Fiser ABSITE Ch. 36-37 Colorectal/Anal Flashcards Preview

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Flashcards in Fiser ABSITE Ch. 36-37 Colorectal/Anal Deck (135)
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1
Q

What embryologic layer does the gut derive from?

A

Endoderm

2
Q

In regards to for-, mid- and hindgut, what portion of the small bowel arises from each?

A

Forgut: Ends at the second portion of the duodenum, uses the celiac artery as blood supply. Midgut: Duodenal ampulla to first two-thirds of the transverse colon, supplied by the SMA. Hindgut: distal transverse colon and descending colon, proximal rectum, supplied by the IMA.

3
Q

What is the distal rectum derived from?

A

The cloaca (also gives rise to the urogenital tract), with branches of the internal iliac system supplying it.

4
Q

What does the anus derive from?

A

Invagination of the ectodermal anal pit and fusion with the distal rectum at the dentate line.

5
Q

How does the longitudinal muscles of the colon and rectum differ?

A

It completely encapsulates the rectum, but makes of teniae coli of the colon. (which are associated with haustra).

6
Q

Where is the end of the colon?

A

Ends at the peritoneal reflection, roughly 15 cm from the anal verge.

7
Q

What is the largest diameter portion of the colon, and most prone to perforation?

A

The cecum, with an average diameter of 7.5 cm.

8
Q

When attempting to identify the left ureter, what is a helpful landmark associated with the sigmoid colon?

A

The intersigmoid fossa, a small recess formed by the mesosigmoid, where it attaches to the pelvic sidewall.

9
Q

At what level do the teniae coli broaden to begin the rectum?

A

The sacral promontory (marks the start of the rectum).

10
Q

What lies just posterior to the rectum? Which layer contains lymphatics, that when dissected around, preserves them?

A

Presacral fascia; The fascia propria is a distinct mesothelial layer that envelops the mesorectum and presacral fascia. Dissection in the plane between the fascia propria and sacrum preserves the lymphatics contained in the mesorectum.

11
Q

What ligament contains the middle rectal artery, and what are its origins?

A

The fascia propria condenses anterolaterally into two rectal ligamentsthat contain the middle rectal artery and mixed autonomic nerves (injury can lead to impotence and bladder dysfunction).

12
Q

What region marks the beginning of the anus? What anatomic structures are found there?

A

The dentate line, where mucosa forms longitudinal folds (Columns of Morgagni).

13
Q

In what order do the arterial branches come off the SMA?

A

Middle colic, then right colic and finally the ileocolic (which branches into the appendiceal artery).

14
Q

What arteries supply the rectum? What are their origins?

A

Superior rectal - off IMA; Middle rectal - from the internal iliac artery; Inferior rectal - arises from the internal pudendal artery

15
Q

What artery connects the proximal SMA and the IMA?

A

The Arc of Riolan.

16
Q

What are the order of veins converging when creating the portal vein?

A

The inferior mesenteric vein joins the splenic vein, then the superior mesenteric vein joins to create the portal vein.

17
Q

How does the inferior rectum’s venous drainage vary from more superior parts of the large intestine?

A

The distal rectum and anus are drained by the middle and inferior rectal veins into the internal iliac veins.

18
Q

When ligating the IMA, what nerve injury has been described and what are its consequences?

A

The Hypogastric nerve, resulting in ejaculatory dysfunction in men.

19
Q

What are the overall physiologic roles of the colon?

A

Extract water (roughly 90% recovered), sodium (90% recovered via active Na/K ATPases), short chain fatty acids (butyrate, propionate, acetate that are made by bacterial fermentation are the PRIMARY ENERGY SOURCE FOR COLONIC EPITHELIUM, also help create an osmotic gradient) and some vitamins.

20
Q

In regard to bacteria, what are the most common colonic anaerobe and aerobe?

A

Anaerobe: Bacteroides; Aerobe: E. coli

21
Q

What are the three primary contractility patterns of the colon?

A

Retrograde: begins at hepatic flexure down to cecum, allows increased stool mixing; Segmental contraction: short distances, further increases stool mixing; Mass movements: longer progression, with pressures rising up to 200 mmHg (highest in the sigmoid colon)

22
Q

What are the two nerve complexes of the colon?

A

Auerbach (myenteric, located between the longitudinal and circular layers of the muscularis propria) and Meissner (submucosal, from nerve fibers that perforate the circular muscle layer).

23
Q

Why are diverticula of the colon pseudodiverticula?

A

They only contain mucosa and submucosa, and not ALL the layers of the colonic wall.

24
Q

What percentage of patients who have an episode of uncomplicated diverticulitis experience a second episode?

A

13%

25
Q

What is Hinchey Stage I diverticulitis?

A

Small confined pericolic abscess (Less than 2 cm). Treated with antibiotic

26
Q

What is Hinchey Stage II diverticulitis?

A

Larger, walled off abscess that is pericolic. Often percutaneously drained

27
Q

What is Hinchey Stage III diverticulitis?

A

Generalized purulent peritonitis.

28
Q

What is Hinchey Stage IV diverticulitis?

A

Generalized feculant peritonitits.

29
Q

What is the most common fistula to form following complicated diverticulitis (specify for men and women)?

A

Men: Colovesicular fistulas, presenting with pneumaturia and recurrent UTIs.

30
Q

What are the two most common causes (in order) of LARGE bowel obstruction?

A

Cancer if first. Benign stricture from diverticular disease is second.

31
Q

How does a competent ileocecal valve change a colonic obstruction?

A

It creates a closed loop obstruction, leading to vascular compromise, pneumatosis and portal venous gas.

32
Q

What populations are at highest risk of sigmoid volvulus?

A

Elderly (> 70 yo), including the debilitated and chronically constipated, and those on psychotropic medications are at highest risk. In these patients the sigmoid colon can lengthen by as much as 70%, predisposing to volvulus. On imaging they’ll have a “bent inner tube on plain film, or a whorl sign on CT.

33
Q

What is the first treatment for sigmoid volvulus?

A

Decompression with a rectal tube placed via proctoscopy or colonoscope. Roughly 80% reduce. They will then eventually need surgical resection of the their sigmoid (nearly 20-50% will recur).

34
Q

What is a cecal bascule (makes up 10% of all cecal volvulus)?

A

A capacious and mobile cecum flips over and is trapped by the fixed ascending colon.

35
Q

What percentage of surgically reduced cecal volvulus cases will recur?

A

20%

36
Q

At what size is colonic dilation considered an emergency due to likely vascular compromise?

A

12 cm.

37
Q

What infectious colitis affects roughly 10% of AIDS patients?

A

Cytomegaloviral colitis. Treat with Gancyclovir.

38
Q

What two toxins are made by C. difficile, and what overall effect do they have?

A

Enterotoxin A and Cytotoxin B, which cause mucosal damage, causing characteristic exudative pseudomembrane. On pathology you see PMN inflammation of mucosa and submucosa.

39
Q

What are some common pathologic findings in both UC and Crohn’s disease?

A

Pseudopolyps (clumps of regenerating mucosa), crypt abscesses (infammatory collections in the base of the Crypts of Lieberkuhn, which contain mucus-secreting Goblet Cells).

40
Q

What are some extra-intestinal manifestations of Ulcerative Colitis?

A

Pyoderma gangrenosum: inflammatory ulcerative skin disease often found around ostomy sites and on arms/legs. Can be controlled once intestinal disease is controlled! Primary sclerosing cholangitis: obliterating inflammatory disease of the small and large bile ducts. Colectomy does NOT improve symptoms. Arthritides, including ankylosing spondylitis and sacroiliitis, linked to UC and HLA-B27. Not improved with colectomy.

41
Q

What is the overall risk of developing colorectal cancer when you have UC?

A

During first 10 years of disease, risk is 2-3%. It rises 2% per year after that with a lifetime risk of 35%. Therefore, annual colonoscopy starts 10 years after age of diagnosis.

42
Q

What is pouchitis, a complication often seen following ileal pouch-anal anastomosis (IPAA)? Treatment?

A

Idiopathic inflammation of the ileal pouch, seen in 50% of patients after an IPAA. Likely due to bacterial overgrowth. Diagnosis confirmed by sigmoidoscopy. Treated with Flagyl (Metronidizole). IF the patient has stump pouchitis from unused rectum, you treat with short chain fatty acid enemas. Salycilates, stool enemas and probiotics have been shown to help.

43
Q

What are indications for surgical intervention in Crohn’s disease?

A

1) Failure of medical therapy 2) Obstruction (from inflammation, abscess or stricture) 3) Intra-abdominal abscess 4) Symptomatic fistulas 5) Severe perianal disease 6) Failure to thrive 7) Colorectal cancer

44
Q

What is sited as adequate margins when resecting Crohn’s disease?

A

2 cm

45
Q

What are the two major types of polyps found in the colon?

A

Neoplastic (adenomatous) and benign (hyperplastic, juvenile, inflammatory).

46
Q

What conditions do you see hyperplastic polyps (benign) in the colon?

A

The most common benign polyp, are usually small and have no malignant potential.

47
Q

What conditions do you see juvenile polyps (benign) in the colon?

A

They are hamartomas, seen throughout the GI tract, often in patients with severe polyposis syndromes (aka Juvenile Polyposis syndrome, an AD disorder). Can often bleed. Not malignant, but patients at increased risk of colon cancer.

48
Q

What conditions do you see inflammatory polyps (benign) in the colon?

A

Heaps of regenerative and inflammatory tissue, seen in BID and some erosive infections.

49
Q

What are the three pathological classifications of adenomatous polyps?

A

Includes tubular (with branching glands, most common [75%] ), villous (with long fingerlike glands), or tubulovillous (mixed features).

50
Q

What are features of adenomatous polyps are harbingers of increased risk for cancer?

A

Increased size (> 2 cm), villous features (40% risk), sessile appearance (flat, as opposed to pedunculated).

51
Q

What constitutes and adequate polypectomy when resecting a cancerous polyp?

A

If malignancy is classified as 3 or below (invasion into the stalk, but NOT the submucosa of the bowel wall), is well or moderately differentiated, and margins are > 2 mm. These patients then require early repeat colonoscopy at 3 years out due to 40% risk of developing another cancerous polyp.

52
Q

Why are polyps classified as a Level 4 (invading colonic submucosa), or with poorly differentiated lesions, not adequately treated by polypectomy?

A

Because risk of nodal metastasis is 10%, and therefore requires surgical resection.

53
Q

What is the most common mutation in Familial Adenomatous Polyposis (FAP)?

A

Most often (80% of the time) due to autosomal dominant APC mutation (a tumor suppressor gene) on chromosome 5. * Remember, that there is a 100% chance of developing cancer by 40 y/o! These patients get total colectomies prophylactically at 20 years old (total abdominal colectomy with IPAA)

54
Q

What is Gardner Syndrome?

A

Genetic disorder causing GI polyposis, ostemoas, sarcomas and epidermoid inclusion cysts.

55
Q

What is Turcot Syndrome?

A

Genetic disorder with associated polyposis and brain tumors.

56
Q

At what age do patients with increased risk of colon cancer (FAP, Turcot/Gardner Syndrome) begin screening?

A

10-12 years old. They get annual sigmoidoscopy, stopping at age 40 IF NORMAL.

57
Q

What is the risk of developing cancer in an FAP patient who underwent total abdominal colectomy with ileorectal anastomosis? What is done about this?

A

25%. Therefore screening of the remaining rectum should be performed frequently.

58
Q

Why do FAP patients need to undergo upper endoscopy every 2 years?

A

They are at risk of developing polyps in the stomach and near the duodenal papilla (periampullary cancer is the second leading cause of death in FAP patients after colon cancer)!

59
Q

What disease is the most common cause of inherited colon cancer, and what is the cause?

A

Hereditary Non-Polyposis Colorectal Cancer (HNPCC, aka Lynch Syndrome), caused by errors in the DNA mismatch repair genes (many varying mutations identified). Associated with disease in many other organ systems (small bowel, ureter and renal pelvis, endometrium)

60
Q

What criteria are utilized for the diagnosis of Lynch Syndrome (aka HNPCC)?

A

Amsterdam Criteria (Three, Two, One): Three affected relatives spanning two generations, with at least one family member diagnosed before 50 y/o.

61
Q

When diagnosed with colon cancer in patients with HNPCC, what is the suggested surgical treatment for men and women?

A

Men: Total abdominal colectomy with ileorectal anastomosis (future rectal monitoring will be needed yearly). Women: Above + TAHBSO (these patients are at increased risk of ovarian, endometrial, bladder and stomach cancer)

62
Q

What genetic mutation characterizes Multiple Polyposis Coli?

A

AD syndrome in the SMAD4 gene. Have juvenile polyps that can bleed or act as lead points for intussusception. Adenomatous elements found in 10% of polyps. Patients at increased risk for gastric, pancreatic and duodenal cancer.

63
Q

What genetic mutation characterizes Peutz-Jeghers Syndrome?

A

AD disease with mutation in tumor suppressor gene STK11. Patients have multiple hamartomatous polyps, as well as hyperpigmentation of the lips and digits. There’s a 2-10% risk of GI cancer as well as extra-intestinal malignancy (gonadal, breast, biliary).

64
Q

What are the screening recommendations for someone at moderate risk for colon cancer (cancer in first degree relative diagnosed > 60 y/o)?

A

Screening every 10 years starting at 40 y/o.

65
Q

What are the screening recommendations for someone at moderate risk for colon cancer (cancer in first degree relative diagnosed > 60 y/o or > 2 relatives with diagnosis)?

A

Every 5 years, starting 10 years before the youngest relative’s age of diagnosis.

66
Q

What are the screening recommendations for someone at high risk with FAP?

A

Start screening at 10 yo with sigmoidoscopy, and continue yearly at least until 40 years old.

67
Q

What are the screening recommendations for someone at high risk with HNPCC?

A

Start screening at 20 y/o (or 10 years earlier than earliest diagnosed relative), then perform every 2 years until 35-40, then yearly.

68
Q

What are the screening recommendations for someone at high risk with inflammatory bowel disease?

A

Begin screening 10 years after onset of symptoms of colitis, then continue every 1-2 years.

69
Q

What percentage of patients who have limited metastases with the diagnosis of colon cancer have curative resections?

A

20%

70
Q

What is the minimally acceptable margins when resecting colon cancer?

A

2 cm.

71
Q

What criteria would allow transanal excision of a rectal tumor?

A
  • Must be less than 4 cm in size - Within 6 cm of anal verge - Involve less than 40% circumference of the bowel - Be T1 or T2 (invade the muscularis propria AT MOST) - Well differentiated without vascular/lymphatic involvement. Rate of recurrence is 8% (T1 lesions) or 20% (T2 lesions).
72
Q

When attempting to identify a GI bleed, what criteria are needed for tagged radionuclide red blood cell scan to be effective?

A

Requires active bleeding at a rate of 1 mL/min. Because labeling of RBCs persists up to 24 hours, intermittent bleeds can identified with serial scans. Only allows regional localization of bleeding. Labeled colloid scans can identify bleeds at a rate of ≥ 0.1 mL/min.

73
Q

When attempting to identify a GI bleed, what criteria are needed for angiography to be effective?

A

Requires active bleeding at a rate of 0.5 mL/min.

74
Q

What percentage of diverticular bleeds resolve spontaneously?

A

75%. It’s the most common cause of lower GI bleeding.

75
Q

What causes the initial vague abdominal pain of appendicitis, as well as nausea and anorexia?

A

Distention of the appendix and stimulation of visceral nerves.

76
Q

What causes the progressively focal pain of appendicitis?

A

Irritation of the peritoneum locally as the inflammation progresses.

77
Q

Following non-operative management of perforated appendicitis, what is the rate of recurrence?

A

35% (Hence the argument for interval appendectomy).

78
Q

What is Goodsall’s rule in regard to relationship between the internal and external openings of fistuals-in-ano?

A

Openings in the skin anterior and within 3 cm of the verge track directly to the anal canal. Those posterior to the line or further than 3 cm will take a curved path and track to the posterior midline.

79
Q

What are the two types of rectovaginal fistula, and how does that change management?

A

Either LOW (involving lower third of the rectum and lower half of the vagina) or HIGH (between middle third of the rectum and posterior vaginal fornix. Low lesions are amenable to transanal approaches (including myocutaneous advancement flap of the rectal mucosa and internal sphincter). High lesions require transabdominal repair.

80
Q

What causes anal fissures?

A

Mucosal ischemia secondary to hyperplasia and hypertonicity of the internal anal sphincter. Ulcers will have an associated heaped up epidermis (sentinel pile). If fissures are away from the midline (particularly the posterior midline) worry about Crohn’s disease.

81
Q

Once medical management has failed (including CCBs or nitroglycerin creams) for anal fissures, what surgical technique can be utilized?

A

Lateral internal sphincterotomy. Recurrence after surgery is less than 10%. Incontinence is a RARE (less than 1%) complication.

82
Q

What are the locations of the highly vascularized, thickened submucosa that lines the anal canal, and can give rise to hemorrhoids?

A

Left lateral, right anterior and posterior. Those ABOVE the dentate are internal and those below are external.

83
Q

Describe the following: First degree hemorrhoid

A

Bleeding, without prolapse

84
Q

Describe the following: Second degree hemorrhoid

A

Prolapse with strain, spontaneously reduces.

85
Q

Describe the following: Third degree hemorrhoid

A

Prolapses with strain, requires manual reduction.

86
Q

Describe the following: Fourth degree hemorrhoid

A

Prolapse and incarcerated. Can become strangulated and thrombosed.

87
Q

Why are no more than two hemorrhoids excised at a time?

A

Decreases the risk of anal stenosis.

88
Q

What is the rate of recurrence of an incised external hemorrhoid if done within 72 hours?

A

50% recurrence.

89
Q

What has been linked to incontinence and rectal prolapse (procidentia)?

A

Proximal pudendal nerve damage causing weakening of the pelvic floor. Can be due to diabetes, obstetric trauma, or iatrogenic injury. Over 50% have constipation, 35% are nullparous, 15% have diarrhea, 75% experience some incontinence.

90
Q

Before surgical intervention for prolapse (procidentia), what study must be performed?

A

Colonoscopy, to rule out more severe pathology.

91
Q

What are the percentages of improvement in regards to incontinence, constipation and prolapse (procidentia) in patients who’ve undergone transabdominal resection rextopexy?

A

Incontinence: 40%; Constipation: 50%; Prolapse: 98%

92
Q

What is the recurrence rate following an Altemeier procedure for rectal prolapse (procidentia)?

A

15%

93
Q

What is the determining factor for T status in patients with anal cancer?

A

Size (duh), with T1 less than 2 cm, T2 is 2 - 5 cm, T3 > 5 cm

94
Q

What disease is an indolent in situ squamous cell carcinoma of the anal verge?

A

Bowen disease! Usually plaque-like, can present with pruritis and burning.

95
Q

What is the treatment for Bowen Disease (in situ squamous cell carcinoma?

A

Wide local excision with minimal margins. Invasion is found in 5% of cases, and requires APR.

96
Q

What is a plaque-like anal lesion (similar in appearance to Bowen disease) that is more common in older patients, and is possibly originating from Langerhans cells or a met from underlying rectal carcinoma?

A

Paget disease (adenocarcinoma in situ). Treated with wide local excision (if primary), or APR (if associated with underlying carcinoma). Adjuvant chemo/radiation is standard.

97
Q

What is the disease caused by HPV, and is the most common perianal STD?

A

Condyloma acuminatum. It is STRONGLY associated with HIV infection. Requires anoscopy (some cases extend into the anal canal).

98
Q

What is the treatment for Condyloma Acuminatum?

A

Fulguration with electrocautery and direct excision.

99
Q

What are Buschke-Lowenstein Tumors, and what are they associated with?

A

Also called verrucous carcinomas, they are larger invasive derivatives of condyloma, and can become infected or fistulize. It is NOT uncommon for it to undergo transformation squamous cell carcinoma. Treat with WLE or APR, with addition of rad/chemo if carcinoma found.

100
Q

In regards to anorectal carcinoid tumors (4th most common site of presentation), what is the size determination in regards to treatment?

A

Tumors less than 2 cm can be locally excised, > 2 cm require APR.

101
Q

What are the transverse bands that form the haustra of the colon?

A

Plicae semilunaris.

102
Q

What major arteries does the Marginal Artery of Drummond connect?

A

The SMA and IMA branches.

103
Q

In regards to the rectum, what do the lateral stalks contain?

A

The middle rectal arteries, which supply the mid-portion of the rectum.

104
Q

Where does the inferior rectal artery branch off of?

A

The internal pudendal artery, which is a branch of the internal iliac.

105
Q

What is the muscular origin of the external sphincter, and what nerves innervate it?

A

Puborectalis (as a continuation of the levator ani muscle). Neural control comes from the inferior rectal branch of the internal pudendal nerve and perineal branch of S4.

106
Q

With regard to colonic polyps, what is another term for high grade dysplasia?

A

Carcinoma in situ (the basement membrane is intact). It becomes invasive once it invades the submucosa (T1).

107
Q

What is the new surveillance in a patient who had the below, and subsequent interval screening: - Had resection of a single adenoma less than 1 cm?

A

5 years post-polypectomy. IF normal, can resume average-risk recommendations.

108
Q

What is the new surveillance in a patient who had the below, and subsequent interval screening: - Following resection ≥ 1 cm or high-risk adenoma?

A

3 years post-polypectomy. Then repeat again in 3 years, if normal can return to normal screening.

109
Q

What is the new surveillance in a patient who had the below, and subsequent interval screening: - Had curative resection of colorectal cancer?

A

Within one year post-op. Repeat again in 3 years, then every 5 years.

110
Q

What is the new surveillance in a patient who had the below, and subsequent interval screening: - Inflammatory bowel disease?

A

Within 8 years of diagnosis. Survey for dysplasia q1-2 years.

111
Q

In patients with colon cancer and liver metastases, if resectable what is the 5-year survival?

A

25%

112
Q

What percentage of colorectal cancer patients have drop metastases to the ovaries?

A

5%

113
Q

What is the significance of Batson’s plexus in regards to colorectal cancer?

A

Rectal cancer can metastasize directly to the the spine via this venous plexus.

114
Q

What are the primary chemotherapeutic agents utilized for Stage II (rectal) and III (colon or rectal) cancers?

A

5FU, Leukovorin and Oxaliplatin

115
Q

What are chemotherapeutic agents used for stage IV colon or rectal cancer?

A

5FU, Leuovorin. Can also use Avastin (Bevacizumab), a monoclonal Ab against VEGF OR Erbitux (Cetaximab), monoclonal Ab against epidermal growth factor. These increase survival but do not cure cancer.

116
Q

What criteria must be met for rectal cancer to get post-op XRT?

A

Needs to be a T3 tumor or have positive nodes (stage II or higher)

117
Q

What is the most common site of injury following radiation treatment for rectal cancer?

A

Rectum, causing vasculitis, thrombosis, ulcers or strictures.

118
Q

For colorectal cancer patients status post resection, what is the interval follow up for PE, CEA and stool guaiac?

A

Every 6 months for 3 years, then annually. They should also get yearly LFTs, abdominal CT, colonoscopy and CXR.

119
Q

In addition to colon screening, what do WOMEN with HNPCC need to undergo?

A

Endometrial biopsy every 3 years, annual pelvic exam, earlier mammograms.

120
Q

What medications have been shown to maintain remission in UC patients?

A

5-ASA, Sulfasalazines.

121
Q

In ulcerative colitis, what is the most likely site of perforation?

A

Transverse colon.

122
Q

In ulcerative colitis, what is the colon cancer risk?

A

1-2% per year starting 10 years after initial diagnosis. High grade dysplasia is an indication to operate.

123
Q

What is Ogilvie’s Syndrome?

A

Pseudo-obstruction of the colon causing massively dilated colon. Treat with colonoscopy and decompression with neostigmine (a reversible acetylcholinesterase inhibitor causing more ACh, leading to more nicotinic/muscarinic stimulation).

124
Q

What is Lymphogranuloma venereum?

A

Caused by Chlamydia, mostly in homosexuals, it causes proctitis, tenesmus and bleeding. Treat with Doxycycline, Hydrocortisone.

125
Q

What is neutropenic typhlitis (enterocolitis)?

A

Following chemotherapy when WBCs are low, it can mimic surgical disease (including pneumatosis), treat with antibiotics.

126
Q

What bacterial infection can mimic appendicitis?

A

Yersinia. Treat with Tetracycline or Bactrim.

127
Q

What is Solitary Rectal Ulcer Syndrome?

A

Chronic straining leads to internal intussusception, frictional damage. You treat with high fiber diets and defecation training.

128
Q

In regards to the anus, what is the venous drainage?

A

Above the dentate line it is via the internal hemorrhoid plexus and below the external hemorrhoid plexus

129
Q

What is the most dreaded complication of internal closed hemorrhoidectomy?

A

Pelvic sepsis (usually in immunocompromised patients), which presents with perianal pain, fever and urinary retention. Treat with IV antibiotics (cover GNR and anaerobes), EUA to rule out necrotizing soft tissue infection.

130
Q

Prior to surgical intervention, what are the various medical treatments for anal fissures?

A

Sitz baths, bulk, lidocaine jelly, stool softeners (90% heal), also topical Diltiazem cream, Nitroglycerine paste or Bethanachol. The BEST non-operative intervention is botulinum injection

131
Q

In regards to anal canal cancers (above the dentate line), what is the primary treatment? This is similar to squamous, basaloid, cloacogenic, and transition cancers (all behave similarly).

A

The Nigro protocol: 5-FU, Mitomycin, as well as radiation (not surgery).

132
Q

In regard to anal melanoma (third most common site after skin and eyes), what is the preferred treatment?

A

APR vs. WLE (no survival benefit).

133
Q

What is the lymphatic drainage of the rectum and anus, which helps explain metastases via nodes in various cancers?

A

Superior and middle rectum = IMA nodes; Lower rectum = primarily IMA nodes, but also internal iliac nodes; Upper 2/3 of anal canal = internal iliac and pelvic nodes; Lower 1/3 of anal canal = inguinal nodes

134
Q

In regards to radiation proctitis, what is the primary treatment? If that fails what is the fall back?

A

Sucralfate enemas. If that fails use argon plasma coagulation or formalin injections.

135
Q

What is the most common bacterial cause of proctitis?

A

Neisseria gonorrhea –> tenesmus, pain, bleeding.