Steve Perry's Pathology Journey Flashcards
Apoptosis
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.
What is a test to check if a cell is undergoing apoptosis
DNA laddering is indicator of apoptosis: during karyorrhexis, endocucleases cleave at internucleosomal regions, yielding 180bp fragments.
Radiation therapy causes apoptosis of tumors and surrounding tissue via
free radical formation and dsDNA breakage. Rapidly dividing cells (e.g. skin and GI mucosa) are very susceptible to radiation therapy-induced apoptosis
Intrinsic pathway of apoptosis
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 Occurs when a regulating factor is withdrawn from a proliferating cell population (e.g. decreased IL-2 after a completed immunological reaction leading to apoptosis of proliferating effector cells).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.
BCL-2
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.
Extrinsic pathway of apoptosis
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
Necrosis: define it
Enzymatic degradation and protein denaturation of a cell resulting from exogenous injury. Intracellular components leak; inflammatory process (unlike apoptosis)
Coagulative necrosis
heart, liver, kidney; occurs in tissues supplied by end-arteries; increase cytoplasmic binding of acidophilic dye. Proteins denature first, followed by enzymatic degradation.
Liquefactive necrosis
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.
Caseous necrosis
TB, systemic fungi, Nocardia
Fatty necrosis
Enzymatic (pancreatitis [saponification]). and nonezymatic (e.g. breast trauma); calcium deposits appear dark blue on staining
Fibrinoid necrosis
Vasculitides (e.g. HSP, churg-strauss), malignant HTN; amorphous and pink on H&E.
Gangrenous necrosis
Dry (ischemic coagulative) and wet (infection); common in limbs and GI tract.
Cell injury: Type that is reversible with O2
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
Cell injury: type that is irreversible with O2
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)
Ischemia: susceptible areas in the brain
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)
Ischemia: susceptible areas in the Heart
Subendocardium (especially LV)
Ischemia: susceptible areas in the Kidney
Straight segment of proximal tubule (medulla); thick ascending limb (medulla)
Ischemia: susceptible areas in the Liver
Area around central vein (zone III, which is where you gind cytochrome p450)
Ischemia: susceptible areas in the Colon
splenic flexure (watershed), rectum (watershed)
Red infarct
Red=hemorrhagic infarct; occur in loose tissue with multiple blood supplies, such as liver, lungs. and intestine
reperfusion injury is due to
damage by free radicals
Pale infarct
occur in solid tissue with a single blood supply, such as heart or kidney or spleen
Shock: what do you see
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.
Distributive shock
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
Hypovolemic/cardiogenic shock
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.
Atrophy
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)
Inflammation is characterized by
rubor-redness, Dolor-pain, calor-heat, tumor-swelling, functio laesa-loss of function
Inflammation: vascular component is doing what
increased vascular permeability, vasodilation, endothelial injury
Inflammation: the cellular component is doing what
Neutrophils extravasate from circulation to injured tissue to participate in inflammation through phagocytosis, degranulation, and inflammatory mediator release.
Acute inflammation
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
Chronic inflammation
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
Chromatolysis
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
Dystrophic calcification
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)
Metastatic Calcification
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.
Leukocyte extravasation: what is it, name 4 steps
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.
Leukocyte extravasation: what mediates margination and rolling
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
Leukocyte extravasation: what mediates Tight-binding
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
Leukocyte extravasation: what mediates Leukocyte Diapedisis
leukocyte PECAM-1 (CD31) binds PECAM-1 (CD31) on vasculature/stroma and guides it through
What chemotactic products released in response to bacteria guide leukocytes in migration
Chemotactic products are: C5a, IL-8, LTB4, kallikrein, platelet-activation factor
Free radicals damages cells via
membrane lipid peroxidation, protein modification, and DNA breakage
What initiates free radical injury
initiated via radiation exposure, metabolism of drugs (phase 1), redox reactions, Nitric oxide, transition metals, leukocyte oxidative burst.
How can you clear free radicals
Eliminated by enzymes (catalse, super-oxide dismutase, glutathione peroxidase), spontaneous decay, antioxidants (vitamins A,C,E)
Pathologies that are due to free radical damage
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)
Inhalation injury
most common pulmonary complication after exposure to fire. Inhalation of products of combustion (carbon particles, toxic fumes) leads to chemical tracheobronchitis, edema, and pneumonia.
Scar formation: tensile strength and timeline
70-80% of tensile strength returns at 3 months following wound; little additional tensile strength will be regained.
Scar formation: hypertrophic scars
Get increased collagen synthesis; Parallel collagen arrangement; scar stays confined to borders of original wound; infrequently reocur following resection
Keloid scar formation
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
Wound healing tissue mediators: PDGF
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
Wound healing tissue mediators: FGF
Fibroblast growth factor stimulates all aspects of angiogenesis (growth of new blood vessels)
Wound healing tissue mediators: EGF
Epidermal growth factor stimulates cell growth via tyrosine kinase (e.g EGFR (EGF receptor) as expressed by ERBB2)
Wound healing tissue mediators: TGF-beta
Transforming growth factor beta stimulates angiogenesis, fibrosis, and cell cycle arrest
Wound healing tissue mediators: Metalloproteinases
stimulates tissue remodeling
Phase of wound healing (mediators and characteristics): Inflammatory (immediate)
Mediators: Platelets, neutrophils, macrophages
Characteristics: clot formation, increased vessel permeability and neutrophil migration into tissue; macrophages clear debris 2 days later.
Phase of wound healing (mediators and characteristics): Proliferative stage (2-3 days after wound
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)
Phase of wound healing (mediators and characteristics): remodeling phase (1 week after wound)
mediators: Fibroblasts
Characteristics: Type III collagen replaced by type I collage, increased tensile strength of tissue
Granulomas and anti-TNF drugs: what is the big deal
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.
Exudate
Thick, cellular, protein rich, with a specific gravity > 1.020; Due to lymphatic obstruction, inflammation/infection, or malignancy
Transudate
thin, hypocellular, protein poor, specific gravity
Erythrocyte sedimentation rate is what
Products of inflammation (E.g. fibrinogen) coat RBCs and cause aggregation. When aggregated, RBCs fall at a faster rate within the test tube.
What can cause an increased ESR
most anemias, infections, inflammation, cancer, pregnancy, autoimmune disorders
What can cause a decreased ESR
Sickle cell (altered shape), Polycythemia (increased RBCs dilute aggregation factors), CHF (unknown)
Iron poisoning
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.
Amyloidosis
abnormal aggregation of proteins (or their fragments) into Beta pleated sheet structures leading to damage and apoptosis
AL (primary) amyloidosis
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)
AA (secondary) amyloidosis
Seen with chronic conditions, such as rheumatoid arthritis, IBD, spondyloarthropathy, protracted infection. Fibrils composed of serum Amyloid A. often multisystem like AL amyloidosis.
Dialysis related amyloidosis
Fibrils composed of beta2-microglobulin in patients with ESRD and/or on long-term dialysis. May present as carpal tunnel syndrome
Heritable Amyloidosis
Heterogenous group of disorders. Example is ATTR neurologic/cardiac amyloidosis due to transthyretin (TTR or prealbumin) gene mutation.
Age-related (senile) systemic amyloidosis
Due to deposition of normal (wild type) TTR in myocardium and other sites. Slower progression of cardiac dysfunction relative to AL amyloidosis
Organ specific amyloidosis
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
Lipofuscin
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
P-glycoprotein
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).
Define: hyperplasia
Increase in number of cells: reversible
Define: metaplasia
one adult cell type is replaced by another. often secondary to irritation and/or environmental exposure: reversible
Define: dysplasia
Abnormal growth with loss of cellular orientation, shape, and size in comparison to normal tissue maturation; commonly preneoplastic: reversible
Define: Anaplasia
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
Define: neoplasia
A clonal proliferation of cells that is uncontrolled and excessive. Neoplasia may be benign or malignant: irreversible
Define: Desmoplasia
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
Tumor grade
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.
Tumor stage
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
Tumor nomenclature: define carcinoma
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
Tumor nomenclature: Sarcoma
denotes mesenchymal origin of malignancy; usually spreads hematogenously.
Name for a benign and malignant epithelium tumor
benign: Adenoma, papilloma;
Malignant: adenocarcinoma, pappilary carcinoma
Name for a benign and malignant: mesenchyme blood cell tumor
benign: no such thing;
Malignant: leukemia, lymphoma
Name for a benign and malignant: mesenchyme blood vessel tumor
Benign is hemangioma;
Malignant is Angiosarcoma
Name for a benign and malignant: mesenchyme smooth muscle tumor
benign is Leiomyoma;
Malignant is leiomyosarcoma
Name for a benign and malignant: mesenchyme striated muscle tumor
benign is Rhabdomyoma;
malignant is Rhabdomyosarcoma
Name for a benign and malignant: mesenchyme Connective tissue tumor
Benign is fibroma;
Malignant is fibrosarcoma
Name for a benign and malignant: Mesenchyme bone tumor
benign is osteoma;
Malignant is Osteosarcoma
Name for a benign and malignant: mesenchyme fat tumor
benign is lipoma; malignant is liposarcoma
What is a benign tumor
Usually well differentiated, low mitotic activity, well demarcated, no metastasis, no necrosis.
What is a malignant tumor
May be poorly differentiated, erratic growth, locally invasive/diffuse, may metastasize, decrease apoptosis (upregulation of telomerase prevents chromosome shortening and cell death)
Cachexia
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
What neoplasm is associated with this disease: Acanthosis nigricans (hyperpigmentation and epidermal thickening)
Visceral malignancy (esp. stomach)
What neoplasm is associated with this disease: Actinic keratosis
Squamous cell carcinoma of skin
What neoplasm is associated with this disease: AIDS
Aggressive malignant lymphomas (non-hodgkin) and kaposi sarcoma
What neoplasm is associated with this disease: Autoimmune diseases (Hashimoto, SLE, thyroiditis)
Lymphoma
What neoplasm is associated with this disease: Barret esophagus
Esophageal adenocarcinoma
What neoplasm is associated with this disease: Chronic atrophic gastritis, pernicious anemia, post-surgical gastric remnants
Gastic carcinoma
What neoplasm is associated with this disease: Cirrhosis
Hepatocellular carcinoma
What neoplasm is associated with this disease:Cushing syndome
Small cell lung cancer
What neoplasm is associated with this disease: Dermatomyositis
Lung cancer
What neoplasm is associated with this disease: Down syndrome
ALL and AML
What neoplasm is associated with this disease: Dysplastic nevus
Malignant melanoma
What neoplasm is associated with this disease: Hypercalcemia
Squamous cell lung cancer
What neoplasm is associated with this disease: Immunodeficiency states
Malignant lymphomas
What neoplasm is associated with this disease: Lambert-Eaton myasthenic syndrome
small cell lung cancer
What neoplasm is associated with this disease: Paget disease of Bone
Secondary osteosarcoma and fibrosarcoma
What neoplasm is associated with this disease:Plummer-Vinson syndrome (decreased iron)
Squamous cell carcinoma of esophagus
What neoplasm is associated with this disease: Polycythemia
Renal cell carcinoma, hepatocellular carcinoma
What neoplasm is associated with this disease: Radiation exposure
Leukemia, sarcoma, Papillary thyroid cancer, and breast cancer
What neoplasm is associated with this disease: SIADH
small cell lung cancer
What neoplasm is associated with this disease:Tuberous sclerosis
Giant cell astrocytoma, renal angiomyolipoma, and cardiac rhabdomyoma
What neoplasm is associated with this disease: Ulcerative colitis
Colonic adenocarcinoma
What neoplasm is associated with this disease: Xeroderma pigmentosum, albinism
Melanoma, basal cell carcinoma, and especially squamous cell carcinoma of skin
Define oncogene
Gain of function mutations that lead to an increased risk of cancer. Need to damage only 1 allele
What tumor is this oncogene associated with and what is its gene product: BRC-ABL
CML, ALL; codes for tyrosine kinase
What tumor is this oncogene associated with and what is its gene product: bcl-2
Follicular and undifferentiated lymphomas; Anti-apoptotic molecules
What tumor is this oncogene associated with and what is its gene product: BRAF
Melanoma; Serine/threonine kinase
What tumor is this oncogene associated with and what is its gene product: c-kit
Gastrointestinal stromal tumor (GIST); codes for cytokine receptor (for stem cell factor)
What tumor is this oncogene associated with and what is its gene product: c-myc
Burkitt lymphoma; transcription factor
What tumor is this oncogene associated with and what is its gene product: HER2/neu (c-erbB2)
Breast, Ovarian and gastric carcinoma; codes for tyrosine kinase
What tumor is this oncogene associated with and what is its gene product: L-myc
Lung tumor; codes for transcription factor
What tumor is this oncogene associated with and what is its gene product: N-myc
Neuroblastoma; codes for transcription factor
What tumor is this oncogene associated with and what is its gene product: ras
Colon cancer, lung cancer, pancreatic cancer; codes for GTPase
What tumor is this oncogene associated with and what is its gene product: ret
MEN 2A and 2B; codes for tyrosine kinase
define tumor suppressor gene
Loss of function of a gene that increases your risk of cancer; both alleles must be knocked out for expression of disease
What tumor is this tumor suppressor gene associated with and what is its gene product: APC
colorectal cancer (associated with FAP);
What tumor is this tumor suppressor gene associated with and what is its gene product: BRCA1
Breast and ovarian cancer; makes DNA repair protein
What tumor is this tumor suppressor gene associated with and what is its gene product: BRCA2
Breast and ovarian cancer; makes DNA repair protein
What tumor is this tumor suppressor gene associated with and what is its gene product: CPD4/SMAD4
Pancreatic cancer; DPC-deleted in pancreatic cancer
What tumor is this tumor suppressor gene associated with and what is its gene product: DCC
Colon cancer; DCC-deleged in colon cancer
What tumor is this tumor suppressor gene associated with and what is its gene product: MEN1
MEN type I;
What tumor is this tumor suppressor gene associated with and what is its gene product: NF1
Neurofibromatosis type 1; RAS GTPase activating protein (neurofibromin)
What tumor is this tumor suppressor gene associated with and what is its gene product: NF2
Neurofibromatosis type 2; Merlin (schwannomin) protein
What tumor is this tumor suppressor gene associated with and what is its gene product: p16
Melanoma; produces cyclin-dependent kinase inhibitor 2A
What tumor is this tumor suppressor gene associated with and what is its gene product: p53
Most human cancers; Li-Fraumeni syndrome; produces transcription factor for p21, blocks G1 going to S phase
What tumor is this tumor suppressor gene associated with and what is its gene product: PTEN
Breast cancer, prostate, cancer, endometrial cancer
What tumor is this tumor suppressor gene associated with and what is its gene product: Rb
Retinoblastoma, osteosarcoma; Inhibits E2F; blocks G1 going to S phase
What tumor is this tumor suppressor gene associated with and what is its gene product: TSC1
Tuberous sclerosis; Hamartin protein
What tumor is this tumor suppressor gene associated with and what is its gene product: TSC2
Tuberous sclerosis; Tuberin protein
What tumor is this tumor suppressor gene associated with and what is its gene product: VHL
von Hippel-Lindau disease; inhibits hypoxia inducible factor 1a
What tumor is this tumor suppressor gene associated with and what is its gene product: WT1
Wilms tumor (nephroblastoma);
What tumor is this tumor suppressor gene associated with and what is its gene product: WT2
Wilms tumor (nephroblastoma);
Tumor markers: what are their use
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.
Tumor marker that tells you what: Alkaline phosphatase
Metastases to bone, liver, Paget disease of bone, seminona (placental ALP)
Tumor marker that tells you what: Alpha-fetoprotein
normally made by fetus. Hepatocellular carcinoma, hepatoblastoma, yolk sac (endodermal sinus) tumor, testicular cancer, mixed germ cell tumor (co-secreted with Beta-hCG)
Tumor marker that tells you what: Beta-hCG
Hydratidiform moles and Choriocarcinomas (Gestational trophoblastic disease), testicular cancer. Commonly associated with pregnancy.
Tumor marker that tells you what: CA-15-3/CA-27-29
Breast cancer
Tumor marker that tells you what: CA-19-9
Pancreatic adenocarcinoma
Tumor marker that tells you what: CA-125
Ovarian cancer
Tumor marker that tells you what: Calcitonin
Medullary thyroid carcinoma
Tumor marker that tells you what: CEA
CarcinoEmbryonic Antigen. Very nonspecific but produced by about 70% of colorectal and pancreatic cancers; also produced by gastric, breast, and medullary thyroid carcinomas
Tumor marker that tells you what: PSA
Prostate specific antigen. Used to follow prostate adenocarcinoma. Can also be elevated in BPH and prostatitis. Questionable risk/benefit for screening
Tumor marker that tells you what: S-100
Neural crest origin (e.g. melenomas, neural tumores, schwannomas, Langerhans cell histiocytosis)
Tumor marker that tells you what: TRAP
Tartrate-Restistant Acid Phosphatase (TRAP). Hairy cell leukemia-a B-cell neoplasm.
TRAP the hairy animal. Largely replaced by flow cytrometry.
Oncogenic microbe that causes what: EBV
Burkitt lymphoma, Hodgkin lymphoma, nasopharyngeal carcinoma, CNS lymphoma (in immunocompromised patients)
Oncogenic microbes that causes what: HBV, HCV
Hepatocellular carcinoma
Oncogenic microbe that causes what: HHV-8 (kaposi sarcoma-associated herpesvirus)
Kaposi sarcoma, body cavity fluid B-cell lymphoma
Oncogenic microbe that causes what: HPV
Cervical and penile/anal carcinoma (16, 18), head and neck or throat cancer
Oncogenic microbe that causes what: H pylori
Gastric adenocarcinoma and MALT lymphoma
Oncogenic microbe that causes what: HTLV-1
Adult T-cell leukemia/lymphoma
Oncogenic microbe that causes what: Liver fluke (clonorchis sinensis)
Cholangiocarcinoma
Oncogenic microbe that causes what: Schistosoma haematobium
Bladder cancer (squamous cell)
Carcinogens, their target and what they cause: Aflatoxins (aspergillus)
Liver; Hepatocellular carcinoma
Carcinogens, their target and what they cause: Alkylating agents
Blood; Leukemia/lymphoma
Carcinogens, their target and what they cause: Aromatic amines
Bladder; Transitional cell carcinoma
Carcinogens, their target and what they cause: Arsenic
Liver, lung, skin; Angiosarcoma, lung cancer, squamous cell carcinoma
Carcinogens, their target and what they cause: Carbon tetrachloride
Liver; centrilobular necrosis and fatty change
Carcinogens, their target and what they cause: cigarette smoke
bladder-transitional cell carcinoma, esophagus-squamous and adenocarcinoma, kidney- renal cell carcinoma, larynx-squamous, lung-squamous and small cell carcinoma, pancreas-adenocarcinoma
Carcinogens, their target and what they cause: Ethanol
liver-HCC
Carcinogens, their target and what they cause: Ionizing radiation
Thyroid; papillary thyroid carcinoma
Carcinogens, their target and what they cause: Nitrosamines
(smoked foods); stomach-gastric cancer
Carcinogens, their target and what they cause: Radon
Lung; lung cancer (second leading cause after cigarettes)
Carcinogens, their target and what they cause: Vinyl chloride
Liver-Angiosarcoma
Paraneoplastic syndrome (hormone/agent, the effect, associated neoplasms): 1,25-(OH)2 D3 (calcitriol)
Effect: hypercalcemia;
neoplasms: Hodgkin lymphoma, some non-hodgkin
Paraneoplastic syndrome (hormone/agent, the effect, associated neoplasms): ACTH
Effect: Cushing syndrome;
Neoplasms are small cell lung carcinoma
Paraneoplastic syndrome (hormone/agent, the effect, associated neoplasms): ADH
effect: SIADH
Neoplasm: Small cell lung carcinoma and intracranial neoplasms
Paraneoplastic syndrome (hormone/agent, the effect, associated neoplasms): Antibodies against presynaptic Ca2+ channels at NMJ
Effect: Lambert-Eaton myasthenic syndrome (muscle weakness)
Neoplasms: small cell lung carcinoma
Paraneoplastic syndrome (hormone/agent, the effect, associated neoplasms): Erythropoietin
Effect: Polycythemia
Neoplasms: Renal cell carcinoma, Thymoma, hemangioblastoma, HCC, Leiomyoma, Pheochromocytoma
Paraneoplastic syndrome (hormone/agent, the effect, associated neoplasms): PTHrP
Effect: Hypercalcemia
Neoplasms: Squamous Cell lung carcinoma, renal cell carcinoma, breast cancer
Psammoma bodies
Laminated concentric, calcific spherules;
SPaMMoma bodies are seen in: Papillary carcinoma of thyroid, Serous papillary cystadenocarcinoma of ovary, Meningioma, Malignant mesothelioma
Leading types of cancers for males
Prostate, lung, colon/rectum (Lung kills the most, then prostate)
Leading types of cancers for females
Breast, lung, colon/rectum (Lung kills most, then breast)
Common sites of metastasis is the brain: where did it come from
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
Common sites of metastasis is the Liver: where did it come from
Colon» Stomach> pancreas;
Liver and lung are the most common site of metastasis after the regional lymph nodes
Common sites of metastasis is the Bone: where did it come from
Postate, breast> lung > thyroid;
Bone metastasis»_space; primary bone tumors. Whole-body bone scan shows tumor predilection for axial skeleton, prostate=blastic, breast=lytic and blastic