GI Exam: The Gut Flashcards
1
Q
What does the upper esophageal sphincter do?
A
Prevents aspiration of esophageal contents
2
Q
What does lower esophageal sphincter do?
A
Prevents reflux of gastric contents, allows food bolus to pass into stomach
3
Q
What phases of swallowing are voluntary? Involuntary?
A
Voluntary: oropharyngeal phase; tongue moves bolus
Involuntary: esophageal phase; peristalsis
4
Q
What is oropharyngeal dysphasia?
A
–Difficulty transferring bolus out of mouth
–Associated w/ coughing & aspiration
5
Q
What are known causes of oropharyngeal dysphasia?
A
–Mechanical/obstructing lesions •Zenker’s diverticulum, tumors, osteophytes –Neurologic disorders •Stroke, ALS, Parkinson’s –Skeletal muscle disorders •Muscular dystrophy –Neuromuscular transmission disorders •Myasthenia gravis
6
Q
What is esophageal dysphasia?
A
–Sense of bolus “sticking in chest”
7
Q
What are known causes of esophageal dysphasia?
A
–Mechanical causes •Tumors, strictures •Eosinophilic esophagitis –Motility disorders •Achalasia •Chagas’ disease •Scleroderma •Diffuse esophageal spasm
8
Q
What happens to swallowing in scleroderma?
A
Characterized by vascular obliteration and fibrosis of the esophageal smooth muscle
Results in aperistalsis and weak lower esophageal sphincter (no contraction)
9
Q
What happens to swallowing in achalasia?
A
Due to ganglion cell loss in myenteric plexus
Impaired relaxation of lower esophageal sphincter (always contracted), aperistalsis
10
Q
How can you treat achalasia?
A
•Pharmacologic:
–Calcium channel blockers
–Botulinum toxin
•Pneumatic balloon dilation
•Heller myotomy (cut through LES), may be accompanied by a “loose wrap” of the fundus
•POEM (peroral endoscopic myotomy), fix w/ endoscopy
11
Q
What is GERD?
A
•Definition: the reflux of gastric contents into the esophagus that results in troublesome symptoms and/or complications
•Most common reason for visit to GI specialist
–Significant health care impact: costs, quality of life, loss of productivity
12
Q
What are typical and atypical symptoms of GERD?
A
•Typical symptoms
–Heartburn
–Regurgitation
•Reflux chest pain
•Atypical symptoms
–Wheezing, cough, hoarseness, globus, dyspepsia, nausea
Typical can occur without atypical; much less common for atypical to occur without typical
13
Q
What are common causes of GERD?
A
Defective esophageal clearance Lower esophageal sphincter dysfunction (transient LES relaxations) Hiatal hernia Increased intra-abdominal pressure Delayed gastric emptying
14
Q
What are transient lower esophageal sphincter relaxations?
A
•Transient LES relaxations (tLESRs)
–Primary mechanism underlying most acid reflux episodes
–Not associated with swallowing
–Last longer than swallow LESRs (10+ seconds)
•Can be caused by certain foods as well as gastric distention
•Can be inhibited by GABA type B agonists (baclofen)
–Clinical trial results disappointing
15
Q
How should mild to moderate GERD be treated?
A
–Dietary modification
•Avoidance of fatty food, alcohol, caffeine, carbonated beverages
•Smaller meals
–Weight loss
–Raise head of bed if pt has nighttime symptoms
–Stop smoking
–Antacids (neutralize refluxate)
•Magnesium trisilicate, aluminum hydroxide, and calcium carbonate
•Neutralize pH of low pH refluxate
16
Q
How should moderate to severe GERD be treated?
A
•Reduce gastric acid production (increase pH of refluxate)
–Histamine-2 receptor antagonists (H2RAs)
•Cimetidine, famotidine, ranitidine
•Block H2 receptor on gastric parietal cells
•pH about 4
-PPIs (pH 6-7); inhibited acid secretion into gastric lumen by binding covalently to cysteine residues of H+/K+ ATPase
17
Q
When should PPIs be used?
A
– h/o erosive esophagitis
• Erosive esophagitis is a chronic condition – high rate of relapse (up to 80%)
– Barrett’s esophagus
– GERD sx responsive to PPIs and not controlled by less potent rx
18
Q
What are the potential adverse effects of PPIs?
A
Higher rates of c diff
Bone fracture rate increases
Vitamin B12 deficiency (gastric acid releases B12 from protein-bound state and can then bind to R proteins)
19
Q
What pathologic changes are seen in GERD?
A
•Inflammation –Eosinophils*, Lymphocytes, Neutrophils •Basal cell hyperplasia •Hyperplasia of stromal papillae •Erosions/ulcers •Barrett’s Esophagus (late complication)
20
Q
What is Barrett’s Esophagus?
A
•Complication of chronic GERD
•Definition:
–Proximal displacement of squamocolumnar junction
–Columnar-lined epithelium with intestinal metaplasia (goblet cells)
•Primary precursor lesion to esophageal adenocarcinoma
–Lifetime esophageal cancer risk is about 5-10%
•Prevalence: is about 1-2% of general population
•Risk factors:
–*GERD, white, male, older age, smoking, obesity, H. pylori (inverse)
21
Q
What is eosinophilic esophagitis?
A
•Allergen mediated esophagitis – assoc autoimmune disorders/atopy
–Most often diagnosed in children and young adults
–70% of cases in males
•Symptoms
–Children: feeding intolerance, heartburn, regurgitation, dysphagia, food impaction, failure to thrive, diarrhea
–Adults: dysphagia (to solids), food impaction, heartburn, chest pain
22
Q
What are the findings of eosinophilic esophagitis on endoscopy?
A
- White papules
- Linear furrows
- Rings (felinization, trachealization)
- Strictures
23
Q
How is eosinophilic esophagitis treated?
A
•Dietary modifcation
–Avoidance of triggers
•Six-food elimination diet: milk, egg, soy, wheat, peanuts/tree nuts, fish/shellfish
•More effective in children than adults
–Elemental diet (amino acid-based formulas)
•Steroids
–Topical (fluticasone, beclomethasone)
–Systemic steroids, other immunosuppressants
•No FDA-approved treatments for EoE
•Frequent relapses when therapy discontinued
24
Q
How is the histology seen in eosinophilic esophagitis?
A
•Diagnosis requires combination of sx of EoE combined with histologic findings: –15+ eosinophils in a high-power field –Basal cell hyperplasia –Subepithelial fibrosis –Eosinophilic microabscesses –Degranulated eosinophils –Superficial clustering
25
What is HSV esophagitis?
* Most common viral esophagitis
* Self limited in healthy pts. Can disseminate in immunosupressed
* Ulcers
* Secondary bacterial and fungal infections common
* Dx generally made by bx
* Primarily infects squamous cells
26
What are the common drugs that can cause esophagitis?
```
NSAID
tetracyclines
bisphosphonates
potassium
vitamin C
iron
```
27
What is radiation esophagitis?
```
•Acute and chronic damage possible
•Acute: within 2-3 wks of RT
–Ulceration, necrosis, mucosal denudation
–Sx: odynophagia, chest pain
–Eventually resolves spontaneously
•Chronic: at least 3-6 months after RT
–Fibrosis and stricturing
–Sx: dysphagia
–Rx: dilation, stents
```
28
What is metaplasia?
Change from 1 cell lineage to another
29
What is a hamartoma?
Malformation
30
What does adeno- mean?
Glandular
31
What is a carcinoma?
Malignant epithelial neoplasm
32
What is a sarcoma?
Malignant mesenchymal neoplasm
33
What do chief cells excrete?
pepsinogen
34
What do parietal cells excrete?
HCl and instrinsic factor
35
What are the layers of the stomach?
1. Mucosa – delineated by muscularis mucosae (thin muscle)
2. Submucosa – between muscularis mucosae and muscularis propria
3. Muscularis propria – thick muscle
4. Serosa – outermost thin lining of the organ
36
What is seen in histo in chronic gastritis?
Increased plasma cells
| Lymphocytes
37
What is seen in active (acute) in chronic gastritis?
PMNs (acute inflammation)
38
What is the progression of h pylori?
1. Infection
2. Acute inflammation
3. Chronic inflammation
- can then cause no atrophy or possible intestinal metaplasia
4. Multifocal atrophy
5. Intestinal metaplasia
6. Dysplasia
7. Adenocarcinoma
39
What is autoimmune atrophic gastritis?
* Caused by autoantibodies to parietal cell (more common) or intrinsic factor
* F more common than M, about 1-2% of population, elderly women about 4-5%
* Stomach body-centered disease (antrum is spared)
* Can lead to iron deficiency anemia or vitamin B12 anemia (“pernicious anemia”)
* Can lead to neuroendocrine tumors and even adenocarcinoma
40
What are the histo features of autoimmune atrophic gastritis?
* Atrophy (loss of oxyntic glands)
* Inflammation (variable)
* “Antralization”
* Intestinal metaplasia
* Enterochromaffin-like cell hyperplasia
41
What is granulomatous gastritis?
• Pattern of injury, not specific disease
• Granuloma = nodular collection of
histiocytes
• Differential includes: Crohn’s disease, Sarcoidosis, Infection (mycobacterial, rarely H. pylori), Drug effect
42
What can cause lymphocytic gastritis?
Celiac disease, lymphoma, H pylori
43
What is CMV gastritis?
• Typically seen in immunosuppressed patients
• Infects epithelial, endothelial and stromal
cells
• Histologic features:
--Large cells, large nuclei
--Red-purple nuclear inclusion (larger)
--Basophilic cytoplasmic inclusion (smaller)
44
What is reactive gastropathy and what does it look like on histo?
•Caused by NSAIDS, duodenal reflux (bile)
•AKA “chemical” gastritis
•Histologic features of:
--Foveolar hyperplasia with mucin reduction
--Smooth muscle proliferation
--Mucosal edema, fibrosis and congestion
--Minimal chronic inflammation
45
What is a hyperplastic polyp?
```
• Benign, likely reparative (very rarely
can see dysplasia)
• Most common
• Usually in antrum
• Dilated and distorted mucous glands
• Serrated epithelium may be seen
```
46
What is a fundic gland polyp?
* Almost always benign, usually secondary to hypochloridia (PPI treatment)
* Considered hamartomatous
* Dysplasia can be seen (esp. patients with FAP)
* Dilated oxyntic glands
47
What is a peptic ulcer?
* A punched-out mucosal defect that can be round or linear, appearing white with depth, which penetrates the wall deeper than the muscularis mucosa, and which occurs in the presence and partly as a consequence of acid and pepsin.
* Usually 3+ mm, distinct from erosions
* Simple or complex, anywhere in upper GI tract
* PUD implies tendency to recur
* Lifetime prevalence of PUD ~ 10%
48
What is the difference between an erosion and an ulcer?
Erosion only gets down to the muscularis mucosa and does not penetrate it; ulcer may go below it
49
How do peptic ulcers typically present?
```
•Simple ulcers
–Symptomatic: Dyspepsia
(Differential diagnosis includes non-ulcer dyspepsia (NUD), GERD, medications, pancreatobiliary disease, gastric cancer.)
–Asymptomatic
•Complicated ulcers
–Bleeding
–Perforation (or penetration).
–Obstruction (gastric outlet obstruction)
–Death
```
50
What is hematochezia?
bright red blood per rectum
51
What are major causes of upper GI bleeding?
–PUD (50%), esophageal varices/portal HTN (20%), Mallory Weiss tears (5-10%; usually caused by vomiting), angiodysplasia/AVM (7%), erosive gastritis (10%), esophagitis (2%), neoplasms (< 1%)
52
What are major causes of peptic ulcer dz?
H pylori
| NSAIDs
53
How is H pylori typically transmitted?
* Universal in developing countries (80-90%) but declining in prevalence (30-40%) in industrialized nations
* In the U.S., higher rates in older adults (cohort effect)
* Infection is acquired primarily in early childhood (younger than 2)
* Transmission is person-to-person (oral-oral vs fecal-oral)
* Infection strongly associated with low socioeconomic status, crowding and poor sanitation
* Familial clustering (passed among siblings older-younger)
54
What GI side effects are seen from NSAIDs?
* Dyspepsia – present in up to 30% of users
* Gastric erosions- seen at EGD in 50%
* Peptic ulcer disease (PUD risk is 20-fold increased in chronic users: GU in 15-20%, DU in 5-10%, lifetime risk 25%)
* GI bleeding, perforation or obstruction
* Intestinal lesions (ulcers, strictures, GIB, IBD exacerbations)
* Other toxicity (renal, liver, rash, HTN)
55
Why do NSAIDs cause GI side effects?
•Systemic effects of COX inhibition
–Depletion of prostaglandins (PGE2) responsible for normal gastric cytoprotection
•Direct topical damage
–“ion trapping” and “enterohepatic circulation”
•Platelet inhibition by aspirin and some other NSAIDs
56
What are the pluses and minuses of coxibs?
Coxibs, particularly COX2 selective drugs, have fewer GI side effects, greatly decrease PUD risk
Chronic use may be associated with cardiovascular issues
57
What is Gastrinoma Syndrome (ZES)?
•Neuroendocrine tumors (NET) that secrete high levels of gastrin
•Triad of hypergastrinemia, massive acid hypersecretion, and peptic ulcer disease
•Rare and <1% of PUD due to gastrinoma
•Most cases sporadic but 25% associated with multiple endocrine neoplasia (MEN1) syndrome.
•MEN1 autosomal dominant inherited disorder characterized by tumors of parathyroid, pituitary and pancreatic islets
Tumors arise from the duodenum and cluster around the "gastrinoma triangle"
58
What are some signs of gastrinoma?
–Recurrent or refractory or respond poorly to meds
–Atypical locations such as multiple duodenal or jejunal
–Associated with diarrhea (30-50%) and/or severe erosive esophagitis (50-70%)
–Associated w/ large gastric folds, excessive gastric secretions
–Diagnosed in patients that have hypercalcemia
59
How is gastrinoma diagnosed?
–Increased serum gastrin
–low gastric pH (no PPI use, r/o pernicious anemia)
–Localize tumor with CT, EUS, octreotide scan
60
How is gastrinoma treated?
–Surgical resection is only chance for cure
–Manage acid hypersecretion/PUD with high dose PPIs
–Chemotherapy/somatostatin analogues only for progressive metastatic disease
61
What are "stress ulcers"?
–Ulcers in setting of hypotension or shock due to ischemia of the gastric wall, often seen in ICUs
–Minor form is “stress gastritis”
62
Where do H2 blockers work?
Basolateral membrane of the parietal cell
| Result in inhibition of HCl secretion
63
Where do PPIs work?
Bind H+/K+ ATPase that are actively secreting H+
64
How is H pylori treated?
PPI triple regimens - PPI + 2 antibiotics
65
How is celiac disease diagnosed?
•Presence of consistent pathology in a duodenal biopsy and response (clinical and histological) to a gluten-free diet
•Serology: autoantibodies to tissue transglutaminase and the endomysium (tTG-IgA, EMA)
•HLA DQ2 or DQ8 required
Inflammation and villous atrophy
66
How do genes affect celiac?
Runs in families (10%)
Twin occurrence rates (70%)
HLA DQ2 92%
DQ8 8%
67
What is the pathophys of celiac?
Gluten/gliadin is poorly digested by gastric, duodenal and pancreatic secretions leaving toxic epitopes
Gliadin enters the mucosa
68
What is the classical presentation of celiac disease?
Pediatric
| Steatorrhea, malabsorption, weight loss`
69
What are less common presentations of celiac disease?
Dermatitis herpetiformis
Dental enamel defects
Apthous ulceration
70
How can celiac present on blood test?
Abnormal LFTs, low ferritin
Hypocholesterolemia (low HDL) Hyperamylasemia
Hypoalbuminemia
Hyposplenism – Howell-Jolly bodies
Elevated ESR, prolonged PT, vitamin deficiency
Hypocalcemia, secondary hyperparathyroidism
71
What are the signs of vitamin E deficiency?
hemolytic anemia
retinopathy
neuropathy
myopathy
72
What are the signs of niacin deficiency?
diarrhea
dementia
dermatitis
painful tongue
73
What are the signs of vitamin b6 deficiency?
```
polyneuropathy
oxalate stones
anemia
glossitis
dermatitis
```
74
What is marasmus?
•The most severe or “end stage” of the process of cachexia
•Clinical setting: decreased energy intake
•All available body fat stores have been exhausted due to starvation
•Cancer, chronic pulmonary disease, anorexia nervosa
Low Cr
Generally immunocompetent; ability to handle short-term stress is relatively conserved
75
How should marasmus be treated?
Nutritional support is required, but go slowly
76
What is Kwashiorkor?
•Happens with acute, life-threatening illnesses like trauma, sepsis
•Physiologic stress leads to increased protein and energy requirements
•Time course: weeks
Patient appears deceptively well-nourished
Low albumin + at least one of the following: poor wound healing, decubitus ulcers, skin breakdown, easy hair pluckability, edema
•Poor prognosis
77
How should Kwashiorkor be treated?
Unlike in Marasmus, aggressive nutritional support indicated to restore metabolic balance quickly
78
What is Marasmic Kwashiorkor?
* When cachectic or marasmic patient subjected to acute stress (surgery, trauma, sepsis)
* Life-threatening situation can occur, high risk of infection and other complications
* Determine major component of PEM
* Kwashiorkor predominant means vigorous nutritional therapy
* Marasmus predominant means more cautious feeding
79
What are the Rome III criteria for IBS?
•Recurrent abdominal pain or discomfort at least 3 days/month in the last 3 months associated 2+ of the following:
–Onset associated with a change in frequency of stool
–Onset associated with a change in appearance of stool
–Improvement with defecation
80
How does normal defecation work?
•Feces distend the rectum causing stretch receptors to be stimulated
–Receptors transmit signals along afferent fibers to spinal cord neurons
–Triggers spinal cord reflex
•parasympathetic (efferent) fibers stimulate internal anal sphincter (IAS) relaxation
–IAS relaxation is “the call to stool": makes the brain aware that the poop is there!
Then under voluntary control
When you want to stool, you relax your external anal sphincter and the puborectalis is relaxed, straightening the angle
81
What is normal transit constipation?
```
–Most common
–Patient self-report
•Normal physical examination
•Normal colonic transit time
Primary constipation
```
82
What is slow transit constipation?
```
–Decreased colonic motility
•Increased colonic transit time
–No increase in peristalsis after meals
–Infrequent “call to stool”
•Internal anal sphincter relaxation
Primary constipation
```
83
What is pelvic floor dysfunction?
```
Primary constipation
–Normal colonic transit
–Outlet problem
•Stool not expelled when it reaches the rectum
–incoordination of pelvic floor muscles during attempted evacuation
–Symptoms:
•prolonged or excessive straining
•soft stools difficult to pass
•feeling of incomplete evacuation
•rectal discomfort
•manual aid to evacuate stool
```
84
What is secondary constipation?
1. Colonic secretion decreases with similar absorption, leading to less stool water and constipation
2. Muscle-based contractions (caused by muscular disorders like muscular dystrophy)
3. Neurological disorders
4. Enteric nervous system disorders
5. Lifestyle, poor diet, meds, etc
85
What is lubiprostone?
•Chloride channels are a driving force for intestinal fluid secretion
–Draw Chloride, sodium and water into gut lumen
•Amitiza activates chloride channel-2
–Enhances intestinal fluid secretion
–Facilitate increased motility
86
What are the 5 layers of the GI tract?
```
Mucosa
Submucosa
Circular muscle
Longitudinal muscle
Serosa
```
87
Where is the colon most likely to perforate?
The cecum (where it's widest)
88
Where is the colon most likely to be obstructed?
The sigmoid colon (where it's narrowest)
89
How should c diff be treated?
Offending antibiotic should be discontinued if possible
Oral antibiotic therapy should be prescribed for 14 days
Patients who cannot take oral medication can be treated with metronidazole 500 mg IV q 8 hours
Severe refractory colitis, toxic megacolon or perforation may necessitate surgical resection
90
How does ischemic colitis present?
•Common event in the elderly
•Generally due to low blood flow state (eg hypotension or dehydration)
•Clinical: severe pain, cramps, bleeding, +/- diarrhea, relatively unremarkable abdominal exam
•Treatment – vigorous hydration, bowel rest
On x ray, looks like "thumbprinting"
91
What is diverticulitis?
* Inflammation, infection of diverticuli most common in the sigmoid
* Rare below age 50
* Clinical – localized pain, fever, WBC elevated, NO diarrhea NO bleeding
* CT scan – ‘gold’ standard for diagnosis; colonoscopy contraindicated
* Treatment – antibiotics, clear liquids, surgery
92
How does appendicitis present?
* History and physical exam still play an major role in diagnosis
* Abdominal pain is the primary symptom and classically peri-umbilical but may be epigastric or suprapubic
* After 1-12 hours pain migrates to RLQ and becomes more intense; anorexia and nausea ensue
* If vomiting precedes abdominal pain question diagnosis
93
What is sigmoid volvulus?
Sigmoid torsion resulting in obstruction
| Men 3:1
94
What is osmotic diarrhea?
•Low volumes (less than 1 liter)
•Resolves with fasting
•Excess stool osmotic gap (greater than 100 mOsm/kg)
•Low stool pH (carbohydrate malabsorption)
-- seen in lactose intolerance, laxative use, malabsorptive states
95
What is secretory diarrhea?
```
•High volumes (more than 1 liter)
•Occurs at night
•Low stool osmotic gap (less than 20 mOsm/kg)
•Can be bloody or non-bloody
Caused by toxins, hormones, inflammation
```
96
How should diarrhea be treated?
* Utilize Na/glucose co-transporters
* Requires intact villus epithelium
* Solution must contain Na and glucose
* Solution must be near isosmolar relative to plasma
97
When should you treat diarrhea with antibiotics?
•Severity: >8 stools/day, volume depletion, symptoms >1 week, considering hospitalization
•Host: immunocompromised (HIV, immunosuppresants, advanced age, chronic organ dysfunction)
•Empiric treatment: fluoroquinolone x 3-5 days
Alternative: azithromycin
•Antimotility agents (lomotil/loperamide) if afebrile and stools non-bloody.
98
What type of stones are associated with fat malabsorption?
Calcium oxalate
•Oxalate is normally bound to calcium in the intestinal lumen
•Malabsorbed fatty acids can bind to calcium
•Oxalate, unbound, is absorbed in the colon
99
When is cholestyramine effective?
•less than 100 cm Terminal Ileum Resected
–Bile salts in the colon leads to increased secretion
–Bile Salt Induced Watery Diarrhea
–Cholestyramine helpful
• more than 100 cm Terminal Ileum Resected
–Bile Salt Pool depleted leads to Fatty Diarrhea
–Cholestyramine makes diarrhea worse
–Rx: low fat diet, MCT oil
100
What is octreotide?
synthetic octapeptide similar to somatostatin with a longer half life, given IV over 3-5 days
–Reduces splanchnic/ portal blood flow and variceal pressure
–Used to treat bleeding varices, other causes of GI bleeding
101
Are cholesterol stones radioopaque or radiolucent?
Radiolucent
| 85% of stones
102
What is cholecystitis?
Inflammation of the gallbladder
103
What is cholangitis?
Inflammation of the bile duct caused by bacterial infection
104
What are the characteristics of biliary colic?
* Steady upper abdominal pain
* Radiation to back or shoulder
* Restlessness
* Duration of 1 to 6 hours
* Onset more than 1 hour after meals
* Onset at night (1 am)
* Unpredictable interval between attacks
105
What are the symptoms of acute cholecystitis?
```
•Symptoms
–Acute abdominal pain, nausea, vomiting
–Begins diffuse, then localizes
–Increases with movement, inspiration, cough, vomiting
–Radiation to back
```
106
What are the PE exam signs of cholecystitis?
```
•Signs
–fever, tachycardia, tachypneic
–abdominal tenderness, guarding, rebound
–Murphy’s
•Labs
–mild LFT elevations in 25%
–leukocytosis
```
107
How should acute cholecystitis be treated?
```
•NPO, supportive care
•Antibiotics
•Surgery
–Laparoscopic or Open
–Early (24 - 72 hours) or delayed
•Cholecystostomy (only in severely ill pts)
•Endoscopic methods
–Endoscopic cystic duct stenting
–EUS guided gallbladder drainage
```
108
What is Marrizzi's syndrome?
cystic duct stone is so large that it obstructs the common hepatic duct or common bile duct
109
What is gallstone ileus?
* Mechanical bowel obstruction caused by the impaction of a gallstone in the ileum after being passed through a biliary-enteric fistula
* Rare but highly morbid
* Older woman with comorbid diseases
* 60% caused by cholecystoduodenal fistulas
* Adhesions then pressure necrosis
* Stones 2+ cms
* Treatment: Enterolithotomy and CCY
110
How can gallstones be treated medically?
* Ursodeoxycholic acid (UDCA) hydrophilic bile acid
* Reduces biliary cholesterol secretion, increases biliary bile acid concentration, and reduces cholesterol saturation index
* Improves GB emptying
* Most cholesterol gallstones contain some calcium salts which limits therapy
111
What is choledocholithiasis?
Blockage of bile duct with 1 or more stones
112
What are causes of acute cholangitis?
```
•Choledocholithiasis
•Tumor
•Biliary instrumentation
•Benign acalculous causes of stasis
–congenital cysts
–pancreatitis
•Parasites
–E.G. Ascaris lumbricoides, Clonorchis sinesis
•HIV
```
113
How does acute cholangitis present?
```
•Clinical Presentation
–Charcot’s Triad 60 - 70% of patients
–Reynolds Pentad
–tenderness less severe than other abd. emergencies
•Labs
–Leukocytosis
–Elevated bili (20% of patients have total bili < 2)
–Elevated AST/ALT and Alk Phos
•Imaging Studies
–Ultrasound, CT
```
114
How should acute cholangitis be treated?
•Antibiotics
–Cipro
–Zosyn
•NPO, Hydration
•Most patients respond within 12 - 24 hour
–Plan for semi-elective drainage
•Toxic patients, or patients who fail to respond to initial treatment require emergency drainage via ERCP
115
What should you think if you see painless jaundice?
Ampullary cancer until proven otherwise
116
What is sphincter of oddi dysfunction?
* Abnormality of SO contractility
* Benign, noncalculous obstruction to the flow of bile or pancreatic juice through the pancreaticobiliary junction
* Pancreaticobiliary pain, pancreatitis or abnormal LFTs
* Made up of SO dykinesia or SO stenosis
* Most commonly occurs after CCY
* Abdominal pain is the most common symptom
* RUQ, radiating to the back
* Abnormal LFTs, dilated CBD on imaging
* SO manometry (40 mm Hg upper limit of normal for basal SO pressure)
* Medical, endoscopic and surgical therapy
117
What does the pancreas do?
```
•Endocrine pancreas – Islets of Langerhans
b cells - insulin
a cells - glucagon
d cells - somatostatin
PP cells - pancreatic polypeptide
```
•Exocrine pancreas (80% of pancreatic mass):
Composed of acini that synthesize and secrete digestive enzymes in the form of zymogen granules
–Secrete 1 L of bicarbonate rich fluid
118
What is acute pancreatitis?
* When the protective mechanisms are overcome, there is inappropriate activation of digestive enzymes within the pancreas
* Resulting in “auto-digestion” of pancreatic cells and subsequent inflammatory reaction (interleukins, TNF, PAF)
* Acinar cells are damaged and leak activated digestive enzymes into the intercellular space resulting in fat necrosis and edema
119
What is the clinical presentation of acute pancreatitis?
```
•History
–Epigastric pain, radiation to the back
–Unbearable in severity
–Alcohol or gallstone history
–New medications (thiazides, 6-MP, statin, DDI)
•Physical
–Abdominal tenderness
–Fever, tachycardia, tachypnea
–Rarely, evidence of retroperitoneal hemorrhage (Grey-Turner’s sign, Cullen’s sign)
```
120
How do you diagnose pancreatitis?
•Requires 2 of the following:
–Abdominal pain characteristic of acute pancreatitis
–Serum amylase and/or lipase 3+ x normal
–Characteristic findings of acute pancreatitis on imaging (US/CT/MRI)
121
How is acute pancreatitis treated?
* Nothing by mouth
* Aggressive fluid hydration
* Pain control
* Assess for complications
* Assess for etiology to prevent future attacks
122
How do you assess whether pancreatitis is caused by gallstones?
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–Abdominal sonogram (CBD > 6 mm)
–ALT > 3x above normal
–GGT > 7x above normal
–Total bilirubin > 3.0
–Cholangitis
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How should severe acute pancreatitis be treated?
* GI and surgical consultation
* Intensive care unit
* Aggressive volume replacement
* Close monitoring, including Swan-Ganz
* ERCP if etiology is gallstones
* Dynamic CT within first 48 - 72 hours
* Initial antibiotics NOT recommended
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How are pancreatic fluid collections defined in pancreatitis?
* Acute peripancreatic fluid collection (APFC) (first 4 week)—no solid component, due to inflammation in the absence of necrosis or pancreatic ductal disruption.
* Pseudocyst—(after 4 weeks) well circumscribed homogeneous fluid collection rich in Amylase
* Post-necrotic pancreatic fluid collection (PNPFC) Begin 2-6 weeks after the onset of pancreatitis, arise from necrosis and contain fluid and necrotic debris
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What can be seen in chronic pancreatits?
•“Classic pain” – epigastric pain, radiating to the back, exacerbated by oral intake and associated with nausea and vomiting and can be relieved by sitting forward
•Prospective natural history study demonstrated two patterns of pain:
–Episodes of pain lasting about 10 days, followed by pain-free periods
–Daily pain with frequent exacerbations and repeat hospitalization
•Up to 20% of patients with CP can present with pancreatic insufficiency and no pain
•Clinical insufficiency occurs when >90% of pancreatic function is lost
•Fat maldigestion leading to steatorrhea
•Diabetes – labile, because glucagon producing a cells are also affected
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What are the parts of the small bowel?
Duodenum, jejunum, ileum
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What is Whipple's Disease?
Found in contaminated soil
•Infection with Tropheryma whippelii
•PAS-positive macrophages in intestinal mucosa
•Most commonly affects the small intestine causing malabsorption
•Arthralgias, cardiac, neurological symptoms common
•Treatment: Penicillin G + streptomycin, then Bactrim for more than 1 yr
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What is SIBO?
Small Intestinal Bacterial Overgrowth
Leads to malabsorption of nutrients due to excessive number of colonic bacteria
Low serum B12, high folate
symptoms: abdominal pain, bloating, excess gas, nausea/vomiting, diarrhea/constipation, weight loss
treat with tetracycline, bactrim, and rifaximin for 10-14 days
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What is Meckel's Diverticulum?
•Most common congenital abnormality of GI tract
•Remnant of embryonic vitelline duct causes outpouching in distal ileum
•May contain ectopic acid-secreting gastric mucosa that can lead to peptic ulceration and GI bleeding or perforation
•Can cause obstruction from intussusception or volvulus
•Rule of 2’s:
–2% of population
–2 inches long
–2 feet from ileocecal valve
–2 types of common ectopic tissue (gastric and pancreatic)
–2 years most common age at presentation
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What is intussusception?
* Telescoping of a proximal bowel segment into a more distal segment causing bowel obstruction
* Can compromise blood supply
* Most common in infants and young children
