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INPATIENT > Gastrointestinal disorders > Flashcards

Gastrointestinal disorders Flashcards

1
Q

What are some etiologies of gastroparesis?

A
  • Idiopathic
  • Diabetes mellitus
  • Medications - a2 agonists, TCAs, CCBs, octreotide
  • Post-surgical - injury to vagus nerve, e.g. fundoplications, Roux-en-Y
  • Neurologic disease, e.g. Parkinson
  • Autoimmune

UpToDate

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2
Q

What are the clinical manifestations of gastroparesis?

A
  • nausea (93%)
  • vomiting (68 - 84%)
  • abdominal pain (46 - 90%)
  • early satiety (60 - 86%)
  • postprandial fullness, bloating
  • in severe cases, weight loss

UpToDate

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3
Q

What is the workup for suspected gastroparesis?

A
  1. Rule out mechanical obstruction: Upper endoscopy, CT, MRI
  2. Assess gastric motility: gastric emptying scintigraphy, wireless motility capsule
    * UpToDate*
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4
Q

What is the initial treatment approach for gastroparesis?

A
  1. Dietary modification:
  • Fats and fiber move more slowly through the GI tract - eat diet low in fat and only soluble fiber
  • Avoid carbonated beverages, alcohol, smoking
  1. Hydration and nutrition - repeated vomiting may lead to electrolyte imbalance and/or dehydration
  2. Optimize glycemic control
  3. Prokinetics - metoclopramide, erythromycin
    * UpToDate*
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5
Q

What is the treatment approach to refractory gastroparesis?

A
  1. Jejunostomy for nutrition
  2. PEG for decompression of upper GI tract
  3. TCAs, gastric electrical stimulation
    * UpToDate*
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6
Q

Diagnostic criteria for spontaneous bacterial peritonitis:

A
  1. presence of ascites (no ascites, no SBP)
  2. Polymorphonuclear cell count in ascitic fluid > 250
  3. Positive culture of ascitic fluid (but don’t wait for results to start treatment - if above are true, start empiric therapy)
    * UpToDate*
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7
Q

Spontaneous bacterial peritonitis almost exclusively occurs in patients with _____.

A

cirrhosis

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8
Q

What are the clinical manifestations of spontaneous bacterial peritonitis?

A
  • Fever
  • Abdominal pain & tenderness
  • Altered mental status
  • Diarrhea
  • Paralytic ileus, hypotension, hypothermia

UpToDate

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9
Q

How is spontaneous bacterial peritonitis treated?

A
  1. Empiric antibiotics: IV third-generation cephalosporin -> cefotaxime, ceftriaxone
  2. Albumin 1.5 g/kg IV reduces mortality
    * UpToDate, Medscape*
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10
Q

What are the complications of spontaneous bacterial peritonitis?

A

SBP *is* the complication - of cirrhosis! It’s bad news - 40-70% mortality

Medscape

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11
Q

What are the 4 main etiologies of ascites?

A
  1. Portal hypertension (e.g. cirrhosis, HF)
  2. Hypoalbuminemia (e.g. nephrotic syndrome, severe malnutrition)
  3. Peritoneal disease (e.g. ovarian cancer)
  4. Other (e.g. myxedema, disrupted pancreatic duct)
    * UTD*
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12
Q

What are the clinical manifestations of ascites?

A
  • abdominal discomfort
  • shortness of breath
  • early satiety
  • weight gain

UTD

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13
Q

What is the diagnostic workup for ascites?

A
  1. Physical exam
  2. Ultrasound
  3. Paracentesis to determine cause of ascites
    * UTD*
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14
Q

How is the cause of ascites determined?

A

Assessing the ascitic fluid:

  • appearance - cloudy, bloody, etc.
  • serum-to-ascites albumin gradient (SAAG) determination
  • cell count and differential
  • total protein concentration

Plus basically every single test available for serum: glucose, LDH, gram stain, triglycerides, etc.

UTD

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15
Q

What is SAAG and what is it for?

A

Serum-ascites albumin gradient -> to help determine cause of ascites

_To calculate: _

(albumin concentration of serum) - (albumin concentration of ascitic fluid)

To use it:

HIGH difference in the two: ascites is due to portal hypertension, e.g. cirrhosis, alcoholic hepatitis, HF, Budd-Chiari syndrome

LOW difference in the two: ascites is not due to portal hypertension, e.g. pancreatitis, nephrotic syndrome

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16
Q

What is the biggest risk factor for gastric adenocarcinoma and gastric lymphoma?

A

H. pylori

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17
Q

Name 4 environmental risk factors for gastric adenocarcinoma.

A

~high nitrate diet

~low vitamin C

~hx pernicious anemia

~hx gastric resection

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18
Q

What are the s/s of gastric cancer?

A
  • Generally asymptomatic until quite advanced
  • Dyspepsia, epigastric pain, anorexia, early satiety, weight loss
  • Ulcerating lesions can lead to bleeding and hematemesis or melena
  • Pyloric obstruction leads to postprandial vomiting
  • LES obstruction leads to dysphagia
  • Palpable gastric mass is NOT COMMON

Sign of metastatic spread:

Virchow node! (left supraclavicular)

~No specific lab findings other than IDA if bleeding or liver test abnormalities if hepatic metastasis

CURRENT

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19
Q

What is the diagnostic workup for suspected gastric cancer?

A

Upper endoscopy for all patients over 55 with new dyspepsia or in any patient with dyspepsia that fails to respond to a PPI trial

CURRENT

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20
Q

What is the management of gastric cancer?

A

Surgical resection is the only therapy with curative potential

CURRENT

21
Q

What is Zollinger Ellison syndrome?

A

a rare cause of peptic ulcer disease

22
Q

What are the s/s of Zollinger Ellison syndrome?

A

Over 90% of patients with ZE have peptic ulcers, and usually the symptoms are indistinguishable from other causes of PUD so ZE may go undetected for years.

CURRENT

23
Q

What is the diagnostic workup for Zollinger Ellison syndrome and when should you do it (when do you suspect possible ZE)?

A
  • If the patient has refractory ulcers, multiple duodenal ulcers, frequent ulcer recurrences, ulcers with diarrhea, giant ulcers, or has ulcers and is negative for H. pylori and NSAID use, then ZE screening should be done.
  • The most sensitive and specific method for identifying ZE is an increased fasting serum gastrin concentration.
  • pH should also be measured, to rule out hypochlorhydria (increased pH, whereas it will be lower with ZE).
  • When testing serum gastrin, need to withdraw H2 antagonists for 24 hours and PPIs for 6 days.
  • Imaging is done to determine the extent of metastasis and to determine the primary tumor site.

CURRENT

24
Q

How is Zollinger Ellison syndrome managed?

A
  1. PPIs – control hypersecretion
  2. Resection of tumor

CURRENT

25
Q

List some causes of gastritis.

A
  • H. pylori
  • NSAIDs
  • Alcohol
  • Autoimmune
  • Serious or life-threatening illness

UpToDate

26
Q

What is the workup for suspected gastritis?

A

Upper endoscopy, biopsy

H. pylori testing

Barium swallow

CBC (anemia)

UpToDate

27
Q

What is the treatment for gastritis?

A
  • PPI and/or H2-receptor antagonists
  • Treat H. pylori as needed
  • Stop offending agents (alcohol, NSAIDs, etc.)

CURRENT

28
Q

What are the 2 major causes of peptic ulcer disease?

A
  1. NSAIDs
  2. H. pylori
29
Q

What are the s/s of peptic ulcer disease?

A
  • EPIGASTRIC PAIN (80-90% of patients)
  • pain is well-localized to epigastrium, is gnawing, dull, aching, and not severe
  • 50% of patients get relief of pain with food or antacids and a recurrence of pain 2-4 hours later
  • 67% of duodenal ulcers and 33% of gastric ulcers cause nocturnal pain that awakens the patient
  • Most patients have symptomatic intervals interspersed with asymptomatic months or years

CURRENT

30
Q

What is the diagnostic workup for peptic ulcer disease?

A

Upper endoscopy

H. pylori testing

31
Q

What is the treatment for peptic ulcer disease?

A
  • PPIs
  • H2-receptor antagonists
  • H. pylori eradication therapy
  • STOP SMOKING

CURRENT

32
Q

List some risk factors for pancreatic cancer.

A
  • Genetic: family history of pancreatic cancer; BRCA1/BRCA2 breast cancer gene
  • Non-type O blood group
  • Chronic pancreatitis
  • DM/insulin resistance
  • Cigarettes
  • Obesity
  • “Western” diet (meat, saturated fat, smoked meat)

UpToDate

33
Q

What are the presenting s/s of pancreatic cancer?

A

The most common presenting symptoms in patients with exocrine pancreatic cancer are pain, jaundice, and weight loss.

UTD

34
Q

What is the workup for suspected pancreatic cancer?

A
  1. Lab tests: LFTs, serum lipase
  2. U/S (if jaundice); abdominal CT if pain without jaundice or if mass seen on U/S
  3. Sometimes tumor marker CA 19-9 (depends on tumor size and patient blood group antigens)
    * UTD*
35
Q

What is the treatment approach for pancreatic cancer?

A

Surgical resection is the only potentially curative treatment. Unfortunately, because of the late presentation of the disease, only 15 to 20 percent of patients are candidates for pancreatectomy.

If not resectable, then use algorithm to determine a combination of chemotherapy and radiation.

UTD

36
Q

Name some common causes of upper GI bleeding.

A
  • Gastric and/or duodenal ulcers (epigastric/RUQ pain)
  • Varices (hx EtOH, portal HTN, jaundice)
  • Esophagitis (odynophagia, dysphagia, GERD)
  • Erosive gastritis/duodenitis (dyspepsia, N/V)
  • Mallory-Weiss syndrome (hx retching, epigastric pain)
  • Angiodysplasia (asymptomatic other than s/s bleeding)
  • Mass lesions (polyps/cancers)

UTD

37
Q

What are the top causes of lower GI bleeding?

A
  • Diverticulosis
  • Colitis
  • Ischemia
  • Anorectal (hemorrhoids, anal fissures, rectal ulcers)
  • Neoplasia (polyps and cancers)
  • Angiodysplasia
  • Postpolypectomy
  • Inflammatory bowel disease
  • Colitis

UTD

38
Q

Describe the treatments for varices:

–prophylaxis

–acute bleeding

A

Prophylaxis: nonselective BB (propranolol), endoscopic variceal ligation

Acute bleeding: octreotide, endoscopic band ligation, abx if cirrhotic (ceftriaxone or norfloxacin)

purple book 3-3, 3-22

39
Q

What is acute liver failure?

A

acute hepatic disease (elevated aminotransferases, often with abnormal bilirubin and alkaline phosphatase levels)

+

hepatic encephalopathy

+

elevated INR/PTT

purple book 3-20, UTD

40
Q

What are the physical exam findings of cirrhosis?

A
  • Hepatomegaly
  • Splenomegaly
  • Spider angiomata/spider telangiectasias
  • Palmar erythema
  • Digital clubbing
  • Dupuytren’s contracture
  • Muehrcke nails, Terry nails
  • Gynecomastia (men)
  • Loss of chest or axillary hair (men)
  • Testicular atrophy (men)
  • Caput medusa
  • Cruveilhier-Baumgarten murmur (venous hum heard best with the stethoscope over the epigastrium)
  • Jaundice
  • Ascites (abdominal distension, shifting dullness, fluid wave)
  • Asterixis
  • Fetor hepaticus

UTD

41
Q

What are the lab findings of cirrhosis?

A
  • Moderately elevated aminotransferases (often with an AST:ALT ratio >1)
  • Elevated alkaline phosphatase (2 to 3 times the ULN)
  • Elevated GGT
  • Thrombocytopenia (splenic sequestration 2/2 portal HTN)
  • Leukopenia/neutropenia
  • Anemia
  • Low serum albumin
  • Prolonged PTT/elevated INR
  • Hyperbilirubinemia
  • Hyponatremia
  • Elevated serum creatinine

UTD

42
Q

What are the imaging findings in cirrhosis?

A
  • Surface nodularity
  • Increased echogenicity (ultrasound)
  • Atrophy of the right lobe
  • Hypertrophy of the caudate or left lobes
  • Small, nodular liver
  • Ascites
  • Hepatocellular carcinoma
  • Portal/splenic/superior mesenteric vein thrombosis
  • Portosystemic collaterals

UTD

43
Q

Review the pathophysiology of hepatorenal syndrome.

A
  • Cirrhosis -> portal hypertension -> splanchnic dilatation -> underfilling of renal arteries -> renin release -> systemic vasoconstriction, including renal arteries -> decrease in renal blood flow -> Cr goes up (hypothesis from purple book 3-22, UTD)
  • Kidneys themselves are normal
44
Q

What are the diagnostic criteria for hepatorenal syndrome?

A
  1. cirrhosis w/ ascites
  2. Cr > 1.5 mg/dL
  3. No improvement in Cr after volume expansion with albumin and stopping diuretics
  4. No shock
  5. No nephrotoxic meds
  6. No organic kidney disease or obstruction
    * purple book 3-22*
45
Q

What are the treatment approaches for hepatorenal syndrome?

A
  1. octreotide + midodrine + albumin

or

terlipressin + albumin

  1. TIPS
  2. liver transplant
    * purple book 3-22, UTD*
46
Q

What are 6 etiologies of hepatitis?

A
  • viral
  • autoimmune
  • alcoholic
  • acetaminophen
  • ischemic
  • nonalcoholic fatty liver disease

purple book 3-17

47
Q

Name 5 classes of antiemetics, examples of each, and what type of nausea they are used for.

A

Anticholinergics (M1 receptor antagonists): scopolamine; motion sickness

Antihistamines (H1 receptor antagonists): diphenhydramine, meclazine, promethazine [Phenergan]; motion sickness

Dopamine D2 receptor antagonists: prochlorperazine [Compazine], metoclopramide [Reglan]; chemo nausea

Serotonin 5-HT3 receptor antagonists: ondansetron [Zofran]; chemo nausea

Neurokinin NK1/Substance P receptor antagonists: aprepitant; chemo nausea

UTD

48
Q

What are the most common causes of small bowel obstruction?

Other causes?

A
  • Most common: postoperative adhesions & hernias
  • Others: tumors, intussusception, gallstones, etc.

UTD

49
Q

What are the clinical manifestations of small bowel obstruction?

A
  • Patients with bowel obstruction can present with an abrupt onset of abdominal pain, nausea, vomiting, and abdominal distention, or with intermittent, acute symptoms that resolve only to recur again.
  • A hallmark of small bowel obstruction is dehydration, which manifests as tachycardia, orthostatic hypotension, and reduced urine output, and if severe, dry mucus membranes.

UTD

INPATIENT (11 decks)

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