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Other GI Flashcards

1
Q

What is the most common site for lymphoma in the gastrointestinal tract?

A

The stomach is the most common site for all GI lymphoma.

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2
Q

Is primary GI lymphoma common?

A

Very rare; usually a manifestation of diffuse nodal disease.

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3
Q

What is a distinguishing feature of lymphoma in the GI tract?

A

Always has significant lymphadenopathy.

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4
Q

What conditions are associated with GI lymphoma?

A

Celiac sprue, Crohn’s disease, Wegner’s, SLE, and AIDS.

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5
Q

What type of lymphoma is most common in the GI tract?

A

Most commonly non-Hodgkin lymphoma (NHL) of B cell type; almost never Hodgkin lymphoma.

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6
Q

What is the diagnostic method for GI lymphoma?

A

Abdominal CT and node sampling.

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7
Q

Treatment for GI lymphoma?

A
  • Treatment for GI lymphoma controversial. Some say GI lymphoma = sign of systemic disease requires chemo
  • However, non-metastatic colonic/small bowel lymphoma involving can be treated with surgery 1st
  • Non-metastatic colon and small bowel lymphoma  resection with lymphadenectomy then CHOP-R
  • If 1st or 2nd portion of duodenum, gastric, anal lymphoma, pancreatic, thyroid, treatment = CHOP-R
  • Metastatic disease  CHOP-R
    Chemo for non-hodgkins lymphoma – CHOP-R – cyclophosphamide, doxorubicin, vincristine, prednisone, rituximab
    40% 5-year survival rate
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8
Q

What are the symptoms of typhoid enteritis in children?

A

RLQ pain, bloody diarrhea, fever, maculopapular rash, and leukopenia. Large mesenteric LN

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9
Q

What is the treatment for typhoid enteritis?

A

Bactrim.

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10
Q

What are plica circulares?

A

They are structures present on all small bowel, wrapping circumferentially around the bowel.

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11
Q

What are plicae semilunares?

A

Transverse bands that form haustra along the colon.

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12
Q

What are taeni coli?

A

Three bands that run longitudinally along the colon. At rectosigmoid junction they become broad

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13
Q

What is a true diverticulum?

A

Meckel’s diverticulum and traction diverticula in the esophagus.

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14
Q

What is Meckel’s diverticulum?

A

A true diverticulum resulting from failure of closure of the omphalomesenteric duct (persistent vitelline duct)

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15
Q

What is the most common type of tissue found in Meckel’s diverticulum?

A

Gastric mucosa is the most common and can lead to symptoms like bleeding.

Pancreas tissue: diverticulitis

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16
Q

What is the Rule of 2’s regarding Meckel’s diverticulum?

A

2 feet from the IC valve, twice as common in males, 2% of the population, 2% symptomatic, presents in the first 2 years of life.

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17
Q

What is the most common cause of painless lower gastrointestinal bleeding in children?

A

Meckel’s diverticulum.

Adults present with obstruction

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18
Q

Meckel’s treatment

A

If bleeding is a symptom (ileum ulcer) = gastric mucosa = ulcer is on the small bowel not in meckel’s  No longer advocated to perform segmental resection of bowel. Diverticulectomy is new standard.
Dx: Meckel’s Tc scan
Tx:
Any Meckel’s found incidentally on imaging without symptoms  do nothing
Asymptomatic found incidentally intra-op don’t resect unless:
- Found in children  diverticulectomy
- Palpable abnormality  formal resection
- > 2 cm  formal resection
Symptomatic – bleeding, hernia, SBO, diverticular inflammation
- Surgery for all
Perform diverticulectomy unless any below, these need formal resection
Need segmental resection for:
* No longer supported to performed segmental resection for bleeding
* Complicated diverticulitis (perf)
* Palpable abnormality at base
* Inflammation/diverticulitis at base
* Large diameter base > 2 cm or Neck > 1/3 diameter of normal bowel. Concern for narrowing lumen with diverticulectomy

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19
Q

What is a carcinoid tumor?

A

A neuroendocrine tumor, most commonly found in the small bowel.

Will see Fibrosis and desmoplastic reaction on CT
Associated with tricuspid regurg  R heart failure
Causes low Niacin (B3) levels so can cause Pellagra diarrhea, dermatitis (rough scaly skin, glossitis, angular stomatitis), dementia, and/or hypoalbuminemia.
Tumor size correlates with likelihood of metastasis, larger the size, more likely it will metastasize
Octreotide scan best for localization
Will also stain positive for synaptophysin
Pathology: Kulchitsky cells (neural crest cells)
Site of highest metastasis rate and highest carcinoid syndrome rate  ileum
Site of highest 5YS 95% - Appendix
If patient has carcinoid syndrome with liver mets  debulking as much tumor as possible is a good treatment. All need cholecystectomy.

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20
Q

What is the most common site for carcinoid tumors?

A

Ileum, followed by rectum and appendix.

MC appendix tumor
MC tumor of small bowel

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21
Q

What are the symptoms associated with carcinoid syndrome?

A

Facial flushing, asthma, hypotension, and diarrhea.

Facial flushing - kallikrein
Asthma and hypotension – bradykinin
Diarrhea - Serotonin

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22
Q

What is the best test for screening carcinoid tumors?

A

Chromogranin A is best test for screening, recurrence, and response to treatment

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23
Q

What is the gold standard test for detecting metastatic carcinoid?

A

24-hour urinary 5-HIAA test is highly specific for detecting metastatic carcinoid and considered the gold standard test to establish the diagnosis
- Not sensitive for detecting non-functional carcinoid
- Not all carcinoid will produce this!!!

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24
Q

What is the treatment for carcinoid syndrome?

A

Octreotide – Used to for both Metastatic carcinoid AND carcinoid syndrome
- If has carcinoid syndrome and operating, need to start octreotide before surgery
- If planning on starting octreotide, patient will need a cholecystectomy (increase stones) will especially need it if liver mets (plan for ablation or embolization)

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25
Q

What is the treatment for gastric neuroendocrine tumors?

A

Nonfunctional: no carcinoid syndrome here
Work up: EGD with Bx, Gastrin level, Gastric pH test
- Need to stop PPI before obtaining gastrin level, otherwise will have elevated gastrin level. Ok to be on H2 blocker.

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26
Q

What is the treatment for Type I gastric neuroendocrine tumors?

A

Type I - MC type 80%. pernicious anemia/chronic atrophic gastritis. High gastrin levels, pH >4.
Tx: If < 2 cm  endoscopic resection or just follow up with EGD surveillance
Tx: If > 2 cm or multifocal  antrectomy

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27
Q

What is the treatment for Type II gastric neuroendocrine tumors?

A

Type II 5% – associated with Zollinger Ellenson. Has small risk of cancer. High gastrin levels, pH < 2.
- Tx: Localize gastrinoma usually EGD resection is sufficient
- Also need to work up for MEN I

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28
Q

What is the treatment for Type III gastric neuroendocrine tumors?

A

Type III – High malignant potential. Normal gastrin level. Often present with mets. Need octreotide scan to stage.
- Tx: Should be treated like gastric CA. Partial/total Gastrectomy with lymphadenectomy
Biopsies should be stained for Chromogranin A and synaptophysin
Get Serum gastrin and Chromogranin A
Endoscopic ultrasound is preferred for assessing both tumor size and depth of penetration

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29
Q

What are the main contributing factors to short gut syndrome?

A

Loss of bowel, particularly the terminal ileum, and hypersecretion of acid.

-hypersecretion of acid decreases pH -> increases intestinal motility-> interferes with fat absorption -> steatorrhea

Sudan red stain checks for fecal fat
Complications of short gut: nephrolithiasis (hyperoxaluria), cholelithiasis (low bili reabsorption), gastric acid hypersecretion (transient), bacterial overgrowth
>180 cm of SB Don’t require TPN
90 cm require TPN for at least a year generally
< 60 cm require TPN for life

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30
Q

Treatment for short gut syndrome?

A

Tx: Antidiarrheal + fluid and electrolyte management + TPN = first line
- Loperamide, diphenoxylate, PPI/H2blocker, b12/FOLATE
- High carb, high protein, low fat diet (Medium chain fatty acid is ok) rich in glutamine
- H2 blocker and PPI  b/c resection of small bowel  causes hypergastrinemia, increases acid, decreases digestion
- Growth hormone and teduglutide (GLP-2 analog) has pro-absorptive effects on intestines
- Octreotide use is off label used to treat diarrhea, should not be used long term. Causes steatorrhea, and gallstones
- Cholestyramine tx for nephrolithiasis and helps with diarrhea, reduces fat

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31
Q

What are the indications for intestinal transplant?

A

Cholestatic liver disease (cirrhosis) from TPN, repeated episodes of bacteremia from central lines, and no availability of veins for TPN (recurrent thrombosis/stenosis).

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32
Q

Appendix mucinous neoplasm

A

2nd MC tumor of appendix, #1 is carcinoid
MCC of death is SBO. Causes SBO by fibrosis
If there is presence of mucin outside the appendix, like mucinous ascites, this is a clinical syndrome called Pseudomyxoma peritonei
Tx for Appendix mucinous neoplasm
- Appendectomy is the operation of choice +/- cytoreductive surgery with HIPEC
- These DO NOT need a right hemicolectomy. Does not confer survival advantage. Low risk of lymph node mets.
- The question is whether the patient will need cytoreductive surgery with HIPEC or not
- If just the appendix, no extra-appendiceal involvement, found incidentally on pathology with negative margins  You are done after appendectomy
- If extra-appendiceal mucin present then you will need cytoreductive surgery with HIPEC
- If Mucinous adenocarcinoma, this is different, (path = signet ring cells) is found  Right hemicolectomy

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33
Q

GI neuroendocrine tumor (carcinoid)
Rectal/colon/small bowel/duodenum

A

GI neuroendocrine tumor (carcinoid)
T1 (<2 cm) lesions confined to the mucosa or submucosa have a low risk of metastatic spread and are amenable to local treatments.
Rectal
- <2 cm, T1 (submucosa) 
o WLE if in low rectum (0-5 cm from anal verge)
o Endoscopic resection (5-15 cm from anal verge)
- > 2 cm or invades muscularis propria, T2  APR vs LAR
Colon
- < 1 cm, T1 – endoscopic resection
- > 1 cm or invasion of muscularis propria  segmental resection with lymph nodes

Small bowel
- On CT this will show classic mesenteric nodes with calcification
- Formal resection with lymph nodes
Duodenal
- Periampullary  very aggressive  whipple
- < 1 cm endoscopic resection
- 1-2 cm WLE with negative margin
- > 2 cm formal resection with LN

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34
Q

What is Pseudomyxoma peritonei?

A

Can come from appendix, ovary or small bowel
- cytoreductive surgery + HIPEC. Remove ALL tumor.
- Need to debulk to < 2.0 mm !!!!!
- Hyperthermic intraperitoneal chemo (mitomycin and 5FU)
- Mucinous ovarian CA will need TAH-BSO
HIPEC is being used for malignant peritoneal mesothelioma

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35
Q

Appendicitis

A

Abdominal pain 1st! then nausea. If it’s the opposite order = gastroenteritis
Periumbilical pain = visceral. RLQ pain = somatic sensory of peritoneum
Children have higher rate of perforation
Laparoscopic is associated with lower incisional infections however, it has increased risk with deep orgain space infection when compared to open
Operate on all appendicitis in pregnancy regardless of trimester
Abscess < 3 cm just do IV abx. > 3 cm  Drain
If going for appendectomy, and you find normal appendix  still perform appendectomy
Normal appendix < 2 mm wall and < 6 mm dilation
Appendicitis with phlegmon = perforated  non-op management
Perforated appendicitis  If not sick, and especially if delayed  non-op management. Most perfs will be managed non-op unless minimal inflammation, no abscess to drain, presented early
If patient has perforated appendicitis  All need colonoscopy at 6 weeks at the minimum
- Routine interval appendectomy is no longer recommended
- If appendicolith is present, offer interval appy

Stool from wound after appendectomy = cecal fistula  non-op. Usually low output. 75% close spontaneously

Incidental appendectomy for:
- Children undergoing chemo
- Crohn’s without gross involvement of cecum
- Disabled Quadriplegic
- Travel to remote area without medical/surgical care

Uncomplicated appendicitis = no perforation AND no appendicolith
Non-op management for uncomplicated appendicitis when compared to an operation
- Has about a 25% failure rate at 1 year  will ultimately require appendectomy
- Complication rate of non-op is lower than appendectomy
- Overall societal (includes time off work) costs are higher with an operation
- Have a higher readmission rate within 1 year recurrent appendicitis
- Higher length of stay

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36
Q

What is the treatment for acute mesenteric adenitis?

A

Acute mesenteric adenitis = ileitis
Associated with MC #1 Yersinia enterocolitica, Helicobacter jejuni, Campylobacter jejuni, and Salmonella or Shigella
Preceded by URI
See lymphadenopathy in small bowel mesentery = key
Don’t biopsy

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37
Q

What is the primary function of the colon?

A

Secretes K and absorbs Na (Na/K ATPase), absorbs water (mostly right colon)
Retroperitoneal – ascending, descending, sigmoid, rectum

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38
Q

What is the marginal artery of Drummond?

A

It connects the superior mesenteric artery (SMA) and inferior mesenteric artery (IMA).
Travels near colon,

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39
Q

What is the significance of the meandering mesenteric artery?

A

Arc of Riolan
connection between proximal SMA and proximal IMA. Becomes enlarged with either IMA or SMA stenosis

40
Q

Rectal arterial supply

A

Superior rectal artery - IMA
Middle rectal artery - branch of internal iliac
Inferior rectal artery - branch of internal pudendal, which is branch of internal iliac

41
Q

What are the drainage patterns for rectal veins?

A

Superior rectal vein - IMV into portal
Middle rectal veins - drain into internal iliac vein
Inferior rectal vein - internal iliac into caval system

42
Q

Where do the superior and middle rectum nodal drainage?

A

They drain into IMA nodes.

43
Q

Where does the lower rectum nodal drainage?

A

Lower rectum drains into both IMA nodes and internal iliac nodes.

44
Q

What is the initial management for Ogilvie’s syndrome?

A

Observation unless failed 24-48 hours or if cecal diameter > 12 cm, then consider neostigmine.

45
Q

What to do if neostigmine fails in Ogilvie’s syndrome?

A

If that fails, perform decompressive colonoscopy.

46
Q

What is the next step if decompressive colonoscopy fails?

A

Go to OR for percutaneous cecostomy. If there is any ischemia or perforation, perform subtotal colectomy, NOT cecostomy.

47
Q

What are the contraindications for neostigmine?

A

Contraindicated in 2nd degree heart block, asthma, acute coronary syndrome, NOT CAD.

48
Q

What is Alvimopan?

A

Alvimopan is an opioid antagonist. Do not give to chronic opioid users due to risk of MI.

49
Q

How is neutropenic colitis diagnosed?

A

Typhlitis
Diagnosis made by neutropenia, abdominal pain, bowel wall thickening.

50
Q

What causes amebic colitis?

A

Amebic colitis is caused by Entamoeba histolytica, transmitted fecal-orally, often in Mexico.

51
Q

What will stool show in amebic colitis?

A

Stool will show trophozoites.

52
Q

What is the treatment for amebic colitis?

A

Treatment is Flagyl.

53
Q

What is the management for parastomal hernia?

A

Placing a mesh at index operation greatly reduces risk of hernia.

  • Do not relocate the stoma, use the same site, just add mesh
  • Use prosthetic mesh
  • Highest in loop colostomy. Least in loop ileostomy.
  • No repair unless symptomatic

Stoma retraction – More likely to cause symptoms in ileostomy than colostomy because of likelihood of leakage from stoma appliance

54
Q

What technique is used for stoma repair?

A
  • Sugarbaker technique – underlay repair. Cover some distal bowel with mesh, and bowel exits laterally. Has less recurrences
  • Keyhole technique – keyhole Is made on mesh and encircled around bowel. MC one used
55
Q

What is the most common stomal infection?

A

Candida is the most common stomal infection.

56
Q

What is the treatment for diversion colitis?

A

Diversion colitis (Hartmann’s Pouch) – due to lack of short chain fatty acids. Tx: Short chain fatty acid enema (acetate, butyrate, and propionate)

57
Q

What is the most common cause of stenosis of stoma

A

Ischemia is the most common cause of stenosis of stoma. Treatment is dilation if mild.

Retracted and fixed stoma- will likely require surgical fixation
Fistula at stoma – MCC by full thickness suture through the bowel and will need operation and place stoma at new site
Abscess: Underneath stoma site, often caused by irrigation device
Ostomy should go through the rectus on the lateral side

58
Q

Ileostomy

A

Ileostomy-> causes cholesterol gallstones (loss of bile salts) and uric acid kidney stones 2/2 to loss of bicarb
Loop ileostomy is superior to end ileostomy, end colostomy and loop colostomy for fecal diversion e.g. protection low rectal anastomosis
#1 complication following loop ileostomy take down is SBO

59
Q

What is the management for stercoral ulcer?

A

Treatment is fecal disimpaction and aggressive bowel care. If perforation occurs, never do primary repair; needs formal resection (Hartmann’s) with end colostomy.

60
Q

What is the role of IR angiography in GI bleeding?

A

IR angiography: can detect bleeding at a rate > 0.5 cc/min
CTA can detect bleeding at a rate > 0.3 cc/min
RBC scan can detect bleeding at a rate of > 0.1 cc/min

61
Q

What is the first step for lower GI bleeds?

A

Place an NGT and do gastric lavage. If you see bile only  ruled out UGI source. If you see no bile, cannot rule out UGI source
colonoscopy is almost always the first step for LGIB, always try to give prep first but never delay colonoscopy just to prep, perform colonoscopy within 12 – 24 hours
If patient is stable  Colonoscopy is ALWAYS the first step
If patient is stable  Colonoscopy failed/inconclusive  next step is CTA then angiography
CTA should always precede angiography if patient is stable, since it is better at identifying bleeds
If the patient is unstable Go for angiography 1st

62
Q

What is the most common cause of obscure GI bleeding?

A

MCC of obscure GIB not found in upper and lower endoscopy is small bowel angiodysplasia.

MCC of UGIB is peptic ulcer disease
MCC of LGIB is #1 diverticulosis, #2 colitis #3 neoplasm #4 angiodysplasia

63
Q

What is the treatment for uncomplicated diverticulitis?

A

Treatment is cipro/flagyl for 7-10 days.

64
Q

Hinchey Classification

A

1a: pericolonic phlegmon and inflammation, no fluid collection
1b: pericolonic abscess < 4 cm
2: pelvic or inter-loop abscess OR abscess > 4 cm
3: purulent peritonitis
4: feculent peritonitis

65
Q

What is the management for complicated diverticulitis?

A

Abscess < 4 cm  treat with abx. > 4 cm need drain  ALL need elective sigmoidectomy
Complicated diverticulitis = perforation, abscess, stricture, obstruction
- If patient has any complicated (above) diverticulitis, they need elective resection

66
Q

What is the preferred treatment for acute diverticulitis with perforation?

A

Acute Diverticulitis with perforation Sigmoidectomy with primary anastomosis and diverting loop ileostomy preferred over Hartmann’s.
- No difference in mortality
- Higher rate of ostomy take down with loop ileostomy
Need to resect all of sigmoid down to normal rectum
If patient has diffuse diverticuli only resect portion that is symptomatic.  Do not perform procto-colectomy
LAR = sigmoidectomy and proximal rectum. Take sigmoidal arteries +/- rectal. LEAVE IMA and left colic.

67
Q

Cowden’s syndrome

A

Cowden’s syndrome – Autosomal dominant
PTEN gene mutation
Colonic and stomach polyps that are – hamartomas, fibromas, adenomas, lipoma, neurofibroma
Multiple hamartomas of the skin, GI, bones, CNS, eye, GU, thyroid, endometrium, and breast
Facial Trichilemmomas and macrocephaly = pathognomonic
Screening colonoscopy at 45 years old, then q 5 years
No real increase in colorectal cancer risk
Highest risk of CA is thyroid, endometrium and breast

68
Q

Mut y homolog-associated polyposis

A

Uniquely autosomal recessive
10 or more synchronous polyps, usually left side, occur at age 50
80% risk of colorectal CA
< 100 polyps
Mutation in MYH gene, not APC

69
Q

Muir-Torre syndrome – Autosomal dominant

A

Sebaceous gland tumors and visceral tumors MC colorectal
Considered a variant of HNPCC
Sebaceous gland tumor is hallmark; presents as yellow facial papules

70
Q

Desmoid tumors

A

Desmoid tumors
Benign, slow growing
Usually found after trauma incident, previous surgical scar or during or after pregnancy
- Desmoid tumors are associated with increased estrogen  OCPs and pregnancy
Arises from connective tissue
Female predominance
Imaging: CT will show: homogenous mass arising from connective tissue. Imaging not enough to Dx:
Diagnosis: with core needle/incisional biopsy
Pathology will show spindle cells with abundant fibrous stroma (high collagen content) with fibroblasts (fibromatosis)
Anterior abdominal wall – MC location.
Intra-abdominal masses  associated with Gardner’s
High risk of local recurrence, no lymphatic or distant spread
- Any resection has 50% chance of recurrence
Most important prognostic factor is negative margins
Treatment:
Abdominal wall and extra abdominal desmoid tumors
- Mainstay of treatment is wide local excision with 1 cm margins, without lymph nodes
- Any extra-abdominal desmoid including abdominal wall that is resectable, should be resected
- Radiotherapy for those who are not surgical candidates or recurrence
Intra-abdominal/retroperitoneal desmoid tumors
- Treat with sulindac (FAP), tamoxifen (FAP)
If desmoid tumor involving mesentery= likely Gardner’s  DO NOT RESECT  Use suldinac and tamoxifen
Non-resectable or incidental, asymptomatic intra-abdominal desmoid (associated with FAP)  treat with suldinac and tamoxifen

71
Q

Retroperitoneal tumors

A

Most are malignant
MC malignant retroperitoneal tumor = #1 lymphoma, #2 liposarcoma
Retroperitoneal sarcoma < 25% resectable, 40% recurrence

72
Q

Gastrin

A

Gastrin – found in stomach. Secreted by G cells.
Stimulated by: protein, vagal input (ACH), calcium, ETOH, antral distension, pH > 3.0
Inhibited by: pH < 3, somatostatin, secretin, CCK
Target: Parietal cell and chief cell
Response: Increase HCl, intrinsic factor, pepsinogen secretion (gastrin is strongest stimulator for all these),

73
Q

Somatostatin

A

Somatostatin - mainly from D cells of antrum, also small bowel and pancreas
Stimulated by acid in duodenum

74
Q

Cholecystokinin

A

Cholecystokinin - Secreted by I Cells of duodenum.
Stimulated by protein and fat in duodenum
Contracts the GB, relaxation of sphincter of oddi, increase pancreatic enzyme secretion (most potent stimulus)
Increases intestinal motility

75
Q

Secretin

A

Secretin released by S cells duodenum
Stimulated by fat, bile and pH < 4
Increases pancreatic bicarb. Inhibits gastrin and HCl release
High pancreatic duct output: high bicarb and low chloride
Slow pancreatic output - low bicarb and high chloride (carbonic anhydrase in duct exchanges HCO3 for Cl)

76
Q

Motilin

A

Motilin
Released by M cells in duodenum
Highest concentration of receptors in gastric antrum
Stimulated by duodenal acid, food
Released during fasting, not while eating
Erythromycin acts on this receptor

77
Q

What does pancreatic polypeptide do?

A

Pancreatic polypeptide
secreted by islet cells in pancreas
Causes decreased pancreatic endocrine and exocrine function
Stimulated by: fasting, exercise and hypoglycemia

78
Q

What stimulates vasoactive intestinal peptide?

A

Vasoactive intestinal peptide - produced by cells in pancreas and gut
Stimulated by fat and ACH
Increases intestinal (water and electrolytes) secretions and motility

79
Q

What is the effect of peptide YY?

A

Peptide YY – released from terminal ileum following fatty meal; inhibits acid secretion and stomach contraction, inhibits GB contraction

80
Q

Appendix Carcinoid

A

Appendiceal carcinoid - < 2 cm, not near the base, mesoappendix not involved, no nodes or mets, and it is T1  appendectomy.
All others require a RHC (including lymphovascular invasion, mod-high grade, goblet cell)

81
Q

Enterocutaneous/colocutaneous fistula

A

Enterocutaneous/colocutaneous fistula
<200 cc/day = low output
>500 cc/day = high output
Enterocutaneous fistula treatment algorithm:
* Restrict oral intake of hypotonic fluids < 1 liter a day  NPO and TPN if still high output
* Initial therapy: Loperamide + PPI
* If refractory  next to add is Codeine
* Then you can consider octreotide. Octreotide is not first line
Must wait 12 weeks or 3 months before considering an operation

82
Q

Actinomyces

A

Actinomyces – can occur in cecum; penicillin or tetracycline

83
Q

Anorexia – mediated by

A

Anorexia – mediated by hypothalamus

84
Q

Bombesin (gastrin-releasing peptide) – increases intestinal motility, pancreatic enzyme secretion, and gastric acid secretion

A

Bombesin (gastrin-releasing peptide) – increases intestinal motility, pancreatic enzyme secretion, and gastric acid secretion

85
Q

Laparoscopic Lavage and drainage for HINCHEY III when compared to Hartmann’s

A

Fallen out of favor, high rates of morbidity
No increase rates of operation
Are at increased risk of requiring additional drainage of abscesses
Decreased risk of having a colostomy at 12 months
Decreased length of stay

86
Q

Inpatient vs outpatient treatment of diverticulitis

A

Inpatient admission:
- any complicated diverticulitis. (abscess, fistula, perforation, obstruction)
- If CT shows uncomplicated diverticulitis, but shows
o Microperforation
o Any sign of SEPSIS
o Failed outpatient tx
o Age >70
All others can be treated outpatient

87
Q

Colovesicular fistula
Colo-vaginal fistula

A

Colovesicular fistula – MC fistula in men. MCC is diverticulitis in men and women. Dx: CT with oral or rectal contrast WITHOUT IV contrast!!!! BEST TEST!!
- All need colonoscopy prior to surgery to rule out cancer
- Tx: If due to diverticulitis  resect involved segment of colon, primary anastomosis, close bladder, without diversion
- Tx: if due to cancer  need en block resection
Colo-vaginal fistula – MC fistula in women from diverticulitis

88
Q

MCC of LGIB

A

Diverticula. Caused by disrupted vasa recta arterial bleed

89
Q

Angiodysplasia

A

MC in right colon. -> venous bleeding. Angiogram shows tufts and slow emptying

-Forms due ot progressive submucosal blood vessel dilation; can be cause of occult lower GI bleeding
-Flat, bright red, stellate shape
-Tx: endoscopic thermal coagulation= argon plasma coagulation ablation

90
Q

Ischemic colitis

A

middle and lower rectum is spared
Dx: Endoscopy with argon beam coagulation

91
Q

Cronkite-Canada

A

GI polyps
Associated with alopecia, cutaneous pigmentation, atrophy of fingernails and toenails
Diarrhea is a prominent symptom

92
Q

Peutz-Jeghers

A

Peutz-Jeghers – autosomal dominant
* Hamartomatous polyps through all of GI. MC jejunum and ileum
* Harmatomatous polyps + mucocutaneus lesions = make the diagnosis
* Mutation is SKT11
* Sx: MC obstruction  intussusception
* Hyperpigmentation mucous membranes and hands, feet
* Significantly increased risk of many extra GI CA- MC is breast, other common colorectal, pancreatic and testicular
* Screening: EGD and colonoscopy yearly starting at 10 years old. Then q 3 years
* Yearly screening for uterus, ovary, cervix, breast, testicles starting at 25 years

93
Q

Familial Juvenile polyposis

A

Familial Juvenile polyposis – Autosomal dominant
More than 10 polyps
Hamartomatous Polyps – upper GI and COLON – before 20
Colon affected 100% of the time
50% rate of colorectal CA
Has significant risk of GI cancer, not as high as FAP
**MOSTLY RIGHT SIDED POLYPS
Need colonoscopy starting at age 15 then q 3 years
Need EGD Q1 year by age 25
No prophylactic resection. MADH4 germ line mutation

94
Q

MC mesenteric malignant tumor

A

liposarcoma

95
Q

MC omental tumor

A

mets

96
Q

C diff treatment

A

First line treatment PO fidaxomicin

97
Q

ERCP position

A

Prone position with head turned right; ease of visulaization/ cannulation of ampulla of vater; better pancreaticobiliary anatomuy image; prevent aspiration

Absite (39 decks)

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