GI Flashcards
orophayngeal vs esophageal dysphagia
Oro: difficulty initiating a swallow, often with coughing, drooling or aspiration. Can have ear pain from hypopharyngeal lesion referred pain. Next test is nasopharyngeal laryngoscopy
Esophageal: delayed sensations of food sticking in upper or lower chest.
Dysphagia that begins with solids and then eventually involves liquids is due to mechanical obstruction.
Dysphagia initially involving both solids and liquids is neuromuscular
If no diagnosis made with laryngoscopy or barium esophagram, then maybe EGD
EGD is most helpful when evaluating lower esophageal symptoms.
Hirschsprung Disease
Full term infants usually pass meconium in 48h. Failure to pass it is pathologic and can lead to distention, poor feeding and bilious emesis.
Initial eval with XR. Multiple dilated loops of bowel and absence of rectail air is concerning for distal bowel obstruction. Contrast enema is performed to delineate level of obstruction
Classic finding in HD (congenital aganglgionic megacolon) is transition zone btw a normal or narrow caliber rectosigmoid colon (aganglionic segment) and a normally innervated but markedly dilated descending colon.
Absence of ganglion cells on rectal mucosal suction biopsy is diagnostic.
Treatment is surgical excision of aganglionic segment followed by anastomosis of normal bowel to anus.
25% of HD patients have another genetic anomaly (like renal) and 10% have a chromosomal issue (Down)
diverticular bleeding
Etiology: Arterial erosion due to colonic mucosal outcropping
Clinical: Painless hematochezia in patients over 40. Bleeding often self-limited but can recur. R sided (more common than left) bleeding can cause melena.
Dx: Colonoscopy or tagged RBCs
Tx: IV volume replacement. Endoscopic therapy or angiographic embolization. Colonic resectionfor persistent bleeding.
Colonic angiodysplasia
AVM. Development of dilated, tortuous submucosal vessels.
Common cause of hematochezia. Predisposing risk factors include ESRD, von Willebrand disease, aortic stenosis.
timing of cholecystectomy during gallstone pancreatitis
Mild case (no organ failure or systemic complications like acute necrotic collecton, HF, etc): surgery within 7 days of symptom improvement
Moderate to severe (persistent organ failure of one or more systems… hypotension not responding to fluids, for ex). Delay surgery for 6-8 weeks. Also get a pre-op ERCP or intraop cholangiogram.
gastric vs duodenal ulcer pain
Gastric ulcers get worse after food. higher risk of malignancy (rec surveillance endoscopy to confirm healing)
Duodenal ulcers get better after food. Also worse at night. H Pylori is seen in 70% of these ulcers.
triple therapy
Treatment for H Pylori
PPI (omeprazole), clarithromycin, amoxicillin.
Confirmation of eradication is recommended in patients with duodenal ulcer. Either a urea breath test or fecal antigen test but neither until 4 weeks after completion of therapy
Eradication should also be confirmed in patients with persistent dyspepsis, MALT lymphoma, or who have had resection of early gastric cancer.
acute pancreatitis
Etiology
- Chronic alcohol
- gallstones
- hypertriglyceridemia, hypercalcemia
- drugs (valproic acid, diuretics)
- Infection (CMV, HIV, ascariasis)
- trauma, ischemia, post-ERCP
Presentation
- acute epigastric pain radiating to back
- fever, nausea, vomiting
- tachypnea, hypoxemia, hypotension if severe
Diagnosis
- Requries 2 of the following:
- characteristic epigastric pain
- serum amylase or lipase more than 3 times normal
- imaging findings consistent with pancreatitis
Treatment
- Aggressive IV volume resuscitation
- Pain control (hydromorphone)
- nothing by mouth until pain resolves, nasojejunal feeds if oral intolerance for more than 3-4 days.
cough predominant GERD tx
lifestyle mod (weight loss, avoid alcohol) and 8 week trial of PPI.
Trial of histamine blocker is avoided in cough predominant GERD
If cough does not respond to PPI, 24h esophageal pH monitoring can further evaluate
GERD
Pathophys
- decreased tone or excessive transient relaxation of LES
- anatomic disruption to GEJ (hiatal hernia)
- Increased risk with obesity, pregnancy, smoking, alcohol
Manifestations
- regurgitation of acidic material in mouth
- heartburn
- odynophagia (often indicates reflux esophagitis)
- Extraesophageal manifestations like cough, hoarseness, wheezing
Complications
- esophageal - erosive esophagitis, Barrett, strictures
- extraesophageal - asthma, laryngitis
Initial tx
- lifestyle (weight loss) and diet change
- H2R blocker or PPI
clinical features of acute diverticulitis
Abdominal pain (usually LLQ), fever, nausea, vomiting, ileus (peritoneal irritation)
Diagnosis with CT (oral and IV)
Manage with bowel rest and antibiotics (cipro, metronidazole)
Complications include ABSCESS, obtruction, fistula, perforation
Patient with acute diverticulitis who does not improve symptomatically after 2-3d of treatment
Get repeat CT to look for complications (abscess, perf, obstruction)
Colonic abscess is number 1. Symptoms resemble diverticulitis and often do not improve with oral antibiotics alone. Will likely need percutaneous drainage and IV antibiotics followed by elective partial colectomy several weeks later.
What test is needed following diveriticulitis after symptoms resolve?
Colonoscopy 6-8 weeks after complete resolution of symptoms to rule out colon cancer.
When should you suspect peritonitis from hollow viscus perforation?
Patient with sudden onset abdominal pain with significant tenderness and guarding. Tend to lay still to minimize peritoneum irritation.
Dx with upright CXR first. If unclear, then maybe CT.
Perforated peptic ulcer is most common etiology
All patients with perforation will need surgery so in preparation, patients with suspected/confirmed peptic ulcer perfoation should receive IV fluids, IV PPI, and broad spectum antibitoics
most common cause of SBO in patients with history of abdominal surgery?
Adhesions
Management of unresponsive patient with hematemsis
Stabilize (intubate) and then EGD for likely bleeding varices
Avoid NGTs in patients with suspected varices bc can lead to rupture
intravenous octreotide
Initiate in patient with UGIB highly concerning for variceal hemorrhage.
It decreases elevated portal venous pressure by decreasing splanchnic flow. Give as patient is being stabilized.
FFP
Can be used to correct coagulopathies due to vitamin K deficiency and is typically given when INR is at least 2.
Associated with risk of volume overload in patients with cirrhosis.
IV H2 blocker vs PPI in acute UGIB
Do not give H2 (worse outcomes), but yes to PPI
BB in primary and secondary prevention of esophageal variceal hemorrhage
Nonselective BBs (nadolol, propranolol) can be used as both, patricularly in combination with endoscopic surveillance and band ligation.
Possible extra benefit with oral nitrate too
Diagnosis of acute cholecystitis
Persistent RUQ pain, fever, nausea, vomiting and leukocytosis.
Confirmed when US reveals choleliths with gallbladder wall thickening or sonographic murphy’s sign. If negative or inconclusive, HIDA is usually confirmatory.
ERCP is used when choledolithiasis is suspected. Abdominal pain, fever, leukocytosis but patients typically have CBD dilation on US and elevated bilirubin and alk phosph.
biliary colic
Transient (less than 6h) RUQ pain, nausea, vomiting. Typically managed with as needed pain control and elective cholecystectomy.
Chronic Hep C infection
Positive HCV antibodies and circulating HCV RNA.
Frequently asymptomatic as many patients only have minimal lab issues.
Mainstay of tx is direct acting antiviral agents (sofosbuvir-velpatasvir) but patients require further strategies to reduce risk of liver damage
Primary concern is superimposed infection with HepA or HepB which really increases risk for hepatic decompensation and liver failure. Patients with chronic hcv should be vaccinated against hav and hbv if they don’t already have immunity
Look for negative HAV antibody (no prior hep a immunity) or positive HBV surface antibody (evidence of HBV immunity)
Note: Positive surface antigen for HBV is suggestive of active infection.
Also screen for comorbidies and complications like liver fibrosis, renal disease, and extrahepatic manifestations (cryoglobulinemia).
Counsel substance use/alcohol cessation
acetaminophen and chronic HCV
it’s OK! as long as it’s less than 2 g a day.
Porcelain gallbladder
development of punctate or curvilinear calcs within gb wall due to chronic cholelithiasis. Most are asymptomatic and dx is usually incidental on imaging
Patients are at increased risk for gallbladder cancer and often require ppx cholecystecomy if they have symptoms of gallbladder disease (biliary colic) or if punctate calcs are present.
Curvilinear calcs minimally increase risk cancerand generally do not need intervention
Chronic diarrhea
Loose stools with or without increased frequency for at least 4 weeks. In high income countries most common causes are IBS, IBD, chronic infection, and malabsorption syndromes (Celiac, lactose).
First step is Hx/PE. In addition to routine labs, get stool analysis
Malabsorptions Syndromes
Lactose intolerance
- Diarrhea after lactose containing meals
- increased stool osmotic gap
- low stool ph
- positive lactose hydrogen breath test
Chronic pancreatitis
- greasy stools
- abdominal pain radiating to back
Celiac
- Increased stool osmotic gap
- microcytic anemia, iron deficiency
- villous atrophy
small intestinal bacterial overgrowth
- macrocytic anemia, B12 deficiency
- positive lactulose breath test
Stool osmotic gap
290 - 2 (stool Na + stool K)
- less than 50 is secretory diarrhea
- 50-125 is indeterminate
- over 125 is osmotic diarrhea
Celiac disease
Large volume, foul smelling stools, excessive flatulance, weight loss, microcytic anemia. osmotic diarrhea.
Patients may not associate it with specific foods.
For most patients with reasonable clinical suspicion, get anti tissue transglutaminase antibdies and small bowel biopsy (usually from distal duodenum during egd)
histo shows villous atrophy, loss of normal villus architecture, intraepithelial lymphocytic infilrates and crypt hyperplasia
Collagenous colitis
chronic, watery diarrhea associated with fecal urgency and nocturnal diarrhea
Secretory diarrhea
Biopsy has thick subepithelial collagen band
Management of Celiac Disease
Gluten free diet/education
- dietary counseling with a dietician
- monitor lifelong adherence to diet
- access to support group
Nutritional deficiency
- most common deficiences are iron, calcium, vit d, folic acid and rarely thiamine
Prevention of bone loss
- increased risk for osteopenia and osteoporosis
- obtain DXA at diagnosis
- Repeat DXA 1 year later if osteopenia present
Vaccination
- pneumococcal
Dermatitis herpetiformis
- dapsone in addition to gluten free diet
Most patients see improvement in 2-3 weeks following starting the diet. Normalizing villous architecture takes several months tho. For patients who do not achieve symptomatic relief the first response is detailed dietary history bc most common reason is lack of diet adherance. If adherent and still no impovement, look for other causes
Alarm symptoms for GERD
Dysphagia, odynophagia, anorexia, weight loss, evidence of GI bleeding
In patients with frequent GERD symptoms (more than twice a week) and no alarm symptoms, initial treatment is daily PPI for at least 8 weeks. Lifestyle changes as well. If symptoms fail to improve after 8 weeks of low dose PPI, PPI should be increased to high dose for at least 8 weeks.
If still persists, then esophageal PH monitoring.
If alarm symptoms or patient has failed both low and high dose PPI… EGD
Acute cholangitis
Etiology - ascending infection due to biliary obstruction
Presentation
- fever, jaundice, RUQ pain (charcot triad)
- hypotension and AMS (Reynolds pentad)
Dx
- cholstatic liver function
- increased direct bili, alk phos
- mildly increased aminotransferases
- bilary dilation on US or CT
Tx
- antibiotic coverage of enteric bacteria (pip/tazo, cipro with metronidazole)
- biliary drainage by ERCP within 24-48h!!! definitive tx
don’t forget to first aggressively administer fluids
Best initial therapy for oral candidiasis
Topical antifungal (nystatin suspension or clotrimazole troches) with an oral antifunal like fluconazole used for resistant cases.
In patients where thrush is secondary to inhaled steroids, proper technique should be assessed by watching them use inhaler
Look out for esophagitis (odynophagia)
First step in management of splenic rupture
Volume resusitation if in hypovolemic shock
Once patient is hemodynamically stable, get CT. Ideally management is nonoperative (observation with serial hemoglobin, embolization) to preserve splenic function. If remain unstable from severe ongoing hemorrhage may need ex-lap and splenectomy
Intussusception (peds)
Risk factors
- recent viral illness or rotavirus vaccine
- Pathologic lead point
- congenital malformation of intestines (meckel diverticulum)
- Henoch-schonlein purpura
- Celiac
- intestinal tumor
- polyps
Presentation
- sudden, intermittent abdominal pain
- currant jelly stools
- sausage shaped abdominal mass
- lethargy or ams
Diagnosis
- taget sign on US
Tx
- air or saline enema
- surgery for removal of lead point
Most cases occur between 6 months and 3 years
US is not required in patients with a classic clinical picture.
Get XRs to rule out perf. Then once ruled out get nonoperative reduction via air or water soluble contrast enema. Diagnostic and therapeutic. If nonoeprative reduction doesn’t work, get srugery.
If pathologic lead point is identified, elective surgery for removal of the lead point may be indicated.
perf is a complication of enema reduction. Patients with acute pain after reduction should get XRs to rule out perforation
Primary Biliary cholangitis
Symptoms/signs
- fatigue and pruritis (most common)
- inflammatory arhritis (40-70%)
- hyperpigmented skin (25-50)
- RUQ discomfort (10%)
- Xanthelesmata (10%) and xanthomata (5%)
Dx
- elevated alk phos
- positive Antimitochondrial antibody
- livery biopsy if AMA neg
tx
- ursodeoxycholic acid (slows progression)
- liver transplant (only curative tx) in advanced cirrhosis.
Progressive autoimmune disease characterized by fibrosis and obliteration of intrahepatic bile ducts leading to cirrhosis. Most common in women of northern european decent with typical onset at age 30-65. Risk higher in family members
Often asymptomatic at diagnosis. Most often symptom is just fatigue and itchiness. Can also have steattoreha, jaundice, hyperlipidemia etc
Patients may also have other autoimmune disorders (CREST, type 1 DM)
Increased risk for osteopenia and osteoporosis. These patients warrant screening with DXA
Alpha 1 antitrypsin deficiency
cirrhosis (with signifant elevation in hepatic transaminases) and emphysema
