GI 1 pt 2 Flashcards
Describe S/Sx of Conjugated hyperbilirubinemia (direct)
1) Possibly asymptomatic (mild)
2) Often with pruritis, light-colored stools (acholic), & jaundice
3) Malaise, anorexia, RUQ discomfort frequent with HC disease
4) Dark urine, jaundice, and in women, amenorrhea can occur
5) Other possible signs: enlarged tender liver, spider telangiectasias (angiomas), palmar erythema, ascites, gynecomastia, sparse body hair, fetor hepaticus, & asterixis
Hyperbilirubinemia initial labs & imaging: What are the first labs you should order?
Sr total & unconjugated bilirubin, ALP, ALT & AST, PT/INR, albumin
Hyperbilirubinemia initial labs & imaging:
1) What does it tell you if ALP, AST, & ALT are normal?
2) What abt if it’s predominant ALP elevation?
3) What if there’s a predominant AST & ALT elevation?
1) Not likely hepatic injury or biliary tract disease
2) Suggests biliary obstruction or intrahepatic cholestasis
3) Suggests jaundice caused by intrinsic hepatocellular disease
1) What does elevated INR that corrects with Vit. K suggest?
2) What if elevated INR does not correct with Vit. K?
1) Suggests obstructive jaundice
2) Suggests hepatocellular disease with impaired synthetic function
Hyperbilirubinemia initial labs & imaging: What are the 3 initial imaging options?
US, CT, MRI
List some potential causes of abd. pain
1) Parietal peritoneal inflammation from bacterial contamination, chemical irritation
2) Mech. obstruction of hollow viscera
3) Vasc. disturbances
4) Distention of viscera
5) Inflammation
True or false: IBS Sx can mimic ovarian CA
True
List some potential causes of referred abd pain
1) Cardiothoracic
2) Metabolic causes
3) Neurologic
4) Toxins
5) Other
Give some DDxs for abd. pain for each location:
1) Upper right quadrant
2) Epigastric
3) Left upper quadrant
Give some DDxs for abd. pain for each location:
1) Right lower quadrant
2) Periumbilical
3) Left lower quadrant
Give some potential causes of diffuse nonlocalized pain
1) Gastroenteritis
2) Mesenteric ischemia
3) Bowel obstruction
4) IBS
5) Peritonitis
6) Diabetes
7) Malaria
8) Metabolic diseases
9) Psych. disease
Describe the patterns of referred abd pain
GERD (non cardiac chest pain):
1) What can it mimic?
2) When may it occur?
3) How is it managed?
1) Angina pectoris with substernal squeezing or burning.
2) After meals, awaken patients from sleep, and be exacerbated by emotional stress
3) Acid suppressive therapy (usually PPIs x 4 weeks)
Non-reflux esophagitis (medications, infections, radiation injury):
1) How does it present?
2) How is it managed?
1) Sternal chest pain, odynophagia
2) Address underlying etiology
Eosinophilic esophagitis (EoE; non card. chest pain):
1) Epidemiology and etiology?
2) Sx?
3) How is it Dx’d?
4) How is it managed?
1) M>F, 20-30 y/o; strong association with food & environmental allergies, asthma, atopic dermatitis
2) Dysphagiawith solids, food impaction, central chest pain, refractory heartburn
3) Sx, endoscopic findings, & histology
4) Dietary modification (SFED,) PPIs, topical glucocorticoids, endoscopic dilatation of strictures, dupilumab (inhibits IL 4 &13)
Esophageal motility disorder (non card. chest pain):
1) Sx?
2) Mgmt?
1) Squeezing retrosternal pain or spasm
Dysphagia with solids and liquids
2) Treat underlying etiology
3 most common causes of infectious esophagitis are what?
1) Esophageal candidiasis
2) Herpes simplex virus (HSV)
3) Cytomegalovirus (CMV)
Esophagitis via esophageal candidiasis:
1) What 2 conditions is it most common in?
2) What may they have simultaneously?
3) What is the hallmark Sx?
4) What is seen on endoscopy?
1) HIV & hematologic malignancies
2) May have concomitant thrush (oral candidiasis)
3) Hallmark symptom is odynophagia (pain in retrosternal area)
4) White mucosal plaque-like lesions on endoscopy
Biopsy shows yeast & pseudohyphae
Esophagitis via esophageal candidiasis:
1) What would a culture show?
2) How do you manage this?
1) Candida spp
2) PO or IV antifungal (ie, fluconazole) x 14-21 days
Esophagitis via HSV
1) Who is it common in?
2) What type of HSV is most common?
3) What may occur during primary HSV infection?
4) What 2 Sx do pts usually present with?
1) Immunocompromised (chemotherapy, transplantation, HIV)
2) Most commonly HSV type 1
3) Reactivation of HSV
4) Odynophagia and/or dysphagia
Esophagitis via HIV:
1) What are 2 possible Sxs?
2) What is the Dx?
3) How is it managed?
1) Fever & retrosternal chest pain
2) Usually via endoscopic visualization confirmed by Bx
3) Acyclovir 400 mg PO 5 times daily x 14-21 days (immunocompromised)
Esophagitis via CMV:
1) What is it an uncommon but serious complication of?
2) When is there a significant decrease in incidence?
3) In what setting does it mostly occur in?
4) Who is it most common in?
1) AIDS
2) Anti-Retroviral Therapy (ART)
3) Advanced immunosuppression (CD4 counts <50)
4) Patients not taking ART
Esophagitis via CMV: Describe the clinical features
1) Odynophagia, nausea, substernal burning pain
2) Commonly causes multiple ulcers at the lower esophageal sphincter
3) May cause diffuse esophagitis
List 2 reasons to endoscopy pts with CMV esophagitis
1) Endoscopy with biopsy for failure of empiric therapy (fluconazole for suspected Candida esophagitis)
2) Endoscopy for initial evaluation of severely symptomatic patients requiring hospitalization
CMV esophagitis:
1) What will be seen in mucosal biopsies?
2) Are CMV in blood, tissue, or antibody indicated for diagnosis in AIDS?
1) Characteristic cytomegalic cells
2) No; does not reliably confirm or exclude end-organ disease
Describe CMV esophagitis management
1) All should receive anti-CMV therapy
2) Start induction antiviral agent (ie, ganciclovir) inj x 3-6 weeks or until asymptomatic
3) IV therapy for severe disease
4) Initiate ART
5) Maintenance therapy: patients with concurrent CMV retinitis & those who relapse after induction therapy (usually with oralvalganciclovir)
Medication/Pill-Induced esophagitis:
1) What is it? Where does it usually occur?
2) What is the most common site for it to occur? Why?
3) What does this type of esophagitis cause?
1) Direct esophageal mucosal injury caused by medications; at anatomical sites of esophageal narrowing
2) Near level of aortic arch; extrinsic compression
3) Physiologic reduction in amplitude of esophageal peristaltic wave
Medication/Pill-Induced esophagitis; give examples of the following etiologies:
1) Abx
2) Aspirin & anti-inflammatories
3) Biphosphates
4) Others
1) Tetracycline, doxycycline & clindamycin (direct irritant effect)
2) Aspirin & anti-inflammatories: ASA, NSAIDs (severe
3) Risedronate, alendronate (esophagitis, ulcers, strictures)
4) Potassium chloride, quinidine preparations, iron compounds, emepronium, alprenolol, pinavarium
Medication/Pill-Induced esophagitis: List the clinical features
1) Retrosternal pain or heartburn
2) Odynophagia
3) Dysphagia
4) Rare (hematemesis, abdominal pain, weight loss)
5) Occurs within a few hours to 1 month after ingestion
6) Common history: swallowing pill without water, commonly at bedtime
Medication/Pill-Induced esophagitis: How is it managed?
1) Discontinue culprit medication
-If unable to discontinue, switch to liquid formulation
2) Consider antacids, PPIs, H2RAs, sucralfate
3) Consider short-term parenteral hydration or alimentation for patients with severe odynophagia with inability to eat or drink
4) Endoscopic dilation possibly needed in patients with esophageal stricture
Esophageal dysmotility:
1) Define GERD
2) Define achalasia
1) Underlying hypotensive/incompetent LES
2) Tight stricture of inferior esophagus
Esophageal dysmotility: achalasia:
1) What kind of dysphagia?
2) What Sx can it cause?
3) What exacerbates it?
4) How is it managed?
1) Dysphagia for solids & liquids
2) Regurgitation of food (undigested, non-acidic, non-bilious); Chest pain
-“Bird beak” distal esophagus on barium-esophagram, dilated upper esophagus
3) Emotional stress & hurried eating
4) Pharmacologic, dilation of LES, surgical or endoscopic myotomy, botulinum toxin injection therapy
Lower esophageal spasm (esophageal dysmotility):
1) What is it?
2) What are some main Sx?
3) What can it mimic?
4) What should be done to rule out common disorders?
1) Non-peristaltic contractions with normal LES relaxation
2) Chest pain, dysphagia with solids & liquids, regurgitation
3) Cardiac angina
4) EGD with biopsies
Lower esophageal spasm (esophageal dysmotility): How is it managed?
1) Reassurance, PPIs, nitrates & CCBs, low-dose TCAs
2) Peppermint oil (Altoid mints) for dysphagia and/or chest pain in patients with no GERD (or well-controlled GERD)
Hypercontractile esophagus (esophageal dysmotility):
1) What is it also called?
2) What does it cause?
3) What can rule out common disorders?
1) Aka Jackhammer esophagus, Nutcracker esophagus
2) Dysphagia with solids & liquids, +/- retrosternal chest pain
+/- heartburn & regurgitation
3) EGD with biopsies
Hypercontractile esophagus (esophageal dysmotility): How is it managed?
1) Management = nitrates or CCB
2) Low-dose TCAs for chest pain
3) Cognitive behavioral therapy
4) Peppermint oil for dysphagia and/or chest pain in patients with no GERD (or well-controlled GERD)
What are some etiologic considerations for dysphagia?
1) Determine acuity (acute onset suggests impaction)
2) Distinguish from odynophagia (pain with swallowing)
3) Not related to rumination or globus sensation
4) Determine phase: oral, oropharyngeal, or esophageal
Define dysphagia
Subjective sensation of difficulty swallowing
List 3 tests for dysphagia and why you’d order each
1) Pre-endoscopic or barium study1
-History/clinical features of proximal esophageal lesion
-Known complex (tortuous) stricture
2) Upper endoscopy/EGD: determine underlying cause, r/o malignancy, perform therapy
3) Esophageal manometry: upper endoscopy unrevealed or suspect motility disorder
Esophageal obstruction:
1) What etiological consideration should you determine?
2) What are the Sx?
1) Food impaction vs non-food objects/foreign body
2) Choking, refusal to eat, hypersalivation, retrosternal fullness, regurgitation, wheezing, blood-stained saliva, odynophagia
Esophageal obstruction: What is the diagnostic and therapeutic approach?
1) Upper endoscopy
a) Remove obstruction (usually meat)
b) Push food into stomach if able
Barrett’s esophagus:
1) Define
2) Pathogenesis?
3) Clinical features?
1) Replacement of the normal stratified squamous epithelium of the distal esophagus with metaplastic columnar epithelium (gastric & intestinal features)
2) Increased exposure & longer periods of acid reflux
3) No specific symptoms
Barrett’s esophagus:
1) How is it managed?
2) What abt for pts w. dysplasia?
1) Once daily PPI (even without symptoms of GERD)
2) Endoscopic eradication therapy and/or endoscopic resection
Gastroesophageal reflux disease (GERD):
1) What is it?
2) What are 2 main causes? Describe each
1) Reflux of stomach contents into esophagus leading topain/burning and/or complications
2)
a) Physiologic (postprandial, short-lived, may be asymptomatic, rarely nocturnal)
b) Pathologic (symptomatic or mucosal injury, often nocturnal)
GERD: List some other misc. Sx
Dysphagia, chest pain, water brash, globus sensation (feeling of lump in the throat from spasm of upper esoph sphincter), odynophagia, extraesophageal symptoms (chronic cough, hoarseness, wheezing), & nausea
Gastroesophageal reflux disease (GERD):
1) Classification?
2) Epidemiology?
3) Pathogenesis?
1) Erosive esophagitis or non-erosive reflux disease
2) Prevalence up to 20% in U.S., <5% in Asia
3) Transient relaxation of the lower esophageal sphincter
List + describe the classic Sx of GERD
1) Heartburn (pyrosis): retrosternal burning sensation (usually postprandial)
-Troublesome if mild symptoms > 2 days/week or moderate-severe symptoms > 1 day/week
2) Regurgitation: perceived gastric contents refluxed into mouth or hypopharynx
GERD:
1) What will you see on PE?
2) How is it diagnosed? What should you test for?
3) What are some alarm features?
1) normal in uncomplicated disease
2) Clinical (must have classic symptoms)
Testing if there are alarm features (upper GI series, EGD, Bravo pH) or failure of PPI therapy
3) Hematemesis/coffe-ground emesis, melena, wt loss, odynophagia or dysphagia.
Describe the initial mgmt of GERD
Based on
a) Frequency & severity of symptoms and
b) Presence of erosive esophagitis or Barrett’s on endoscopy
1) Lifestyle & dietary modifications for all
2) Antacids, H2-blockers, and/or PPIs
List some lifestyle modifications for GERD
1) Weight loss
2) Elevate head of bed
3) Eliminate dietary triggers (caffeine, chocolate, spicy foods,citrus, high-fat or fried foods, carbonated drinks, and alcohol)
4) Avoid tight-fitting clothing
5) Give Oral lozenges/chewing gum
6) Avoid tobacco & alcohol
List the first, second, and third line Txs for GERD. What 2 things should you avoid?
1) 1st line: lifestyle & dietary modification
2) 2nd line: antacids followed by sucralfate
-Avoid sodium bicarbonate & magnesium trisilicate (Gaviscon)
3) 3rd line: H2RAs followed by PPIs
When do you do an EGD (upper endoscopy) for GERD?
Only if strong indication (ie, significant GI bleeding)
True or false: You should do empiric acid suppression for patients with GERD, even if EGD indicated
True
What are 3 referral criteria for GERD?
1) Failure of once daily PPI therapy (refractory GERD)
2) Intolerant to long-term PPIs
3) Desire to discontinue therapy
Mallory-Weiss Tear:
1) What is it? What is the usual cause?
2) What is this tear a cause of?
3) What do lacerations often lead to?
1) Longitudinal mucosal lacerations (intramural dissection) in the distal esophagus and proximal stomach, which are usually associated with forceful retching
2) Upper GI bleeding
3) Lacerations often lead to bleeding from submucosal arteries
What are some possible risk factors for Mallory-Weiss Tears?
1) Heavy alcohol use: bleeding usually worse when associated with portal hypertension & esophageal varices
2) Hiatal hernia
3) Age: unclear, as most MWT occur in patients under 40
What are some precipitating factors for Mallory-Weiss tears?
Vomiting, straining or lifting, seizures, blunt abdominal trauma and nasogastric (NG) tube placement
What are some clinical features of Mallory-Weiss tears?
1) Acute onset of hematemesis coffee-ground emesis
2) May have epigastric or back pain
3) May have history of non-bloody emesis, prolonged retching or coughing prior to onset
4) If significant bleeding, may have signs of hypovolemia & hemodynamic instability (resting tachycardia, hypotension)
(typically pts with MW are pretty stable tho)
Mallory-Weiss tear:
1) DDxs?
2) Dx?
1) Reflux esophagitis, medication-induced esophagitis, infectious esophagitis
2) Via upper endoscopy (EGD); also rules out other etiologies
Define dyspepsia
Acute, chronic, or recurrent predominant epigastric pain/discomfort for at least 1 month
List a bunch of etiologies of dyspepsia
1) Food intolerance (overeating, excess alcohol or coffee)
2) Drug intolerance (ASA, NSAIDs, antibiotics, DM drugs, ACE-I, SSRIs, steroids, iron, opioids)
3) Functional dyspepsia (FD): no organic etiology found
4) Peptic Ulcer Disease (PUD): 5-15%
5) GERD: up to 20%
6) Gastric or esophageal cancer: <1%
7) Gastroparesis
8) Parasitic infection: Giardia
9) Helicobacter pylori infection (+ PUD)
10) Pancreatic carcinoma & chronic pancreatitis
11) Biliary tract disease
12) Others (DM, thyroid, CKD, cardiac, malignancy, hernia, intestinal ischemia, pregnancy)
Dyspepsia:
1) What should you do for alarm features?
2) What cause is common in young pts with multiple complaints, h/o anxiety or depression, h/o psychotropic meds?
3) What is rarely helpful?
1) Endoscopy or abdominal CT for alarm features
2) FD (functional dyspepsia)
3) Physical exam
Dyspepsia:
1) What tests should you do for >/= 60?
2) What abt <60?
3) What is the study of choice to diagnose gastroduodenal ulcers, erosive esophagitis, & upper GI malignancy?
1) CBC, CMP (liver, calcium), thyroid function, EGD
2) Test for H. pylori first (urea breath test, fecal antigen test)
3) EGD
Dyspepsia:
1) When should you endoscopy?
2) What should you consider for refractory symptoms or progressive weight loss?
3) What should you do when pancreatic, biliary tract, vascular disease, or volvulus are suspected?
1) Pts <60 with prominent alarm features + pts ~45 with higher incidence of gastric cancer
2) Celiac Ab, stool testing (O&Px3, Giardia), or fecal fat (elastase)
3) Abdominal US or CT
Dyspepsia:
1) When should you empirically Tx?
2) What are other pharmacologic agents?
1) Pts <60 without alarm features; general treatment measures
2) Nortriptyline, buspirone, metoclopramide, prucalopride
Helicobacter pylori induced injury:
1) What is it?
2) What is the etiology?
3) What causes the injury?
1) Direct alteration of signal transduction in mucosal and immune cells leading to increased acid secretion and diminished mucosal defenses
2) Noninvasive organism, but renders underlying mucosa vulnerable to acid damage
Releases proteases that degrade the protective mucus
2) Host inflammatory/immune response
NSAID induced injury:
1) How does this happen?
2) How much NSAID is needed to cause this?
3) What amount increases risk of duodenal ulcers?
1) Inhibits cyclo-oxygenase activity (COX-1 & COX-2) which impairs mucosal-protecting prostaglandin & nitric oxide leading to microscopic and macroscopic injury
2) As little as 10 mg ASA daily
3) 325 mg ASA QOD
NSAID induced injury:
1) What is microscopic injury?
2) Give examples of macroscopic injury
1) Damage of surface cells by gastric acid
2) Edema, erythema, erosions, subepithelial hemorrhage, ulcers
NSAID induced injury:
1) What may interact withH pyloriand NSAIDs to increase mucosal injury?
2) When is there an increased risk of injury w NSAIDs?
3) NSAID-induced PUD _____________ with age
1) Cigarette smoking
2) Increased risk of injury within first 3 months (<1 week unlikely to cause injury in healthy adults)
3) increases
NSAID induced injury: List some other misc risk factors
1) Dose of NSAID
2) H/o PUD
3) Comorbidities: disability (osteoarthritis), ASA/anticoagulant use, concurrent use of glucocorticoids & SSRIs
Esophageal strictures:
1) What is it?
2) What are two different presentations?
1) Benign or cancerous narrowing or tightening of esophagus
2) Simple vs complex
Esophageal strictures: Give examples of benign etiologies
1) Peptic stricture (more common) as complication of GERD (systemic sclerosis, NG tube)
2) Radiation therapy (thoracic or head/neck tumors)
3) Caustic ingestions, postsurgical resection, drug-induced, EoE
Esophageal strictures: Give 2 examples of cancerous etiologies
1) Adenocarcinoma
2) SCC/ Squamous cell carcinoma
Describe benign esophageal strictures
Usually short & contiguous with gastroesophageal junction; possible solid food dysphagia with progressive symptoms & episodic food impaction; management with endoscopic dilation & acid-suppressive therapy (PPIs)
Describe cancerous esophageal strictures
Stricture indicates advanced lesion; rapidly progressing dysphagia (solids, then liquids); may have chest pain, odynophagia, anemia, anorexia, weight loss; management depends on staging
Esophageal varices:
1) What is it? When is it most common?
2) How do pts present?
3) What is the prognosis?
1) Dilated veins due to portal hypertension; in setting of cirrhosis
2) W. hematemesis and/or melena
3) 15% of those who bleed from varices will die from the bleed
Esophageal varices:
1) Is primary prophylaxis recommended?
2) What can Tx bleeding? What is the ultimate Tx?
1) Primary prophylaxis (prevention of 1st bleeding episode) is recommended with β-blocker
2) Bleeding is treated with rubber banding, sclerotherapy; transjugular intrahepatic portosystemic shunt (TIPS)
Esophageal varices: variceal hemorrhage:
1) Why do they develop?
2) Where is the thinnest layer of supporting tissue and most likely to rupture & bleed?
3) What result in large increase in wall tension?
1) To decompress the hypertensive portal vein & return blood to systemic circulation
2) Gastroesophageal junction
3) Small increases in vessel radius
Esophageal varices variceal hemorrhage
1) Why does Dx & management differ from other forms of GI bleeding?
2) There’s a poor prognosis; why?
1) Different underlying cause (increased pressure gradient vs AVM, vs mucosal injury)
2) High rates of rebleeding, even in patients with spontaneous resolution (70% will rebleed over long term)
Describe esophageal varices management
1) Hemodynamic resuscitation
2) Airway protection
3) Address coagulopathies
4) IV octreotide or somatostatin
5) Endoscopic variceal ligation; or endoscopic sclerotherapy
6) Balloon tamponade for continued bleeding
7) Trans-jugular intrahepatic portosystemic shunt (TIPS)
-90-100% patients achieve hemostasis following TIPS
90-100% of esophageal varices patients achieve hemostasis following _____________
Trans-jugular intrahepatic portosystemic shunt (TIPS)
