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74 Cards in this Set
- Front
- Back
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Endometrial polyps
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Often asymptomatic, estrogen sensitive, possible genetic relationship, benign
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Endometrial Hyperplasia
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Pre-malignant, high estrogen stimulation. Risk factors all related to high estrogen: PCOS, >40 years old, estrogen treatment, early menarche, granulosa-teca cell tumor, late menopause, nulliparity, obesity, DM, hypertension
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Endometrial carcinoma
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#1 invasive, CA of female genital tract. Develops from hyperplasia.
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Cervix non-neoplastic disorders
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cervicitis - inflammation of the cervix, typically due to Trichomonas vaginalis, chlamydia trachomatis, gardnerella vaginalis and candida albicans
Cervical polyps - not neoplasms, represent proliferation of cervical epithelium in response to inflammation |
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Cervic Pre-cancerous
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CIN - cervical intraepithelial neoplasia. Associated with HPV 16, 18. Show disorganized epithelial growth due to HPV's inhibition of tumor suppressor genes p53 and RB. Precancerous. May regress or may become invasive. CIN III is carcinoma in situ.
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Invasive cervical carcinoma
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Represents neoplastic development of cervical epithelium with invasion through underlying basement membrane. Stage 0 = carcinoma in situ. Stage 4 = invasive carcinoma has extended beyond the pelvic wall or has involved blader or rectal mucosa.
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Endometrial polyps
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benign focal endometrial development
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Polycystic ovrian syndrome
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Chronic anovulation with symptoms of androgens excess along with obesity. thought to be due to excess LH. The high LH stimulates ovarian theca cells to produce androstenedione, which causes acne and hirsutism.
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Endometriosis
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Presence and proliferation of non-neoplastic endometrial tissue outside of the uterine cavity. Develop multiple nests of endometrial cells throughout structures in the peritoneal cavity. Usually proliferation in the ovary, but also can occur in uterine ligaments, rectrovaginal area, and pelvic peritoneum. Bleeding can occur into the extopic endometrial tissue, and if on the ovary, can develop chocolat ecysts. See dysmenorrhea, dyschezia (painful bowel movements), and dyspareunia (painful sex).
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Uterine leiomyoma
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Fibroid. #1 uterine tumor and overall #1 tumor in women, benign, estrogen sensitive, growing during reproductive years and regressing during menopause. See whorled pattern of smooth muscle bundles. Can cause abnormal menstrual bleeding, urinary frequency, impaired fertility, increased risk of spontaneous abortion/fetal malpresentation, and postpartum hemorrhage.
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Hydatidiform mole
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AKA mole, molar pregnancy, gestational trophobalstic neoplasm. due to abnormal ovum fertizliation that ultimately causes excessive trophoblastic development in the form of grape-like cysts. A complete mole is formed with 2 xchromosome containing sperm that have fertilized 1 enucleate ovum. An incomplete mole is formed from the fertilizaiton of 1 ovum with 2 or more sperm. Very high bhcg. Uterus is larger than expected for gestational age.
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Choriocarcinoma
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Frequent and early metastases. Dx is too late for intervention. Very high bhcg. Malignant neoplasm of trophoblastic cells. Initially asymptomatic. Late findings: irregular spotting of brown, bloody foul-smelling fluid. Risk factors: retained GTN, retained placenta after delivery or abortion, may alternatively develop spontaneously in ovary as a type of germ cell tumor.
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Fibrocystic change
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Multiple bilateral nodules. The lumpy, bumpy breast. Fluctuate in size and tenderness with menstrual cycle. Benign.
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Breast cancer
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Typically sone solitary nodule. Typically unilateral, often non-tender in early stages. Does nto fluctuate with menstrual cycle.
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Fibroadenoma
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Fibrous and glandular tissue. A stromal tumor. Single, sharply circumscribed, mobile, and marble-shaped and sized. Occur usually at <30 years of age. Midly increased risk of subsequently developing breast cancer.
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Phylloides tumor
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stromal tumor, beign, grows quickly, rapidly becomes a huge, log shaped tumor.
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Intraductal papilloma
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Epithelial tumor, benign, tumor comprised of ductal epithelial cells, nipple discharge is frequently bloody or serous.
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Ductal carcinoma in situ
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an in situ carcinoma. Neoplasm of ductal epithelial cells.
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Invasive ducal carcinoma
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neoplasm of ductal epithelium. The most common breast cancer. Often scirrhous, may see peaud'orange, nipple retraction, dimpling, fixed mass.
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Lobular carcinoma in situ
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tumor of the lobules/terminal ducts. Never forms calcifications or mases, tend to be bilateral and rare. Signet-ring cells common.
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Invasive lobular carcinoma
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Uncommon, bilateral, diffusely invasive through breast, making detection difficult. High met rate to CSF, ovary, bone marrow, and uterus. Usually confers a rubbery consistency to the breast. Signet ring cells common.
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Paget's disease of the nipple
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A form of DCIS that actually extends from the nipple ducts into the contiguous nipple skin and areola. Fissured, ulcerated, oozing, hyperemic, edematous nipple.
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Mammographic density
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If it is invasive ductal or tubular breast cance,r there is usually a spiculated density with irregular infilatration of surrounding tissue. If it is a cyst or fibroadenoma, there is usually a well circumscribed density with smooth borders.
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Architectrual distortion
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If it is a lobular carcinoma, usually a distortion of the breast without a discrete density is appreciated.
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Calcifications
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If there is a malignant lesion, usually small, irregular, numerous, and clustered or linear and branching calcifications are seen. DCIS is the most common malignant breast disease associated with calcifications.
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Most common metastatic sites for breast cancer are
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lungs, bone, liver, adrenals, brain, meninges
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estrogen and progesterone receptors
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Common in breast tumors, more common in post menopausal patients.
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Glossitis
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Inflammation of the tongue, associated with B2 and B12 vitamin deficiency
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Cheilosis
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Drying and scaling of lips with fissuring at corners of the mouth. Associated with vitamin B2 deficiency.
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Smooth beefy red tongue
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Atrophy of papillae and mucosa, exposing underlying vasculature; associated with advanced vitamin B12 deficiency.
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Strawberry tongue
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white coaated tongue through which hyperemic papillae poke, giving an appearance akin to bumps on a strawberry; associated with scarlet fever.
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Koplik's spots
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Ulceration on buccal mucosa, the first sign of measles.
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Esophageal diverticula location
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Zenkers - above the upper esophageal sphincter
Traction - midpoint of the esophagus epiphrenic - occurs above the lower eophageal sphincter |
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Number of layers of the esophageal diverticulua
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Pulsion of herniation of mucosa only - false
True diverticula involve all layers of the esophagus. |
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Gastritis: acute erosive
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focal damage, risks: ETOH, NSAIDS, stress, cancer drugs, smoking
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Gastritis: Chronic type A
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glandular destruction and mucosal atrophy. affects fundus, autoimmune: Ab against gastric glands, parietal cells, and intrinsic factor, results in pernicious anemia and achlorhydria (no HCl). Usually associated with Hashimoto's disease or addison's disease or vitiligo
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Gastritis: Chronic type B
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Chronic irritation due to H. pylori. Affects antrum, infection with helicobacter pylori, chronic irritation leads to eventual mucosal atrophy and metaplasia, and then eventual carcinoma.
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Gastritis: Menetrier's
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Mucosal hyperplasia, mucosa becomes thickened with concomitant atrophy of glands.
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Hyperplastic intestinal polyps
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The most common type of colinic polyp. Due to decreased epithelial cell turnover in the bowel, occurs in 50s and 60s, has little to no risk fo rmalignat transformation.
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Hamartomatous polyps
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Represent malformations of the glands and stroma of the epithelium, causing overgrowth of mature tissue natural to the area. Have little to no risk for malignant transformation. See with peutz-Jegher's sundrome.
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Inflammatory polyps
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inflamed regenerating tissue surrounded by ulceration, associated with inflammatory bowel disease.
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lymphoid polyps
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large but normal variants of intramucosal lymphoid tissue
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adenomatous polyps
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also known as adenomas. Neoplastic, pre=malignant, acting as a precursor lesion for invasive colorectal carcinoma. All raise from proliferative dysplasia of epithelial cells lining the colon.
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Peutz-jeghers syndrome
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Inherited autosomal dominant hamartomatous polyp disoder that is a familial polyposis syndrome of the entire bowel. See harmartomatous polyps and spotted melanin hyperpigmentation of lips, palms, and soles. Have very lower cancer potential. The risk of colon cancer not related to these polyps is greater than that of the general population.
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Familial adenomatous polyposis
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Due to a loss of tumor suppressor gene, apc. Once polyps develop, there is almost 100% chance of colon cancer development. All polyps are adenomatous.
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Gardner's syndrome
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FAP colon polyps and benign mandible and skull tumors and epidermal cysts and high risk for abnormal dentition. Autosomal dominant.
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Turcot's syndrome
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FAP and malignant brain tumors. Autosomal dominant.
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Hereditary nonpolyposis colorectal cancer aka Lynch Syndrome
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Autosomal dominant. Due to defective DNA mismatch repair genes, associated with microsatellites. Increased risk for colon cancer and multiple other cancers, including cancer of the stomach, liver, brain, prostate, skin, biliary ducts, small intestine, and especially the endometrium and ovary. Cancer develops NOT from adenomatous polyps.
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Colon cancer
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Most arise sporadically, from adenomas. Usually due to the APC gene becomes inactivated OR the RAS gene is mutation and P53 is inactivated.
Risk factors: excessive dietary caloric intake, high refined carbohydrate diet, intake of red meat, reduced consumption of dietary fiber. Metastatses to liver and lungs. |
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Right colon cancers
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Cause iron deficiency anemia and positive hemoccult stool, not stool changes are noted.
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Left colonic cancers
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Cause positive hemoccult stool, change in bowel haits, and crampy left lower quadrant discomfort or tenesmus, pencil stools may also be produced.
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Diverticular disease
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Chronic or recurrent elevated intraluminal pressures in the colon can cause small areas of the colon wall to form outpouchings. Greatest in sigmoid colon. Endangered areas are areas where blood vessels penetrate the entire bowel wall thickness.
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Diverticulosis
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Diverticuli are present. Blood vessels at the sites of diverticuli are now more exposed, yielding a positive hemoccult stool and often gross bleeding. Painless, diagnosed with barium enema and x-ray.
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Diverticulitis
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Inflammation of diverticuli. A complication of diverticulosis. Due to seeds, nuts, or other small objects lodging in the diverticulum orifice, causing bacteria to be trapped and to cause infection. Lower left quadrant pain, fever, elevated neutrophils, often diarrhea but hemoccult negative. Can cause abscess formation, bowel perforation, and/or sepsis, is potentially life-threatening. Diagnosis made by CT scan. Treatment is ciprofloxacin and metronidazole..
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Irritable bowel syndrome
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recurrent, unpredictable bowel habits and abdominal cramping, exacerbated by emotional stress. Thought to be a dysregulation of the enteric nervous system, it activates and inhibits itself, without regard to signals from the autonomic nervous system.
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Crohn's Disease
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Rectum spared, ielum usually most involved. Skip lesions, transumural, noncaseating granulomas, crypt abscesses, strictures, fissures, and fistulas, + string sign on barium study. moderate colon cancer risk, more pain, less bleeding.
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Ulcerative colitis
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Begins at rectum and progresses proximally. can progress through colon to ileocecal junction. Continuous lesions, mucosa/submucosa only. Nongranulomatous lesions, crypt abscesses, pseduopolyps, lead pipe colon on raiologic study. High risk of colon cancer and toxic megacolon, more bleeding and less pain.
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Malabsoprtion
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Most common symptom is steatorrhea +/- diarrhea. labs: stool fat analysis, sudan III stool stain, D-xylose absorption test, and schilling test.
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Sudan III stain of stool
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Qualitatively determines if there is an increase in stool fat or not. Screening test.
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Stool fat analysis
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Measures the QUANTITY of fat after eating a certain amount. Gold standard.
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D-xylose absorption test
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Patient is fed d-xylose, a non-digestible sugar and it is later measured in the patient's urine. It should have been absorbed from the gut and entered the boodstream and excreted with the urine. If there is malabsorption, only small quantities will be recovered in the urine.
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Schilling test
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Used to identify the cause of vitamin B12 deficiency. Feed B12 and test, then B12 and intrinsic factor and test. If the IF doesn't help, indicates chronic pancreatitis, bacterial overgrowth, or disease of the ileum.
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Celiac sprue
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affects the small intestine. See flat villi upon biopsy. See weight loss, steatorrhea, diarrhea and bloating after wheat, rye, barley, oat indigestion. Labs: anti-gliadin, anti-gluten, anti-endomysial Ab, anti-reticulum. Some develop dermatitis herpetiformis and all are at risk for MALT lymphoma.
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Tropical Sprue
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Probably infectious etiology. Chronic diarrhea, steatorrhea, weight loss.
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Whipple's Disease
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Affects any organ, primarily the intestine, CNS, and joints. See steatorrhea, arthralgia, and fever. Biopsy findings of the small bowel, PAS + macs in mucosa due to gram positive actinomyces. Etiologic agent: tropheryma whippelii. Abx therapy has to be administered for at least 4-6 months, preferably for 1 year.
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Cholesteral stones
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Due to high cholesterol that ultimately saturates the bile, allowing the excess cholesterol to precipiatate out into the bilary system. Fat, forty, female, fertile.
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Mixed stones
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Combination of cholesterol and bilirubin
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Pigment stones
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stones formed from excess bilirubin. Each stone represents an ccumulation of bilirubin --> insoluble Ca2+ salts of bilirubin and inorganic calcium. Excess bilirubin is a feature of hemolysis.
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Cholelithiasis
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Gallstones in the gallbladder, usually asymptomatic and all labs are normal.
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Cholecysitis
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gall bladder infection. Fever, RUQ pain, murphy's sign, NV. Elevated neutrophils and alkaline phosphatase. On ultrasound see gallbladder wall thickening, pericholecystic fluid, gallstones.
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Choledocholithiasis
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Obstruction of the common bile duct. Elevated alkaline phosphatase and conjugated bilirubin. On US see dilated common bile duct.
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Ascending cholangitis
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Infection of the common bile duct. Complication of choledocholithiasis. RUQ pain, jaundice, clay colored stool, tea colored urine, fever. Elevated alkaline phosphatase and conjugated bilirubin, elevated neutrophils.
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Primary schlerosing cholangitis
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Non-infectious inflammation and sclerosis of bile ducts with eventual obliteration of all biliary ducts. See pruritis, RUQ pain, jaundice, and later cirrhosis. Elevated conjugated bilirubin and lkaline phosphatase.
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Primary biliary cirrhosis
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Autoimmune destruction of intrahepatic bile ducts. Starts with pruritis, followed by jaundice, steatorrhea, xanthelasmas. + AMA plus elevated alkaline phosphatase and GGT. later elevated bilirubin. Features anti-mitochondiral antibody (AMA).
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