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Surgery MS3 Clerkship > GI system > Flashcards

GI system Flashcards

Excluding Hernia and hepatopancreaticobiliary

1
Q

Test to help determine GERD

A

pH monitoring

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2
Q

Two things that can develop in chronic GERD

A

Damage to lower esophagus (peptic esophagitis) and Barrett’s esophagus

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3
Q

Indicated test for esophageal damage due to GERD

A

Endoscopy and biopsy

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4
Q

Usual surgery for gastoesophageal reflux

A

Laparoscopic Nissen fundoplication

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5
Q

Tests for motility problems of the esophagus

A

Barium swallow, manometry

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6
Q

Achalasia

A

Dysphagia that is worse for liquids.

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7
Q

Diagnostic test for achalasia, and treatment

A

Manometry. Tx with balloon dilatation done with endoscopy

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8
Q

Classic progression of symptoms s/p esophageal cancer

A 
Dysphagia starting with meat, then other solids, then soft foods, eventually liquids,
and finally (in several months) saliva. Significant weight loss is always seen.
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9
Q

What type of esophageal cancer is most common with smokers and drinkers? With gastroesophageal reflux?

A

Smoking, drinking -> Squamous Cell Carcinoma.

GERD -> Adenocarcinoma

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10
Q

Tests for esophageal cancer

A

Barium swallow first to prevent inadvertent perforation, then endoscopy and biopsy

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11
Q

What are Mallory-Weiss tears?

A

Tears in the esophagus following prolonged, forceful vomiting. Will see bright red blood.

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12
Q

Test and Tx for Mallory-Weiss tears

A

Endoscopy, tx with photocoagulation (lasers)

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13
Q

Boerhaave syndrome

A

Starts with prolonged, forceful vomiting leading to esophageal perforation. There is continuous, severe, wrenching epigastric and low sternal pain of sudden onset, soon followed by fever, leukocytosis, and a very sick-looking patient.

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14
Q

Test and Tx for Boerhaave syndrome

A

Contrast swallow (Gastrografin first, barium if negative) is diagnostic, and emergency surgical repair should follow. Delay in diagnosis and treatment has grave consequences

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15
Q

Instrumental perforation of the esophagus

A

The most common reason for esophageal perforation. Shortly after completion of endoscopy, symptoms resembling Boerhaave syndrome will develop. There may be emphysema in the lower neck (virtually diagnostic in this setting).

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16
Q

Symptoms of gastric adenocarcinoma

A

Anorexia, weight loss, and vague epigastric distress or early satiety. Occasionally hematemesis.

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17
Q

Diagnosis and treatment for gastric adenocarcinoma

A

Endoscopy and biopsies are diagnostic. CT scan helps assess operability. Surgery is the best therapy.

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18
Q

Diagnosis and treatment for gastric lymphoma

A

Chemotherapy and radiotherapy. Surgery is done if perforation is feared as tumor melts away.

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19
Q

Presentation of Small Bowel Obstruction (SBO)

A

Colicky abdominal pain and protracted vomiting, progressive abdominal distention (if it is a low obstruction), and no passage of gas or feces. Early on, high pitched bowel sounds coincide with the colicky pain (after a few days there is silence).

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20
Q

X-ray findings for SBO

A

Distended loops of small bowel, with air fluid levels.

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21
Q

Most common cause of SBO in adults

A

Adhesions secondary to prior laparotomy

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22
Q

Treatment for SBO

A

NPO, NG suction, and IV fluids hoping for spontaneous resolution. Surgery if conservative treatment fails.

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23
Q

Strangulated SBO

A

Starts with same presentation as normal SBO, but then patient develops fever, leukocytosis, constant pain, signs of peritoneal irritation, and ultimately full blown peritonitis and sepsis. Emergency surgery is required.

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24
Q

Carcinoid syndrome

A

Seen in patients with a small bowel carcinoid tumor with liver metastases. See diarrhea, flushing of the face, wheezing, and right-sided heart valvular damage (look for prominent jugular venous pulse)

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25
Q

Diagnostic test for carcinoid syndrome

A

Twenty-four-hour urinary collection for 5-hydroxyindoleacetic acid provides the diagnosis

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26
Q

Classic picture of acute appendicitis

A

Anorexia, followed by vague periumbilical pain that several hours later becomes sharp, severe, constant, and localized to the right lower quadrant of the abdomen. Tenderness, guarding, and rebound are found to the right and below the umbilicus (not elsewhere in the belly). There is modest fever and leukocytosis in the 10,000–15,000 range, with neutrophilia and immature forms. Emergency appendectomy should follow.

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27
Q

Presentation, dx, and tx of cancer of the right colon

A

Anemia (hypochromic, iron deficiency) typically in the elderly, for no good reason. Stools will be 4+ for occult blood. Colonoscopy and biopsies are diagnostic; surgery (right hemicolectomy) is treatment of choice.

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28
Q

Presentation, dx, and tx of cancer of the left colon

A

Bloody bowel movements. Blood coats the outside of the stool, there may be constipation, stools may have narrow caliber. Flexible proctosigmoidoscopic exam (45 or 60 cm) and biopsies are usually the first diagnostic study. Before surgery is done, full colonoscopy is needed to rule out synchronous second primary. CT scan helps assess operability and extent. Pre-op chemotherapy and radiation may be needed for large rectal cancers.

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29
Q

Colonic polyps in descending order of probability of malignancy

A

Familial polyposis (and variants such as Gardner), familial multiple inflammatory polyps, villous adenoma, and adenomatous polyp. Polyps that are not premalignant include juvenile, Peutz-Jeghers, isolated inflammatory, and hyperplastic.

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30
Q

Indications for surgery to treat chronic ulcerative colitis

A

Disease present for longer than 20 years (high incidence of malignant degeneration), severe interference with nutritional status, multiple hospitalizations, need for high-dose steroids or immunosuppressants, or development of toxic megacolon.

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31
Q

Surgical tx for chronic ulcerative colitis

A

Removal of affected colon, including all of the rectal mucosa (which is always involved)

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32
Q

What causes pseudomembranous enterocolitis

A

Overgrowth of Clostridium difficile in patients on antibiotics

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33
Q

Treatment of choice for pseudomembranous enterocolitis

A

Discontinue antibiotic at fault, and tx with Metronidazole, with vancomycin as an alternate. Do not use antidiarrheals.

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34
Q

Clinical presentation and dx of pseudomembranous enterocolitis

A

Profuse, watery diarrhea, crampy abdominal pain, fever, and leukocytosis. The diagnosis is best made by identifying the toxin in the stool. Pseudomembranes are not always seen on endoscopy.

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35
Q

Internal vs. External Hemorrhoid clinical presentation

A

Bleed when internal (tx w/ rubber band ligation).
Hurt when external (may need surgery if
conservative treatment fails).
Internal hemorrhoids can become painful and produce itching if they are prolapsed.

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36
Q

Typical clinical picture of anal fissures

A

Young women, exquisite pain with defecation and blood streaks covering the stools. The fear of pain is so intense that they avoid bowel movements (and get constipated) and sometimes refuse proper physical examination of the area. Exam may need to be done under anesthesia. The fissure is usually posterior, in the midline.

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37
Q

Pathology and tx of anal fissures

A

A tight sphincter is believed to cause/ perpetuate the problem, so therapy is directed at relaxing it: stool softeners, sitz baths, and topical lidocaine and nifedipine / nitroglycerin (UWorld).

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38
Q

Clinical presentation of Crohn disease when it affects the anus

A

Starts with a fissure, fistula, or small ulceration, but the diagnosis should be suspected when the area fails to heal and gets worse after surgical interventions. Surgery fact, should not be done in Crohn disease of the anus. A fistula, if present, could be drained with setons while medical therapy is underway. Remicade helps healing.

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39
Q

Tx of Crohn disease affecting the anus

A

Surgery is contraindicated. A fistula, if present, could be drained with setons while medical therapy is underway. Remicade helps healing.

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40
Q

Clinical presentation and management of Ischiorectal abscess

A

Very common. Pt is febrile, w/ exquisite perirectal pain that does not let him sit down or have bowel movements. Physical exam shows all the classic findings of an abscess (rubor, dolor, calor, and tumor) lateral to the anus, between the rectum and the ischial tuberosity.

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41
Q

Tx of ischiorectal abscess

A

Incision and drainage are needed, and cancer should be ruled out by proper examination during the procedure. If patient is severely diabetic, horrible necrotizing soft tissue infection may follow: watch him closely.

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42
Q

Potential complication following drainage of ischiorectal abscess

A

Fistula-in-ano

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43
Q

Fistula-in-ano clinical presentation and management

A

Physical exam shows opening(s) lateral to the anus, a cordlike tract may be felt, and discharge may be expressed. Rule out necrotic and draining tumor, and treat with fistulotomy.

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44
Q

Squamous cell carcinoma of the anus: Who is at risk, what does it look like, how to diagnose, and how to treat.

A

At risk: HIV+ and people who practice receptive anal sex. Fungating mass grows out of the anus, metastatic inguinal nodes are often felt. Diagnose with biopsy.
Tx w/ Nigro chemoradiation protocol, followed by surgery if there is residual tumor. However, the 5-week chemo-radiation protocol has a 90% success rate, so surgery rarely is required.

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45
Q

Blood in the vomit comes from what part of the GI tract?

A

Upper GI tract (tip of the nose to the ligament of Treitz)

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46
Q

Melena

A

Black tarry stools. Indicates digested blood.

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47
Q

Red blood per rectum: Where does it come from? What do you do?

A

It can come from anywhere, as it could go through GI too fast to be digested. Pass an NG tube; if bloody, an upper source is established. If not sanguinous or bilious, do upper GI endoscopy. If bilious, entire upper GI is excluded.

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48
Q

Workup for bright red blood per rectum, and upper GI is excluded.

A

Anoscopy (exclude hemorrhoids); if negative, and bleeding is profuse, do angiography. If bleeding is not profuse, do a colonoscopy once the bleeding stops. If in the middle, do a red-cell study.

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49
Q

Blood per rectum in a child: most likely cause, and workup

A

Meckel diverticulum. Technetium scan, looking for ectopic gastric mucosa.

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50
Q

Massive upper GI bleeding in stressed, trauma, or post-op patient: most likely cause, and workup.

A

Stress ulcer. Endoscopy to confirm.

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51
Q

Acute Abdomen in right upper quadrant: differential diagnosis

A

Cholecystitis, symptomatic colelithiasis, cholangitis, duodenal ulcer, acute hepatitis,

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52
Q

Acute Abdomen in left upper quadrant: differential diagnosis

A

Splenic rupture, irritable bowel syndrome, splenic flexure syndrome

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53
Q

Acute Abdomen midepigastrum: differential diagnosis

A

Peptic ulcer disease, Pancreatitis, Dissected aorta, Myocardial Infarction

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54
Q

Diffuse Acute Abdomen: differential diagnosis

A

Peritonitis (i.e. perforated bowel, hemorrage into peritoneum), obstructed bowel, strangulated bowel, acute hepatitis

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55
Q

Clinical signs and radiologic findings of perforated bowel

A

Peritoneal irritation (guarding, rebound tenderness, silent abdomen). Will see free air under diaphragm on upright X-ray

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56
Q

Tx for generalized acute abdomen

A

Ex lap

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57
Q

Lower quadrant Acute Abdomen: differential diagnoses

A

LLQ: appendicitis, salpingitis
RLQ: Sigmoid volvulus, sigmoid diverticulitis
Either or Both: renal calculi, pyelonephritis, ectopic pregnancy, ovarian torsion

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58
Q

X-ray findings: air-fluid levels in small bowel, very distended colon, and a huge air-filled loop in the RUQ that tapers down towards the LLQ in the shape of a “parrots beak”

A

Diagnostic for Sigmoid Volvulus

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59
Q

What should you think when you see coffee-ground emesis or melena, and how did blood come to look like that?

A

Upper GI bleed. When the iron in blood is exposed to gastric acid, it oxidizes and looks like coffee grounds.

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60
Q

What should you think when you see bright red bloody stool or maroon-colored stool

A

Lower GI bleed. Rarely, bright red blood per rectum will be upper GI if the volume of bleeding is super high.

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61
Q

What are esophageal varices, and what causes them?

A

Dilated tortuous veins located in the submucosa of the distal third of the esophagus. They form as a result of portal hypertension.

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62
Q

Acute gastritis vs Chronic gastritis

A

Acute gastritis: erosive, superficial inflammation in the lining of the stomach due to dysfxn of mucosal defenses (e.g. prostaglandins, bicarbonate, and somatostatin). NSAIDs (COX-1 and COX-2 inhibitors), reduce the production of prostaglandins and their protective mechanisms on the stomach lining.
Chronic gastritis: non-erosive inflammation of the gastric mucosa. Type A (fundus-dominant) chronic gastritis is assc. w/ pernicious anemia (autoantibodies to parietal cells –> megaloblastic anemia & vitamin B12 deficiency). Type B (antral-dominant) chronic gastritis is most common and is caused by a H. pylori infection leading to peptic ulcer disease & increased risk of gastric cancer and MALT lymphoma

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63
Q

Dieulafoy’s lesion

A

A vascular malformation in which a large tortuous artery that is aberrantly located in the submucosa, often in the lesser curvature of the stomach, is eroded by gastric acid.

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64
Q

Endoscopic finding: small, pinpoint defect in the gastric mucosa, described as a visible vessel without an underlying ulcer present.

A

Dieulafoy’s lesion: not a primary ulcer but likely a result of the mechanical pressure from the pulsating large artery that progressively erodes through the mucosa

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65
Q

Branches of the celiac trunk that are at risk of erosion when a gastric ulcer penetrates the mucosa (list 3)

A

Splenic artery, Left gastric artery, gastroduodenal artery

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66
Q

What happens to BUN/Creatinine ratio during a GI bleed?

A

BUN/Cr ratio increases, due to absorption of degraded blood products during intestinal transit and prerenal azotemia secondary to hypovolemia.

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67
Q

What is prerenal azotemia

A

Most common cause of acute renal failure. It is an excess of nitrogen compounds in your blood stream due to a lack of blood flow to each kidney.

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68
Q

What is considered the upper GI

A

Oropharynx to the distal duodenum (at the ligament of Treitz), which marks the transition from the retroperitoneal duodenum to the intraperitoneal jejunum

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69
Q

3 intravenous PPIs

A

Pantoprazole, lansoprazole, and esomeprazole

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70
Q

Triple therapy for H. pylori

A

Proton pump inhibitor such as omeprazole, along with clarithromycin and amoxicillin. Treat 1 week.

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71
Q

Best test for H. pylori eradication

A

Urea Breath Test (UBT)

72
Q

Esophageal varices bleeding management

A

Short term antibiotic prophylaxis, then endoscopic band ligation. Somatostatin (octreotide) or vasopressin are given to reduce portal flow. If everything fails, transjugular intrahepatic portosystemic shunting (TIPS) may be considered to lower portal pressure.

73
Q

Best way to stop recurrent bleeding from esophageal varices

A

long-term ß-blocker (propranolol) (not useful in the acute setting)

74
Q

Management of Mallory-Weiss tears

A

Usually self-limited. Rare cases need sclerosing therapy or electrocautery.

75
Q

Best way to manage stress-related mucosal damage

A

IV PPIs to keep gastic pH greater than 5

76
Q

Most common symptoms of peptic ulcer disease

A

Abdominal pain, burning in the epigastric region, non-radiating. Gastric ulcers often have pain during food consumption, while duodenal ulcers have pain 2–3 h post-prandially. Other symptoms include N/V, abdominal distention, melena, and weight loss.

77
Q

How will a perforated peptic ulcer present

A

Acute onset sharp abd. pain in epigastric region, rapidly becomes diffuse. May c/o shoulder pain due to diaphragm irritation (referred pain from the phrenic nerve). On PE, pt lying motionless, peritonitis (seen as exquisite tenderness to palpation, abdominal guarding, and rigidity). The abdomen is usually not distended

78
Q

Epidemiology of perforated gastroduodenal ulcers

A

Gastroduodenal perforations occur in 2–10% of patients with PUD and account for more than 70 % of deaths associated with PUD.

79
Q

How do NSAIDs lead to Peptic Ulcer Disease (PUD)

A

By inhibiting both COX-1 and COX-2 production, NSAIDs inhibit the secretion of prostaglandins and thromboxanes. Prostaglandins regulate inflammatory rxs w/in gastric mucosa and reduce the production of acid by parietal cells of the stomach. The chronic use of NSAIDs results in the unopposed secretion of acid and a reduction in mucosal defense.

80
Q

How Does Vomiting Change a Patient’s Acid/Base Balance?

A

Vomiting results in the loss of potassium and hydrochloric acid. The loss of the hydrogen ions leads to a metabolic alkalosis. If the vomiting continues, the patient will also start losing sodium. Hyponatremia is sensed by the macula densa of the kidneys and results in the activation of the renin-angiotensin-aldosterone system. This results in reabsorption of sodium and water within the renal tubules at the expense of hydrogen ions. This is also known as contraction alkalosis.

81
Q

Lab findings of perforated PUD

A

CBC and blood chemistries should be ordered. Blood test abnormalities may include leukocytosis with a left shift, elevated C reactive protein (CRP), decreased albumin, and elevated BUN and creatinine.

82
Q

Possible X-ray findings for perforated PUD

A

Pneumoperitoneum; free air under diaphragm on upright X-ray

83
Q

If perforation of ulcer is suspected, what two procedures are contraindicated?

A

Barium swallow (causes barium peritonitis) and endoscopy (air insufflation can exacerbate pneumoperitoneum)

84
Q

Graham patch

A

Tying a patch of omentum to a repaired perforated ulcer. The omentum acts as a nidus for an inflammatory reaction as well as fibrin formation

85
Q

Surgical tx for perforated gastric ulcer

A

Wedge resection. do pathology for malignancy.

86
Q

Most common type of gastric cancer

A

Gastric adenocarcinoma

87
Q

Consider this in a pt who presents with weight loss and epigastric abdominal pain, dysphagia, nausea, early satiety, and rarely a palpable mass. Common only c/o dyspepsia, vague abdominal pain, and fatigue.

A

Gastric cancer

88
Q

Three “nodes” associated with gastric cancer

A

Virchow’s nodes (left supraclavicular nodes), Sister Mary Joseph nodes (periumbilical lymphadenopathy), Irish’s nodes (left axillary node)

89
Q

Two histological types of gastric adenocarcinoma, and key facts about them

A

Intestinal-type: well differentiated, assc w/ environmental factors, more common, step-wise progression.
Diffuse-type: poorly differentiated, no discrete mass, congenital (read: younger pts), progression jumps straight from chronic atrophic gastritis to adenocarcinoma

90
Q

What Is Linitis Plastica?

A

Diffuse-type gastric cancer, highly metastatic and aggressive –> rapid progression –> cancer seen in the esophagus or duodenum, infiltration of the entire gastric wall, known as “linitis plastica” (plastic lining) named after the stiff, undistensible gastric wall that develops after it is infiltrated with tumor.

91
Q

Arterial supply to stomach (4 vessels) which branch off of what vessel?

A

Left and right gastric arteries (lesser curve) and left and right gastroepiploic arteries (greater curve). All of the vessels that supply the stomach are derived from the celiac artery

92
Q

Test for suspected gastric cancer

A

Upper endoscopy, multiple biopsies from ulcerated lesions (98% sensitivity)

93
Q

Workup for gastric cancer after diagnosis

A

Endoscopic ultrasound helps with staging, CT of abdomen to see if pt is a surgical candidate, possibly PET scan to look for metastasis. If favorable conditions, resect tumor.

94
Q

Suspect this in a pt who c/o chest pain after forceful retching, who has crepitus to palpation around the sternum, left sided pleural effusion, SIRS

A

Boerhaave syndrome

95
Q

Mackler’s triad

A

Vomiting, thoracic pain, and subcutaneous emphysema. Highly suggestive of Boerhaave’s syndrome

96
Q

Most Specific Sign of an Esophageal Rupture

A

Subcutaneous emphysema after forceful retching

97
Q

Workup for suspected Boerhaave’s syndrome

A

Chest X-ray (look for left pleural effusion, atelectasis). If questionable, CT with a water-soluble (NOT BARIUM) oral contrast (high sensitivity, gives you extent of rupture).

98
Q

What test should you NOT do if you suspect Boerhaave’s syndrome?

A

Endoscopy. Insufflation of esophagus with air could worsen the perforation.

99
Q

Management of Boerhaave’s syndrome

A

Aggressive IVF resuscitation, NPO, broad spectrum antibiotics, antifungals. Follow with H2-blocker or PPI to reduce gastric acid secretions. Then surgury.

100
Q

Two options for surgery for Boerhaave’s syndrome

A

Primary closure of the perforation, and esophageal resection. Primary closure is preferred esp. if the perforation is small and recent.
All devitalized tissue should be debrided, including in the mediastinum and pleura, (pleural decortication).

101
Q

Most common causes of lower GI bleeding

A 
"H-Drain":
Hemorrhoids
Diverticular bleeds
Radiation colitis
Angiodysplasia
Infectious/Ischemic/IBD
Neoplasms/polyps
102
Q

What is an occult bleed? What might it mean for a patient?

A 
The patient does not see any blood per rectum. The bleeding is only detected by fecal occult blood testing or by finding iron-deficiency anemia. 
Occult bleeding (esp. in older patients) could mean malignancy (esp. colorectal cancer).
In younger patients, could mean inflammatory bowel disease or familial cancer syndromes (e.g., FAP, Hereditary nonpolyposis colorectal cancer).
103
Q

What medications can exacerbate GI bleeding?

A

Anticoagulants such as warfarin, aspirin, clopidogrel, and NSAIDs can exacerbate GI bleeding.

104
Q

What should you suspect if a patient presents with abdominal pain along with their blood per rectum

A

Suspect IBD, ischemic colitis, or infectious diarrhea.

Stuff like angiodysplasia and diverticulosis is painless.

105
Q

What might iron-deficiency anemia mean in the context of a lower GI bleed?

A

Malignancy (especially colorectal cancer, particularly if the patient has never had screening).

106
Q

Suspect this in an elderly patient with left sided abdominal pain and bloody diarrhea (esp in the setting of low-flow states, like severe dehydration, heart failure, shock, and trauma)

A

Ischemic colitis

107
Q

Two genres of people more at risk for diverticulosis

A

Old, fat people.

People with connective tissue disorders, like Marfan or Ehlers-Danlos.

108
Q

A saclike protrusion through the colonic wall

A

A diverticulum

109
Q

Most common site of diverticula, and why?

A

90% occur in Sigmoid colon. The combination of harder stool and decreased lumen diameter causes increased pressure and makes diverticulum formation more likely.

110
Q

How common is a diverticular bleed

A

3-5% of diverticula will cause bleeds

111
Q

Natural history of a diverticular bleed

A

75% stop bleeding spontaneously. Each episode of a diverticular bleed increases the risk of a future bleed.

112
Q

Focal submucosal areas of thin, weak, and dilated (ectatic) vessels in the GI tract, most commonly in the cecum and right colon in individuals over age 60. Most common vascular abnormality of the GI tract.

A

Angiodysplasia

113
Q

Risk factors for angiodysplasia

A

Age. Also assc with von Willebrand’s disease, aortic stenosis, and chronic kidney disease

114
Q

What causes ischemic colitis

A

Decreased blood flow to the colon, causing non-occlusive (meaning not due to arterial thrombosis or embolism) ischemic colitis. Mucosa is affected first and may progress through all layers of the colon. The most common areas to be affected are “watershed” areas which have relatively poor perfusion as they are in between two areas of the colonic blood supply (e.g., splenic flexure).

115
Q

What factors can precipitate ischemic colitis?

A

dehydration, heart failure, shock, cardiovascular surgery, hypercoagulable states, extreme exercise, hemodialysis, and certain drugs (e.g., digitalis, vasopressors, cocaine)

116
Q

Natural history of ischemic colitis

A

Most cases will resolve with supportive measures, while a minority of cases will require resection for transmural (i.e., full thickness of the colonic wall) infarction

117
Q

Pathophysiology of acute mesenteric ischemia

A

arterial embolus or thrombosis

118
Q

Initial management of lower GI bleed

A

Two large-bore IV’s, labs (type and cross, CBC, chemistry, INR/PTT), and if pt needs it, resuscitation with crystalloid and pRBC. Place an NG tube to rule out upper GI bleed.

119
Q

Best diagnostic tests for lower GI bleed

A

Colonoscopy, ideally after a bowel prep. May not see anything; if so, do arteriography or tagged RBC scan using technetium-99 m.

120
Q

most common cause of lower GI bleed

A

Diverticulosis

121
Q

Left vs Right Colon diverticula

A

Right bleeds,

Left gets infected

122
Q

“Red currant jelly” stool

A

Think Intussusception

123
Q

Classic sequence of symptoms: anorexia, vague periumbilical abdominal pain, vomiting, and then a shift to localized right lower quadrant pain.

A

Appendicitis

124
Q

Why might you find absent bowel sounds in cases of appendicitis?

A

Absent bowel sounds indicate a paralytic ileus which in this setting would be secondary to inflamed/infected bowel.

125
Q

Hamburger sign in setting of appendicitis

A

Most pts w/ appendicitis will have anorexia. If pt is hungry, acute appendicitis is less likely. Inquire about pt’s favorite food (e.g., hamburger, pizza), and ask if they’d like to eat it. They’ll decline their favorite food (positive hamburger sign).

126
Q

Appendicitis signs: Rovsing’s, Psoas, and Obturator Signs and McBurney’s Point Tenderness

A

Rovsing’s sign: RLQ pain with palpation of the LLQ (palpation stretches the abdominal wall triggering pain in the inflamed RLQ peritoneum).
Psoas sign: RLQ pain on passive extension or active flexion of the right hip.
Obturator sign: RLQ pain on internal rotation of the hip (can occur with a pelvic appendix).
McBurney’s sign is maximal tenderness at McBurney’s point.

127
Q

Most common cause of appendiceal obstruction. What else can happen in children?

A

fecaliths.

Lymphoid hyperplasia.

128
Q

Lab values to watch in appendicitis

A

WBC, C-reactive protein

129
Q

Pseudoappendicitis causative agent, and how do you treat?

A

Yersinia enterocolitica. Treat with doxycycline

130
Q

Pencil thin stools: where is the cancer most likely located?

A

Left sided colon

131
Q

USPSTF recommended ages of screening for colon cancer for a person of average risk

A

ages 50 to 75, colonoscopy every 10 years

132
Q

USPSTF recommended ages of screening for colon cancer for a person with a first degree relative who had colon cancer

A

starting at 40, or 10 years younger than when the family member was diagnosed, then every 5 years

133
Q

Risk factors for colon cancer

A

Age, African American race, IBD, family history, low fiber/high fat diet, sedentary lifestyle, obesity, smoking, alcohol, type 2 diabetes, and radiation therapy to the abdomen

134
Q

In which side of the colon is cancer more commonly found? And where?

A

Left side. Near the rectosigmoid junction.

135
Q

If patient has melena, and colon cancer is suspected, in which side is the cancer more likely to be?

A

Right side

136
Q

Two types of non-neoplastic polyps

A

Juvenile, Hyperplastic (most common)

137
Q

Three genes lost or mutated in the development of adenocarcinoma of the colon

A

APC, KRAS, p53

138
Q

Suspect this when a large number of hamartomatous polyps in the stomach and colon develop in children

A

Juvenile Polyposis

139
Q

Suspect this when multiple hamartomatous polyps develop alongside with mucocutaneous hyperpigmentation spots on the lips and genitalia

A

Peutz-Jeghers syndrome

140
Q

What is the most common site of local and distant metastasis of colorectal cancer?

A

Local: mesenteric lymph nodes.
Distant: Liver

141
Q

Two main heritable diseases associated with colon cancer

A

Hereditary Non-Polyposis Colorectal Cancer (HNPCC) (aka Lynch syndrome).
Familial Adenomatous Polyposis (FAP). Gardner syndrome. Turcot syndrome.

142
Q

HNPCC: what type of heredity, most common cancers, what age, which side of the colon, and what do the polyps look like?

A

Autosomal dominant, colorectal and endometrial cancers, in the 40’s, right side of the colon, polyps look flat instead of polypoid

143
Q

FAP: what type of heredity, what does the colon look like, what age, what to do for prophylaxis?

A

Autosomal dominant, colon develops hundreds to thousands of polyps, which can develop into cancer if left untreated, usually starts mid-teens but as early as 7, and prophylactic colectomy is often recommended because 100% of patients get cancer by the 4th or 5th decade of life.

144
Q

Gardner’s syndrome: type of heredity, what do you get, and what happens if left untreated, and it is a variant of what disorder?

A

Autosomal dominant with variable penetrance, associated with osteomas and colonic polyps, 100% of patients will get cancer in their 4th or 5th decade of life. Variant of FAP.

145
Q

Turcot Syndrome: what do you get, and it is a variant of what disorder?

A

Assc. w/ cafe-au-lait spots, CNS malignancies, and neoplastic colon polyps that progress to cancer. Variant of FAP.

146
Q

Synchronous vs Metachronous tumors

A

Synchronous tumors: primary tumors (not a metastasis) that were all present at the time of initial diagnosis.
Metachronous tumors: primary tumors that developed elsewhere 6 months after resection of another tumor. Not a recurrence, which would be at the margin of resection.

147
Q

Work-up for suspected colon cancer

A

Colonoscopy with biopsy

148
Q

After confirmation of colon cancer, what lab tests should you get?

A

Carcinoembryonic antigen (CEA), liver enzyme tests (elevated AlkPhos suggests liver metastasis)

149
Q

CEA as a screening tool for colon cancer

A

NOT RECOMMENDED. Low sensitivity and specificity; also caused by a laundry list of other conditions.

150
Q

After confirmation of colon cancer, what imaging should you get?

A

CT of chest, abdomen, pelvis to look for metastasis.

151
Q

What imaging should you get before surgery for rectal cancer, and why?

A

Transrectal ultrasound (TRUS) and MRI, because it’s important to see how close the tumor is to sphincter muscles, if they’re good candidates for sphincter-preserving resection, etc.

152
Q

Adjuvant vs Neoadjuvant therapy

A

Adjuvant: chemotherapy after surgery to prevent recurrence and metastasis.
Neoadjuvant: chemotherapy before surgery to shrink tumor before resection.

153
Q

Staging of colorectal cancer

A

TNM: Tumor (size, depth of invasion), Nodes (extent of spread to regional lymph nodes), Metastasis (if it has spread remotely)

154
Q

What Is a “Bowel Prep” and Why Is It Done?

A

Essentially prepares the colon for surgery. The premise is that it removes all stool from the colon, theoretically preventing stool spillage into the peritoneum when the colon is divided at surgery. For colonoscopy, it permits better visualization of polyps. Most bowel preps consist of orally ingested polyethylene glycol that the patient drinks on the day prior to the procedure.

155
Q

Two physical features of the large bowel

A

Taenia coli (longitudinal white lines), taenia epiploica (fat appendages)

156
Q

Screening tool for colorectal cancer

A

Colonoscopy

157
Q

Suspect this in a patient with obstipation, severe abdominal distension, “coffee bean” dilated sigmoid on CT

A

Sigmoid volvulus

158
Q

Suspect this in a patient with progressive massive abdominal distention over several days, nausea, and vomiting (similar to an LBO). However, unlike LBO, the classic setting is in someone who is already hospitalized and often in the postoperative setting. No mechanical obstruction.

A

Ogilvie’s syndrome

159
Q

5 F’s of abdominal distention

A

Fat (obesity), feces (fecal impaction), fetus (pregnancy), flatus (ileus or obstruction), and fluid (ascites)

160
Q

Most common causes of large bowel obstruction

A

In the US, malignancies (primarily colon cancer) are the most common, followed by diverticulitis (either acute or chronic with a stricture) and then volvulus

161
Q

Where in the colon is a cancer most likely to cause an obstruction?

A

In the left side, as it has a narrower lumen. Right side more likely presents with iron deficiency anemia.

162
Q

Malrotation of the colon

A

Congenital condition in which the bowel does not reside in its normal anatomic position. As a result, the bowel and its mesentery are not properly fixed/attached and are therefore prone to twisting and becoming obstructed.

163
Q

Volvulus of the bowel

A

Twisting of the bowel. Volvulus can be a manifestation of malrotation. If the small bowel twists, the term used is midgut volvulus. Volvulus can also occur in the absence of malrotation (i.e., sigmoid volvulus).

164
Q

Suspect this in a patient with severe diffuse abdominal pain, fever, tachycardia, altered mental status, marked tenderness to palpation with peritoneal signs, and laboratory evidence of infection.

A

Complicated volvulus

165
Q

Imaging for suspected large bowel obstruction

A

Plain abdominal and upright chest radiographs. Look for free air

166
Q

Imaging signs of volvulus

A

“coffee bean” or “bend inner tube” sign on X-ray. “Bird’s beak” or “ace of spades” sign on contrast enema. “Whirl sign” on CT with oral and IV contrast

167
Q

After initial treatment (IVF, NG tube etc), how can you treat sigmoid volvulus?

A

Untwisting (detorsion) of the volvulus via endoscopy. Can be flexible sigmoidoscopy, rigid proctoscopy, or colonoscopy. Contrast enema is another option, but does not allow mucosal inspection. If detorsion fails, the patient must undergo urgent surgery. After that, semi-elective sigmoid resection.

168
Q

Surgical treatment for complicated sigmoid volvulus

A

Resect the colon. Don’t detorse, as it could release bacteria and toxins into systemic circulation.

169
Q

Treatment for cecal volvulus

A

Right colectomy, as it has a high rate of failure, necrosis, and recurrence.

170
Q

Tx for Ogilvie’s syndrome

A

neostigmine, or colonic decompression

171
Q

Risk factors for diverticulosis

A

Obesity, diet low in fiber and high in fat and red meat, and advanced age

172
Q

Where in the Colon Do Diverticula Occur Most Frequently? Which Diverticula Are More Prone to Infection? Bleeding?

A

The vast majority of diverticula occur in the sigmoid colon. Diverticula in the left or sigmoid colon are more likely to become infected. Diverticula in the right colon are more likely to bleed.

173
Q

True vs false diverticula

A

There are three primary layers of the intestinal wall: the mucosa, submucosa, and muscularis. In a true diverticulum, all layers are part of an outpouching of the intestine. In a false diverticulum (such as sigmoid diverticula), only the mucosa and submucosa are part of the outpouching.

174
Q

Colovesical fistula: most common etiologiy, and presentation

A

Diverticulitis is the most common etiology. Can present with fecaluria (feces in the urine), pneumaturia (air in the urine), recurrent UTIs that are refractory to treatment, or by a UTI caused by multiple enteric organisms or anaerobes (most UTIs are single organism and aerobes).

175
Q

Two imaging studies contraindicated in diverticulitis

A

Barium enema, and colonoscopy. These may aggravate already inflamed tissue and may cause a new perforation or exacerbate an old one.

176
Q

What should you do in the setting of a 5 cm ring enhancing lesion (read: abscess) you find in a pt w/ diverticulitis?

A

Drain the abscess with CT-guided percutaneous drainage.

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