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GENSURG ROTATION > Abdominal Surgery: Small and Large Intestine Part II > Flashcards

Abdominal Surgery: Small and Large Intestine Part II Flashcards

1
Q

the formation of abnormal outpouchings of the colonic mucosa

A

Diverticula

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2
Q

These can develop due to a combination of chronically elevated intraluminal pressures due to chronic constipation (e.g., due to low-fiber diets, lack of physical exercise) and age-related weakening of connective tissue.

A

Diverticula

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3
Q

What contributes to the formation of diverticula?

A

These can develop due to a combination of chronically elevated intraluminal pressures due to chronic constipation (e.g., due to low-fiber diets, lack of physical exercise) and age-related weakening of connective tissue.

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4
Q

What part of the GI tract is most involved in the formation of diverticula?

A

The sigmoid colon is most commonly involved.

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5
Q

When is colonoscopy warranted in the evaluation of diverticula?

A

Colonoscopy is the diagnostic modality of choice for symptomatic diverticulosis but is contraindicated if acute inflammation of the diverticula (i.e., diverticulitis) is suspected.

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6
Q

type of diverticulum that involves only the mucosa and submucosa and does not contain muscular layer or adventitia.

A

False diverticulum

Most common type of gastrointestinal diverticula
Typically acquired
particularly in the sigmoid colon

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7
Q

The presence of multiple colonic diverticula without evidence of infection

A

Diverticulosis

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8
Q

Contributing factors to diverticulosis

A

Diet (low-fiber, rich in fat and red meat)
Obesity
Low physical activity

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9
Q

Is the most common cause of lower GI bleeding in adults.

A

Diverticulosis is the most common cause of lower GI bleeding in adults.

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10
Q

________________is defined as the twisting of a loop of bowel on its mesentery and is one of the most common causes of intestinal obstruction but not the most common cause.

A

Volvulus

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11
Q

How do patients with a volvulus typically present?

A

Patients typically show features of bowel obstruction (abdominal pain, distension, bilious vomiting) or of bowel ischemia and gangrene (tachycardia, hypotension, hematochezia, peritonitis) in severe cases

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12
Q

__________________ is the investigation of choice in infants with suspected midgut volvulus

A

Upper GI series

A diagnostic imaging test which can be used to diagnose anatomic and/or functional abnormalities (e.g., strictures, dilatation) in the esophagus, stomach, and small intestines. A radiopaque fluid (e.g., barium or gastrografin) is swallowed and radiographs are taken to visualize the lumen of the alimentary tract.

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13
Q

Ladd procedure

A

Surgical procedure to treat intestinal malrotation, consisting of division of Ladd’s bands, widening of the small intestinal mesentery, appendectomy, and correcting the location of cecum and colon.

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14
Q

Surgical procedure to treat intestinal malrotation, consisting of division of Ladd’s bands, widening of the small intestinal mesentery, appendectomy, and correcting the location of cecum and colon.

A

Ladd procedure

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15
Q

Volvulus of the ________________ is more common in infants while in __________________ is more common in adults

A

infants–> midgut
adults–> sigmoid

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16
Q

What is the difference between intestinal alroation and a midgut volvulus?

A

Intestinal malrotation: arrest in the normal rotation of the gut in utero, resulting in an abnormal orientation of the bowel and mesentery within the abdominal cavity

Midgut volvulus: torsion of a malrotated midgut causing mechanical bowel obstruction, mostly in neonates and infants

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17
Q

Pathophys of volvulus

A

Closed-loop mechanical bowel obstruction → accumulation of gas and feces within the loop → increased intraluminal pressure → impaired capillary perfusion of bowel → bowel strangulation, ischemia, and gangrene

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18
Q

an abnormal rotation of the stomach of more than 180° → closed-loop obstruction → possible incarceration and strangulation → intestinal ischemia and perforation
Intestinal malrotation
Intestinal malrotation

A

Gastric volvulus

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19
Q

Features of gastric volvulus

A

severe abdominal pain, retching, and inability to pass a nasogastric tube

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20
Q

Signs of a midgut volvulus

A

Bilious vomiting with abdominal distension in a neonate/infant
Signs of bowel ischemia: hematochezia

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21
Q

Corkscrew duodenum

A

Midgut volvulus on an upper GI series

Upper GI Series=A diagnostic imaging test which can be used to diagnose anatomic and/or functional abnormalities (e.g., strictures, dilatation) in the esophagus, stomach, and small intestines. A radiopaque fluid (e.g., barium or gastrografin) is swallowed and radiographs are taken to visualize the lumen of the alimentary tract.

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22
Q

A radiologic sign characterized by a whorled appearance created by the twisting of one structure around another (e.g., from cecal volvulus, malrotation with midgut volvulus, ovarian torsion, testicular torsion). Can be seen on ultrasonography and CT scan.

A

Whirlpool sign, abdominal ultrasound will show this in a midgut volvulus

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23
Q

What might we see with a brium enema in a midgut volvulus?

A

Bird’s beak sign at the site of the twist

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24
Q

is the dilation of the colon in the absence of a mechanical obstruction (e.g., colonic tumor/stricture). There are three etiological types.

A

Megacolon

The 3 types: acute, chronic, and toxic megacolon

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25
Q

Chronic megacolon is often caused by…

A

colonic dysmotility due to neuropathic or myopathic etiology

Chronic megacolon is the permanent dilation of the colon caused by chronic colonic dysmotility due to an underlying neuropathic (Hirschsprung’s disease, chronic Chagas disease) or myopathic (Duchenne’s muscular dystrophy) disorder.

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26
Q

Acute megacolon is seen in/caused by…

A

characteristically seen in severely medically/surgically ill patients, probably secondary to an electrolyte/metabolic imbalance

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27
Q

How do we treat megacolon?

A

Patients with acute/chronic megacolon can often be treated conservatively with bowel rest, dietary modifications, prokinetic drugs, and/or neostigmine.

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28
Q

When is surgical intervention warranted in acute/chronic megacolon?

A

Surgical intervention for acute/chronic megacolon (colectomy and ileorectal anastomosis) is indicated if conservative treatment fails.

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29
Q

When is surgery indicated in toxic megacolon?

A

Conservative management of toxic megacolon includes bowel rest, IV antibiotics (for infectious colitis), IV steroids (for inflammatory bowel disease). There is a high risk of colonic perforation in patients with toxic megacolon. Hence, no improvement to medical therapy within 24–72 hours is an indication to perform surgery (subtotal colectomy and end ileostomy).

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30
Q

Etiology of chronic megacolon

A

Congenital (e.g., Hirschsprung disease)

Acquired:
diabetic neuropathy
Duchenne’s muscular dystrophy
Chronic Chagas disease

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31
Q

Etiology of toxic megacolon?

A

Infectious colitis
Bacterial: C. difficile (pseudomembranous colitis), Salmonella, Shigella, Campylobacter infections

Ulcerative colitis, Crohn disease

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32
Q

In which megacolon do we get loss of haustration observed on xray

A

Loss of haustration

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33
Q

What are some differences in the clinical features of the megacolons?

A

Acute: constipation/diarrhea

Chronic: constipation

Toxic: bloody diarrhea

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34
Q

How do patients with colonic polyps typically present?

A

Affected individuals are typically asymptomatic but may present with gastrointestinal (GI) bleeding, iron deficiency anemia, and/or mechanical bowel obstruction (e.g., due to intussusception)

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35
Q

Colonic polyps are classified histologically as adenomatous (most common), hyperplastic, inflammatory, serrated, or hamartomatous. Which ones have the highest malignancy potential?

A

Adenomas (e.g., adenoma-carcinoma sequence) have the highest malignancy potential (∼ 5%).

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36
Q

What subtype of adenomas have the highest malignant potential?

A

villous

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37
Q

An autosomal dominant syndrome characterized by > 10 hamartomatous polyps throughout the gastrointestinal tract. Typically manifests within the first 2 decades of life with hematochezia. Patients have an increased risk of developing colorectal and/or gastric malignancies.

A

Juvenile polyposis syndrome

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38
Q

An autosomal dominant, hamartomatous polyposis syndrome characterized by the presence of polyps (typically < 20) throughout the gastrointestinal tract (mainly the jejunum). Associated with mutation of the STK11 gene on chromosome 19p13.3. Manifests with hematochezia, constipation, diarrhea, mucocutaneous hyperpigmentation, and an increased risk of colorectal, ovarian, breast, and pancreatic cancer.

A

Peutz-Jeghers syndrome

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39
Q

Polyps tend to be asymptomatic. If a patient has polyps, what might you expect to observe clinically?

A

Hematochezia
Change in bowel habits
Mucus in stool
Pallor

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40
Q

Hamartomatous polyposis syndromes

A

A subtype of hereditary polyposis syndrome. Characterized by hamartomatous polyps. Includes Peutz-Jeghers Syndrome (PJS), Juvenile polyposis syndrome (JPS), and PTEN-Hamartoma Tumor syndromes (PHTS).

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41
Q

A subtype of hereditary polyposis syndromes. Characterized by numerous adenomatous polyps and an increased risk of colon cancer and other intestinal and extraintestinal tumors. Comprises classic familial adenomatous polyposis (FAP), FAP subtypes (e.g., Gardner syndrome, Turcot syndrome, attenuated FAP), and MUTYH-associated polyposis.

A

Adenomatous polyposis syndromes

42
Q
A
43
Q

For pts with recurrent intussusception, what should we evaluate them for?

A

A pathologic lead point like a meckel diverticulum, a tumor, a polyp. The most common lead point is a Meckel Diverticulum so be astute if you see a patient with recurrent intussusception with iron deficiency/anemia (a sign of occult bleeding possible due to meckels).

44
Q

What are complications of diverticulitis?

A
44
Q

a 99m technetium scan/nuclear scintigraphy is the modality we use to evaluate…

A

meckel diverticulum

44
Q

What is the difference in approach for pts with asynmptomatic femoral hernias versus inguinal hernias?

A
45
Q

What are the different kinds of ascitic fluid characteristics?

A
46
Q

What is the typical appearance of ascitic fluid?

A

Straw-colored&clear

47
Q

What does bloody ascitic fluid indicate?

A

suggests trauma or malignancy

48
Q

What does cloudy ascitic fluid mean?

A

infection

49
Q

What does milky ascitic fluid indicate?

A

lymphatic disruption

50
Q

How could ordering a cell count and differential of ascitic fluid be helpful in dx?

A

Cell count can help narrow down somethings…
Lymphocyte predominance indicates malignancy or tuberculosis while neutrophil predominance suggests spontaneous bacterial peritonitis

51
Q

Major risk factors for hepatocellular carcinoma

A

cirrhosis
chronic hep B

52
Q

Elevated alpha fetoprotein in an adult male who has cirrhosis should raise concern for…

A

hepatocellular carcinoma

53
Q

What is severe acute pancreatitis?

A

defined as pancreatitis that causes failure of greater than or equal to one organ system lasting more than 48 hours.

54
Q

What are important clinical predictors of severe acute pancreatitis (associated with a worse prognosis)?

A

SIRS criteria, elevated BUN/signs of volume depletion due to third spacing, and radiologic signs of third spacing

55
Q

What is emphysematous cholecystitis?

A

A lifethreatening form of acute cholecystitis that occurs more commonly in patients with immunosuppression or vascular disease. It arises due to infection of gallbladder wall with gas-forming bacteria and requires emergency cystectomy.

56
Q

How is dx confirmed for emphysematous cholecystitis?

A

imaging demonstrating air fluid levels in the gall bladder, gas in the gall bladder wall, and occasionally pneumobilia.

57
Q

What is the next step in managment of a biliary cyst dx’d w/MRCP?

A

Surgery!
There is a 30x increase in chance of malignancy so take that sucker out.

58
Q

What lab values should you look for in acute pancreatitis?

A

amylase/lipase levels >3 times the upper limit of normal

59
Q

55 yo m presenting with a year of progressive gatigue and frequenct loose stools. He describes voluminous foul smelling stools that are difficult to flush. He has lost about 20 pounds without trying this past year. On multiple occastions, he has been hospitalized for epigastric pain radiating to the back.

What is this describing most likely?

A

Pancreatic insufficiency due to pancreatitis.

Chronic pancreatitis can be due to alcohol abuse, cystic fibrosis, or autoimmune.

Pancreatic cancer can also cause pancreatic insufficiency.

60
Q

What is the most likely caused of small bowel intestinal bleeding in a 10 yo boy?

A

meckel diverticulum, dx with t 99m scan

61
Q

Ischemic colitis commonly affects what watershed areas?

A

the splenic flexure and rectosigmoid junction

62
Q

How do we dx toxic megacolon?

A

ab ct, showing colonic dialation of greater than 6 cm

63
Q

How does the presentation of left vs right sided colon adenocarcinoma present?

A

Left: obstruction of the outflow of stool leading to altered bowel habits, hematochezia

Right: bleeding is NOT likely visible so it has OCCULT bleeding and iron deficiency anemia
Right is more insidious

64
Q

What do we mean by loss of haustrations on abdominal xray in the setting of toxic megacolon?

A
65
Q

Systemic toxicity presenting as fever, tachycardia, hypotension as well as ab pain and distention following a diarrheal illness or in suspected IBD is concerning for…

A

Toxic megacolon

66
Q

How do we treat toxic megacolon in an IBD pt?

A

Methyprednisolone!
Fluids, electrolyte repletion, bowel rest and decompression (NG tube) and broad spec abx.

67
Q

What is the difference in presentation of a small bowel obstruction vs an ileus?

A
68
Q

How do we manage c. diff?

A
69
Q

DRE with bright red blood inthe rectum, colonoscopy with muscosal pallow, friability, and multiple telangienctasias in the setting of a pt with a hx of rdjuvant radiation therapy for cervical cancer is concerning for…

A

Radiation proctitis

70
Q

How might a SBO develop in a pt with crohn?

A

Severe uncontrolled inflammation can lead to fibrotic strictures

71
Q

How does abdominal compartment syndrome impact preload?

A

DECREASED preload (abdominal pressure decreases venous return to the heart)

72
Q

Abdominal distention, colonic dialation, in the setting of electrolyte derrangements or medications…

A

Acute colonic pseudo obstruction (ogilvie syndrome) arises from autonomic dysruption of the colon

73
Q

is the dilation of the colon in the absence of a mechanical obstruction (e.g., colonic tumor/stricture).

A

Megacolon

74
Q

etiological factors → impairment/destruction of the autonomic nervous system → imbalance between sympathetic and parasympathetic control of intestinal motility–> megacolon

A

Pathophysiology of acute megacolon (ogilvie’s syndrome)

75
Q

What can contribute to acute megacolon? (acute colonic pseudoobstruction, ogilvie’s syndrome)

A

Its idiopathic but can happen in the setting of very ill patients who recently underwent a surgical procedure, have electrolyte imbalances, or are on anticholinergic drugs, opioid analgesics, antipsychotics, calcium channel blockers

76
Q

What are the risk factors for toxic megacolon?

A

infections colitis as seen in c diff, UC, Crohns

77
Q

How may colonic polyps lead to bowel obstruction?

A

The polyps can cause intussusception

78
Q

Most common type of nonneoplastic polyp among those with low malignant potential, common in the distal colon

A

hyperplastic polyp

79
Q

red flags for CRC

A

change in bowel habits, lower GI bleeding, and weight loss. These features as well as iron deficiency anemia in men older than 50 years of age and postmenopausal women

80
Q

What labratory marker do we track in colorectal cancer?

A

CEA, which is a prognostic marker and should not be used to screen for colorectal cancer. Think of it as the CA125 of CRC.

81
Q

Lynch syndrome (hereditary nonpolyposis colorecta cancer) increases risk for what other kinds of cancer?

A

endometrial, gastric, and ovarian cancer.

82
Q

What criteria do we use to ID individuals at increased risk for lynch syndrome?

A

Amsterdam II criteria

83
Q

When is screening recommended for patients with family members who have lynch?

A

Preventative screening for colorectal cancer and associated tumors is recommended in individuals with family members known to have a Lynch syndrome gene mutation; it should occur every 1–2 years, starting at 20–25 years of age, or 2–5 years before the earliest recorded case of a tumor in the family.

84
Q

presence of Lynch syndrome-related CRC and brain tumors (especially gliomas)

A

Turcot syndrome

85
Q

What is the 3-2-1 rule with lynch syndrome?

A

3-2-1 rule: (3 affected family members, 2 generations, 1 relative under 50 years of age).

86
Q

How does the manifestation of familial adenmatous polyposis differ from lynch?

A

Lynch syndrome typically manifests with colorectal cancer of the proximal colon, with only a few adenomatous polyps, in contrast to familial adenomatous polyposis, in which hundreds of adenomatous polyps are present.

87
Q

painless rectal mass that protrudes through the anus
Fecal incontinence
Pruritus ani
Rectal bleeding

A

rectal prolapse

88
Q

The main risk factors for developing anal cancer are …

A

The main risk factors for developing anal cancer are immunosuppression and human papillomavirus (HPV) infection.

89
Q

This condition is the most common cause of lower gastrointestinal bleeding in adults.

A

Diverticulosis

90
Q

Tx of choice for anal SCC

A

The combination of chemotherapy and radiation is the treatment of choice for patients with anal canal SCC; it has been shown to be superior to surgery, with a 5-year survival rate of ∼ 80%. Subsequent surgery is only indicated if a residual tumor is confirmed with biopsy after the completion of radiochemotherapy.

91
Q

How does prophylaxis differ in pts with FAP versus lynch?

A

Patients with Lynch syndrome are at high risk of gastrointestinal malignancies and should receive an annual colonoscopy beginning at 20–25 years of age to screen for colorectal cancer, but prophylactic proctocolectomy is not recommended.
Prophylactic subtotal or total proctocolectomy with ileoanal anastomosis is recommended in patients with familial adenomatous polyposis (FAP). A family history of gastrointestinal malignancy is also seen in FAP. However, patients with FAP would have numerous polyps on colonoscopy by adolescence, and germline testing would show a mutation in the adenomatous polyposis coli (APC) gene rather than in MLH1 and MSH2.

92
Q

Prophylactic proctocolectomy with ileoanal anastomosis is for…

A

Familial Adenomatous Polyposis

93
Q

Which is worse: villous or tubular adenomatous polyp

A

villous; A villous adenomatous polyp has the highest risk (∼ 50%) of malignant transformation of the three types of adenomatous polyps.

94
Q

An autosomal dominant, hamartomatous polyposis syndrome characterized by the presence of polyps (typically < 20) throughout the gastrointestinal tract (mainly the jejunum). Associated with mutation of the STK11 gene on chromosome 19p13.3. Manifests with hematochezia, constipation, diarrhea, mucocutaneous hyperpigmentation, and an increased risk of colorectal, ovarian, breast, and pancreatic cancer.

A

Peutz-Jeghers syndrome

95
Q

This patient presents with a protruding rectal polyp and multiple hamartomatous polyps. In combination with mucocutaneous hyperpigmentation, what is the most likely dx?

A

Peutz-Jeghers syndrome

96
Q

is a variant of familial adenomatous polyposis that manifests with multiple colonic polyps and may cause hematochezia together with extracolonic bone and/or soft tissue lesions, such as osteomas, epidermal cysts, and congenital hypertrophy of the retinal pigment epithelium, all of which are seen here. A family history of colon cancer at a young age furthermore supports this diagnosis.

A

Gardner Syndrome

97
Q

Conservative measures such as sitz baths and topical therapy with calcium channel blockers (e.g., nifedipine, diltiazem) are recommended as the initial treatment for most…

A

anal fissures

98
Q

What are the firstline Conservative measures for anal fissures?

A

Conservative measures such as sitz baths and topical therapy with calcium channel blockers (e.g., nifedipine, diltiazem) are recommended as the initial treatment for most anal fissures. These measures reduce anal sphincter tone and promote mucosal healing by increasing blood flow to the anal mucosa.

99
Q

Frank blood in stool and DRE shows no masses is concerning for…

A

likely diverticulosis

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