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USMLE Step I Pathology > GI Pathology (Pathoma) > Flashcards

GI Pathology (Pathoma) Flashcards

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USMLE® Step 1 flashcards
1
Q

Cleft Lip an Palate

A

Full-thickness defect of lip and/or palate.

*Due to failure of facial proiminences to fuse

Usually occur together.

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2
Q

Apthous Ulcer

A

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

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3
Q

Behcet Syndrome

A

Recurrent apthous ulcers, genetial ulcers, and uveitis.

Due to immune complex vasculitis of small vessels.

Can follow viral infx.

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4
Q

Oral Herpes

A

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

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5
Q

Squamous Cell Carcinoma

A

Malignant squamous cells lining oral mucosa

Tobacco and alcohol are syntergistic risk factors.

Floor of mouth is MC location.

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6
Q

Leukoplakia and Erythroplakia

A

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

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7
Q

Hairy Leukoplakia

A

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

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8
Q

Mumps

A

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.
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9
Q

Sialadenitis

A

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

Usually unilateral

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10
Q

Pleomorphic Adenoma

A

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

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11
Q

Warthrin Tumor

A

Benign cystic tumor.

2nd mc tumor of salivary gland

Always parotid

Lymph tissue

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12
Q

Mucoepidermoid Carcinomaq

A

Malignant tumor composed of mucinous and squamous cells.

Usually in parotid. Commonly involves facial nerve.

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13
Q

TE Fistula

A

Congenital defect resulting in connection of esophagous and trachea.

MC = proximal esophageal atresia w/ distal fistula

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

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14
Q

Esophageal Web

A

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

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15
Q

Plummer-Vinsion Syndrome

A

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

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16
Q

Zenker Diverticulum

A

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.

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17
Q

Mallory-Weiss Syndrome

A

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).

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18
Q

Esophageal Varices

A

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)

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19
Q

Achalasia

A

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.

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20
Q

GERD

A

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.
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21
Q

Barrett’s Esophagus

A

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.

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22
Q

Esophageal Carcinoma

A

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
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23
Q

Gastroschisis

A

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

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24
Q

Omphalocele

A

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)

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25
Q

Pyloric Stenosis

A

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

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26
Q

Acute Gastritis

A

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)
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27
Q

Chronic Autoimmune Gastritis

A

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,
  2. )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)

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28
Q

Chronic H. Pylori Gastritis

A

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.

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29
Q

Peptic Ulcer Disease

A

Solitary mucosal ulcer involving proximal duodenum (90%) or distal stomach (10%).

DDX of ulcers includes cancer.

30
Q

Duodenal Ulcer

A

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

31
Q

Gastric Ulcer

A

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
32
Q

Gastric Carcinoma

A

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

33
Q

Intestinal Type Adenocarcinoma

A

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.

34
Q

Diffuse type Adenocarcinoma

A

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

35
Q

Duodenal Atresia

A

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.

36
Q

Meckel Diverticulum

A

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

37
Q

Volvulus

A

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)

38
Q

Intussusception

A

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
39
Q

Small Bowel Infarction

A

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
  3. ) decreased bowel sounds
40
Q

Lactose intolerance

A

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)

41
Q

Celiac Disease

A

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

42
Q

Dermatitis herpetiformis

A

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

Looks like herpes.

43
Q

Topical Sprue

A

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

44
Q

Whipple Disease

A

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

45
Q

Abetalipoproteinemia

A

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_

46
Q

Carcinoid tumor

A

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.

47
Q

Carcinoid syndrome

A

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.

48
Q

Carcinoid Heart Disease

A

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

49
Q

Acute Appendicitis

A

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.

50
Q

Inflammatory Bowel Disease

A

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

51
Q

Ulcerative Colitiis

A

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

52
Q

Crohn’s Disease

A

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.

53
Q

Hirschsprung Disease

A

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.

54
Q

Colonic Diverticula

A

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)
55
Q

Angiodysplasia

A

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

56
Q

Hereditary Hemorrhagic Telangiectasia

A

AD disorder resulting in thin-walled blood vessels esp. in nasopharynx and GI

Rupture presents as bleeding.

57
Q

Ischemic Colitis

A

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

58
Q

Irritable Bowel Syndrome

A

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

59
Q

Colonic Polyps

A

Raised protrusion of colonic mucosa

MC types are hyperplastic, adenomatous

60
Q

Hyperplastic polyp

A

Due to hyperplasia of glands, “serrated” appearance on microscopy

MC polyp; usually in left (rectosigmoid) colon

Benign w/ no malignant potential.

61
Q

Adenomatous polyps

A

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)

62
Q

Adenoma-Carcinoma sequence

A

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!

63
Q

FAP

A

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

64
Q

Gardner Syndrome

A

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

65
Q

Turcot syndrome

A

FAP w/ CNS tumors (medulloblastoma and glial tumors)

66
Q

Juvenile polyp

A

Sporadic hamartomous polyp that arises in chilren (

67
Q

Juvenile polyposis

A

Multiple juvenile polyps in the stomach and colon

Large numbers of juvenile polyps increases risk of progression to carcinoma

68
Q

Puetz-Jeghers Syndrome

A

Hamaratomatous polyps throughout GI tract

Mucocutaneous hyperpigmentation on lips, oral mucosa, and genital skin

AD disorder

Increased risk for CRC, breast, and GYN cancer

69
Q

Colorectal carcinoma

A

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.

70
Q

HNPCC

A

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.

USMLE Step I Pathology (14 decks)

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