Gastroenterology Flashcards

1
Q

What is the differential for ascites?

A

Cirrhosis

Alcoholic Hepatitis

Heart Failure

Cancer (peritoneal carcinomatosis, liver cancer with mets)

Pancreatitis

Nephrotic Syndrome

Budd-Chiari Syndrome

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2
Q

What is the SAAG?

How dos this help in the differential of ascites?

A

Gradient > 1.1 g/dL (portal hypertension)

  1. Cirrhosis
  2. Alcoholic Hepatitis
  3. Cardiac Ascites
  4. Portal Vein Thrombosis
  5. Budd-Chiari Syndrome
  6. Liver Metastases

Gradient < 1.1 g/dL

  1. Peritoneal carcinomatosis
  2. Tuberculous peritonitis
  3. Pancreatic ascites
  4. Biliary ascites
  5. Nephrotic syndrome
  6. Serositis
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3
Q

How do you manage ascites?

A
  1. Sodium restriction < 2 grams / day
  2. Aldactone / Furosemide
    1. Aim for a 100:40 ratio, IE 100 mg to 40 mg daily, can increase to 400 mg and 160 mg daily.
  3. Counsel on aclohol and NSAID avoidance
  4. Large volume paracentesis, contraindications: SBP, recent GI bleed, azotemia, sepsis, hypotension.
  5. TIPS; however no benefits if Child-Pugh > 11, INR > 2, TBili > 5, progressive renal failure.
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4
Q

How do you diagnose spontaneous bacterial peritonitis?

A

Paracentesis that shows > 250 PMNs

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5
Q

What are the common pathogens in spontaneous bacterial peritonitis (SBP)? How do you treat?

A

The common pathogens are; GNB, ecoli and GPC, mainly streptococcus and enterococci: Three most common being: Ecoli, Klebsiella, Strep Pneumomia.

Once the diagnosis of SBP has been made the non-selective beta blocker should be held.

Antibiotic therapy with a third generation cephalosporin (cefotaxime) should be initiated for a five day treatment duration.

Cefotaxime vs cefotaxime plus albumin 1.5g per kg day 1 and 1g/kg day 3, decrease in mortality from 29% to 10%

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6
Q

What are the indications for SBP prophylaxis?

A

1) Cirrhotic with GI bleeding- 7 days of antibiotics
2) After episode of SBP- norfloxacin vs Bactrim
3) Ascites with Tprotein <1.5 AND impaired renal function

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7
Q

What is the differential for upper GI bleeding?

A

Peptic Ulcer Disease (Most common), Variceal (second most common), AV malformation, Mallory-Weiss Tear, Neoplastic, Dieulafoy’s lesion.

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8
Q

What are risk factors for peptic ulcer disease?

A

Risk Factors: H. pylori infections, NSAIDs/Low dose ASA, stress

Risk of re-bleeding is high if on endoscopy active bleeding is observed. If there is a clean based ulcer then the risk of re-bleeding is less than 5%.

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9
Q

What is empiric medical management and treatment of an upper GI bleed?

A

2 Large Bore IV’s (16 gauge or 18 gauge), fluid and blood product administration.

PPI in GI bleeding works by increasing GI pH which facilitates platelet aggregation and clotformation:

  1. IV PPI prior to endoscopy has shown to have shorter lengths of stay, fewer active bleeding ulcers, and more ulcers with a clean base.
  2. Bolus 80 mg of IV Pantoprazole, followed by IV drip to continue 72 hours post endoscopy.
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10
Q

What adjunctive therapy should be added to a variceal bleed besides a PPI?

A

Octreotide 50 mcg IV bolus, followed by 50 mcg/Hr.

Octreotide causes splanchnic vasoconstriction, which decreases portal blood flow.

Ceftriaxone should be added as this prevents early re-bleeding rates.

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11
Q

In what patients with an upper GI bleed should prophylactic antibiotics be added to?

A

All patients with cirrhosis and patients with suspected variceal bleed.

Ceftriaxone 1 gram daily for 7 days.

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12
Q

What is the differential for causes of lower GI bleed?

A

The most common causes of lower GI bleed are diverticulosis and hemorrhoids. However, other causes such as angiodysplasia, ischemic, radiation induced, and inflammatory are causes to consider.

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13
Q

What is the etiology of acute mesenteric ischemia?

A
  • Arterial obstruction is most common
    • Embolic occlusion in 40 to 50% of cases
    • Thrombotic occlusion of a previously stenotic mesenteric vessel in 20 to 35% of cases
    • Dissection or inflammation of the artery in less than 5% of cases
  • Mesenteric venous thrombosis accounts for 5 to 15% of cases
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14
Q

What are the risk factors for messenteric ischemia?

A
  • •Risks of embolism
    • A-fib
    • Mechanical valve
    • Infective endocarditis
    • Ventricular aneurysm
  • Risks of thrombotic occlusion
    • PVD
    • Advanced age
  • Acquired and hereditary thrombotic conditions
  • Poor cardiac output
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15
Q

How does messenteric ischemia present clinically?

A
  • Acute abdominal pain, “pain out of proportion to examination”
  • Abdominal tenderness
  • Bloody diarrhea in advanced ischemia
  • Absent bowel sounds and peritoneal sign at late stage
  • Metabolic acidosis
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16
Q

How do you diagnose messenteric ischemia if it is suspected?

A
  • Abdominal CTA is the recommended method of imaging
  • Endoscopy does not reach the majority of sections of the small bowel that are most frequently involved in mesenteric ischemia.
    • Most useful in rule out conditions other than mesenteric ischemia
17
Q

How do you treat and manage messenteric ischemia?

A
  • Heparin treatment should be initiated as soon as possible
  • Broad-spectrum antibiotics should be administered early
  • Vasodilators may play a role
  • Needs revascularization ASAP:
    • Revascularization with open surgery if patient needs immediate laparotomy
    • Patients without advanced intestinal ischemia may be candidates for a primary endovascular approach
18
Q

What is the etiology of colonic ischemia?

A
  • In most cases, no specific cause for ischemia is identified, and such episodes are attributed to localized nonocclusive ischemia, likely a result of small-vessel disease
  • Abnormalities seen on angiography rarely correlate with clinical manifestations
    • IMA is occluded in up to 10% of asymptomatic patients over 60 years of age
  • Colonic blood flow is supplied by three vessels: the superior mesenteric artery (SMA), IMA, and the superior hemorrhoidal artery. Vascular anatomy, however, is variable and oft en individually unique. Watershedareas of the colon are regions that are particularly susceptible to ischemic insult as a result of their location between two diff erent vascular supplies. These areas include the splenic flexure and sigmoid colon.
19
Q

What are the risk factors for colonic ischemia?

A
  • CAD
  • Diabetes mellitus
  • HTN
  • CKD on dialysis
  • PVD
  • Irritable bowel syndrome
  • A-fib
  • Female
20
Q

What is the clinical presentation of colonic ischemia?

A
  • Acute abdominal pain
  • Abdominal tenderness
  • Urgent desire to defecate
  • Rectal bleeding or bloody diarrhea within 24 hours
  • Absent bowel sounds and peritoneal sign at late stage
  • Metabolic acidosis
  • Of note, patients with isolated right-colon ischemia present most commonly with acute abdominal pain without rectal bleeding
21
Q

How do you diagnose colonic ischemia?

A
  • CT with intravenous and oral contrast should be the first imaging modality
    • Classic findings include bowel wall thickening, edema, fat stranding, etc.
  • CTA are not indicated in most patients with suspected CI
  • CTA should be performed when suspecting isolated right colon ischemia or when possibility of mesenteric ischemia cannot be excluded
  • Early colonoscopy (within 48h of presentation) should be performed in suspected CI to confirm the diagnosis
22
Q

How do you manage and treat colonic ischemia?

A
  • Most cases of ACI resolve spontaneously and do not require specific therapy
  • Antimicrobial therapy should be considered for patients with moderate or severe disease
  • No role for anticoagulation
  • When should emergent surgery be considered?
    • Peritoneal signs
    • Massive bleeding
    • Fulminant colitis with or without toxic megacolon
    • Portal venous gas or pneumatosis intestinalis on imaging
    • Deteriorating clinical condition
23
Q

What is the definition of gastroparesis?

A

Gastroparesis is a syndrome of objectively delayed gastric emptying in the absence of a mechanical obstruction and cardinal symptoms of nausea, vomiting, early satiety, bloating, and/or upper abdominal pain.

24
Q

What disease is the most common cause of gastroparesis?

A

Diabetes Mellitus. In the course of 10 years patients with Type I and Type II have an incidence of gastroparesis at 5 and 1 percent.

25
Q

What are common medications that cause gastroparesis?

A
  • Narcotics (affecting mu opiate receptors alone or combined with inhibition of norepinephrine reuptake [eg, oxycodone and tapentadol, respectively]
  • Alpha-2-adrenergic agonists (eg, clonidine)
  • Tricyclic antidepressants
  • Calcium channel blockers
  • Dopamine agonists
  • Muscarinic cholinergic receptor antagonists
  • Octreotide
  • Glucagon-like peptide (GLP)-1 agonists and amylin analogues
  • Cyclosporine (but not tacrolimus, which is derived from macrolide molecule like erythromycin, and does not inhibit gastric emptying)
26
Q

How do you evaluate a patient with suspected gastroparesis?

A
  • Need to exclude mechanical obstruction; careful upper endoscopy, CT or MR enterography to exclude mechanical obstruction should also be reommended.
  • Scintigraphy should then be performed to assess gastric motility.
27
Q

How do you manage gastroparesis?

A
  • Optimize glycemic control
  • Dietary modifications; fatty, acidic, spicy foods increase symptoms
  • Prokinetics; Metoclopramide, domperidone, erythromycin
    • Increase gastric emptying, should be given 10 to 15 minutes before meals
28
Q

What are the indications for a gastric bypass procedure to be performed?

A

American Association of Clinical Endocrinologists/Obesity Society/American Association of Metabolic and Bariatric Surgery (AACE/OS/ASMBS) recommendations on patient selection for bariatric surgery (grade A)

—Adults with a BMI ≥40 kg/m2 without co morbid illness

—Adults with a BMI 35.0 to 39.9 kg/m2 with at least one serious co morbidity

29
Q

What is dumping syndrome? How many patients are affected?

A
  • Occurs in 15% of patients
  • Can be early or late
  • Early Dumping Syndrome
    • Usually within 15 minutes secondary to rapid emptying of food into the small bowel. Due to the hyperosmolality of the food it results in hypotension and activation of the sympathatic nervous system.
    • Hypotention
    • Tachycardia
    • Abdominal cramping and diarrhea
    • Nausea and vomiting
  • Late Dumping Syndrome
    • Postprandial hyperinsulinemic hypoglycemia (PHH) of unclear pathophysiology.
    • Patients present with dizziness, fatigue, diaphoresis, and weakness, usually occur one to three hours after ingestion of a carbohydrate-rich meal, typically months to years after surgery.
30
Q

How do you treat dumping syndrome?

A

—Patients should avoid foods that are high in simple sugar content and replace them with a diet consisting of high fiber, complex carbohydrate, and protein rich foods.

—Behavioral modification, such as small, frequent meals, and separating solids from liquid intake by 30 minutes.

—Usually, early dumping is self-limiting and resolves within 7 to 12 weeks

31
Q

What type of nutritional deficiencies develop in patients with gastric bypass?

A
  • Iron Deficiency Anemia; 30%
    • —Low gastric acid levels prohibit iron cleavage from food
    • —It’s normally absorbed in duodenum or proximal jejunum
    • —Decrease in iron-rich food consumption due to intolerance
  • Fat soluble vitamin deficiency; 30-50%
  • Can also see Zinc, Copper, and Selenium deficiency.
32
Q
A