Carcinogens, their target and what they cause: Ionizing radiation

A

Thyroid; papillary thyroid carcinoma

173
Q

Carcinogens, their target and what they cause: Nitrosamines

A

(smoked foods); stomach-gastric cancer

174
Q

Carcinogens, their target and what they cause: Radon

A

Lung; lung cancer (second leading cause after cigarettes)

175
Q

Carcinogens, their target and what they cause: Vinyl chloride

A

Liver-Angiosarcoma

176
Q

Paraneoplastic syndrome (hormone/agent, the effect, associated neoplasms): 1,25-(OH)2 D3 (calcitriol)

A

Effect: hypercalcemia;
neoplasms: Hodgkin lymphoma, some non-hodgkin

177
Q

Paraneoplastic syndrome (hormone/agent, the effect, associated neoplasms): ACTH

A

Effect: Cushing syndrome;

Neoplasms are small cell lung carcinoma

178
Q

Paraneoplastic syndrome (hormone/agent, the effect, associated neoplasms): ADH

A

effect: SIADH
Neoplasm: Small cell lung carcinoma and intracranial neoplasms

179
Q

Paraneoplastic syndrome (hormone/agent, the effect, associated neoplasms): Antibodies against presynaptic Ca2+ channels at NMJ

A

Effect: Lambert-Eaton myasthenic syndrome (muscle weakness)
Neoplasms: small cell lung carcinoma

180
Q

Paraneoplastic syndrome (hormone/agent, the effect, associated neoplasms): Erythropoietin

A

Effect: Polycythemia
Neoplasms: Renal cell carcinoma, Thymoma, hemangioblastoma, HCC, Leiomyoma, Pheochromocytoma

181
Q

Paraneoplastic syndrome (hormone/agent, the effect, associated neoplasms): PTHrP

A

Effect: Hypercalcemia
Neoplasms: Squamous Cell lung carcinoma, renal cell carcinoma, breast cancer

182
Q

Psammoma bodies

A

Laminated concentric, calcific spherules;
SPaMMoma bodies are seen in: Papillary carcinoma of thyroid, Serous papillary cystadenocarcinoma of ovary, Meningioma, Malignant mesothelioma

183
Q

Leading types of cancers for males

A

Prostate, lung, colon/rectum (Lung kills the most, then prostate)

184
Q

Leading types of cancers for females

A

Breast, lung, colon/rectum (Lung kills most, then breast)

185
Q

Common sites of metastasis is the brain: where did it come from

A

Lung> breast> genitourinary> osteosarcoma> melanoma> GI;
50% of brain tumors are from metastases, commonly seen as multiple well-circumscribed tumors at gray/white matter junction

186
Q

Common sites of metastasis is the Liver: where did it come from

A

Colon» Stomach> pancreas;

Liver and lung are the most common site of metastasis after the regional lymph nodes

187
Q

Common sites of metastasis is the Bone: where did it come from

A

Postate, breast> lung > thyroid;
Bone metastasis&raquo_space; primary bone tumors. Whole-body bone scan shows tumor predilection for axial skeleton, prostate=blastic, breast=lytic and blastic

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