Gastroenterology Flashcards
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
- Stop all NSAID use.
- Start treatment with PPI
- 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:
location
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?
- Radionuclide (i.e., nuclear medicine) scans can detect slow or intermittent bleeds if a source cannot be found with endoscopy
- Angiography can detect more rapid bleeds, and embolization of bleeding vessels can be done during the procedure.
- 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.
- Celiac disease (look for dermatitis herpetiformis)
- Crohn disease
- 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
progression
location
bowel habit changes
classic lesions
colon cancer risk
surgery
.
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.
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)
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?
How are omphalocele and gastroschisis differentiated?
Omphalocele
- midline
- abdominal organs sealed with intact sac
- absent umbilical ring
- other anomalies are common
Gastroschisis
- located to the right of the midline
- only small bowel is exposed (no true hernia sac)
- umbilical ring is present
- other anomalies are rare
