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GI 1 > Clin Med Diverticulosis/litis & Colon Polyps > Flashcards

Clin Med Diverticulosis/litis & Colon Polyps Flashcards

1
Q

Large Intestine Anatomy

A
  • The Colon and Rectum are considered the Large Intestine
  • U-shaped Tube of several layers
  • Approximately six (6) feet in length
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2
Q

Cecum

A

a pouch like passage that connects ileum to the proximal ascending colon.

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3
Q

Where is the ascending colon located?

A

begins in the right lower quadrant and ascends to the right upper quadrant where it terminates at the hepatic flexure.

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4
Q

Where is transverse colon?

A
  • Transverse colon is situated across the upper abdomen.
  • Starts at the hepatic flexure and ends at the splenic flexure.
  • Mid transverse colon may sag as low as the umbilicus.
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5
Q

Which part of the colon is retroperitoneal?

A

Ascending colon

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6
Q

Which part of the colon is peritoneal?

A

Transverse colon

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7
Q

Where is descending colon? Is it retro or peritoneal?

A
  • left side of abdomen

- retroperitoneal

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8
Q

Sigmoid colon characteristics

A
  • S-shaped
  • Last part of the colon.
  • Lies in the pelvis about 40 cm long
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9
Q

The gastrointestinal tract ends with…

A

Rectum – 6” long

Anus = exit

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10
Q

Define diverticulum

A

Saclike protrusion in the colonic wall that develops as a result of herniation of the mucosa and submucosa through the muscularis propria, through points of weakness in the muscular wall of the colon

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11
Q

Define diverticular disease

A
  • symptomatic and asymptomatic disease with underlying pathology of colonic diverticula
  • Diverticulosis is an acquired disease
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12
Q

Population affected by diverticular disease

A
  • In the US, < age 40 uncommon
  • Up to 50% of the population by age 60; 70% by age 80
  • Mean age at presentation of the disease is 59 years
  • More common with Western diet (aka low fiber)
  • Dubbed a “disease of Western Civilization”
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13
Q

Diverticular disease incidence/epidemiology

A
  • Prevalence among females and males is similar (males tend to present at a younger age)
  • In Western countries: left-sided, in Asia: right-sided
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14
Q

What are the 6 parts of diverticular disease pathophysiology?

A
  1. Segmentation
  2. Protrusion
  3. Mychosis
  4. Colonic wall changes
  5. Chronic inflammation
  6. Dietary fiber deficiency
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15
Q

Pathogenesis - Segmentation

A
  • Contractions of the circular muscles of the colon produces a closed segment of colon with increased intraluminal pressure.
  • Elevated intraluminal pressures may ultimately result in herniation of the mucosa and submucosa at sites of weakness
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16
Q

Pathogenesis - Protrusion

A

Protrusion occurs in weak areas of the bowel wall where blood vessels (vasa recta) penetrate through the muscularis propria

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17
Q

Pathogenesis - Mychosis

A

Myochosis (thickening of muscle layer and resultant lumina narrowing) is seen in most patients with sigmoid diverticula.

  • -Results from increased deposition of collagen and elastin within the muscle
  • -Also decreases the resistance of the colon wall
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18
Q

Pathogenesis - Colonic Wall Changes

A
  • With age, tensile strength of the collagen and muscle fibers of the colonic wall decreases
  • -Contribute to the creation of more distensible muscle fibers
  • With age, collagen fibers in the left colon become smaller and more tightly packed.
  • -Lower colonic compliance in the sigmoid and descending colon
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19
Q

Pathogenesis - Chronic Inflammation

A
  • Chronic low grade inflammation - Segmental colitis.
  • Inflammatory process that is localized to the portion of the colon with diverticula, sparing the rectum and right colon.
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20
Q

Pathogenesis - Dietary Fiber Deficiency

A
  • Fiber binds water and salt in the colon, leading to bulkier and more voluminous stools.
  • -Therefore, fiber decreases the frequency of contractions and prevents an exaggerated form of segmentation
  • Dietary fiber also influences growth and maintenance of colonic cellular function
  • -deficient diet increases the chances of intense, more frequent segmentation, thus predisposing to herniation of mucosa by allowing isolated increases of intraluminal pressure
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21
Q

Define diverticulosis

A
  • Diverticulosis refers to presence of one or multiple diverticula and generally implies an absence of symptoms.
  • Often incidental finding and no further w/u.
  • Approximately 80-85% patients with diverticula are asymptomatic.
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22
Q

Symptomatic diverticular disease is characterized by

A

attacks of (LLQ) abdominal pain without evidence of inflammatory process

  • -Colicky pain, often relieved by passing stool or flatus.
  • -Often precipitated by eating
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23
Q

Other symptoms found with symptomatic diverticulosis

A
  • Bloating, nausea, irregular bowel movements (intermittent diarrhea or constipation – MC)
  • Bleeding alone can sometimes be the only sign of diverticulosis!
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24
Q

Symptomatic diverticulosis on physical exam

A
  • fullness or tenderness to LLQ with possible voluntary guarding on exam
  • No abnormal vital signs, such as tachycardia or fever (which would indicate an inflammatory/infectious process)
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25
Q

Imaging/Diagnosis - Symptomatic Diverticulosis

A
  1. Barium enema - will demonstrate the presence, localization, and number of diverticula.
  2. Colonoscopy is the preferred diagnostic study to r/o other causes that are on DDx, such as IBD, colorectal cancer, and ischemic colitis.
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26
Q

When is colonoscopy contraindicated?

A
  • can be difficult to perform d/t narrowing of the colonic lumen and possible colonic fixation from fibrosis.
  • in patients in whom acute diverticulitis is suspected, d/t increased risk of colonic perforation.
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27
Q

Treatment/Management – Diverticulosis

A

-Therapies used to treat uncomplicated diverticular disease include fiber-rich diets, nonabsorbable antibiotics, mesalazine, probiotics, and prebiotics.

Note: Nothing encourages regression of the diverticuli.

28
Q

Treatment/Management: Fiber - Diverticulosis

A
  • Shortens gut transit time, reduces intracolonic pressure and helps with constipation.
  • Recommended daily fiber intake for adults is 20–35 g/day
  • High fiber foods – whole grain breads/cereals, fresh fruits and vegetables, beans
  • Fiber supplements available contain either soluble fiber (psyllium, ispaghula, calcium polycarbophil) or insoluble fiber (corn fiber, wheat bran)
29
Q

Treatment/Management: Non-Absorbable Antibiotics

A

Rifaximinis a broad-spectrum antibiotic (80 to 90%remains within the gut)

30
Q

Treatment/Management: Mesalazine

A
  • Anti-inflammatory drug that acts topically on the gut mucosa
  • May help symptoms related to chronic mucosal inflammation
31
Q

Treatment/Management: Probiotics

A
  • Probiotics contain microorganisms with the goal to reestablish the normal bacterial flora (BifidobacteriaandLactobacilliare used most frequently)
  • Normal bacterial flora may be altered by slowed colonic transit and stool stasis.
  • Theorized that reestablishing normal gut flora may lead to symptomatic improvement.
32
Q

Treatment/Management: Prebiotics

A
  • substances that promote the growth and metabolic activity of beneficial bacteria, especially BifidobacteriaandLactobacilli.
  • Frequently indigestible complex carbohydrates.
  • Bacteria ferment these substances, leading to a more acidic luminal environment, which suppresses the growth of harmful bacteria.
  • -Substances shown to promote the growth ofBifidobacteriaandLactobacilli- psylliumfiber,lactulose, fructose, oligosaccharides, germinated barley extracts, and inulin
33
Q

Acute Diverticulitis results from…

A

Results from the micro- or macroperforation of a diverticulum, resulting in anything from subclinical inflammation to feculent peritonitis

34
Q

Acute Diverticulitis Characteristics

A

-Male predominance younger than 45 years; equal distribution between 45 and 54; female predominance after the age of 54.

35
Q

Pathogenesis – Acute Diverticulitis: Elevated Colonic Pressure

A
  • Erosion of the diverticular wall d/t increased intraluminal pressure or thickened/congealed food particles.
  • Leads to inflammation and focal necrosis, with resultant perforation of the thin-walled diverticulum.
36
Q

Pathogenesis – Acute Diverticulitis: Changes in Bacterial Flora

A
  • Altered microbial composition within the gut may impair the mucosal barrier, resulting in chronic low-grade inflammation.
  • Growth ofBifidobacteriais promoted by soluble fiber, the fermentation of which leads to the generation of short-chain fatty acids, the preferred energy source for colonocytes.
  • -The increased production of short-chain fatty acids may aid in maintaining the colonic barrier.
37
Q

Which drug class is associated with acute diverticulitis and perforation? Mechanism?

A
  • NSAIDs

- Postulated to be d/t decreased prostaglandin synthesis and direct topical mucosal damage and irritation.

38
Q

What role do prostaglandins play in the colon?

A

Prostaglandins aid in maintaining colonic mucosal barrier by stimulating mucin and bicarbonate secretion and increasing mucosal blood flow. (NSAIDs decrease these)

39
Q

Other role of NSAIDs in acute diverticulitis

A

NSAIDs are weak acids that may denude epithelial cells, resulting in increased mucosal permeability, ulceration, and the translocation of bacteria and toxins

40
Q

Pathogenesis - Diet (Acute Diverticulitis)

A
  • Diet low in fiber may not only predispose to formation of diverticula, but may also predispose to the development of diverticulitis.
  • By increasing stool weight and water content, fiber helps reduce colonic segmentation pressures, which may protect against perforation.
41
Q

What role does red meat play in acute diverticulitis?

A

Heterocyclic amines, products of cooking meat, have been associated with apoptosis of colonic epithelial cells - may predispose to perforation.

42
Q

Pathogenesis - Perforations (Acute Diverticulitis)

A
  • After micro-perforation, infection contained by pericolonic fat, mesentery and/or adjacent organs.
  • -Localized area of infection/inflammation occurs.
  • Macro-perforation – infection less restricted.
  • -Peritonitis or pericolic abscess can occur.
  • If septic process erodes into adjacent structures, results in fistula formation.
43
Q

Clinical Findings – Acute Diverticulitis

A
  1. LLQ pain (MC complaint) - gradual onset. It is constant, with intermittent exacerbations
  2. Fever
  3. Leukocytosis
  4. Nausea and vomiting (20–62%)
  5. Constipation (50%)
  6. Diarrhea (25–35%)
  7. Urinary symptoms (10–15%)
44
Q

Acute Diverticulitis on Physical Exam

A
  • Tenderness in the LLQ, with a tender mass being present in 20% (possible guarding and rebound tenderness)
  • Tenderness in the RLQ - from either a large sigmoid loop or from right-sided diverticulitis.
  • Fever
  • Diffuse tenderness suggests free perforation and peritonitis.
  • Abdominal distention and hypoactive bowel sounds may be present if an ileus has developed.
  • In free perforation, hemodynamic instability may develop, along with a rigid, distended abdomen
45
Q

Lab Findings – Acute Diverticulitis

A
  1. Leukocytosis most common.
    - -Marked leukocytosis suggestive of peritonitis or abscess.
  2. Liver function tests are usually normal.
  3. Serum amylase - normal or mildly elevated.
    - -If amylase elevated, suggestive of possible peritonitis or perforation.
46
Q

Imaging Studies – Acute Diverticulitis

A
  1. Plain radiograph normal except with ileus, bowel obstruction or larger perforation
  2. CT - radiographic test of choice for diagnosing diverticulitis.
47
Q

Which forms of imaging are no longer recommended for acute diverticulitis?

A
  1. Barium enema – no longer recommended d/t risk of extravasation of contrast material if perforation.
  2. Rigid proctoscopy, flexible sigmoidoscopy, and colonoscopy are relatively contraindicated (required air insufflation can unseal or worsen a perforation!)
48
Q

Outpatient Treatment – Acute Diverticulitis

A

If patient has uncomplicated case & is stable:
1. Bowel reset and antibiotics
(to cover gram-negative rods and anaerobes - Metronidazole + Quinolone; Metronidazole + Trim-Sulfa; Augmentin)
2. Clear liquid diet, with slow advancement of the diet.

49
Q

Inpatient Treatment – Acute Diverticulitis

A

considered for patients with more severe presentations, older pts, inability to tolerate oral intake, or comorbid illnesses:

Bowel rest, IV fluids, and IV antibiotics

50
Q

Antibiotics for inpatient acute diverticulitis

A
  1. Metronidazole OR Clindamycin PLUS Aminoglycoside (Gentamicin or Tobramycin or Aztreonam) or Third-generation Cephalosporin (Ceftriaxone, Ceftazidime, Cefotaxime)
  2. Alternatively – IV Second generation Cephalosporin (Cefoxitin, Cefotetan)
  3. Alternatively – IV Ampicillin-Sulbactam, Ticarcillin-Clavulanate
51
Q

Complicated Diverticular Disease - Abscess

A

when pericolic tissues fail to control spread of inflammatory process.

  • High fever, leukocytosis or both despite adequate trial of appropriate antibx.
  • Localized peritonitis and possible tender mass on exam
52
Q

Complicated Diverticular Disease - Fistula

A

abscesses can progress to this between colon and surrounding structures.

  • Bladder (most common esp men), cutaneous, vaginal.
  • Passage of stool through the skin or vagina or the presence of stool or air in the urinary stream (pneumaturia).
  • -Colovaginal fistulas more common in women s/p hysterectomy
53
Q

Complicated Diverticular Disease - Intestinal Obstruction

A

caused by adhesions, luminal narrowing from inflammation or compression by abscess.

  • Severe abdominal distention with nausea and vomiting.
  • Generally self-limited with conservative tx, but persistent may require endoscopic or surgical techniques.
54
Q

Complicated Diverticular Disease - Perforation with peritonitis

A

increases mortality rate as high as 35% and needs urgent surgical intervention.

  • -Diffuse peritonitis - generalized tenderness, involuntary guarding, or decreased or absent bowel sounds.
  • -Linked with NSAID, and maybe glucocorticoid steroid use.
55
Q

Uncomplicated vs. Complicated Diverticular Disease

A

Uncomplicated:

  • abdominal pain
  • fever
  • leukocytosis
  • anorexia/obstipation

Complicated:

  • abscess
  • perforation
  • stricture
  • fistula
56
Q

Diverticular Hemorrhage

A

Most common cause of major lower GI bleed, yet only 15-20% of patients with diverticulosis will have gastrointestinal bleeding.
*At times first (and only) sign of diverticular disease!

57
Q

Risk of Diverticular Hemorrhage

A

Increased risk if hypertensive, have h/o atherosclerosis, and regularly use aspirin and NSAIDs.

58
Q

Diverticular Hemorrhage – Imaging

A

Colonoscopy and angiography (diagnostic and therapeutic – can cauterize, vasoconstrict, etc.), and nuclear bleeding scans (diagnostic only).

  • 75–90% of patients, bleeding stops spontaneously.
  • Surgery required when medical management not successful!
59
Q

Colon Polyps

A

Considered a cancer precursor - majority of colorectal cancers are believed to arise within benign adenomatous polyps

60
Q

Colon polyps characteristics

A

-They can be symptomatic or asymptomatic, pedunculated or sessile, and range in size from millimeters to many centimeters in diameter

+/- 10 yrs time interval to transition to invasive cancer

-Removal of these precursor adenomatous polyps decreases the risk for lethal colorectal cancer significantly!

61
Q

National polyp study predictors for development of future advanced adenomas or cancers as High-Risk Adenomas (HRAs):

A

(1) three or more adenomas,
(2) adenoma size greater than 1 cm, and
(3) adenoma with villous features or high-grade dysplasia

62
Q

Management of colon polyps

A

Current recommendation is surveillance colonoscopy in 3 years!

63
Q

Familial Adenomatous Polyposis

A
  • Hundreds to thousands of adenomatous polyps in the colon.
  • Nearly 100% risk of developing CRC by middle age if affected colon is not surgically removed.
  • Autosomal-dominant inheritance, but 30% of cases emerge as de novo gene mutation.
64
Q

When is familial adenomatous polyposis discovered?

A

Second or third decade of life- usually discovered during endoscopic evaluation for bleeding or diarrhea, or during routine screening in individuals with a known family history.

65
Q

What other malignancies are associated with familial adenomatous polyposis?

A

Extracolonic malignancies associated with papillary thyroid cancer, adrenal carcinomas, and central nervous system tumors.

66
Q

When should you begin screening for familial adenomatous polyposis?

A

Age 11.

GI 1 (16 decks)

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