Chronic GI and GI Bleeds Flashcards

1
Q

Iron deficiency anemia in __ or __ should make you consider colon cancer with GI bleeding.

A

Iron deficiency anemia in a man or a post-menopausal woman should make you consider colon cancer with GI bleeding.

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2
Q

R sided vs L sided colon cancer presentations

A
  • R sided: Stool is still loose and fluid, so there is no obstuction. Rather, these will present with bleeding or anemia
  • L sided: Stool is firm and obstructable. Will present with constipation or with intermittent constipation and diarrhea.
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3
Q

Low-risk polyps

A
  • Small
  • Pednuculated
  • Biopsy shows tubular adenoma
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4
Q

High-risk polyps

A
  • Large
  • Sessile (no stalk)
  • Villous
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5
Q

Colon cancer Tx

A
  • CT for staging
  • Surgical resection where appropriate
  • FOLFOX/FOLFIRI + rad, + bevacizumab if metastatic
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6
Q

When to come back for endoscopy w/ common endoscopy findings

A
  • Nothing: 10 y
  • Benign polyp: 5 y
  • Carcinoma-in-situ or dysplasia: 1-3 y depending upon features
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7
Q

Fistulotomies in Crohn’s

A
  • Indications: Refractory to medical therapy OR patient wants it done (elective)
    • HIGHLY likely to recur in Crohn’s – this is why it is not routinely done.
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8
Q

Internal hemorrhoids ___, but don’t ___.

External hemorrhoids ___, but don’t ___.

A

Internal hemorrhoids bleed, but don’t hurt.

External hemorrhoids hurt, but don’t bleed.

This is easy to remember if you recall that the more external portion of the rectum will be somatically innervated.

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9
Q

Diagnosing and treating hemorrhoids

A
  • Dx is clinical.
    • If you can see them, you’re done
    • If you can’t see them (suspected internal), do anoscopy
    • DO NOT do a flexible sigmoidoscopy. Too invasive and too far.
  • Tx:
    • Initial management: Conesrvative w/ Sitz baths, preparation H cream
    • If above fails:
      • Internal: Banding
      • External: Resection
  • Note: We don’t resect internal hemorrhoids because they may scar and obstruct the rectum.
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10
Q

Anal fissure

A
  • Path: Tight sphincter
  • Pres: Pain on defecation, lasts for hours. Patients often avoid stooling, poop gets dehydrated, when they eventually do have to poop it is abbrasive to the bowel wall.
  • Dx: Clinical
  • Tx:
    • Conservative: Nitroglycerin paste, Sitz baths
    • Lateral internal sphincterotomy
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11
Q

Anal cancer

A
  • Essentially cervical cancer of the anus
  • Pathology: HPV, squamous cell carcinoma
  • Pres: In someone who has anal receptive sex, increased risk in MSM and those w/ HIV
    • People who have HIV must be screened w/ Pap
  • Dx: Anal Pap followed by biopsy
  • Tx: Nigro protocol of chemo and radiation.
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12
Q

Pilonidal cyst

A
  • Path: Abscessed hair follicle
  • Pres: Congenital cyst. Hair follicle grows into it. Leads to abscess.
  • Dx: Clinical
  • Tx: Incision and drainage. Then, take to OR to resect.
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13
Q

Indications for colectomy in ulcerative colitis

A
  • If on presentation:
    • Toxic megacolon
    • Colonic perforation
    • Life-threatening GI hemorrhage
  • Otherwise, only if refractory to medical therapy.
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14
Q

“Resectable” Pancreatic adenocarcinoma criteria

A
  • No involvement of arteries
  • < 180 degree involvement of veins
  • No metastases
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15
Q

Division of upper and lower GI bleeds

A

Ligament of Treitz

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16
Q

Melena means that. . .

A

. . . the blood was in the GI tract for at least 14 hours

May be upper GI, maybe not

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17
Q

Hematochezia usually indicates. . .

A

. . . lower GI bleed OR profuse upper GI bleed (ruptured varix, etc)

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18
Q

Workup for GI bleed with tachycardia

A
  • 2 large bore IV needles
  • Blood labs (CBC, CMP, coags)
    • Follow-up with q4h Hgb
  • Blood type, screen, crossmatch
  • Start a PPI (stabilizes clot by raising pH of the gastric lumen)
  • IF CIRRHOTI: Octreotide + Abx
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19
Q

It takes __ for Hgb to adjust to acute blood loss

A

It takes 12-17 hours for Hgb to adjust to acute blood loss

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20
Q

Dieulafoy lesion

A

Vein abberantly grows to flow through the mucosa, then develops a pinpoint breech in the vessel wall through which

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21
Q

While most diverticulosis occurs in ___, a bleeding diverticulosis is more likely to be ___.

A

While most diverticulosis occurs in the sigmoid colon, a bleeding diverticulosis is more likely to be on the right side.

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22
Q

Most sensitive and specific test for GI bleed

A

Angiography

BUT, they need to be bleeding more than 1 mL / minute.

This is used for patients who are unstable and actively bleeding and for whom initial workup has failed.

Usually preceded by CT-A so that the lesion location is relatively known, then angiography can be used diagnostically and therapeutically

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23
Q

Tagged RBC scan

A

Most sensitive test for GI bleed, even if < 1 mL/minute.

Tag is with Tc.

Problem is that it is nonspecific: It does not show if he is bleeding from a specific area, more like “he’s bleeding vaguely in the LUQ”

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24
Q

Friends mnemonic for fistula risk factors

A
  • Foreign body
  • Radiation
  • Infection
  • Epithelialization
  • Neoplasm
  • Distal obstruction
  • Steroids
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25
Q

Bladder rupture

A
  • Another possibility in extreme blunt pelvic trauma
  • Often presents as severe lower abdominal/pelvic pain and frank blood upon Foley catheterization
  • Dx: Retrograde cystography
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26
Q

Most common cause of lower GI bleed

A

Diverticulosis

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27
Q

In hemodynamically unstable patients with profuse GI bleed and negative EGD, ___ may be preferred over colonoscopy.

A

In hemodynamically unstable patients with profuse GI bleed and negative EGD, angiography may be preferred over colonoscopy.

Since it can be interventional through microvascular embolization to achieve hemostasis. Colonoscopy is too slow.

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28
Q

Risk factors for AV malformation bleeds

A
  • Advanced age (> 60)
  • End-stage renal disease
    • In ESRD, ~30% of lower GI bleeds are due to angiodysplasia
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29
Q

Sinistral portal hypertension

A
  • Etiology: Splenic vein thrombosis
  • Causes portal hypetension only distal to the splenic vein. This manifests as isolated gastric varices arising from the short gastric veins.
  • Treatment is with splenectomy
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30
Q

ATLS classes of hemorrhagic shock severity

A
  • Class I: Well compensated
    • Vitals basically normal
    • Up to 15% blood loss (750 mL in average adult)
  • Class II: Moderate blood loss
    • Slight tachycardia, normal SBP, elevated DBP
    • Up to 30% blood loss (750-1500 mL in average adult)
  • Class III: Severe blood loss
    • Tachycardia to 120 bpm associated with hypotension
    • Often anxious, diaphoretic
    • Up to 40% blood loss (1500-2000 mL in average adult)
  • Class IV: Life-threatening blood loss / hemorrhagic shock
    • Tachycardia to 140 bpm associated with severe hypotension
    • Often unresponsive with decreased mentation
    • >40% blood loss (>2000 mL in average adult)
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31
Q

If a patient with acute upper GI bleed presents with hematemesis, ___ is indicated

A

If a patient with acute upper GI bleed presents with hematemesis, NG tube placement is indicated

This will prevent aspiration on blood

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32
Q

If you’re going to use epinephrine to stop an upper GI bleed. . .

A

. . . you have to combine this with a second treatment modality.

Typically coagulation therapy or clipping. Epinephrine is great for achieving that initial hemostasis, but it doesn’t last.

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33
Q

A patient has an upper GI bleed treated with therapeutic upper endoscopy.

If they start bleeding again, what is the next step?

If they bleed again after that, what is the next step?

A

If they bleed again, they just get another upper endoscopy. Always give upper endoscopy a second chance.

If they bleed a third time, now it’s time to consult IR or surgery.

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34
Q

___ improves gastric motility and visualization during endoscopy

A

Predosing with IV erythromycin improves gastric motility and visualization during endoscopy

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35
Q

ED discharge criteria without need for endoscopy for a patient who presents with uncomplicated upper GI bleed

A
  • SBP > 110 mmHg
  • HR < 100 bpm
  • Hgb > 13g/dL (men) or >12g/dL (women)
  • BUN < 18.2
  • Absence of melena, syncope, heart failure, liver disease
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36
Q

Ideal fluids to resuscitate a patient with variceal-related upper GI hemorrhage

A

Blood products in a ratio of 1:1:1

If not available, colloid is preferred over crystalloid (due to the risk of hepatorenal syndrome)

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37
Q

PPI protocol for nonvariceal upper GI bleed

A
  • Done to minimize contribution of stomach acid to the problem, particularly for suspected PUD or pill-induced irritation
  • 80 mg omeprazole IV bolus followed by 8 mg/hr for 72 hours
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38
Q

Antibiotic ppx for a patient presenting with variceal bleed

A
  • Third generation cephalosporine (eg, ceftriaxone, cefotaxime, or ceftazidime) OR flouroquinolone
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39
Q

Patient presents in fulminant upper GI bleed. No time for an endoscopy. They are unstable. What do you do?

A
  • Place a Sengstaken-Blakemore tube
    • Type of balloon tamponade device
    • Allows temporary control of bleeding, but not for more than 24 hours
    • Purely a temporizing measure
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40
Q

Definitive therapies for variceal hemorrhage

A
  • Therapeutic endoscopy
  • TIPS
  • Self-expanding intraesophageal stent placement
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41
Q

What is the best prophylactic beta blocker to prevent variceal hemorrhage and why?

A

Carvedilol

It is nonselective, enabling it to also act as an alpha-1 blocker and induce vasodilation of the portal venous system.

Typically used over the old standard, propranolol, nowadays

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42
Q

Red Wale Sign

A

Finding of linear red streaks on an esophageal varix. Sometimes called “varices of the varix.”

Represent a thinned portion of the varix wall. Suggets impending GI variceal rupture and need for urgent prophylaxis.

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43
Q

For cirrhotic patients or patients with other etiology of portal hypertension, surveillence endoscopy is recommended every __ with no Hx of varices or every __ with Hx of varices.

A

For cirrhotic patients or patients with other etiology of portal hypertension, surveillence endoscopy is recommended every 2-3 years with no Hx of varices or every year with Hx of varices.

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44
Q

Ppx for varices in patients with portal HTN

A
  • Done for:
    • ​Grade II or III varix on screening endoscopy
    • Presence of Red Wale sign
    • Presence of Red Spot sign
  • Consists of:
    • Propranolol or Carvediolol
    • If the above cannot be tolerated, prophylactic banding
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45
Q

Variceal diameter greater than ___ is associated with a higher risk of variceal bleed

A

Variceal diameter greater than 5 mm is associated with a higher risk of variceal bleed

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46
Q

Ileal brake

A
  • When nutrients enter the ileum, a feedback inhibition occurs which slows bowel peristalsis and delays gastric emptying
    • This enables maximal absorption of nutrients within the ileum
  • Loss of the ileal brake in short gut syndrome results in rapid gastric emptying and decreased intestinal transit time
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47
Q

The complications of TPN

A
  • Catheter-associated complications (infection)
  • Vascular-associated complications (thrombosis)
  • Toxicities of various components (hypercalcemia, hyperkalemia, etc)
  • Liver and biliary effects: cholestasis, liver fibrosis, fatty liver
  • Renal effects: hyperoxaluria and associated nephrolithiasis
  • Osteoporosis
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48
Q

TPN vs PPN

A
  • TPN is by definition delivered centrally, meaning that hyperosmolar solutions may be utilized
  • PPN is by definition delivered peripherally, precluding the use of hyperosmolar solutions. This thereby limits the amount of calories and proteins that may be passed through the catheter.
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49
Q

Workload hypothesis

A

Suggests that delivery of more complex nutrients to the intestinal lumen has beneficial trophic effects on the intestinal remnant in short gut syndrome

For instance, administering polysaccharides is better than administering monosaccharides

50
Q

Pharmacologic therapies for patients with short gut syndrome

A
  • Teduglutide: GLP agonist that increases intestinal absorption and slows gastric emptying and GI transit time
  • Somatropin: Human growth hormone analog. non-GI-tract specific growth stimulant. Drawbacks are excess fluid retention and glucose intolerance.
51
Q

Surgical therapy for SBS

A
  • For selected patients with SBS and poor adaptation and response to medical therapy:
    • Longitudinal gut lengthening
    • Serial transverse enteroplasty
    • Bowel segment reversal
  • For only patients with TPN-related liver insufficiency or history of severe TPN-line complications:
    • Small bowel transplant
    • Small bowel + liver transplant
52
Q

Role of the colon in someone with short gut syndrome

A
  • Absorbs water and electrolyets
  • Converts carbohydrates to short-chain fatty acids and absorbs the fatty acids
53
Q

Gut length associated with short gut syndrome

A

<200 cm of small intestine remaining (~1/3 of original)

54
Q

Most common sources of acute lower GI bleed

A
  • Diverticulosis
  • AV malformation
  • Neoplasm
  • Meckel’s diverticulum (pediatrics/young adults)
  • IBD (young adults)
55
Q

Role of NG tube in suspected lower GI bleed

A

Can be done early on to aspirate and rule out the possibility of upper GI bleed masquerading as lower bleed.

This is useful since treatment of upper GI bleed can be much more rapid in terms of achieving hemostasis.

56
Q

Surgeries assocaited with unique lower GI bleed scenarios

A
  • Prior surgery for GI malignancy
  • Prior abdominal aortic surgery
  • Recent colonoscopy with polypectomy
57
Q

Workflow for lower GI bleed management

A
  1. Stabilize patient
  2. CT with contrast to attempt localization
  3. Colonoscopy if above fails
  4. Tc99-tagged RBC scan if above fails
58
Q

Most important causes of slow, oozing, occult GI bleed

A
  • Malignancy
  • Gatritis
  • Esophagitis
59
Q

Bleed rate detection threshold for CT with IV contrast

A

0.3-0.5 mL/min

60
Q

Bleed rate detection threshold for Tc99-tagged RBC scan

A

0.1 mL/min

However, poorer localization than CT

61
Q

Bleed rate detection threshold for mesenteric angiography

A

0.5-1.0 mL/min

62
Q

Colonoscopy requires ____. Rigid proctosigmoidoscopy does not.

A

Colonoscopy requires sedation. Rigid proctosigmoidoscopy does not.

63
Q

Angiodysplasia

A
  • ie, AV malformations
  • Typically cause low-grade, chronic, self-limiting bleeding, but can present with acute bleed as well
  • Common acquired degenerative vascular condition leading to formation of small, dilated, thin-walled veins in the submucosa
  • Most common in the cecum and ascending colon in those over 60 years old
  • 50% of patients have associated cardiac disease
  • 25% of patients have aortic stenosis
64
Q

If you suspect aorto-duodenal fistula, the appropriate studies are. . .

A

Either CT of upper abdomen or upper GI endoscopy

These procedures cannot be delayed, as these patients are at risk of rapid exsanguination.

Often the initial presentation is with intermittent episodes of “herald bleeds” prior to the development of complete patency of the fistula and exsanguination.

65
Q

Most episodes of upper GI bleed. . .

A

. . . will self resolve

Our work is then to determine the etiology and prevent recurrence by addressing underlying issues

66
Q

When do you need to operate on a patient with ischemic bowel disease?

A
  1. When there is evidence of perforation
  2. When there is transmural necrosis on CT or endoscopy
67
Q

The only concerning types of polyp

A
  • Serrated adenoma / serrated polyp OR villous adenomas
  • Can be considered a pre-cancerous lesion (~15% progress to cancer)
  • Mostly found in R colon
  • More common in females, peak incidence in mid-to-late 70’s.
68
Q

Why does rectal cancer have a much higher rate of recurrence than other colon cancers?

A

Because the rectum is extraperitoneal!

It does not have that nice peritoneal lining to keep it insulated, and is much more likely to invade the surrounding tissue.

69
Q

Where do rectal metastases go?

A

The lung

Think about the venous system

The rectum’s venous supply is to systemic circulation, not to the portal system. So, unlike colon cancers which metastasize to the liver, rectal cancer will metastasize to the lung.

70
Q

Standard therapy for colorectal cancer

A

If local in the colon, surgical treatment alone

If local in the rectum, surgical treatment + adjuvant radiation

If node positive, adjuvant therapy with FOLFOX4 or FOLFIRI

If metastatic, forgo surgery and opt for chemotherapy and biologics

71
Q

Prophylactic surgery for patients with FAP

A

Total proctocolectomy is recommended for FAP patients by age 20-25

72
Q

Chemoprevention of adenomatous polyps

A
  • Sulindac or celecoxib (COX-2 inhibitors) taken chronically
  • Also associated with regression of smaller polyps
73
Q

Role of antibiotics in Crohn’s

A
  • Metronidazole or ciprofloxacin may be used effectively to treat acute intestinal or perianal disease in mild cases
  • Long-term metronidazole mainteane therapy can induce remission in mild Crohn’s disease
  • Think of these as an alternative to 5-ASA
74
Q

Antimetabolites in IBD therapy

A

Main 3 used are azathioprine, 6-mercaptopurine, and methotrexate. Used for moderate to severe disease.

AZT and 6MP are generally preferred to methotrexate due to their less severe side effect profiles, so methotrexate is reserved for those who fail AZT and 6MP.

All can induce bone marrow suppression, nausea, fever, rash, hepatitis, pancreatitis. Methotrexate can also cause stomatitis and pneumonitis.

75
Q

Adenocarcinoma of the small bowel

A

Rare in general population, not too uncommon in Crohn’s

76
Q

Behavioral modification in Crohn’s patients to prevent flareups

A
  • Stop smoking (associated in 50% reduction in recurrences)
  • Avoid NSAIDs
    • Both of the above shown to increase rate of recurrence
77
Q

Crohn’s disease has a wide array of different presentations, however for a given patient. . .

A

. . . the anatomic locations involved remain fairly stable over the course of disease progression

78
Q

A patient who requires one operation for Crohn’s. . .

A

. . . has a ~25% chance of requiring a second at a later date

For this reason, the first surgery shoud be relatively conservative – since you don’t know where the disease will pop up next and you want to avoid short gut syndrome in the long-term.

79
Q

In the setting of Crohn’s disease, a spontaneous enterocutaneous fistula can be initially treated with. . .

A

. . . biologic therapy such as inflixumab or adalimumab.

It turns out that in Crohn’s a good portion of these will self-resolve if you are aggressive in your early management of the IBD. You may be able to spare ~30% of these patients an operation by trialing this conservative management first.

80
Q

Effects of proctocolectomy for UC

A
  • If complete, may cause fecal incontinence
  • Will likely cause chronic diarrhea
  • Eliminates most inflammation and risk of cancer, with the exception of any retained rectum
  • Improves systemic symptoms of UC as well (erythema nodosum, arthritis, eye changes)
81
Q

Radiographic correlate of toxic megacolon

A

Transverse colon > 8 cm in diameter

82
Q

Eye manifestations of IBD

A

Uveitis

Scleritis

Optic neuritis

83
Q

GI manifestations of IBD (apart from IBD itself)

A
  • Primary sclerosing cholangitis
  • Autoimmune hepatitis
  • Pancreatitis
84
Q

Arthritis in IBD

A
  • Three main forms:
    1. Type I peripheral arthropathy: Acute, flares with the colitis
    2. Type II peripheral arthropathy: Chronic, often polyarticular, migratory
    3. Axial arthropathy: Ankylosing spondylitis and sacroiliitis
85
Q

Continent ileostomy / Koch pouch

A
  • Option for preservation of continence in the setting of total proctocolectomy with elimination of internal and external sphinceters and anus
  • Terminal ileum fashioned into pouch with 500-1000 mL volume
  • Emptied via self catheterization
  • Unfortunately, drainage mechanisms often prone to failuire. Rarely done today.
86
Q

Pouchitis

A
  • Inflammation of the J pouch in individuals who have undergone Ileal-J-pouch reconstruction.
  • Happens at least once to 50% of patients who receive this operation.
  • Bacterial overgrowth is a common culprit, and so a course of antibiotics is the first-line therapy
87
Q

Vedolizumab

A
  • anti-α₄β₇ integrin (the mucosal addressin receptor)
  • New biologic used in treatment of UC
88
Q

Diet and diverticulosis

A

Low-fiber, high-fat diets are high risk for development of diverticuli

89
Q

Diverticular phlegmon

A
  • Describes an inflammatory mass related to diverticulitis
  • Clinically and radiographically this appears very simlar to colorectal cancer – so patients with a diverticular phlegmon will need to have colonoscopy to evaluate the area after acute inflammation as resolved
    • Colonoscopies are generally done 4-6 weeks following resolution of diverticulitis.
90
Q

Colovesicular fistula

A
  • Hallmark signs:
    • Pneumaturia, fecaluria, recurrent UTI
  • May be due to a bowel process (Crohn’s, colon cancer, diverticulitis) or a bladder process (cystitis, bladder cancer)
91
Q

Hinchey classification of complicated diverticulitis

A
  • Hinchey I-II (not involving peritonitis) can generally be treated nonoperatively with abx +/- drainage
  • Hinchey III-IV (involving peritonitis) are unlikely to resolve with medical therapy and should proceed to surgical intervention
92
Q

Similar to appendicitis, a classic presentation of uncomplicated diverticulitis may be treated. . .

A

. . . empirically, without obtaining a CT scan

If they fail initial therapy or there is suspicion of complicated diverticulitis, a CT scan is warranted

93
Q

What imaging studies should you definitely not do for a patient with diverticulitis?

A
  • Colonoscopy
  • Barium enema
    • These may increase the pressure in the affected area and worsen disease
94
Q

Physiologic role of hemorrhoids

A
  • Fibrovascular cushions that are normal parts of the anal canal
  • Locatios are right-anterior, right-posterior, and left-lateral
  • Contribute to 15-20% of resting anal pressure
  • Fill with blood upon valsalva in order to help maintain fecal continence
  • Sensory function allows for differentiation of stool consistency (hard, soft, liquidy, firm)
95
Q

Reasons that hemorrhoids might enlarge

A
  • Diarrhea
  • Constipation
  • Obesity
  • Increased intraabdominal pressure
96
Q

Fistula-in-ano

A
  • An anal-to-anal fistula through surrounding tissue
    • May be intersphincteric, transsphincteric, or extrasphincteric
  • Approximately 50% of patients with perirectal abscesses go on to develop fistula-in-ano after abscess resolution (including spontaneous resolution)
  • Often initially addressed with a seton
97
Q

Goodsall rule

A
  • With a transverse line drawn between the anterior half and posterior half of the anus, external openings anterior to this line track straight into the rectum, while posterior openings track curvilinear into the posterior midline
  • Helpful to identify the internal opening of fistulous tracts
98
Q

Seton

A

Loop of plastic or silicone that is placed into a fistula-in-ano. Can be a helpful mechanism of drainage, or can serve as a marker, or cause chronic granulation/fibrosis along the fistula.

Helpful as the initial stage of fistula-in-ano management when subsequent ligation of interphincteric fistula tract (LIFT) procedure is anticipated.

99
Q

Definitive therapy options for fistula-in-ano

A
  • Fustolotomy: Simple unroofing and removal of epithelial lining of a fistula followed by healing by secondary intention.
  • LIFT (ligation of intersphincteric fistula tract) procedure: For treatment of mature trans-sphincteric fistula tracts (6-12 weeks after seton placement). Fistula is incised and then ligated distally and proximally, then excised/unroofed.
100
Q

Why is hemorrhoid banding or ablation an option for internal hemorrhoids, but not external hemorrhoids?

A

Because it induces ischemia, by definition

This would be extremely painful for external hemorrhoids, since they have sensation. Internal hemorrhoids have no sensation, so this is fine.

101
Q

Dentate line

A

Line between rectal mucosa and anal epithelium

Rectal mucosa has no pain sensation, while anal epithelium does. So, above this line is painless, below it is painful.

102
Q

Anal fissure vs hemorrhoids vs fistula-in-ano

A
103
Q

Treatment for fissure-in-ano, hemorrhoids, fistula-in-ano

A
104
Q

Prolapsed hemorrhoids

A

Hemorrhoids are a fairly common cause of rectal prolapse, especially a circumferential mucosal mass.

This form of hemorrhoids would be treated with circumferential stapled hemorrhoidectomy, which accomplishes resolution of the hemorrhoids and increasing structural support in one procedure.

105
Q

Constellation of symptoms for anal fissure

A
  • Severe anal pain, especially with defecation
  • Tear in posterior anoderm
  • Bleeding
  • Increased rectal sphincter tone
106
Q

___ are almost never palpable on digital rectal exam, and everything palpable on digital rectam exam is ___ until proven otherwise.

A

Hemorrhoids are almost never palpable on digital rectal exam, and everything palpable on digital rectam exam is malignant until proven otherwise.

107
Q

A thrombosed external hemorrhoid that does not respond to medical therapy should be treated with. . .

A

. . . excision, NOT INCISION AND DRAINAGE

Excision alone has better outcomes. Drainage is associated with high rates of recurrence.

108
Q

Gardner syndrome

A

Colon cancer

Osteomas

Desmoid tumors

109
Q

Lynch I vs Lynch II

A

Lynch I: Just colon cancer

Lynch II: Colon, stomach, ovarian

110
Q

Turcot’s syndrome

A

Colon cancer

Brain tumors

111
Q

Cowden syndrome

A

Colon cancer/polyps

Breast cancer

Thyroid cancer

112
Q

Gatrointestinal stromal tumor (GIST)

A
  • Sarcoma of the GI smooth muscle
    • Most originate from stomach
    • GI bleed is the most common presenting symptom, often due to tumor necrosis
  • CT will demonstrate a mass circumscribed by mucosa and serosa of the GI tract, often with some central necrosis
  • Specific genetic profiles:
    • KIT GoF mutations (~80% of GISTs)
    • PDGFRA GoF mutations (~6% of GISTs)
    • Some associate with Carney’s Pentad
  • Treatment: Surgical resection with adjuvant or neoadjuvant TKI therapy IF c-Kit POSITIVE (adjuvant generally 1 year duration)
    • TKIs are only effective for c-Kit positive GISTs
113
Q

Carney’s pentad

A
  • Co-occurence of several tumors, often in young women (original Carney’s triad is bolded):
    • GIST
    • Paraganglioma
    • Pulmonary chondroma
    • Esophageal leiomyoma
    • Adrenal adenoma
  • Underlying etiology unclear, considered to be adjacent to the MEN syndromes
114
Q

RTK inhibitors

A
  • Used in treatment of GISTs, CML, and other known RTK GoF mutations in malignancy
  • First-line: imatinib
  • Second-line: sunitinib
  • Third-line: regorafenib
115
Q

Complications of recurrent/chronic diverticulitis

A
  • Fibrosis of bowel
  • Fistulization
  • Cancer
116
Q

With chronic fecal impaction, you are most at risk for perforation of the. . .

A

. . . cecum

~9 cm, it’s a real risk

~11 cm, perforation is imminent

117
Q

Stercolitis

A
  • Chronic irritation of the rectum due to distension from chronic fecal impaction
    • Risk of tissue ischemia, perforation
  • Often in elderly patient on anticholinergic, presenting with encopresis and lower left abdominal pain in the context of chronic constipation
118
Q

Treating Ogilvie syndrome

A

Try stool softeners, pro-motility agents first

If that doesn’t work, neostigmine

If you give neostigmine to someone who actually had a true obstruction, you might cause perforation. Be sure they have TRUE Ogilvie’s

119
Q

Patients who DO get abx following rectal abscess drainage

A
  • Diabetic
  • Systemic illness (fever, chills, sepsis)
  • Immunocompromised
  • Prophylactically for high-risk endocarditis
120
Q

H. pylori and stomach cancers

A

Treating H. pylori can cure 70% of cases of H. pylori-associated MALT lymphoma.

However, it cannot cure H. pylori-associated gastric adenocarcinoma

121
Q

Surveillance after colon resection for colon cancer

A
122
Q

Risk factors for colon cancer

A

Risk derived from obesity and T2DM is thought to be due to hyperinsulinemia, which increases circulating ILGF-1 levels and in turn inhibits colorectal epithelial apoptosis.