Cancer

通報

問題一覧

Any swelling caused by inflammation

Tumor

New, abnormal growth, following uncontrolled proliferation serving no physiological purpose

Neoplasm

Slow growth, well-defined capsule, not invasive, well differentiated, no metastasis, low mitotic index

Benign Tumor

Rapid growth, not encapsulated, invasive, poor differentiation (anaplasia), high mitotic index, can spread distally (metastasis)

Malignant Tumor

Abnormal, uncontrolled, spread

Cancer

-Constantly replace selves -Regenerate using adult stem cells -Stem cells are multi/pluripotent

Normal cells

-Heterogeneous (diverse character/content) -Cancer stem cells

Cancer Cells

Pre-invasive cancer; atypical cells. “In its original place”, cancer cells have not spread beyond where they were first formed, and have not penetrated the basement membrane (no local invasion)

Carcinoma in situ

Tumors and other abnormal growths (morbid growth)

-oma

Cancer from epithelial cells

Carcinoma

Cancer from mesenchymal cells

-sarcoma

Cancer from ductal or glandular tissue

Adenocarcinoma

Cancer from blood forming cells

Leukemia

Cancer from lymphatic cells

Lymphoma

Cancer in precursor cells (blasts); common in children

-blastoma

Mutated or over-expressed proto-oncogenes, which are independent of normal regulatory mechanisms. May amplify, making numerous copies of mutated genes that are important in prognosis and therapy.

Oncogenes

Genes that inhibit or decelerate proliferation-> suppress oncogenes (decrease cell growth, mutation, replication)-> end result of gene changes = loss of caretaker gene function (TP53)

Tumor suppressor gene role in cancer suppression

-Cancer cells use inflammation to their benefit to support growth and progression -Have ability to produce chemotactic signals -> attract macrophages-> produce mediators -> decrease inflammation and increase proliferation and angiogenesis, recruit macrophages, decrease cytotoxic response to not kill cancer cells -T-regulatory cells change -> no cell destruction + produce cytokines -> proliferation/spread

Inflammation role in cancer progression

Muscle wasting, loss of lean body mass with or without adipose tissue, multi-organ syndrome, systemic inflammation, negative protein energy balance -Changes in mitochondrial Ca+ signaling, loss of myofibrils -Increased apoptosis and decrease regeneration -White adiopose tissue breakdown -> conversion to brown adipose tissue with increased thermogenesis (IL-6) -Changes in appetite hormones —>(Orexin < Anorexin levels)

Cachexia

-(Rare) triggered by immune system response to neoplasm -Involves non-metastatic systematic effects that accompany malignant disease -Collection of symptoms produced by tumor occurring remotely from the tumor origin -Can effect neuromuscular, CV, cutaneous, hematologic, GI, renal, miscellaneous Examples - -SIADH <- intracranial neoplams -> release ADH -Venous thrombosis <- pancreatic carcinoma -> tumor products activate clotting

Paraneoplastic Syndrome

It measures liver and germ cells

Alpha Fetoprotein

It measures prostate cells

PSA

It measures germ cell choriocarcinoma (for numerous cancers - colon, lung, and breast)

Carcinoembryonic antigen

It measures urine marker for multiple myeloma

Bence Jones Protein

It measures marker for small cell lung cancer and neuroblastoma

Neuron-specific enolase

-The higher number the worse the prognosis - (T) indicates tumor spread - (N) indicates node involvement - (M) indicates presence of distal metastasis

Process of staging cancers

Most common cancers - leukemia and brain tumor, solid tumors

Cancer in Children

Lymphoma most common. Leukemia, thyroid carcinoma, brain tumors, and germ cell tumors are also common

Cancer in Adolescents

Incidence increases with age, changes in immune system, immunocompetence, longer time exposed to potential gene mutations. More likely to develop solid organ tumor.

Cancer in Elderly

Diagnosis during active growth periods, and approximately 85% are cured

Cancer in Adolescents and Children

-Risk factors: smoking , COPD -Manifestations: non-productive cough, hemoptysis, PNA, atelectasis -Site of Metastasis: hila and project into bronchi

Squamos cell carcinoma (lung)

-Risk factors: women, Asians, non-smokers -Manifestations: asymptomatic, and usually found on unrelated CXR -Site of metastasis: periphery of lung parenchyma

Adenocarcinoma (lung)

-Risk factors: men > 60 yo, Asians -Manifestations: non-productive cough, hemoptysis, chest pain, PNA, SOB, orthopnea -Site of metastasis: central and distal trachea

Large cell carcinoma (lung)

-Risk factors: smoking (strong relation) -Manifestations: Hyponatremia, Cushing’s, hypocalcemia, gyneomastia, carcinoid syndrome, Lambert-Eaton myasthenic syndrome -Pathophysiology: neuroendrocrine tumors derived from neuro-secretory granules in tracheobronchial trees -Site of metastasis: central portion of the lung

Small cell carcinoma (lung)

-Risk factors: smoking, ETOH, low intake of fruit/vegetables, low zinc intake, hot food beverages -Manifestations: Chest pain and dysphagia -Pathophysiology: r/t chronic inflammation and metaplastic changes -Site of metastasis: upper portion of esophagus

Squamous cell carcinoma (esophagus)

-Risk factors: Barrett’s esophagus, GERD, obesity, smoking, sliding hiatal hernia -Site of metastasis: lower esophagus

Adenocarcinoma (esophagus)

-Risk factors: familial adenomatous polyposis, age 50+, black, family Hx, smoking, obesity, inactivity, high fat and low fiber diet, IBD, genetics, DMII -Etiology: arise from polyps in intestinal mucosal epithelium -Manifestations: if large enough-> bowel obstruction; pain abdominal mass, anemia, occult blood, distension -Pathophysiology: polyps with frequency in size

Colon Cancer

-Risk factors: increase with age, ETOH, family Hx, non-O blood type, DMII, chronic pancreatitis, smoking, BRCA-2, Lynchburg and FAMMM Syndromes, K-ras (proto-oncogene) -Etiology: tumors arise from exocrine (more likely) and endocrine cells -Manifestations: obstruction of portal vein and common bile duct -> jaundice, dull black stool, protein and fat malabsorption, lethargy; weight loss, N/V, new onset DM, pruritis, light-colored or floating stools, dark urine, flank or back pain, abdominal pain, DVT

Pancreatic cancer

-Risk factors: Family Hx, ovarian, breast, or uterine cancers, IVF, post-menopausal, infertility, early menarche, late menopause, endometriosis, BRCA1>BRCA2, Turners Syndrome -Etiology: unclear -Manifestations: vague, non-specific; Early -> decreased appetite, abdominal and pelvic pain, Late -> pain, ascities, dyspepsia, vomiting, change in bowel habits

Ovarian cancer

-Risk factors: white > black (higher mortality), early menarche, late menopause, nulliparity, family Hx, personal Hx of breast or ovarian cancers, tamoxifen use, failure to ovulate, obesity, DMII, HTN, gallbladder disease -Etiology: prolonged estrogen exposure in absence of progesterone -Manifestations: post-menopausal bleeding, pain, weight loss (late sign), Metastasis -> lungs! -Pathophysiology: arises from glandular epithelial of the uterine lining (75% are Adenocarcinoma)

Endometrial cancer

-Risk factors: early age at onset of sexual activity, multiple high risk partners, high risk HPV (strains 16 and 18), smoking, oral contraceptives, immunodeficiency -Etiology: HPV strains 16, 18 are higher risk; 6 & 11 are lower risk -Manifestations: no symptoms in early stage; large absent, may have post-coital vaginal bleeding, malodorous discharge, and abdominal uterine bleeding (late sign) -Pathophysiology: pre-cancerous dysplasia and cervical carcinoma in situ

Cervical cancer

-Risk factors: early age (15-35 yo), white, Hx of undescended testicle, family Hx, HIV, Klinefelter Syndrome, genetics -Etiology: unknown -Manifestations: painless right testicular mass and heavinesses, dull ache in lower abdomen and lumbar, gynecomastia, CNS symptoms; Metastasis -> lung and brain! -Pathophysiology: malignant neoplasm of the testicle

Testicular cancer

-Risk factors: age 50+, black, vasectomy, family Hx, high fat diet, smoking, obesity, ingestion of proinflammatory oils (corn and safflower oils), other tumor suppressors-> Genes BRCA2>BRCA1 -Etiology: unknown -Manifestations: not present until advanced stage - slow urinary stream, incomplete bladder emptying, low back pain, nocturia, dysuria, erectile dysfunction, increased alkaline phosphatase, rectal obstruction, pelvic pain; Metastasis-> vertebrae and pelvic bones! -Pathophysiology: imbalance of estrogen-androgen in epithelial cells

Prostate cancer

-Risk factors: metabolic syndromes - dyslipidemia, insulin resistance, obesity, genetics, thyroid syndromes -Defining characteristics: irregular ovulation, increased androgen levels, polycystic ovaries -Manifestations: anovulation, hyperandrogenism, insulin dysfunction, bleeding/amenorrhea, hirsutism, acne, acanthosis nigricans, infertility -Pathophysiology: altered FSH results in failure of follicules to fully mature and alters ovulation

Polycystic Ovarian Syndrome

-Risk factors: common during reproductive years in women -Defining characteristics: benign unilateral cysts

Ovarian cysts

Follicle stimulated but does not mature, rupture, or regress. Symptoms- bloating, breast tenderness and swelling, heavy/irregular menses. Most are fluid-filled and reabsorpted with next “normal” hormone cycle

Follicular cysts

Formed by granulosa cells “left behind” after ovulation (more prone to rupture) Symptoms-dull, unilateral pelvic pain, amenorrhea-> heavy irregular bleeding. Most regress spontaneously in non-pregnant women

Corpus Luteum Cysts

Triggers a tissue-remodeling matrix -> makes new blood vessels for cancer cells

Metalloproteinases

4 known genetic mechanisms of oncogenes

1) point mutations 2) translocation with excess production of proliferation factor 3) translocation with production of proteins with growth-promoting properties 4) gene amplification

Sensitive but not specific

AFP

Specific but not sensitive

PSA

Metastasis-> vertebrae and pelvic bones!

Prostate Cancer

Metastasis -> lung and brain!

Testicular Cancer

Metastisis -> lungs!

Endometrial Cancer

Patho Renal

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Pathophysiology

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