Gastrointerology Flashcards
Spontaneous Bacterial Peritonitis
- infection without perforation of the bowel
- E.coli is most common organism
- Anaerobes rarelt causes
- Pneumococcus (respiratory pathogen) associated with SBP
Best initial test for SBP
- Cell count with more than 250 neutrophils
Dx options for SBP
- Gram stain is almost always negative
- Fluid cx is best test but is usually never a
Treatment of spontaneous bacterial peritonitis
- ceftoxamine or ceftriaxone
-
Pt has low albumin. Prophylaxis for SPBP
- Prophylactic norfloxacin or trimethoprim/sulfamethoxazole
Dysphagia
difficulty swallowing
Odynophagia
pain with swallowing due to abnormalities in orpharynx or esophagus
Oropharyngeal dysphagia
- usually involves aspiration of food into the lungs
liquids more than solids
Causes of oropharyngeal dysphagia
- Neuro disease (e.g. stroke)
- Myasthania gravia
- Prolonged intubuation
- Zenker’s diverticulum
Obstructive causes of esophageal dysphagia
Difficulty swallowing solids more than liquids
- Strictures
- Schatzki rings
- Esophageal webs
- Esophageal carcinoa
Motility disorder causes of esophageal dysphagia
- Achalasia
- Scleroderma
- Esophageal spasm
Dx of oropharyngeal dysphagia
Video fluorosopy
Dx of esophageal dysphagia
Barrium swallow (aka esophagram) followed by endoscopy, manometry and/or pH monitoring
- if obstructive causes suspected, proceed directly to endoscopy w/ biopsy
Causes of infectious esophagitis
- Candida albicans
- HSV
- CMV
Candida albicans esophagitis
- cause of 90% of esophagitis in AIDS patients
- oral thrush CAN be present but not always
- upper endoscopy shows yellow white plaques ADHERENT to mucosa
Tx of Candida albicans esophagitis
Nystatin oral suspension or Fluconazole
HSV esophagitis
- oral ulcers found on exam
- upper endoscopy shows small, deep ulderations, multinucleated giant cells w/ intranuclear inclusions on biopsy + Tzanck smear
Tx of HSV esophagiti
Acyclovir IV
CMV esophagitis
- associated with retinitis and colitis esp in AIDS patients
- on endoscopy, large, superficial ulcerations
- Intranuclear and intracytoplasmic inclusions on biopsy
Tx of CMV esophagitis
Gancyclovir IV
Esophageal webs associated with which syndrome?
Plummer Vinson syndrome
- esophageal webs
- glossitis
- iron deficiency anemia
Musculature of esophagus
- Upper 1/3 is skeletal
- Middle is mixed skeletal and smooth muscle
- Lower 1/3 is smooth muscle
Esophageal Spasm
- motility disorder in which normal peristalsis is periodically intermittent by high amplitude nonperistaltic contractions
- aka nutcracker esopagus
Hx and PE: esophageal spasm
- sudden onset of chest pain not related to exertion
- can be precipitated by drinking hot or cold liquids
- relieved by nitroglycerin
- EKG and stress test will be normal
Dx of esophageal spasm
Barrium swallow shows corkcrew shaped esophagus
- Manometry shows high-amplitude simultaneous contractions
Tx of esophageal spasm
Nitrates
Calcium channel blockers for symptomatic relief
Esophageal myometry for severe incapacitating symptoms
Achalasia
impaired relaxation of lower esophageal sphincter
- loss of peristalsis in distal 2/3 of esophagus
- due to generation of neurons in myenteric (Auerbach’s) plexus
Achalasia: Hx and PE
- often in young patient < 50
- progressive dysphagia to BOTH solids and liquids at same time
- no association w/ tobacco or alcohol use
- regurgitation of undigested food
Achalasia: Dx
- Barium swallow shows “bird’s beak” tapering of distal esophagus
- Manometry shows increased LES resting pressure, incomplete LES relaxation upon swallowing, and decreased peristalsis
- CXR shows widening of esophagus
- Upper endoscopy shows normal mucosa to r/o malignancy
Tx of Achalasia
- Nitrates, CCBs
- pneumatic dilitation
- botulinium toxin injection
- surgical resectioning or myometry
Zenker’s diverticulum
cervical outpouching of cricopharyngeal muscle
Hx and PE; Zenker’s diverticulum
- presents with chest pain, dysphagia, halitosis, regurgitation of undigested food
Dx of Zenker’s diverticulum
Barium swallow will show outpouchings
Tx of Zenker’s diverticulum
IF symptomatic, treat w/ surgical resection of diverticulum
For Zenker’s diverticulum, myotomy of cricopharygeus is required to relieve high pressure zone
Schatzki ring
- peptic stricture or scarring/tightening of distal esophagus
- associated with acid reflux and hiatal hernia
- associated with intermittent dysphagia
Dx and Tx of Schatzki ring
- seen on Barium swallow
- treated with pneumatic dilitation
Scleroderma
presents with symptoms of reflux and have clear hx of scleroderma or progressive systemic sclerosis
Dx of scleroderma
Manometry shows decreased LES pressure from inability to close LES
Mgmt of GI associated scleroderma
PPIs to manage reflux symptoms
Mallory Weiss tears
- NONPENETRATING tear of only mucosa
- presents with upper GI bleeding after severe vomiting or retching
- repeated retching followed by bright red blood or black stool
- no dysphagia is presents
Tx of Mallory Weiss tears
Often M-W tears resolve spontaneously
- severe cases managed with epinepherine or electrocautery
Boerhaave syndrome
full thickness esophageal rupture
Manometry is diagnostic criteria for which 3 GI disease
- Achalasia
- Esophageal spasm
- Scleroderma
Most common esophageal cancer worldwide
Squamous cell carcinoma
Most prevalent esophageal cancer in Western World
Adenocarcinoma
Risk factors for SCC
Alcohol and tobacco
Risk factors for Adenocarcinoma
Barrett’s esophagus (columnar metaplasia of distal esophagus 2/2 to chronic GERD)
Esophageal Cancer: Hx and PE
- patients > 50 y/o
- dysphagia first for SOLIDS the progressive dysphagia for liquids
- more than 5 - 10 years of GERD symptoms
Best initial test for esophageal cancer
Barium study
- will show narrowing of esophagus with irregular border protruding into lumen
Confirmation of esophageal cancer
Endoscopy with biopsy can only confirmcancer
Tx for Esophageal Cancer
- No resection = no cure
- Chemotherapy and radiation used in addition to surgical resection
- Stent placment for lesions that can’t be resected surgically
GERD
inappropriate relaxation of LES sphincter that allow reflux of gastric contents
- can be due to incompetent LES, gastroparesis, or hiatal hernia
GERD symptoms can be worsened by…
Nicotine Alcohol Caffeine Chocolate Peppermint Late night meals Obesity
Hx and PE: GERD
- patients present w/ heartburn that occurs 30 - 90 minutes after meal, worsens with reclining and improves with antacids
- sour taste, sore throat, hoarseness, or cough
- PE exam is usually normal
Dx of GERD
Primarily clinical diagnosis
empiric trial of lifestyle mods and treatment if attempted first
- if empiric tx fails then EGD w/ biopsy is indicated
Indications for EGD in setting of GERD
- Signs of obstruction
- Weight losss
- Anemia or heme-positive stools
- More than 5 - 10 years of symptoms to exclude Barrett sesophagus
Tx of GERD
Lifestyle modifications
- Avoid alcohol, caffeine, chocolate, late time snacks
- pharm meds
-
Pharm tx in mild GERD
Antacids or H2 blockers (e.g. ranitidine_
Pharm tx in persistent GERD
PPIs (omeprazole, lansoprazole)
Surgical tx of GERD
- when medical treatment is not working
- Nissen fundoplications: wrapping the stomach around LES
Complications of GERD
- Erosive esophagitis
- Esophageal peptic stricture (Schatzki rigns)
- Aspiration pneumonia
- Upper GI bleeding
- Barrett’s esophagus
Barrett’s esophagus
- histological changes in lower esophagus (columnar metaplasia)
- needs at least 5 years of reflux to develop
Dx of Barrett’s esophagus
EGD with biopsy
- has great risk of turning into adenocarcinoma
Hiatal hernia
- herniation of stomach into the ches through the diaphragm
Sliding hiatal hernia
GE junction and portion of stomach are displaced ABOVE diaphragm
Paraesophageal hiatal hernia
GE junction remains below diaphragm while fundus herniates into thorax
Hiatal hernia: PE and Hx
May be asymptomatic
- patients with sliding hiatal hernias may present with GERD
Hiatal hernia: Dx
incidental finding on CXR
- diagnosed with Barium study or EGD
Tx of sliding hernia
Medical therapy and lifestyle modifications to decrease GERD symptoms
Tx of paraeophageal hernia
Surgical gastropexy (attachment of stomach to rectus sheath and closure of hiatrus) is recommended to prevent gastric volvulus
Acute gastritis
rapidly developing, superficial lesions that often due to NSAID use, alcohol, H. pylori, infxn and stress from severe illness
Type A gastritis
- subset of chronic gastritis (10%)
- occurs in fundus and due to AUTOANTIBODIES TO PARIETAL CELLS
- causes pernicious anemia and associated w/ other autoimmuen disorders
- increased risk of gastric cancers
Type B gastritis
- subset of chronic gastritis (90%)
- occurs in antrum and may be caused NSAIDS or H. pylori infection
- often asymptomatic but associated with inc risk of PUD and gastric cancer
Gastritis: HE and PE
- can be asymptomatic
- can present with GI bleeding w/o pain
Dx of Gastritis
- UPPER ENDOSCOPY to evaluate GI mucosa
H. pylori infection diagnosis
- EGD with biopsy
- Urease breath tests
- serum IgG antibodies (show hx of exposure but no current infxn)
- H. pylori stool antigen
Treatment of gastritis
- Decrease intake of exacerbating agents
- Triple therapy (amoxicillin, clarithromycin, omepraxole)
- give prophylactic PPIs for stress ulcers
Curling ulcers
- stress ulcers associated with burns
Cushing ulcers
- stress ulcers associated with traumatic brain injury
Krukenberg tumor
gastric cancer that metastasizes to ovary
Gastric cancer
malignant tumor with poor prognois
- seen in Korea and Japan
- most are adenocarcinomas with two morphologies: intestinal type and diffiuse type
Intestinal gastric cancer
differentiated cancer that originates from intestinal metaplasia of gastric mucosal cells
- diet hih in nitrites and salt
- diet low in antioxidants
- H. pylori colonization
- chronic gastritis
Diffuse gastric cancer
- undifferentiated cancer not associated w/ H. pylori or chronic gastritis
- unknown risk facors
- “signet ring cells on biopsy”
MALT (mucosa-associated lymphoid tissue) lymphoma
- rare gastric tumor that presents in patients with H. pylori infection
- only malignancy that can be cured with abx
- treat with triple therapy (amoxicillin, clarithromycin, and omeprazole)
Gastric Cancer: Hx and PE
- early stages are usually asymptomatic, but may be associated with indigestion and loss of appetite
- late stage disease presents with abdominal pain, weight loss, and upper GI bleeding
Dx of Gastric Cancer
Upper endoscopy with biopsy
Tx of Gastric Cancer
If detected early, treatment is surgical resection Late stage (most patients), usually incurable
Peptic Ulcer Disease
- result from damage to gastric or duodenal mucosa caused by impaired mucosal defense or increase in acidic gastric contents
Most causative agent of PUD
H. pylori - responsible for 90% of duodenal ulcers and 70% of gastric ulcers
Other causes of PUD
- Corticosteroid use
- NSAIDS
- Alcohol
- Tobacco
PUD: Hx and PE
presents with chronic or periodic dull, burning epigastric pain that is related to meals and can radiate to back
- may complain of nausea, hematemesis or bloody stools
- exam may be normal but epigastric tenderness and positive guiaic stools
- acute perforation presents with rigid abdomen, rebound tenderness
Gastric ulcers vs. Duodenal ulcers Hx
Gastric ulcers have “GREATER” pain with eating
Duodenal ulcers have “DECREASED” pain with eating
Diagnostic test for PUD
Upper endoscopy is most accurate test to confirm and rule out bleeding
Diagnosis of PUD
- rule out performations
- upper endoscopy
- H. pylori testing
- in recurrent cases, check serum gastrin to r/o Zollinger- Ellison syndrome
Perforations in Gastric Ulcers
Abdominal X-ray shows free air under the diaphragm
Perforations in Duodenal Ulcers
CT scan with contrast shows air in the retroperitoneal space.
- Order CBC to detect GI bleeding
Upper GI Bleeding: Hx and PE
- Hematemesis (“coffee-ground emesis”)
- Melena > Hematachezia
- Hypovolemia (e.g. tachycardia, lightheadedness, hypotension)
Upper GI Bleeding: Dx
NG tube and lavage
If stable, endoscopy
Upper GI Bleeding: Etiology
PUD (** most important**)
Esophagitis/gastritis
Mallory Weiss Tear
Esophageal varices
Upper GI Bleeding: Initial Management
Protect airway (intubation may be needed) Stabilize patient w/ IV fluids and packed red blood cells
** hematocrit may be normal in early acute blood loss**
Upper GI bleeding: long-term management
Endoscopy followed by therapy directed at the underlying cause
Lower GI Bleeding
Hematochezia > melena, but can be either
Lower GI Bleeding: Dx
- Rule out upper GI bleding with NG lavage if brisk
- Anoscopy/sigmoidoscopy for patients < 45 y/o with small volume bleeding
- Colonoscopy if stable; arteriography or exploratory laparotomy if stable
Lower GI Bleeding: Etiologies
Diverticulosis (60%) **** Angiodysplasia IBD Hemorrhoids/fissures Neoplasm AVM
Lower GI Bleeding: Initial Management
Protect airway (intubation may be neede) Stabilize pt with IV fluids and packed RBCs
Lower GI Bleeding: Long-term management
Depends on the underlying etiology
Endoscopic therapy (e.g. epinepherine injection)
Intra-arterial vasopressin infusion or embolization or surgery for diverticular disease
Most common cause of upper GI bleeding
PUD
Most common cause of lower GI bleeding
Diverticulosis
Common features seen in variceal bleeding
- Vomiting +/- black stool
- Spider angiomata and caput medusa
- Splenomegaly
- Palmar erythema
- Asterixis
Treatment of Variceal Bleeding
- Fluid replacement w/ high volumes
- PRBCs if Hct < 30
- Fresh frozen plasma if PT or INR is elevated
- Platelets if below < 50K
- Octreotide for variceal bleeding
- Endoscopy to determine diagnosis and administer some treatment
- IV PPI for upper GI bleeding
- Surgery if med treatment is refractory
Management of variceal bleeding in addition to fluids, blood, platelets, plasma
- Octreotide to reduce portal pressure
- Banding to obliterate esophageal varices
- TIPS to decrease portal pressure in those not controlled by octreotide and banding
- Propranolol to prevent subsequent episodes of bleeding
- Abx to prevent SBP with ascites
Mesenteric Ischemia
- insufficient blood supply to small intestine resulting in ischemia and potentially necrosis
Two most common causes of mesenteric ischemia
- Acute arterial occlusion from thrombosis
2. Embolism
Risk factors for acute arterial occlusion induced mesenteric ischemia
Atherosclerosis
- commonly occurs in SMA
Risk factors for embolism
Atrial fibrillation and stasis from reduced ejection fraction
Mesenteric Ischemia: Hx and PE
severe abdominal pain out of proportion to exam
- patient has prior episodes of abdominal pain after eating (intestinal angina)
- other symptoms include nausea, vomiting, diarrhea, and bloody stools
- abdominal exam unremarakable until late in disease
Mesenteric ischemia: Dx
- MESENTERIC ANGIOGRAPHY
- Labs show leukocytosis, metabolic acidosis (with increased lactase, amylase, LDH, CK
- AXR shows bowel wall edema (“thumbprinting”) and air wihin bowel
Mesenteric ischemia
- Volume resuscitation, broad spectrum abx
- For acute arterial thrombosis or emboli, treat with anticoagulation and either laparotomy or angioplasty
Cirrhosis
fibrosis and nodular regeneration resulting from chronic livery injury (intrahepatic or extrahepatic)
Intrahepatic causes of cirrhosis
- All causes of chronic hepatitis
Extrahepatic causes of cirrhosis
- Biliary tract disease (primary biliary cirrhosis, primary sclerosing angitis)
- Posthepatic causes (including right sided HF, constrictive endocarditis, Budd-Chiari syndrome)
Cirrhosis: Hx and PE
- presents with JAUNDICE, ASCITES, SPONTANEOUS BACTERIAL PERITONITIS, HERPATIC ENCEPHALOPATHY (asterixis, AMS), GASTROESOPHAGEAL VARICES, coagulopathy, and renal dysfunction
- exam reveals large palpaple or firm liver or signs of portal hypertension and liver failure
Spontaneous bacterial peritonitis
diagnosed as > 250 PMNs/ml in the ascitic fluid
Effects of portal hypertension
- Esophageal varices –> hematemesis
- Peptic ulcer –> melena
- Splenomegaly
- Caput medusa
- Hemorrhoids
Effects of liver cell failure
- Coma
- Scleral icterus
- Fetor hepaticus (breath smells like open corpse)
- Spider nevi
- Gynecomastia
- Jaundice
- Loss of sexual hair
- Liver “flap” - asterixis
- Bleeding tendency (decreased prothrombin)
- Anemia
- Testicular atrophy
- Ankle edema
Diagnosis of cirrhosis
- Liver biopsy shows bridging fibrosis and nodular regeneration
- labs show decreased albumin, increased INR/PT and increased bilirubin
- if ascites is present, etiology determined by SAAG (serum- ascites albumin gradient)
SAAG
serum albumin - ascites albumin
SAAG > 1.1
Related to portal hypertension
- Presinusoidal: splenic or portal vein thrombosis
- Sinusoidal: cirrhosis
- Postsinusoidal: right heart failure, constrictive pericarditis, Budd-Chiari
SAAG < 1.1
Not related to portal hypertension
- Nephrotic syndrome
- TB
- Malignancy with peritoneal carcinomatosis (e.g. ovarian cancer)
36 y/o F with PMH of hypercholesteremia and type 2 DM presents with intermittent dull RUQ discomfort. Pt doesn’t drink alcohol. PE is unremarkable. Labs show elevated AST and ALT but otherwise normal. Hepatitis serologies are negative. Likely diagnosis?
Nonalcoholic fatty liver disease
- condition associated with insulin resistance and metabolic syndrome
- in earliest stage, can be reversed with weight loss and fat-restricted diet
- in later stages, irreversible and can lead to nonalcoholic steatohepatitis and cirrhosis
Complications of cirrhosis
- Ascites
- Spontaneous bacterial peritonitis
- Hepatorenal syndrome
- Hepatic encephalopathy
- Esophageal varices
- Coagulopathy
Ascites: Mechanism
- Increased portal hypertension results in transudative effusion
- Portal exam reveals abdominal distention, fluid wave, and shifting dullness for percussion
Ascites: Management
Sodium restriction and diuretics (furosemide and spironolactone); large-volume paracentesis
- Treat underlying liver disease
Spontaneous bacterial peritonitis: Mechanism
- presents with fever, abdominal pain, chills, nausea, and vomiting
- diagnostic paracentesis shows > 250 PMNs/ml and positive gram stain
SBP: Management
IV antibiotics (3rd generation cephalosporin)
IV albumin
Prophylaxis with fluoroquinolone to prevent recurrence
Hepatorenal syndrome
acute prerenal failure in setting of advanced cirrhosis
Diagnosis of exclusion
Urinary sodium < 10 mEq/L
Hepatorenal syndrome management
Difficult to treat
Often requires dialysis
Only cure is liver transplantation
Hepatic encephalopathy
decreased clearance of ammonia
often precipitated by dehydration, infection, electrolyte abnormalities, and GI bleeding
Hepatic encephalopathy management
Protein restriction, lactulose and/or rifaximin
Correct underlying triggers (e.g. replete potassium)
Esophageal varices
portal hypertension leads to increased flow through portosystemic anastamoses
Esophageal varices management
Endoscopic surveillance in all patients with cirrhosis
- medical prophylaxis with B-blockers to prevent bleeding
- for acute bleeding, endoscopy with band ligation or sclerotherapy is needed
Coagulopathy
impaired synthesis of all clotting factors except Factor VIII
Coagulopathy management
For acute bleeding, administer fresh frozen plasma
Vitamin K will not correct coagulopathy
Primary Biliary Cirrhosis
autoimmune disorder characterized by destruction of intrahepatic bile ducts
- seen in middle aged women with autoimmune conditions
Primary Billiary Cirrhosis: Hx and PE
presents with progressive jaundice, pruritis, and fat-soluble vitamin deficienies (A,D,E, K)
Primary Biliary Cirrhosis: Dx
Lab findings include increased alk phosphatase, increased bilirubin,
positive antimitochondrial antibody
increased cholesterol
Tx of Primary Biliary Cirrhosis
Ursodeoxycholic acid (slows progression of disease)
Cholestyramine for pruritis
Liver transplantation
Hepatocellular Carcinoma
in US, primary risk factor are
- CIRRHOSIS from alcohol
- CHRONIC HEPATITIS
- AFLATOXINS (in various food sources)
- HBV infections
Hepatocellular Carcinoma: Hx and PE
- presents with RUQ tenderness, abdominal distention, and signs of chronic liver disease (jaundice, easy bruisability, and coagulopathy)
- exam shows enlarged liver
Hepatocellular Carcinoma: Dx
Ultrasound or CT
abnormal LFTs
significantly elevated alpha-fetoprotein levels
Hepatocellular Carcinoma: Surgical Tx
Surgical: partial hepatectomy for single lesions < 5cm with no cirrhosis; orthotopic liver transplant for cirrhotic patients
Hepatocellular Carcinoma: Nonsurgical Tx
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Hemochromatosis
state of Fe overload in which hemosiderin accumulates in liver, pancreas (islet cells), heart, adrenals, testes, and pituitary
Primary hemachromatosis
autosomal recessive disease characterized by mutations in HFE chene that results in excessive absorption of dietary Fe
Secondary hemachromatosis
Occurs in patients receiving chronic transfusions therapy (alpha thalassemia)
Hemachromatosis: Hx and PE
presents with abdominal pain, DIABETES MELLITUS, ARTHROPATHY OF MCP joints, HEART FAILURE, or cirrhosis
- exam shows bronze pigmentation, cardiac dysfunction (CHF), hepatomegaly, and testicular atrophy. labs show DM
- hemachromatosis doesn’t affect lung, kidney, eye
Hemachromatosis: Diagnosis
- increased serum Fe, percent Fe saturation, and ferritin with decreased transferrin
- transferrin > 45% is highly suggestive of Fe overload
- perform liver biopsy, MRI, and HFE
Hemachromatosis: Tx
- WEEKLY PHLEBOTOMY to normalize serum Fe levels, then maintain phlebotomy every 2-4 months
- DEFEROXAMINE can be used for maintenance therapy
Hemachromatosis: Complications
- CIRRHOSIS
- HEPATOCELLULAR CARCINOMA
- Restrictive cardiomyopathy
- Arrhythmias
- DM
- Impotence
