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Flashcards in Gastroenterology Deck (92):

Define gastroesophageal reflux disease (GERD). What causes it?

In which patient population is it highest in?

stomach acid refluxes into the esophagus due to inappropriate, intermittent relaxation of the lower esophageal sphincter.

incidence is increased greatly in patients with a hiatal hernia.


Describe the classic symptoms of GERD. How is it treated?

“heartburn,” often related to eating and lying supine

Initial treatment: elevate the head of the bed and to avoid coffee, alcohol, tobacco, spicy and fatty foods, chocolate, and medications with anticholinergic properties. If this approach fails, antacids, H2 blockers, or PPIs may be tried.

Note: many patients have already tried OTC remedies, and many physicians begin empirical treatment at the first visit because “lifestyle modifications” usually fail.


What are the sequelae of GERD?

  • esophagitis
  • esophageal stricture (which may mimic esophageal cancer)
  • esophageal ulcer
  • hemorrhage
  • Barrett esophagus, and esophageal adenocarcinoma


What is a hiatal hernia? How is it different from a paraesophageal hernia?

hiatal hernia - sliding hernia, the whole gastroesophageal junction moves above the diaphragm, pulling the stomach with it; may predispose to GERD.

paraesophageal hernia - the gastroesophageal junction stays below the diaphragm, but the stomach herniates through the diaphragm into the thorax; may become strangulated


What are the signs of peptic ulcer disease (PUD)?

chronic, intermittent, localized epigastric pain (burning, gnawing, or aching); often relieved by antacids or milk.

occult blood in the stool and nausea or vomiting


Explain the classic differences between duodenal and gastric ulcers.



What is the diagnostic study of choice for PUD?

endoscopy (gold standard, most sensitive), but an upper GI barium study is cheaper and less invasive. If endoscopy is done, a biopsy of any gastric ulcer is mandatory to exclude malignancy.


What is the most feared complication of PUD? How should these be managed?

Other complications?

What should you suspect if an ulcer does not respond to treatment?

perforation - look for peritoneal signs, history of PUD, and free air on an abdominal radiograph. Treat with antibiotics (e.g., ceftriaxone, metronidazole) and ex lap to repair the perforation

GI bleeds - second most feared complication

If ulcers are severe, atypical (e.g., located in the jejunum), or nonhealing, think about stomach cancer or Zollinger-Ellison syndrome (gastrinoma; check gastrin level).


How is PUD treated initially? 3

  1. Stop all NSAID use.
  2. Start treatment with PPI
  3. Test for Helicobacter pylori infection, and if positive treat with triple therapy with a proton-pump inhibitor, clarithromycin, and amoxicillin 


List the surgical options for ulcer treatment.

What complications may occur from these procedures?

antrectomy, vagotomy, and Billroth I or II procedures

watch for: 

  • dumping syndrome (weakness, dizziness, sweating, N/V after eating)
  • hypoglycemia 2-3 hrs after a meal, which causes recurrence of the same symptoms
  • afferent loop syndrome (bilious vomiting after a meal relieves abdominal pain)
  • bacterial overgrowth
  • vitamin deficiencies (vitamin B12 and/or iron, causing anemia)


Define achlorhydria. What causes it?

What other findings would be associated with this?

absence of hydrochloric acid (HCl) secretion

caused most commonly by pernicious anemia, in which antiparietal cell antibodies destroy acid-secreting parietal cells and thus cause achlorhydria and vitamin B12 deficiency.

May also be caused by surgical gastric resection.


What are the classic differences between upper and lower GI bleeds in terms of:


common etiologies

how the stool looks

what an NGT aspirate looks like


How is a GI bleed treated?

First - assess ABCs [airways, breathing, circulation]) and give IV fluids and blood, if needed

Then, place NGT and test aspirate for blood to determine if a patient has an upper vs lower GI bleed

Endoscopy is usually performed (upper or lower, depending on symptoms and nasogastric tube aspirate). Endoscopically treatable lesions include ulcers, polyps, vascular ectasias, and varices.


What 2 radiologic imaging studies can be done to localize a GI bleed? 

Does surgery have a role?

  1. Radionuclide (i.e., nuclear medicine) scans can detect slow or intermittent bleeds if a source cannot be found with endoscopy
  2. Angiography can detect more rapid bleeds, and embolization of bleeding vessels can be done during the procedure.
  3. Surgery is reserved for severe or resistant bleeds and typically involves resection of the affected bowel (usually colon).


Define diverticulosis. What causes it? What are its complications?

saclike mucosal projections through the muscular layer of the colon and/or rectum

causes: age, low-fiber, high-fat diet

complications: GI bleeding (painless) and diverticulitis (inflammation of a diverticulum), which can lead to abscess, fistula formation, sepsis, or large bowel obstruction.


How do you diagnose and treat diverticulitis?

What test should a patient have after a treated episode of diverticulitis?

Signs and symptoms: LLQ pain or tenderness, fever, diarrhea or constipation, and elevated WBC

Diagnostic study: CT

Treatment:  antibiotics (e.g., a fluoroquinolone plus metronidazole), bowel rest (i.e., no oral intake), surgery indicated for perforation or abscess

After a treated episode of diverticulitis, all patients need a colonoscopy, as colon carcinoma with perforation can mimic diverticulitis clinically and on CT. These studies should be avoided during active diverticulitis, however, because of an increased risk for perforation.


How is diarrhea categorized according to etiology?

  • Systemic. Any illness can cause diarrhea as a systemic symptom, especially in children (e.g., infection).
  • Osmotic
  • Secretory
  • Malabsorptive
  • Infectious
  • Exudative
  • Altered intestinal transit


How does osmotic diarrhea occur? How can an easy diagnosis be made?

Caused by nonabsorbable solutes that remain in the bowel, where they retain water (e.g., lactose or other sugar intolerance).

When the patient stops ingesting the offending substance (e.g., avoidance of milk, a trial of not eating), the diarrhea stops—an easy diagnosis.


What causes secretory diarrhea?

How do you differentiate between this and osmotic diarrhea?

Results when the bowel secretes too much fluid; often caused by

  • bacterial toxins (cholera, some species of Escherichia coli )
  • VIPoma (pancreatic islet cell tumor that secretes vasoactive intestinal peptide)
  • bile acids (after ileal resection)

Secretory diarrhea continues even when the patient stops eating, compared to osmotic diarrhea, where the diarrhea stops when the patient stops ingesting the offending substance (ie milk)


What are the 3 common causes of malabsorptive diarrhea? How does this differentiate from osmotic diarrhea and secretory diarrhea.

  1. Celiac disease (look for dermatitis herpetiformis)
  2. Crohn disease
  3. Postgastroenteritis (because of depletion of brush-border enzymes)

Similar to osmotic diarrhea, the diarrhea stops when the patient stops eating. Secretory diarrhea continues even when the patient stops eating.


What are the common clues to infectious diarrhea?

What are the common causes?

  • (+) fever
  • (+) white blood cells in the stool (only with invasive bacteria such as Shigella, Salmonella, Yersinia, and Campylobacter spp)
  • (+) travel history
    • ETEC
    • Hikers and stream-drinkers may have Giardia (steatorrhea) -> treat with metronidazole
  • (+) antibiotic use 
    • Clostridium difficile -> treat with PO metronidazole (vancomycin is a second-line agent if metronidazole is not an option)


What causes exudative diarrhea?

How do these patients normally present?

results from inflammation in the bowel mucosa that causes seepage of fluid. Mucosal inflammation is usually because of IBD (Crohn disease or UC) or cancer

Clues: (+) fever and (+) WBC in the stool, as in infectious diarrhea, lacks pathogenic organisms, chronicity, and nonbowel symptoms


What are the 5 common causes of diarrhea caused by altered intestinal transit?

  • bowel resections
  • medications that interfere with bowel function
  • hyperthyroidism
  • neuropathy (e.g., diabetic diarrhea)
  • factitious diarrhea, which is caused by secret laxative abuse.


Define irritable bowel syndrome. How do you recognize it?

common cause of GI complaints.

look for anxious or neurotic patients with a history of

  • diarrhea aggravated by stress
  • bloating
  • abdominal pain relieved by defecation
  • mucus in the stool
  • psychosocial stressors in the history
  • normal physical findings and test results.

IBS is a diagnosis of exclusion; you must do at least basic lab tests, rectal examination, stool examination, and sigmoidoscopy. Because it is so common, however, it is the most likely diagnosis if the question gives no positive findings, especially in young adults (female-to-male ratio = 3:1).


What should you do if a patient has diarrhea? 

watch for and treat dehydration and electrolyte ∆s, especially metabolic acidosis and hypokalemia

Do a rectal examination, look for occult blood in stool, and examine the stool for bacteria (Gram stain and culture), ova and parasites, fat content (steatorrhea), and white blood cells.


What should you watch for in children after a bout of diarrhea?

How should these patients be managed?

watch for hemolytic uremic syndrome, which is characterized by:

  • thrombocytopenia
  • hemolytic anemia (schistocytes, helmet cells, and fragmented red blood cells on peripheral blood smear) 
  • acute renal failure

Treatment: supportive; may need dialysis and/or transfusions


Specify the classic differences between Crohn disease and ulcerative colitis in terms of:

place affected

thickness of pathology



bowel habit changes

classic lesions

colon cancer risk




Describe the extraintestinal manifestations of inflammatory bowel disease.

Both forms of IBD can cause:

  • uveitis
  • arthritis
  • ankylosing spondylitis
  • erythema nodosum
  • erythema multiforme
  • primary sclerosing cholangitis
  • failure to thrive or grow in children
  • toxic megacolon
    • Toxic megacolon is more common in UC; look for a markedly distended colon on abdominal radiograph.
  • anemia of chronic disease
  • fever


How is inflammatory bowel disease treated?

5-aminosalicylic acid +/- sulfa drug (e.g., sulfasalazine) when stable

Steroids + immunemodulators (azathioprine) during severe disease flare-ups


What causes toxic megacolon?

What preciptiates it?

How do these patients present?

How is it treated?

classically seen with IBD (especially UC) and infectious colitis (especially C. difficile)

may be precipitated by antidiarrheal medications, which for this reason are usually not given for infectious diarrhea

presentation: high fever, leukocytosis, abdominal pain, rebound tenderness, and a dilated segment of colon on abdominal xray

treatment: discontinue all antidiarrheal meds; make NPO, place NGT, start IV fluids, give antibiotics to cover bowel flora (ceftriaxone plus metronidazole) + steroids if the cause is IBD. Surgery indicated if perforation occurs.


List the 5 common findings of acute liver disease.

  • Elevated liver function tests (AST, ALT, bilirubin, alkaline phosphatase, and/or PT/INR)
  • Jaundice
  • Nausea and vomiting
  • RUQ pain or tenderness
  • Hepatomegaly


List the 6 common causes of acute liver disease.

  • Alcohol
  • Medications
  • Infection (usually hepatitis)
  • Reye syndrome
  • Biliary tract disease
  • Autoimmune disease


What is the classic abnormality on liver function tests in patients with alcoholic hepatitis?

An elevated AST that is more than twice the value of ALT, although both may be elevated.


What clues suggest hepatitis A? Describe the diagnostic serology.

How long is the incubation period?

Look for outbreaks from a foodborne source.

IgM anti-hepatitis A virus (HAV) is positive during jaundice or shortly thereafter.

The incubation period is about 4 weeks, although IgM may be detected by the time symptoms begin.


How is hepatitis B acquired? 4

What is the best treatment?

perinatally, sexual transmission, contaminated needles, transfused blood

IFNa-2b, peg-IFNa-2a, adefovir, dipivoxil, entecavir, telbivudine, or tenofovir can be tried in patients with chronic hepatitis and elevated liver enzymes.


Describe the serology of hepatitis B infection, including the surface, core, and “e” markers.

hepatitis B surface antigen (HBsAg) is (+) with any unresolved infection (acute or chronic)

(+) HBsAb means that the patient is immune (as a result of either recovery from infection or vaccination); HBsAb never appears if the patient has chronic hepatitis.

hepatitis B “e” antigen (HBeAg) is a marker for infectivity

patients with hepatitis B “e” antibody (HBeAb) have a low likelihood of spreading disease.

The first antibody to appear is the IgM hepatitis B core antibody (HBcAb), which appears during the “WINDOW PHASE” when both HBsAg and hepatitis B surface antibody (HBsAb) are negative.


What are the possible sequelae of chronic hepatitis B or C?

Cirrhosis and hepatocellular cancer (only with chronic, not acute, infection).


What should be given to persons acutely exposed to hepatitis B?

Hepatitis B Ig + hepatitis B vaccination


hepatitis B vaccination alone

BOTH been demonstrated to be effective in preventing transmission after exposure to hepatitis B virus.


Which type of viral hepatitis is the new king of chronic hepatitis?

What the screening guidelines for this?

Hepatitis C

  • most likely cause of hepatitis after a blood transfusion
  • more likely than hepatitis B to progress to chronic hepatitis, cirrhosis, and cancer.

Because of the relatively high prevalence in the “baby boomer” generation and lack of symptoms, the CDC and Prevention has recommended that all Americans born between 1945 and 1965 have a one-time screening test for hepatitis C.


Describe the serology, diagnosis, and treatment for hepatitis C.

(+) hepatitis C antibody means that the patient has had an infection in the past, but does not mean the infection has been cleared. Many patients become chronic carriers of the virus.

A test for hepatitis C virus RNA can detect and quantify the virus.

Treatment: pegylated IFNa + ribavirin (plus a protease inhibitor for those with genotype 1)

  • Success rates depend on the type of infection: Genotype 1 is the most common in the United States, but treatment success rates are higher with genotypes 2 and 3.


When is hepatitis D seen/acquired? Describe the serology.

seen only in patients with Hep B; acquired in the same ways as Hep B (perinatally, by sexual transmission, contaminated needles, blood transfusions)

IgM antibodies to the Hep D antigen = resolution of recent infection

(+) Hep D antigen, Hep D virus RNA, and IgM antibodies to Hep D = chronicity


How is hepatitis E transmitted? What is special about the infection in pregnant women?

Hepatitis E is transmitted like hepatitis A (via food and water; no chronic state); often fatal in pregnant women (for unknown reasons).


What are the 3 classic causes of drug-induced hepatitis?

What is the first step in management?

  • Acetaminophen
  • tuberculosis drugs (e.g., rifampin, isoniazid, pyrazinamide)
  • halothane
  • HMG CoA-reductase inhibitors
  • carbon tetrachloride

first step in treatment is to stop the drug.


When should you suspect idiopathic autoimmune hepatitis?

What is the serologic marker?


Idiopathic autoimmune hepatitis is classically seen in 20- to 40-year-old women with antismooth muscle or antinuclear antibodies and no risk factors or lab markers for other causes of hepatitis.

Treat with steroids.


What are the usual causes of chronic liver disease?

What are the physical evidence of this?

Alcohol, hepatitis, and metabolic diseases.

Watch for the stigmata of chronic liver disease:

  • gynecomastia
  • testicular atrophy
  • palmar erythema
  • spider angiomas on skin
  • ascites


Which species of viral hepatitis can lead to chronic liver disease?

Hepatitis B, C, and D.


What is hemochromatosis and what is its inheritance pattern?

How do you recognize it?

Which sex tends to be affected more?

How do you treat it?

Autosomal recessive mutation that results in excessive iron absorption by the intestine and subsequent deposition in the

  • liver (potentially causing cirrhosis and/or hepatocellular carcinoma)
  • pancreas (potentially causing diabetes)
  • heart (resulting in dilated cardiomyopathy)
  • skin (causing pigmentation classically known as bronze diabetes)
  •  joints (arthritis)

Men are symptomatic earlier and more often because women lose iron with menstruation.

Treatment: phlebotomy


What is Wilson disease and what is its inheritance pattern?

How do you recognize it clinically and diagnostically?

How is it treated?

Autosomal recessive disease resulting in excessive serum copper -> deposition all over

Patients classically have liver disease with CNS/psychiatric manifestations (caused by copper deposits in the basal ganglia) and Kayser-Fleischer rings in the eye.

Serum ceruloplasmin (copper transport protein) = low or absent; serum copper = normal.

Liver biopsy = excessive copper deposition

Treat with penicillamine (copper chelator).


What are the clues to a diagnosis of alpha-1 antitrypsin deficiency?

What is the inheritance pattern?

young adult who develops cirrhosis and/or emphysema without risk factors for either; diagnosis requires a serum A1AT


What metabolic derangements accompany liver failure?

  • Coagulopathy: Prolonged PT and/or PTT (in severe cases); non-responsive to Vitamin K because it cannot be utilized by the damaged liver
    • Symptomatic patients must be treated with fresh frozen plasma.
  • Jaundice/hyperbilirubinemia: Elevated conjugated and unconjugated bilirubin 
  • Hypoalbuminemia
  • Ascites: due to portal HTN +/- hypoalbuminemia;  (+) shifting dullness or a positive fluid wave
    • possible complication: spontaneous bacterial peritonitis
      • ​​caused by infected ascitic fluid that can lead to sepsis; culprits: E. coli, Streptococcus pneumoniae, and other enteric bugs
      • Sx: fever +/- AMS
      • Dx: paracentesis, examine the ascitic fluid for elevated WBC (especially PMNs), and do Gram stain, culture, and sensitivity tests, as well as glucose (low with infection), and protein (high with infection) tests.
      • Treat with broad-spectrum antibiotics (cefotaxime is a common choice).
  • Portal HTN: causes hemorrhoids, varices, and caput medusae
  • Hyperammonemia: The liver clears ammonia.
    • Treat with decreased protein intake (source of ammonia) and lactulose (prevents absorption of ammonia). The last choice is neomycin (which is not used as much as it once was), which kills bowel flora that make ammonia.
  • Hepatic encephalopathy: caused by hyperammonemia; often precipitated by protein intake, GI bleed, or infection. Look for asterixis and/or mental status changes.
  • Hepatorenal syndrome: Liver failure may cause kidney failure (idiopathic).
  • Hypoglycemia: The liver stores glycogen.
  • Disseminated intravascular coagulation: Activated clotting factors are normally cleared by the liver.


What signs and symptoms suggest biliary tract obstruction as a cause of jaundice?

  • Elevated conjugated bilirubin. Conjugated bilirubin is more elevated than unconjugated bilirubin because the liver still functions and can conjugate bilirubin, but conjugated bilirubin cannot be excreted because of biliary tract disease.
  • Markedly elevated alkaline phosphatase
  • Pruritus
  • Clay-colored stools
  • Dark urine, which is strongly positive for conjugated bilirubin. Unconjugated bilirubin is not excreted in the urine because it is tightly bound to albumin.


What are the commonly tested types of biliary tract obstruction?

  • Bile duct obstruction
  • cholestasis
  • cholangitis
  • primary biliary cirrhosis
  • primary sclerosing cholangitis


What are the two major causes of common bile duct obstruction?

How are they distinguished?

How are they detected and treated?


obstruction with a gallstone (choledocholithiasis)

  • four Fs (female, forty, fertile, and fat)
  • detection: US, MRCP, ERCP
  • trmt: endoscopic removal

malignancy (ie pancreatic cancer, cholangiocarcinoma, bowel cancer)

  • weight loss, courvoisier sign (jaundice + palpable gallbladder)


What are the two common causes of cholestasis?

  • Medications (e.g., birth control pills, trimethoprim-sulfamethoxazole, phenothiazines, androgens)
  • pregnancy


What clues suggest a diagnosis of primary biliary cirrhosis?


  • milddle aged women w/o risk factors for liver/biliary disease
  • marked pruritus
  • jaundice
  • positive antimitochondrial antibodies

treatment: Cholestyramine (bile acid sequestrant, which binds bile in the GI tract to prevent its reabsorption) helps with symptoms, but the only treatment is liver transplantation.


Who gets primary sclerosing cholangitis?

How do these patients normally present?

young adults with inflammatory bowel disease (usually ulcerative colitis)

symptoms: fever, chills, pruritus, and RUQ pain


What is cholangitis?

What usually precipitates it?

What is the tip-off to its presence?

How is it treated?

precipitated by a gallstone that blocks the common bile duct with subsequent infection of the bile duct system.

The tip-off is the presence of Charcot triad: fever, RUQ pain, and jaundice

Treatment: antibiotics + remove gallstones surgically or endoscopically


What are the 2 classic symptoms of esophageal disease?

Dysphagia (difficulty in swallowing) and/or odynophagia (painful swallowing).

Patients may also have atypical chest pain.


Define achalasia.

What is it usually associated with?

What are the symptoms?

How is it diagnosed and treated?

What are these patients at high risk for?

incomplete relaxation of the lower esophageal sphincter + loss/derangement of peristalsis; usually idiopathic but may be secondary to Chagas disease (Reduviid bug)

sx: intermittent dysphagia for solids and liquids, but no heartburn because the lower esophageal sphincter stays tightly closed and does not allow acid to reflux

dx: Barium swallow reveals a dilated esophagus with distal “bird-beak” narrowing, confirmed with esophageal manometry

Treatment: Ca channel blockers, pneumatic balloon dilatation, or botulism toxin injection. Surgery (myotomy) is a last resort. 

Risk: esophageal carcinoma


What are the symptoms and signs of esophageal spasm? How is it diagnosed and treated?

diffuse esophageal spasm and nutcracker esophagus (best thought of as a special variant of esophageal spasm) are characterized by irregular, forceful, and painful esophageal contractions that cause intermittent chest pain.

Dx: esophageal manometry.

Trmt: calcium channel blockers and, if needed, surgery (myotomy)


What clues/symptoms suggest scleroderma as the cause of esophageal complaints?

How is it diagnosed?

Scleroderma causes esophageal fibrosis + atrophy of smooth muscle; lower esophageal sphincter becomes incompetent and patients can experience heartburn (in contrast to achalasia). Other associated symptoms include: masklike facies, CREST (calcinosis, Raynaud phenomenon, esophageal dysmotility, sclerodactyly, and telangiectasias)

Dx: (+) ANA


What do you need to know about the epidemiology of esophageal cancer?

adenocarcinoma is now more common than squamous cell carcinoma.

  • Adenocarcinoma - caused by the long-standing effects of gastric acid reflux and thus occurs in the distal esophagus.
  • Squamous cell carcinoma - caused by alcohol + tobacco (synergistic effect); classically seen in black men > 40 yo who smoke and drink alcohol; (+) weight loss, food “sticking” in the chest; tumor usually in the proximal esophagus


What is the relationship between Barrett esophagus and esophageal cancer?

Which type does it normally cause?

What does the pathology show?

How is it diagnosed and managed?

Barrett esophagus, usually is caused by longstanding GERD, predisposes to esophageal adenocarcinoma

pathology: columnar metaplasia of the normal squamous cell esophageal mucosa

diagnosis & management: endoscopy + endoscopic biopsy, with periodic biopsies to monitor for the development of esophageal cancer


What causes acute pancreatitis?

What are the signs and symptoms of acute pancreatitis?

alcohol or gallstones (most common)

Others: hypertriglyceridemia, viruses (mumps, coxsackie virus), trauma, hypercalcemia, PUD, medications (isoniazid, furosemide, simvastatin, steroids, azathioprine), and scorpion stings

Acute Signs: epigastric abdominal pain that radiates to the back, nausea with vomiting that fails to relieve the pain, leukocytosis, and elevated amylase/lipase

Severe Signs: Grey Turner sign (blue-black flanks) and Cullen sign (blue-black umbilicus), both of which are because of a hemorrhagic pancreatic exudate


What is the difference between the Grey Turner sign and Cullen sign? What do they both indicate and what causes it?

Severe signs of pancreatitis:

  • Grey Turner sign (blue-black flanks)
  • Cullen sign (blue-black umbilicus), both of which are because of a hemorrhagic pancreatic exudate


How is acute pancreatitis treated? 4

NPO + NGT (optional) + IVF + pain meds (hydromorphone or fentanyl)


What are the 3 complications of acute pancreatitis?

How are these generally managed?

  1. pseudocyst formation (drain surgically if symptomatic and persistent for several weeks)
  2. abscess or infection (treat with antibiotics and drainage if needed)
  3. chronic pancreatitis


What causes chronic pancreatitis? How is it treated?

What is the sequelae of this?

What is the management of patients with chronic pancreatitis?


note: gallstones do not cause chronic pancreatitis


  • diabetes
  • steatorrhea 
  • pancreatic calcifications
  • ADEK deficiencies 
  • increased risk of pancreatic cancer


  • alcohol abstinence
  • PO pancreatic enzyme replacement
  • fat soluble vitamin supplements


Distinguish between Mallory-Weiss and Boerhaave tears in the esophagus.

How do they present? How are they diagnosed and treated

Mallory-Weiss tears - superficial erosions in the esophageal mucosa

  • usually stop bleeding on their own or with endoscopic treatment

Boerhaave tears - full-thickness esophageal ruptures

  • require immediate surgical repair and drainage

Sx: GI bleed, vomiting + retching (alcoholics and bulimic patients) if they are not iatrogenic (endoscopy)

Dx: endoscopically (bleeding vessels should be sclerosed) and/or CT with contrast


What is the rule about bowel contrast when a GI perforation is suspected and what is the rationale behind this?

What is the alternative and what are the caveats to using this? 

With suspected GI perforation, do not use barium for contrast studies because it can cause chemical peritonitis or mediastinitis

Alternative: water-soluble contrast (gastrografin) with one caveat: can cause chemical pneumonitis in patients with a significant aspiration risk (but oddly, the lungs tolerate barium well)


When does pyloric stenosis usually present?

What are some typical findings of patients who present with this?

What does the vomit usually look like?


When does Intestinal atresia usually present?

What are some typical findings of patients who present with this?

What does the vomit usually look like?


When does tracheoesophageal fistula usually present?

What are some typical findings of patients who present with this?

What does the vomit usually look like?


When does hirschsprung disease usually present?

What are some typical findings of patients who present with this?

What does the vomit usually look like?


When does anal atresia usually present?

What are some typical findings of patients who present with this?

What does the vomit usually look like?


When does choanal atresia (back of the nasal passage, choana, is blocked) usually present?

What are some typical findings of patients who present with this?

What does the vomit usually look like?


When does intussusception usually present?

What are some typical findings of patients who present with this?

What does the vomit usually look like?


When does necrotizing entercolitis usually present?

What are some typical findings of patients who present with this?

What does the vomit usually look like?


When does meconium ileus usually present?

What are some typical findings of patients who present with this?

What does the vomit usually look like?


When does midgut vovulus usually present?

What are some typical findings of patients who present with this?

What does the vomit usually look like?


When does meckel's diverticulum's usually present?

What are some typical findings of patients who present with this?

What does the vomit usually look like?


When does strangulated hernia usually present?

What are some typical findings of patients who present with this?

What does the vomit usually look like?


Which GI malformation primarily causes respiratory problems? What is a complication of this? 


How do these patients present?

Is it more common in males or female infants? left side or right side?

diaphragmatic hernia - results in bowel herniation into the thorax and causing lung compression, which results in pulmonary hypoplasia

sx: respiratory distress with bowel sounds in the chest, bowel loops in the thorax on CXR 


left side 


How are omphalocele and gastroschisis differentiated?


  • midline
  • abdominal organs sealed with intact sac
  • absent umbilical ring
  • other anomalies are common


  • located to the right of the midline
  • only small bowel is exposed (no true hernia sac)
  • umbilical ring is present
  • other anomalies are rare


What is Henoch-Schönlein purpura? 

How do these patients present and what symptoms are common with this?



  • may present with GI bleeding + abdominal pain
  • history of URIs
  • characteristic rash on lower extremities and buttocks
  • swelling in hands and feet
  • arthritis
  • hematuria and proteinuria

Treatment: hydration, rest, and pain relief


What is the most common cause of diarrhea in children?

viral gastroenteritis (Norwalk virus, rotavirus)

should be noted that diarrhea is often a nonspecific sign of any systemic illness (e.g., otitis media, pneumonia, urinary tract infection).


True or false: Children may develop IBD and IBS

True - diarrhea, fever, bloody stools, anemia, joint pains, and poor growth are more concerning for IBD.

GI complaints may be caused by anxiety or psychiatric problems; watch for separation anxiety, children who do not want to go to school, depression, and child abuse.


What is the first step in evaluating neonatal jaundice?

Why is jaundice of concern in a neonate?

determine if jaundice is physiologic or pathologic - measure total, direct, and indirect bilirubin

Concern: kernicterus (caused by high levels of unconjugated bilirubin with subsequent deposit in the basal ganglia); poor feeding, seizures, flaccidity, opisthotonos, and apnea in the setting of severe jaundice.

  • opisthotonos - spasm of the muscles causing backward arching of the head, neck, and spine, as in severe tetanus


What causes physiologic jaundice of the newborn? Who gets it? When does it resolve?

  • occurs because of incomplete maturation of liver functioning
  • 50% of normal infants get experience this, higher incidence in premature infants
  • peaks 2 days after birth, resolves in 2 weeks for normal infants
  • peaks 3 days after birth, resolves in 3 weeks for preemies


How is pathologic jaundice recognized?

What are the 6 potential causes of this?

pathologic jaundice - jaundice present at birth or <24 hours post-partum; may be caused by:

  • Breast milk jaundice: cause peak bilirubin levels at 2-3 wks; temporarily stop breastfeeding until it resolves.
  • Illness: Infection or sepsis, hypothyroidism, liver insult, cystic fibrosis, and other illnesses may prolong neonatal jaundice and lower the threshold for kernicterus
  • Hemolysis: From Rhesus (Rh) incompatibility or congenital RBC diseases that cause hemolysis in the neonatal period. Look for anemia, peripheral smear abnormalities, (+) family hx, and higher levels of unconjugated bilirubin.
  • Metabolic disorders:
    • ​​ Crigler-Najjar cause severe unconjugated hyperbilirubinemia, whereas Gilbert cause a mild form
      • (both are ConjuGation problems) 
    • Rotor and Dubin-Johnson cause conjugated hyperbilirubinemia
  • Biliary atresia: Full-term infants with clay- or gray-colored stools and high levels of conjugated bilirubin. Treat with surgery.
  • Medications: Avoid sulfa drugs in neonates; they displace bilirubin from albumin and may precipitate kernicterus.


How is pathologic jaundice treated?

Unconjugated hyperbilirubinemia that persists, rises above 15 mg/dL, or rises rapidly is treated with phototherapy to convert unconjugated bilirubin to a water-soluble form that can be excreted.

A last resort is exchange transfusion, but should not be implemented unless the level of unconjugated bilirubin is > 20 mg/dL.


What should you do if an infant is born to a mother with active Hep B?

infant should receive first immunization shot PLUS hepatitis B Ig at birth