GI Pathology (Pathoma)

Question 1

Cleft Lip an Palate

Answer 1

Full-thickness defect of lip and/or palate.

*Due to failure of facial proiminences to fuse

Usually occur together.

Question 2

Apthous Ulcer

Answer 2

Painful superficial ulceration of the oral mucosa

Arises in relation to stress. Resolves spontaneously and recurs.

Characterized by grayish base surrounded by erythema.

AKA cancer core.

Can be a part of Behcet Syndrome

Question 3

Behcet Syndrome

Answer 3

Recurrent apthous ulcers, genetial ulcers, and uveitis.

Due to immune complex vasculitis of small vessels.

Can follow viral infx.

Question 4

Oral Herpes

Answer 4

Vesicles involving oral mucosa that ruptures. Shallow painful, red ulcers.

HSV-1

*Primary infection in childhood –> remains dormant in the ganglia of the trigeminal (V) nerve.

Stress and sunlight cause reactivation.

AKA cold sore

Question 5

Squamous Cell Carcinoma

Answer 5

Malignant squamous cells lining oral mucosa

Tobacco and alcohol are syntergistic risk factors.

Floor of mouth is MC location.

Question 6

Leukoplakia and Erythroplakia

Answer 6

Precursor lesion that doesn’t scrape off (vs. candidiasis)

Can be precursor to scc —> biopsy.

Erythroplakia is vascularized leukoplakia (more commonly a precursor for SCC/dysplasia).

DDX vs. Hairy Leukoplakia is on SIDE of tongue and caused by EBV in immunocomprised pts. Hyperplasia only

Question 7

Hairy Leukoplakia

Answer 7

White plaque on SIDE of tongue and caused by EBV in immunocomprised pts. Hyperplasia only (not dysplasia)

Question 8

Mumps

Answer 8

Infection w/ Mumps virus

Bilateral inflamed parotid glands

Orchitis, pancreatitis, and aseptic meningitis may also be present.

1. ) Serum Amylase is increased due to salivary gland or pancreatic involvement
2. )Orchitis carries risk of sterility, especially in teens.

Question 9

Sialadenitis

Answer 9

Obstruction (Sialolithiasis) causing inflammation of salivary gland secondary to infx. (S. aureus)

Usually unilateral

Question 10

Pleomorphic Adenoma

Answer 10

Benign tumor composed of stromal (caritlage) and epithelial tissue (glands).

AKA biphasic or mixed tumor

MC tumor of salivary gland

Parotic is MC

Mobile, painless, circumscribed mass at angle of jaw. (Key sx for bengn –> no invasion)

High Rate of recurrence –> irregular margins.

Rare transformation into scc

Question 11

Warthrin Tumor

Answer 11

Benign cystic tumor.

2nd mc tumor of salivary gland

Always parotid

Lymph tissue

Question 12

Mucoepidermoid Carcinomaq

Answer 12

Malignant tumor composed of mucinous and squamous cells.

Usually in parotid. Commonly involves facial nerve.

Question 13

TE Fistula

Answer 13

Congenital defect resulting in connection of esophagous and trachea.

MC = proximal esophageal atresia w/ distal fistula

Clinical findings: Vomiting, Polyhramnios, abdominal distension, and aspiration.

Question 14

Esophageal Web

Answer 14

Thin protrusions of mucosa, most often in UPPER esophagous.

Presents w/ dysphagia of poorly chewed food.

Increased risk for esophageal SCC

Can be a part of Plummer-Vinson syndrome

Question 15

Plummer-Vinsion Syndrome

Answer 15

Severe IDA, Esophageal web, and beefy red tongue due to atrophic glossitis.

Question 16

Zenker Diverticulum

Answer 16

Outpouching of pharyngeal mucosa through an acquired defect in the muscular wall (false diverticulum –> not entire wall)

Arises above UES at the junction of esophagus and pharynx.

Presents w/ dysphagia, obstruction, and halitosis.

Question 17

Mallory-Weiss Syndrome

Answer 17

Longitudinal laceration of mucosa at GE junciton.

Caused by severe vomiting (alcoholics and bulimia)

Presents w/ painful hematemesis.

Risk for Boerhaave syndrome - rupture of esophagus leading to air in mediastinum causing subcutaneous emphysema (crackling upon pressing –> Hammond’s sign).

Question 18

Esophageal Varices

Answer 18

Dilated submucosal veins in lower esophagus

Arises secondary to portal HTN

Asx, but risk of rupture exists –> painless hematemesis (vs. Mallory Weiss)

MCC of death in cirrhosis (synergism w/ coagulopathy due to liver failure)

Question 19

Achalasia

Answer 19

Disordered esophageal motility w/ inability to relax LES.

Dysphagia of solids and liquids (no peristalsis).

Due to damaged ganglion cells in myenteric plexus

1. ) Located between inner circular and outer longitudinal muscular layers. Important for bowel motility and relaxing LES.
2. ) Damage can be idiopathic or secondary to insult (i.e. Chagas)

Birdbeak sign on barium study

Presents /w dysphagia to solids and liquids, putrid breath, High LES pressure, Bird beak sign, Increased risk for SCC.

Question 20

GERD

Answer 20

Due to relaxed LES tone.

Risk factors: alcohol, tobacco, obesity, fat-rich diet, caffeine, and hiatal hernia (sliding type is MC –> hour glass stomach. Paraesophageal hernia is also possible –> less common and bowel sounds in lung field w/ possible lung hypoplasia).

Clinical features:

1. ) Heartburn (mimics cardiac chest pain
2. )Asthma (adult onset) and cough
3. ) Damage to enamel of teeth
4. )Ulceration with stricture (fibrosis and narrowing)) and Barrett esophagus (metaplasia) are late complications.

Question 21

Barrett’s Esophagus

Answer 21

Metaplasia of lower esophageal mucosa from stratified squamous epithelium to nonciliated columnar epithelium w/ goblet cells; seen in 10% of GERD patients.

Response of lower esophageal stem cells to acidic stress.

May progress to dysplasia and adenocarcinoma.

Question 22

Esophageal Carcinoma

Answer 22

Sublassified as adenocarcinoma or SCC.

Adenocarcinoma is a malignant proliferation of glands; MC type of esophageal carcinoma in the West. –> After Barrett’s and in lower 1/3.

SCC is a malignant proliferation of squamous cells; most common esophageal worldwide.
1.) Usually arises in upper or middle third of esophagous.

Major risk factor is IRRITATION

1. ) Alcohol and Tobacco (MC)
2. )Very hot tea (China and Iran)
3. ) Achalasia
4. ) Esophageal Web
5. ) Esophageal injury (lye injestion)

Presents late (poor prognosis)

1. ) Progressive dysphagia (solids and liquids), weight loss, pain, and hematemesis
2. ) SCC may additionally present w/ hoarse voice (recurrent laryngeal nerve) and cough (tracheal involvement.

Location determines lymph node/spread:

1. ) Upper 1/3 = cervical
2. ) Middle 1/3 = Mediastinal or tracheobronchial
3. ) lower 1/3 = celiac or gastric

Question 23

Gastroschisis

Answer 23

Congenital malformaiton of abdominal wall –> exposure of abdominal contents.

Question 24

Omphalocele

Answer 24

Pesistent herniation of bowel into umbilical cord.

Due to failure of herniated intestines to return to body cavity during development.

Contents are covered by peritoneum and amnion (in bubble vs. gastroschisis)

Question 25

Pyloric Stenosis

Answer 25

Hypertrophy of pyloric smooth muscle. More common in males. Results in stenosis of pyloric sphincter. *Normal at birth, and develops 2 weeks after birth. Projectile nonbilious vomiting. Can see intense peristalsis on PE. Can palpate olive-like structure. Rx = myotomy

Question 26

Acute Gastritis

Answer 26

Acidic damage to mucosa due to: 1. ) Increase in acid production or 2. )Decreased protection of mucosa. Risk factors: 1. ) Severe burn (Curling ulcer) --> secondary to severe hypovolemia 2. ) NSAIDs --> lack of PGE2 which decrease acid produciton, increase mucosal blood flow, and increase bicarb/mucus production 3. ) Heavy Alcohol consumption 4. ) Chemotherapy - death of regenerating cells 5. ) Increased ICP (Cushing ulcer) --> increased vagal stimulation --> increased Ach stimulation of parietal cells --> increased acid production 6. ) Shock (same as mech as Curling ulcer) - also known as stress ulcer --> usually multiple --> PPI if in ICU Acid damage results in: 1. )Superficial inflammation 2. )Erosion of epithelium 3. ) Ulcer (loss of mucosal layer)

Question 27

Chronic Autoimmune Gastritis

Answer 27

Autoimmune destruction of the parietal cells *(fundus and body esp.) T-cell mediated (Type 4 HS) --> creates ABs in blood vs. parietal cells. Clinical features: 1. )Atrophy of mucosa, 2.)Achlorhydria w/ increased gastrin levels and antral G-cell hyperplasia, 3. )Megaloblastic (pernicious) anemia due to lack of IF --> no B-12 absorbtion in ileum. MCC of B-12 deficiency. Increased risk for gastric adenocarcinoma --> Chronic inflammation induces intestinal metaplasia (goblet cells)

Question 28

Chronic H. Pylori Gastritis

Answer 28

H pylori-induced acute and chronic inflammation; MC form of gastritis H pylori ureases and proteases and inflammation weaken mucosal defenses. Antrum is most common site (vs. autoimmune) Presentation - 1. )Epigastric abdominal pain 2. ) Increased risk for ulceration, gastric adenocarcinmoa, and MALT lymphoma (B cell lymphoma in stomach wall) Rx: Triple Therapy = Amoxocillin or Clarithromycin + Metronidazole + Omeprazole (for three complication). Resolves gastritis/ulcer, and reverses intestinal metaplasia. Negative urea breath test and lack of stool antigen confirm eradication.

Question 29

Peptic Ulcer Disease

Answer 29

Solitary mucosal ulcer involving proximal duodenum (90%) or distal stomach (10%). DDX of ulcers includes cancer.

Question 30

Duodenal Ulcer

Answer 30

Duodenal ulcer almost always due to H. pylori; rarely may be due to ZE syndrome Presents w/ epigastric pain that improves w/ meals. Diagnositc endoscopic biopsy shows ulcer w/ hypertrophy of Brunner glands Leads to bleeding from gastroduodenal artery (esp. posterior duodenal wall) or acute pancreatitis (again posterior ulcers) Duodenal ulcers are almost never malignant --> don't biopsy

Question 31

Gastric Ulcer

Answer 31

Gastric ulcers due to H pylori; other causes include NSAIDs and bile reflux. Presents w/ epigastric pain that worsens w/ meals. Ulcer usually located on lesser curvature of antrum; rupture carries risk of bleeding from left gastric artery. Gastric ulcers can be caused by gastric carcinoma Benign features: 1. ) Small 2. ) Punched out 3. ) Margins aren't piling up of mucosa on edge of ulcer. Malignant feature: 1. ) Larger 2. ) Irregular shaped 3. ) Mucosa piling up on edge - must biopsy

Question 32

Gastric Carcinoma

Answer 32

Malignant proliferation of surface epithelial cells (adenocarcinoma) Intestinal Type Diffuse Type Often presents late w/: Weight loss, abdominal pain, anemia, and early satiety Rarely presents w/ acanthosis nigricans (darkening of patch of skin, esp. sub axillary) or Leser-Trelat sign (many seborrheic keratosis that rapidly appear) Spreads to left supraclavicular node (Virchow's node) Metastasis most commonly involves the liver. Periumbilical region (Sister Mary Joseph nodule) seen w/ intestinal type. Bilateral ovaries (Krukenburg tumor) seen w/ diffuse type

Question 33

Intestinal Type Adenocarcinoma

Answer 33

Presents as large, irregular ulcer w/ heaped up margins. MC on lesser curvature of antrum Risk factors: 1. ) Intestinal metaplasia 2. ) Nitrosamines in smoked foods (important for increased risk in Japan) 3. ) Blood type A. Often presents late w/: Weight loss, abdominal pain, anemia, and early satiety Rarely presents w/ acanthosis nigricans (darkening of patch of skin, esp. sub axillary) or Leser-Trelat sign (many seborrheic keratosis that rapidly appear) Metastasis most commonly involves the liver. Periumbilical region (Sister Mary Joseph nodule) seen w/ intestinal type.

Question 34

Diffuse type Adenocarcinoma

Answer 34

Signet ring cells (cells w. nucleus on edge due to mucus production form malignant cells) that diffusely infiltrate gastric wall. Desmoplasia results in thickening of stomach wall (linitis plastica). Not associated w/ H pylori, intestinal metaplasia, or nitrosamines Often presents late w/: Weight loss, abdominal pain, anemia, and early satiety Rarely presents w/ acanthosis nigricans (darkening of patch of skin, esp. sub axillary) or Leser-Trelat sign (many seborrheic keratosis that rapidly appear) Metastasis most commonly involves the liver. Bilateral mucinous tumors of the ovaries (Krukenburg tumor) seen w/ diffuse type

Question 35

Duodenal Atresia

Answer 35

Congenital failure of small bowel to canalize *Associated w/ Down Syndrome Clinical Features: Polyhydramnios, Distesnion of stomach and blind loop of duodenum (double bubble sign). Bilious vomiting.

Question 36

Meckel Diverticulum

Answer 36

Outpouching of all three layers of bowel wall (true) Arises due to failure of vitelline duct to involute/persist --> complete failure results in mechonium passing via umbilius Can palpate stool near umbilius Rules of 2s - 1. )Seen in 2% of the population (MC GI anomaly), 2. ) 2 inches long 3. ) Located in small bowel 2 feet from IC valve 4. )Presents in first 2 years of life Clinical features: Usually asymptomatic. Can result in bleeding, volvulus (twisting of bowel), intussusception (telescoping of bowel), or blockage. Can have heterotopic gastric mucosa --> acidic damage to diverticulum --> bleeding

Question 37

Volvulus

Answer 37

Twisting of bowel along its mesentery Results in obstruction and disruption of blood supply (infarction) MC locations are sigmoid colon (elderly) and cecum (young adults)

Question 38

Intussusception

Answer 38

Telescoping of proximal segment of bowel into distal segment. (drag in w/ peristalsis). Results in obstruction or infarction Can present w/ currant jelly stools. Associated w/ leading edge: 1. )Children MCC is lymphoid hyperplasia, usually post viral infection --> TI into cecum 2. ) In adults, MCC is tumor

Question 39

Small Bowel Infarction

Answer 39

Highly susceptible (needs a lot of ATP Transmural infarction occurs w/ embolism/thrombosis of SMA (can follow vasculitis, i.e. polyarteritis nodosa) or thrombosis of mesenteric vein (i.e. hypercoaguable) Mucosal infarction occurs w/ marked hypotension. Clinical features: 1. ) abdominal pain 2. ) bloody diarrhea 2. ) decreased bowel sounds

Question 40

Lactose intolerance

Answer 40

Due to decreased function of the lactase enzyme found in the brush border of enterocytes. Presents w/ abdominal distension and diarrhea (osmotic) upon consumption of milk products Deficiency may be congenital (rare) or acquired either w/ age (permanent) or post GI infection (temporary)

Question 41

Celiac Disease

Answer 41

Immune-mediated damage of small bowel villi due to gluten exposure (type 4 hypersensitivity reaction) Gluten is present in wheat and grains. Most pathogenic component is gliadin which is deamidated by tTG --> eamidated gliadin is presented by APCs via MHC II --> Helper T cells mediate tissue damage Clinical presentation: Children: Abdominal distension, diarrhea, and FTT Adults: Chronic diarrhea and bloating Associated w/ dermatitis herpetiformis Labs: IgA antibodies vs. endomysium, tTG, or gliadin. IgG antibodies are useful for dx in IgA deficiency (common in celiac's) Duodenal biopsy: 1. ) Flattening of villi, hyperplasia of crypts, and increased intrepithelial lymphocytes 2. ) **Damage is most prominent in duodenum; J and I are less involved. . Symptoms resolve w/ gluten-free diet. Small bowel carcinoma and T-cell lymphoma (EATL) present w/ refractory disease despite good dietary control. Associated w/ HLA DQ2 and DQ8

Question 42

Dermatitis herpetiformis

Answer 42

Due to IgA deposition at tips of dermal papillae which resolves w/ gluten-free diet. Looks like herpes.

Question 43

Topical Sprue

Answer 43

Damage to small bowel villi due to unknown organism resulting in malabsorbtion. Similar to celiac's except: 1. ) Occur in tropical regions 2. ) Arises after infectious diarrhea and responds to antibiotics 3. ) *Damage is most prominent in jejunum and ilium; duodenum is less involved Results in folic acid and B12 deficiencies

Question 44

Whipple Disease

Answer 44

Systemic disease damage characterized by macrophages loaded w. Trophyeryma whipplei organisms (incomplete killing of organisms and thus present in mphage lysosomes --> PAS +) Usually involves small bowel lamina propria resulting in fat malabsorption and statorrhea. (loss of lacteals to absorb chylomicrons) Other common sites of involvement: Synovium of joints (arthritis), cardiac valves, lymph nodes, and CNS

Question 45

Abetalipoproteinemia

Answer 45

AR deficiency of apoprotein B-48 and B-100. Clinical features: Malabsorbtion due to defective chylomicron formation (requries B-48) Absent plasma VLDL and LDL (requires B-100_

Question 46

Carcinoid tumor

Answer 46

Malignant proliferation of neuroendocrine cells; low grade malignancy *Positive for chromogranin Small bowel is MC site (every site has cancer pneumonic) Grows as submucosal polyp-like noducle Often secrete serotonin --> MAO in liver makes 5-HIAA (metabolite is excreted in the urine.) Thus does not cause carcinoid syndrome unless metastatic. If metastasized (i.e. liver) serotonin in systemic circulation --> carcinoid syntrome --> bronchospasm, diarrhea and flushing of skin Can also cause carcinoid heart disease.

Question 47

Carcinoid syndrome

Answer 47

Bronchospasm, diarrhea, and flushing of the skin. Can cause pellagra due to 5-HT consumption of TRP --> inability to produce Niacin --> pellagra --> DDD Sx can be triggered by EtOH or stress.

Question 48

Carcinoid Heart Disease

Answer 48

Right sided valvular fibrosis due to collagen deposition. Leads to tricuspid regurge and pulmonary valve stenosis. *Lung also has MAO ---> converts 5-HT --> no left sided lesions

Question 49

Acute Appendicitis

Answer 49

Acute inflammation of appendix; MCC of acute abdomen. Related to obstruction of the appendix by lymphoid hyperplasia (children) or fecolith (adult) Clinical features: Periumbilical pain, fever, and nausea --> pain eventually localizes to RLQ --> rupture results in peritonitis that presents w/ guarding and rebound tenderness. Periappendiceal abscess is common complication.

Question 50

Inflammatory Bowel Disease

Answer 50

Chronic relapsing inflammation of the bowel. Possibly due to abnormal immune response to enteric flora. Presentation: young women (teens to 30s) w/ recurrent bouts of bloody diarrhea and abdominal pain. More prevalent in the West, particularly caucasians and Eastern European Jews. Dx of exclusion (symptoms mimic other causes of bowel inflammation --> i.e. infx or ischemic) Two types: Ulcerative Colitis or Crohn's Disease

Question 51

Ulcerative Colitiis

Answer 51

Mucosal and submucosal ulcers. Always starts in rectum and can extend proximally up to the cecum (involvement is continuous). Remainder is unaffected. LLQ pain w/ bloody diarrhea Crypt abscess w/ neutrophils Pseudopolyps, loss of haustra (Iead pipe sign on imaging) Complications: Toxic megacolon and *carcinoma. Risk of carcinoma is based on colonic involvement and duration of disease. Generally not a concern until > 10 years. Associated w/ primary sclerosing cholangitis and p-ANCA (also positive in microscopic polyangitis and Churg-Strauss) Smoking protects vs. ulcerative colitis

Question 52

Crohn's Disease

Answer 52

Knife like fissures causing full-thickness inflammaiton. Anywhere in GI tract w/ skip lesions; terminal ileum is MC. Rectum is least common. Presents w/ RLQ pain (ileum) w/ non-bloody diarrhea. Histologically: lymphoid aggregates w/ *granulomas (40% of cases) Cobblestone mucosa, creeping fat, and strictures (string-sign on imaging) Complications: Malabsorption w/ nutritional deficiency (if small bowel is involved), calcium oxalate nephrolithiasis (inflammation increases oxalate absorption), fistula formation, and carcinoma if colonic disease present. Associations: Ankylosing spondylitis, sacroilitis, migratory polyarthritis, erythema nodosum, and uveitis Smoking increases risk.

Question 53

Hirschsprung Disease

Answer 53

Defective relaxation and peristalsis of rectum and distal colon. *Associated w/ Downs Syndrome Caused by congenital failure of ganglion (from both nervous ganglia Submucosal and Myenteric) cells from neural crest to descend. Sx: Failure to pass meconium, Empty rectal vault on DRE, massive dilitation of bowel proximal to obstruction w/ risk of rupture. *Rectal suction (gets submucosa and mucosa) biopsy reveals lack of ganglion cells Rx: Resection of involved bowel. Ganglion cells are present in bowel proximal to the diseased segment.

Question 54

Colonic Diverticula

Answer 54

Outpouchings of mucosa and submucosa through muscularis propria Related to wall stress (constipation, low fiber diet) esp. in older adults. Arises where vasa recta traverse muscularis propria (weak point in colonic wall); sigmoid colon is MC Usually asymptomatic but complications include: 1. )Rectal bleeding due to proximity of vasa recta to pouch (hematochezia) 2. )Diverticulitis (right sided appendicitis) 3. )Fistula (usually colovesicular --> air or stool in urine)

Question 55

Angiodysplasia

Answer 55

Acquired malformation of mucosal and submucosal capillary beds Usually arise in cecum and right colon due to high wall tension Presents w/ hematochezia in older adult

Question 56

Hereditary Hemorrhagic Telangiectasia

Answer 56

AD disorder resulting in thin-walled blood vessels esp. in nasopharynx and GI Rupture presents as bleeding.

Question 57

Ischemic Colitis

Answer 57

Ischemic damage to the colon, usually at the splenic flexure due to atherosclerosis of SMA Presents w/ postprandial pain and weight loss (think angina of colon) Infarction results in pain and bloody diarrhea

Question 58

Irritable Bowel Syndrome

Answer 58

Relapsing abdominal pain w/ bloating, flatulence, and change in bowel habits (diarrhea or constipation) Improves w/ defecation Classically seen in middle aged females Related to disturbed intestinal motility. Fiber may improve sx

Question 59

Colonic Polyps

Answer 59

Raised protrusion of colonic mucosa MC types are hyperplastic, adenomatous

Question 60

Hyperplastic polyp

Answer 60

Due to hyperplasia of glands, "serrated" appearance on microscopy MC polyp; usually in left (rectosigmoid) colon Benign w/ no malignant potential.

Question 61

Adenomatous polyps

Answer 61

Neoplastic proliferation of glands. 2nd MC type of colonic polyp *Benign, but premalignant; may progress to adenocarcinoma via adenoma-carcinoma sequence. All polyps are removed and examined microscopically. Risk for progression from adenoma to carcinoma is related to size >2cm, sessile growth (grow along wall), and villous histology (vs. tubular)

Question 62

Adenoma-Carcinoma sequence

Answer 62

APC (tumor suppressor) mutations (sporadic or germline) increase risk. Mutated in FAP. On chromosome 5. K-ras mutations leads to formaiton of polyp. p53 mutation and increased expression of COX allow for progression to carcinoma. *Aspirin protects against this sequence!

Question 63

FAP

Answer 63

AD disorder characterized by 100s to 1000s of adenomatous colonic polyps Due to inherited mutation of APC on chromosome 5. Marilyn Monroe Fapped Joe Dimaggio (5) Colon and rectum are removed. Otherwise all patients develop carcinoma by age 40

Question 64

Gardner Syndrome

Answer 64

FAP w/ fibromatosis (non-neoplastic proliferation of fibroblasts in retroperitoneum) and osteomas (benign neoplasm of skull)

Question 65

Turcot syndrome

Answer 65

FAP w/ CNS tumors (medulloblastoma and glial tumors)

Question 66

Juvenile polyp

Answer 66

Sporadic hamartomous polyp that arises in chilren (

Question 67

Juvenile polyposis

Answer 67

Multiple juvenile polyps in the stomach and colon Large numbers of juvenile polyps increases risk of progression to carcinoma

Question 68

Puetz-Jeghers Syndrome

Answer 68

Hamaratomatous polyps throughout GI tract Mucocutaneous hyperpigmentation on lips, oral mucosa, and genital skin AD disorder Increased risk for CRC, breast, and GYN cancer

Question 69

Colorectal carcinoma

Answer 69

Peak Incidence is 60-70 years MC arises from adenoma-carcinoma sequence Second MC molecular pathway is microsatellite instability (MSI) --> problems w/ repair mechanisms (HNPCC) Patients w/ ulcerative colitis and Puetz-jahger also have increased risk. Screening via colonoscopy and fecal occult blood. Begins at age 50. Goal is to remove adenomatous polyps before carcinoma develops. Cancer can develop on any part of colon. Left sided = napkin ring lesion w/ *decreased caliber and LLQ pain w/ blood-streaked stool. Adenoma-carcinoma sequence. Right sided = raised lesion --> IDA (slow chronic bleeding) and vague pain. Microsatellite. Increased risk for Streptoccus bovis endocarditis Staging: TNM MC site of metastasis is liver CEA is serum tumor marker. Not useful for screening, but is for response/recurrence.

Question 70

HNPCC

Answer 70

Inherited mutation in DNA mismatch repair enzymes. Increased risk for crc, ovarian, and endometrial carcinoma CRC arices de novo at a relatively young age; usually right sided. AD disorder. Marshawn Lynch is a dominant mismatch who is right handed.