GI Path Flashcards
Common signs and symptoms of GI problems
Pain
Malabsorption
Bleeding
-Pay attention to the pattern of bleeding for clues to origin
Usual locations for severe upper GI bleeding (in descending order of frequency)
Duodenum -duodenal ulcer Stomach -gastric ulcer Esophagus -esophageal varices Note that all of these are above the ligament of Treitz. They make up 90% of major GI bleeds.
Signs of bleed
hematemesis
melenemesis
melena
Hemoglobin converted to hematin by stomach acid
Hematochezia
bright red blood in the stool
sign of distal small bowel (10%) or bleeding originating below the ileocecal valve (90%)
-most commonly the colon (usually diverticulosis)
Guaiac Tests
based on detection of endogenous peroxidase in RBCs
false positives: foods (rare red meat, cruciferous veggies, horseradish), myoglobin
false negatives: ascorbic acid or other reducing agents
Apt test
used to evaluate newborns with blood in stool or vomit
-fetal hemoglobin is resistant to acid and alkaline denaturation
positive test = blood is derived from newborn
Diseases of the esophagus
Heartburn (pyrosis)
Dysphagia
-Pay attention to location of dysfunction and food type for clues to origin
*Just solid food = obstruction
*Solids and liquids = motility disorder
+Upper esophagus involved = skeletal muscle problem
e.g., myasthenia gravis, stroke
+Lower esophagus involved = smooth muscle problem
e.g., CREST syndrome
Odynophagia
Atresias and Fistulas
developmental defects that must be corrected early because incompatible with life
-starvation, aspiration and pneumonia, paroxysmal suffocation from food
Atresias and Fistulas when discovered
usually discovered soon after birth
-regurgitation after first feed
-impossible to pass nasogastric catheter to stomach
may be identified before birth by ultrasound
-polyhydramnios
-association with other congenital anomalies
VATER Syndrome
Vertebral abnormalities
Anal atresia
TE fistula
Renal disease and radial agenesis
cause unknown
Esophageal Webs and Rings
main symptom: dysphagia with solid food
most common in women >40 yoa
Esophageal Mucosal Webs
uncommon ledgelike protrusions of mucosa into esophageal lumen
usually in upper esophagus and semicircumferential
congenital, or in association with long-standing reflux esophagitis, GVHD, or blistering skin diseases
Plummer-Vinson Syndrome(Paterson-Brown-Kelly Syndrome)
web accompanied by Fe-deficiency anemia, glossitis, leukoplakia in oral cavity and esophagus, cheilosis
risk for postcricoid esophageal squamous cell carcinoma
Esophageal Rings
plates of tissue protruding into lumen
in lower esophagus and concentric
-A ring = above squamocolumnar junction of esophagus and stomach
-B ring (Schatzki ring) = at this junction
Esophageal Stenosis
main symptom: progressive dysphagia (starts with solids, then liquids)
fibrous thickening of the esophageal wall, usually due to inflammatory scarring after injury
-gastroesophageal reflux, radiation, scleroderma, caustic injury
Achalasia
progressive dilation of the esophagus above the lower esophageal sphincter (LES), due to
- aperistalsis
- partial or incomplete relaxation of the LES with swallowing
- increased resting tone of the LES
primary achalasia
uncertain (may be autoimmune in origin)
dysfunction of inhibitory neurons containing NO and VIP?
degenerative changes in neural innervation of distal esophagus?
secondary achalasia
Chagas disease
Trypanasoma cruzi infection destroys myenteric plexus of esophagus, duodenum, colon, and ureter, with resulting dilation
Achalasia:Clinical Features
main symptom: progressive dysphagia (first solids, then liquids)
nocturnal regurgitation and aspiration of undigested food
frequent hiccups, difficulty belching
primary form usually occurs in adulthood in bimodal distribution
-20s-40s, and after age 60
Manometry Test
detects aperistalsis and failure of LES to relax
An esophageal manometry test measures the motility and function of the esophagus and esophageal sphincter. A tube is usually inserted through the nose and passed into the esophagus. The pressure of the sphincter muscle is recorded and also the contraction waves of swallowing are recorded. The manometry test is a tool used to help evaluate swallowing disorders.
Hiatal Hernia
protrusion of a portion of the stomach above the diaphragm due to separation of the diaphragmatic crura and widening of the space between the muscular crura and esophageal wall (etiology unknown)
most common is sliding hernia
Hiatal Hernia:Clinical Features
bowel sounds heard over left lung base
usually asymptomatic
heartburn or nocturnal epigastric distress (only ~9% of patients)
much less commonly, ulceration, hematemesis, dysphagia due to stenosis
Diverticula
outpouchings of the alimentary tract that contain all visceral layers (mucosa, submucosa, muscularis propria, and adventitia)
-a false diverticulum (pulsion diverticulum) does not have all four layers
*outpouching of mucosa and submucosa into area of weakness in the wall
any diverticula can undergo inflammation (diverticulitis), ulceration, bleeding, and perforation
Zenker Diverticulum
pulsion diverticulum located in upper esophagus, just above UES
-cricopharyngeus muscle is area of weakness
clinical findings:
-odynophagia, halitosis (due to food entrapped in the diverticulum), regurgitation
Midesophageal Diverticulum
pulsion diverticulum located near midpoint of esophagus (near tracheal bifurcation)
-usually due to motor dysfunction (e.g., PSS) or congenital
-Can see these as true diverticula in the setting of tuberculosis
Usually asymptomatic
Epiphrenic Diverticulum
immediately above the LES
clinical findings: nocturnal regurgitation of massive amounts of liquid
Lacerations:Mallory-Weiss Syndrome
longitudinal tears at the esophagogastric junction or gastric cardia
-usually due to retching in alcoholics and bulimics
*hiatal hernia is a predisposing factor in those without this history
produces hematemesis
-usually stops without surgical intervention, but supportive therapy might be required (vasoconstrictive meds, transfusions, balloon tamponade)
Lacerations:Boerhaave Syndrome
rupture of distal esophagus
-Endoscopy causes ~75% of cases (but not Boerhaave)
-retching, bulimia
complications:
-pneumomediastinum
*air dissects subcutaneously into the anterior mediastinum
*crunching sound (Hamman’s crunch) on auscultation
-pleural effusion containing food, acid, amylase
Esophageal Varices
portal hypertension induces formation of collateral bypass channels where the portal and caval systems communicate
develop in 90% of cirrhotic patients, most often those with alcoholic cirrhosis
-most common cause of death in this group
Esophageal Varices:Clinical Findings
asymptomatic until rupture, then massive hematemesis
~50% die during first bleed; of remainder, 50% will have another bleed within the year (with similar mortality rate)
can monitor at-risk patients with endoscopy and treat varices when found (sclerotherapy
GERD
most important cause of esophagitis
usually limited to adults, but sometimes in infants and children
due to reflux of gastric contents into lower esophagus
GERD causes
decreased LES tone
CNS depressants, pregnancy, hypothyroidism, sclerosing disorders, tobacco or alcohol exposure, nasogastric tube, etc
sliding hiatal hernia
present in ~70% of people with GERD
inadequate or slowed esophageal clearance of refluxed material
delayed gastric emptying and increased gastric volume
reduction in reparative capacity of esophageal mucosa
GERD morphology
inflammatory cells (particularly eosinophils) in the squamous epithelium basal zone hyperplasia elongation of lamina propria papillae and capillary congestion
GERD Clinical Features
heartburn, indigestion nocturnal cough and/or asthma -GERD is most common cause of this symptom early satiety, abdominal fullness bloating with belching when severe: hematemesis or melena
GERD labs
Esophageal pH monitoring
Endoscopy
Manometry
-LES pressure < 10 mm Hg
Esophageal pH monitoring is a test that measures how often and how long stomach acid is entering the esophagus. A small thin tube is introduced through the nose or mouth and into the stomach, which is then drawn back up into the esophagus. The tube is attached to a monitor which records the level of acidity in the esophagus. The patient records symptoms and activity while the tube is left in place for the next 24 hours. The information from the monitor is compared to the diary the patient provides. This test is helpful in determining the amount of stomach acid entering the esophagus.
Eosinophilic Esophagitis
increasing incidence, for unknown reasons (more common in those with atopic history)
symptoms
-children = feeding intolerance, GERD-like symptoms
-adults = dysphagia, fodd impaction
hallmarks: abundant eosinophils at sites away from gastroesophageal junction; absence of acid reflux/no response to high-dose proton pump inhibitor treatment
Infectious Esophagitis
most commonly caused by viruses and fungi, and the most common cause of odynophagia
usually limited to immunosuppressed patients
HSV Esophagitis
most common in patients with leukemia and lymphoma
produces “punched out” lesions on endoscopy; biopsy confirms nuclear inclusions of herpesvirus
CMV Esophagitis
most common in AIDS patients
-AIDS patients can have ulcers in esophagus that mimic CMV without infection
linear ulcerations; biopsy confirms basophilic nuclear and cytoplasmic inclusions
Candida esophagitis
immunocompromised and diabetes mellitus
entire esophagus covered with patches of gray-white fungal hyphae
Chemical Esophagitis
ingestion of mucosal irritants
-alcohol, corrosive acids or alkali, excessively hot fluids, heavy smoking, cytotoxic anticancer therapy
pill-induced esophagitis
-Taking meds without water or lying down increases risk
-NSAIDS, antibiotics, iron tablets, Vit. C, potassium, quinidine, etc
Barrett Esophagus
distal squamous mucosa is replaced by metaplastic columnar epithelium
-complication of long-standing GERD (seen in 10% of symptomatic patients)
Single most important factor predisposing to esophageal adenocarcinoma
Barrett Esophagus diagnosed by
endoscopic evidence of columnar epithelium above the gastroesophageal junction
-appears as red, velvety mucosa
intestinal metaplasia in biopsy specimens
SCC
Older African-American men Developing countries Dietary & environmental link-strong no association w barrets anywhere in esophagus involved- middle & upper most common
Adenocarcinoma
Older Caucasian men More common in the US No dietary & environmental factors Association w Barretts Lower esophagus involved
Signs and Symptoms of Stomach Disease
Hematemesis -most commonly due to peptic ulcer disease (PUD) -usually as melenemisis Melena Gastric analysis includes measurement of -BAO (basal acid output) *output of gastric juice collected in 1 h via nasogastric tube on empty stomach -MAO (maximal acid output) *same as BAO, but this time stimulate with pentagastrin -BAO:MAO ratio normally ~0.20:1
Pyloric Stenosis
progressive hypertrophy of the circular muscles in the pyloric sphincter
treatment: myotomy
Congenital Pyloric Stenosis Epidemiology
likely genetic: affected parents have increased risk of child with CPS, and high rate of concurrence with monozygotic twins
males>females
associated with Turner and Edward’s syndrome, esophageal atresia
Congenital Pyloric Stenosis path & clinical features
Pathogenesis: recent evidence implicates NO synthase deficiency
Clinical features:
-NOT present at birth, but shows up within 2-5 weeks
-projectile vomiting of non-bile-stained fluid
-the hypertrophied pylorus (“olive”) is commonly palpated
Gastritis
inflammation of the gastric mucosa
is a histologic diagnosis, but clinically is applied to any gastric complaint without doing a confirmatory biopsy.
-Often a missed diagnosis, bc most patients with chronic gastritis are asymptomatic
types of inflammation
-neutrophils: acute gastritis
-lymphocytes and/or plasma cells: chronic gastritis
Acute Gastritis
acute (usually transient) inflammation of the mucosa, sometimes with hemorrhage
unifying features of factors known to incite acute gastritis:
-increased acid secretion with back-diffusion
-decreased production of bicarbonate buffer
-direct damage to the epithelium
Acute Gastritis morphology
can range from mild neutrophilic invasion of the epithelial layer to erosion of the epithelial layer with hemorrhage (note there is no breach of muscularis mucosa)
Acute Gastritis clinical
asymptomatic, or epigastric pain, nausea, vomiting
may present with overt hemorrhage, massive hematemesis, melena, or fatal blood loss
Acute Gastric Ulceration(Stress Ulcers)
differ from PUD in timing is acute, there are multiple lesions (mainly in the stomach), and there is no association with H. pylori infection
-these are NOT precursors to chronic PUD
Acute Gastric Ulceration(Stress Ulcers)
follow severe physiologic stress, usually in patients with
- shock, extensive burns, sepsis, or severe trauma
- gastric cells hypoxic due to stress-induced splanchnic vasoconstriction
- intracranial injury
- hypersecretion of gastrin due to stimulation of vagal nuclei by increased intracranial pressure
Ulcers types
Curling ulcers:
arise in proximal duodenum
associated with severe burns, trauma
Cushing ulcers:
arise in stomach, duodenum, and esophagus
associated with intracranial injury, operations, or tumors
high incidence of perforation
Acute Gastric Ulceration(Stress Ulcers) morphology & clinical
Morphology:
-usually multiple, small (<1 cm) ulcers, frequently stained dark brown by acid digestion of extruded blood
clinical features:
-1-4% of critically ill patients will require transfusion due to bleeding
Chronic Gastritis
chronic mucosal inflammation that leads to mucosal atrophy and intestinal metaplasia
-metaplasia can develop into dysplasia, creating a background for cancer
in contrast to acute gastritis, erosions rarely occur
Chronic Gastritis:Helicobacter pylori Infection
THE most important association
most infected adults have associated gastritis but are asymptomatic
-Estimated 50% of American adults >50 yoa are infected
gastritis results from combination of bacterial enzymes and toxins, and chemicals released from recruited neutrophils
gastritis develops in two patterns
antral type
- high acid production
- high risk of duodenal ulcer
pangastric type
- multifocal mucosal atrophy
- increased risk of gastric carcinoma and lymphoma
Autoimmune Gastritis and Pernicious Anemia
<10% of chronic gastritis cases
due to autoantibodies against components of gastric gland parietal cells (e.g., H+,K+- ATPase, gastrin receptor, intrinsic factor)
-loss of acid production, intrinsic factor no longer produced
leads to atrophy and dysplasia
increased risk of gastric carcinoma and carcinoid tumors
