Disorders of the colon Flashcards

1
Q

diverticular disease of the colon

A

-Colonic diverticulosis increases with age in Western societies:
-<20% in those under age 40
-60% by age 60
-More than 70% over age 80
-Very uncommon in developing countries
-asymptomatic
-vary in size- few mm to several cm
-vary in number
-almost all pts have involvement in sigmoid colon -> smaller diameter -> intraluminal pressures
-common in pts with not enough fiber, processed foods
-areas of inherit weakness

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2
Q

anti-mesenteric

A

-lateral colon
-most common for diverticulosis
-The prevalence of diverticular disease affecting the left colon is higher in Western countries compared to Asia

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3
Q

diverticulosis pathogenesis

A

-Years of diet deficient in fiber
-Undistended contracted segments of colon have higher intraluminal pressures: -> More common in sigmoid-> increase intraluminal pressures
-Abnormal motility and hereditary factors may contribute
-left sided more common in US
-Connective tissue ds:
Ehlers- Danlos syndrome, Marfan’s syndrome, scleroderma

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4
Q

diverticulosis complications

A

-Bleeding and diverticulitis
-Approx 4% develop diverticulitis
-5-15% have diverticular bleed -> 50% of acute lower GI bleeding is attributable to diverticulosis
-diverticular bleeds are bad

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5
Q

diverticulitis

A

-Perforation of a colonic diverticulum:
-Microperforation (most common) with localized paracolic inflammation
-Macroperforation with abscess or generalized peritonitis -> catastrophe
-Erosion of the diverticular wall by increased intraluminal pressure or inspissated food particles
-Inflammation and focal necrosis ensue -> resulting in perforation
-S&S- mild to moderate LLQ pain, constipation, nausea and vomiting **

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6
Q

diverticulitis PE and labs

A

-Low-grade fever
-Left lower quadrant tenderness, +/-palpable mass (rare)
-Stool occult blood- common, hematochezia (rare)
-Leukocytosis

-Free/Macroperforation:
Dramatic picture of generalized abdominal pain and peritoneal signs
-imaging- plain abdominal films (usually only with macroperforation)
-CT of abdomen and pelvis***
-colonoscopy and barium enema -> contraindicated bc of perforation

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7
Q

diverticulitis differential dx

A

-Perforated colonic carcinoma** -> 6-8 weeks after do colonoscopy bc it can be a perforated colonic carcinoma
-IBD
-Appendicitis
-Ischemic colitis
-C difficile–associated colitis
-Gynecologic disorders (ectopic pregnancy, ovarian cyst or torsion)

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8
Q

diverticulitis complications

A

-Abscess or phlegmon (early abscess)
-Bleeding
-Fistula
-Stricturing of colon

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9
Q

outpatients tx diverticulitis***

A

-uncomplicated disease:
-Pain medication
-Liquid then low residue diet
- +/- Antibiotics- reassess every three days
-Reassess in 3 days, then follow closely

-complicated disease:
-Metronidazole* 500 mg three times daily plus Ciprofloxacin* 500 mg twice daily x 10 days or augmentin*
-Liquid then low residue diet (low fiber at first) -> then high fiber

-Antibiotic treatment can be used selectively rather than routinely in immunocompetent patients with mild acute uncomplicated diverticulitis -> Antibiotic treatment is strongly advised in immunocompromised pts

-fu with clinical exam NOT imaging

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10
Q

diverticulitis hospitalize and tx

A

-Increasing pain, fever, or inability to tolerate oral fluids
-Elderly or immunosuppressed
-Serious comorbid ds
-Treatment:
-NPO with intravenous fluids
-If ileus -> nasogastric tube for decompression
-IV antibiotics to cover anaerobic and gram-negative bacteria

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11
Q

surgical management: diverticulitis

A

-20–30%
-Elective vs. Emergent
-Surgical consultation*:
-Complicated/Severe disease
-Fail to improve after 72 hours of medical management
-Recurrent disease- not # episodes
-Fistulas, colonic obstruction, abscess

-Emergent* surgical management- Free perforation/peritonitis and large abscesses

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12
Q

diverticulitis prognosis

A

-16 to 42 % risk of developing recurrent diverticulitis
-Obesity, sedentary lifestyle, smoking, NSAIDs, genetics
-Number of prior attacks is no longer used as a criterion for elective surgery
-Future care:
-Colonoscopy 6-8 weeks after to make sure perf wasnt from colon cancer
-High fiber diet

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13
Q

why is colorectal cancer screening important

A

-Facts about colorectal cancer:
-Colorectal cancer is # 2 cause of cancer death in the US and affects both men and women.
-Preventable
-More preventable than breast or prostate cancer
-Screen for colorectal cancer in all adults aged 45-75 years
-Adults aged 76-85 years: determine whether is appropriate in individual cases
-pts and clinicians should consider the patient’s overall health, prior screening history, and preferences

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14
Q

colorectal cancers start in polyps

A

-A polyp is a warty growth on the inner lining of the colon (mucosa)
-Polyps are usually benign
-Polyps that can turn into cancer are called adenomas; not all polyps are adenomas
-Polyps can be removed during colonoscopy
-Removal of polyps prevents the development of colorectal cancer

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15
Q

screening for colon cancer

A

-screen for colorectal cancer in all adults aged 45-75 years
-adults aged 76-85 -> determine whether appropriate in individual cases
-pts and clinicians should consider the pts overall health, prior screening history and preferences

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16
Q

polyps of colon and small intestine

A

-Discrete mass lesions that protrude into lumen
-3 major pathologic groups:
-Mucosal neoplastic: adenomatous polyps***
-Mucosal nonneoplastic polyps: hyperplastic, juvenile polyps, hamartomas, inflammatory polyps (mostly not cancer)
-Submucosal lesions: lipomas, lymphoid aggregates, carcinoids (non cancerous except carcinoids)

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17
Q

nonfamilial adenomatous polyps

A

-Tubular, tubulovillous, villous or serrated
-Sessile (flat) or pedunculated (on stalk) - always
-pedunculated - stalk is non cancerous but the tip is adenomatous
-Present in 25% of adults over 50 years of age
->95% of cases of colon adenocarcinoma are believed to arise from adenomatous polyps
-Small (< 1 cm) have low risk of becoming malignant- less than 5% of these enlarge with time
-“Advanced” adenomas:
- ≥ 1 cm
-Villous features
-Dysplasia
-Higher risk of harboring or progressing to malignancy

-5 years for a medium-sized polyp to develop from normal-appearing mucosa
-7-10 years for a gross cancer to arise

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18
Q

symptoms of adenomatous polyps

A

-Most pts completely asymptomatic
-people dont know until they start bleeding -> melena or rectal bleeding -> Iron deficiency anemia
-Intermittent hematochezia

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19
Q

malignant polyp tx

A

-Histologic assessment found to contain cancer that has penetrated through muscularis mucosae into submucosa
-Malignant polyps considered adequately treated by polypectomy alone if:
-(1) polyp is completely excised and submitted for pathologic examination
-(2) well differentiated
-(3) margin is not involved (clear margins)
-(4) no tumor budding vascular invasion

-excision site of “favorable” malignant polyps should be checked in 3 months for residual tissue

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20
Q

colonoscopy recheck (chart)

A

-10 years- normal colonoscopy / < 20 HP < 10mm
-7-10 years- 1-2 adenomas <10 mm
-5-10 years- 1-2 SSPs < 10mm
-3-5 years- 3-4 adenomas < 10 mm, 3-4 SSPs <10 mm, HP > 10 mm
-3 years- 5-10 adenomas, 5-10 SSPs, adenomas or SSP > 10 mm, adenoma with villous or tubulovillous histology and/or high grade dysplasia, SSP with dysplasia, traditional serrated adenoma
-1 year- > 10 adenomas

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21
Q

colonoscopy

A

-goes to the cecum (unless you have IBD it goes to ileum?)

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22
Q

screening frequency

A

-45-75 years- average risk - every ten years
-stool based tests
-direct visualization- colonoscopy, CT colonography every 5
-personal hx or polyps, IBD, polyposis syndrome -> more frequent
-family history, genetic syndromes - more frequent
-colonoscopy - most specific and detects the smallest

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23
Q

hereditary colorectal cancer and polyposis syndromes

A

-3-4% of all colorectal cancers are caused by genetic mutations* that impose a high lifetime risk of developing colorectal cancer
-rare
-Consider these disorders in patients with:
-family history of colorectal cancer that has affected >1 family member (first degree)
-personal or family history of colorectal cancer < 50yo
-personal or family history of multiple polyps (> 20)
-personal or family history of multiple extracolonic malignancies

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24
Q

familial adenomatous polyposis (FAP)

A

-Affects 1:10,000 people
-0.5% of colorectal cancer- rare
-Hundreds to thousands of colonic adenomatous polyps and a variety of extracolonic manifestations
-Autosomal dominant inherited mutations in the adenomatous polyposis coli (APC) gene on chromosome 5q21
-Attenuated variant produces less polyps
-Colorectal polyps develop by a mean age of 15 years and cancer at 40 years.
-Colorectal cancer is inevitable by age 50 years
-colon removal
-genetic counseling and testing- first degree family members of pts with the disease

25
monitoring FAP
-Annual colonoscopy till colectomy deemed appropriate -Complete proctocolectomy with ileoanal anastomosis or colectomy with ileorectal anastomosis is recommended, usually before age 20 years -> If retain rectum flex sig q 6-12 mos -EGD every 1–3 yrs to look for adenomas or carcinoma
26
hamartomatous polyposis syndromes
-Rare, < 0.1% of colorectal cancers -Peutz-Jeghers syndrome -Familial juvenile polyposis -PTEN multiple hamartoma syndrome (Cowden disease)
27
peutz-jeghers syndrome
-Autosomal dominant condition on gene 19p13.3 -Hamartomatous polyps throughout the GI tract -Mucocutaneous pigmented macules on the lips, buccal mucosa, and skin* -dark spots -Hamartomas may become large -> bleeding, intussusception (telescoping), or obstruction -Not malignant but adenomatous change can occur within the hamartomas-> lifetime risk is 39% for CRC -Extracolonic malignancies: GI malignancies 40%, breast cancer 50%, testicular, pancreatic cancer -Screening every 2-3 yrs with EGD, Colon, MRE -Genetic testing for family
28
familial juvenile polyposis
-Rare, 1/3 familial -Autosomal dominant germline mutation in SMAD4 gene on chromosone 18q21.1 -Several (>10) juvenile hamartomatous polyps located most commonly in colon -Increased risk ( 20%) of adenocarcinoma due to synchronous adenomatous polyps/cancer*** or adenomatous change within hamartomatous polyps -2 types at once -Genetic testing is available -Colonoscopy q 1-2yrs starting at 15-18yo
29
PTEN multiple hamartoma syndrome (Cowden disease)
-Hamartomatous polyps and lipomas throughout the GI tract -Trichilemmomas*: -Slow-growing flesh-colored flat-topped facial papules or plaques 1-5 mm in diameter -Grow, warty appearance -Cerebellar lesions -Increased malignancy- Thyroid, breast, and urogenital tract
30
lynch syndrome
-3% of all colorectal ca -Autosomal dominant- Defect in one of several genes that are important in the detection and repair of DNA base-pair mismatches: MLH1, MSH2, MSH6, and PMS2 -Increased risk of colorectal ca, endometrial ca** + others -Few adenomas, but aggressive*, larger, sessile, villous features, dysplastic, right sided* - Rapid transformation
31
who to suspect lynch syndrome
-pts with synchronous or metachronous CRC -CRC or endometrial cancer prior to 50 years of age -multiple Lynch-associated cancers (eg, CRC and endometrial, ovarian, stomach, small intestine, or renal pelvis/ureter) -familial clustering of Lynch-associated cancers. -Thorough family history is essential to identify families - genetic screening -Screened with colonoscopy every 1–2 years beginning at age 25 (or 2-5 years younger than the age at diagnosis of the youngest affected family member) -> dont need to know age
32
colorectal cancer
-3rd mc cancer in males and in females- 2nd leading cause of death due to malignancy in the US -Almost all adenocarcinomas -Gradual increase in incidence of cancers in cecum and ascending colon. - >50% of cancers now develop proximal to the splenic flexure -risk factors: -age -family hx -personal or family hx of polyps -race -hereditary polyposis syndromes -IBD
33
colorectal cancer S&S and PE
-Right-sided colon cancer- Iron deficiency anemia -> Obstruction uncommon -no obstruction and liquid goes around on right side -> not symptomatic until bleeding, anemic, SOB -Left sided colon cancer: -Often involve bowel circumferentially -Obstructive symptoms -Anemia/Heme+ stool -catch earlier -Rectal cancers: Tenesmus, urgency, recurrent hematochezia -PE- usually normal except in advanced disease -> +/- palpable mass, +/- hepatomegaly, digital exam, rectal exam
34
differential dx colorectal cancer
-Irritable bowel syndrome -Diverticular disease -Ischemic colitis -Inflammatory bowel disease -Infectious colitis -Hemorrhoids
35
colorectal cancer labs
-Complete blood count -Liver function tests (metastases) -Carcinoembryonic antigen (CEA)- tumor marker -> monitor
36
colorectal cancer imaging
-Inspection of the colon: -CT colonography or colonoscopy -+ CT warrants colonoscopy for removal -Colonoscopy: diagnostic procedure of choice -Imaging: Once establish have cancer*: -Chest, abdominal and pelvic PET CT for preoperative staging- -Rectal Ca: Endorectal ultrasonography -> Depth of penetration of cancer through rectal wall and pararectal lymph nodes -Staging: TNM
37
follow up after surgery
-Optimal cost-effective strategy is not clear -Evaluated every 3–6 months for 3–5 years with history, physical, CEA -Annual CT Scan at least for 3 years -Colonoscopy: -1 year after surgical resection -Surveillance colonoscopy performed every 3–5 years -Rectal cancer- Sigmoidoscopy every 3–6 months for 3 years
38
5 year relative survival rates for colon cancer
-localized- 90% -regional- 72% -distant- 13% -all SEER stages combined- 63%
39
anal cancer
-Relatively rare -Squamous cancers make up majority -Increased among people practicing receptive anal intercourse and history of STDs -In over 80%: HPV detected -bleeding, pain are MC symptoms -testing- bx, MR scan and endoluminal rectal US -tx- depends on tumor stage -> excision +/- chemo and radiation
40
lower GI bleeding
-Arising below the ligament of Treitz -Severity ranges from mild anorectal bleeding to massive, large-volume hematochezia -Spontaneous cessation: >85% of cases -Hospital mortality < 3% -to determine the cause -> consider age of pt and severity of bleed -if under 50 -> infectious colitis, anorectal disease, and IBD -older pts -> significant hematochezia is most often diverticular -> other causes: vascular ectasias, malignancy, ischemia
41
diverticular bleed
-Acute hemorrhage occurs in 3–5% of pts with diverticulosis -MC cause of overt major lower GI bleeding (50%) -Bleeding more commonly originates on the right side -**Presents as acute, painless, large-volume maroon or bright red blood in pts over age 50 -Spontaneously resolves in 80% -May recur in up to 25%
42
vascular ectasis (angiodysplasias)
-5–10% of cases of lower GI bleeding -Occur throughout the upper and lower intestinal tracts -MC in patients >70 years and in those with chronic renal failure -Mucosal capillaries* in colon dilate and become incompetent -> Most often in cecum and ascending colon -Painless bleeding ranging from occult to melena to hematochezia
43
neoplasms and polyps
-Colonic neoplasms may cause up to 10% of acute lower gastrointestinal hemorrhage. -MC cause of slow occult bleed, chronic ooze. -Post polypectomy bleed: -After endoscopic removal of colonic polyp significant overt (heavy) bleeding may occur up to 2 weeks later in 0.3% of patients
44
inflammatory bowel disease
-Diarrhea with variable amounts of bright red blood -Abdominal pain, tenesmus, and urgency are often present
45
anorectal disease
-Small amounts of bright red blood noted on toilet paper, streaking of stool, or dripping into toilet bowl -Bleeding is slight & seldom results in sig blood loss -Painless bleeding associated with BM- Hemorrhoids -Bleeding & pain during BM- Anal fissure
46
ischemic colitis
-Commonly in older patients, with ASHD -5% of patients after surgery for ileoaortic or abdominal aortic aneurysm -In young patients, may develop due to vasculitis, coagulation disorders, estrogen therapy, and long distance running -Hematochezia or bloody diarrhea with mild cramps -Typically, bleeding is mild and self-limited -Other causes: Radiation-induced proctitis and Acute infectious colitis
47
approach to pt with lower GI bleed (chart)
-pt with acute, severe hematochezia -initial eval and resucitation -nasogastric tube aspiration- rule up upper GI bleed -if aspirate copious bile and no blood -> colonoscopy -> arteriography is severe -if aspirate blood -> EGD
48
evaluation and management of significant acute bleed
-Initial stabilization, blood replacement, & triage managed same way as acute UGI bleed -Exclusion of an Upper Tract Source: NGT (hemodynamically compromised patients)
49
color of stool helps distinguish upper from lower bleed
-Large volumes bright red blood -> colonic source -Brown stools mixed/streaked with red blood -> rectosigmoid or anus -Maroon stools -> right colon or small intestine -Black stools (melena) ->proximal to ligament of Treitz
50
small volume bleeding
-Under age 45 with small-volume bleeding -> DDX: anorectal disease, inflammatory bowel disease, or infectious colitis, tumor but less likely -Over age 45 years with small-volume bleeding or anemia -> DDX: exclude tumor, vascular ectasias, plus above -All will have a colonoscopy, CBC, additional diagnostic w/u depends on presentation and findings
51
large volume bleeding that has stopped
-stable vital signs -colonoscopy within 24 hours of admission
52
large volume active lower GI bleed tx
-Urgent colonoscopy within 6–12 hours of admission -Probable site of bleeding ID in 70-85% of patients -tx- therapeutic colonoscopy- epinephrine injection, cautery (bipolar or heater probe), or metallic endoclips -intra-arterial vasopressin or embolization: -Selective mesenteric arterial angiography followed by embolization of bleeding lesion provides definitive control of bleeding in up to 90%
53
unable to ID site with colonoscopy or too severe
-Nuclear Bleeding Scan: -Technetium-labeled red blood cell scanning can detect significant active bleeding and localize it to the small intestine, right colon, or left colon. -Less than half of studies are diagnostic -Accuracy of a positive study is only 78% -Angiography: -Angiograms: in patients with positive technetium scans or with hemodynamically significant, ongoing bleeding. Localization of an actively bleeding vessel in up to 80% High complication rate
54
lower GI bleed treatment
-Therapeutic Colonoscopy Epinephrine injection, cautery (bipolar or heater probe), or metallic endoclips -Intra-arterial Vasopressin or Embolization -Selective mesenteric arterial angiography followed by embolization of bleeding lesion provides definitive control of bleeding in up to 90%
55
bleeding diverticulum or vascular ectasia surgical treatment
-Bleeding diverticulum or vascular ectasia -Localized resection: -Preoperative localization of bleeding site by nuclear scan or angiography -Indicated: ongoing excessive bleeding -Total abdominal colectomy with ileorectal anastomosis: very rare -Accurate localization is not possible or emergency surgery is required for massive hemorrhage -Significantly higher morbidity and mortality
56
occult lower GI bleed
-Bleeding that is not apparent to the pt -Chronic gastrointestinal blood loss of less than 100 mL/d may cause no appreciable change in stool appearance -Identified by a positive FOBT or iron deficiency anemia in the absence of visible blood loss -In US 2% of men and 5% of women have iron deficiency anemia -Premenopausal women: MC menstruation and pregnancy -GI source is present in 10% of premonopausal women -Men and postmenopausal women: -Upper gastrointestinal tract in 35–55% -Colonic source in 15–30% -Malignancy is present in 10%
57
MC causes of occult bleed are
-Acid-peptic lesions -Colon Neoplasms -Vascular abnormalities -Infections -Medications -Inflammatory bowel disease -Celiac ds
58
evaluation and treatment of occult bleed
-Colonoscopy and EGD- For all adults over age 40–45 years with positive FOBTs or iron deficiency anemia -Remains unexplained in 30–50% of patients -Unexplained bleeding: -Capsule endoscopy -Double balloon enteroscopy- Treatment of vascular ectasias, bleeding ulcers, polyp removal etc
59
lower GI bleed: massive, moderate, occult
-massive bleeding: -pt > 65 with multiple medical problems -hematochezia or bright red blood -hemodynamically unstable -hmg level = 6 -mc due to diverticulosis or angiodysplasias -mortality rate may be as high as 27% -moderate: -any age -hematochezia or melena -hemodynamically stable -benign anorectal, congenital inflammatory, and neoplastic diseases may cause moderate amount of acute or chronic bleeding -occult: -any age -pts present with microcytic hypochronic anemia due to chronic blood loss -congenital, inflammatory, and neoplastic diseases may cause chronic occult bleeding