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74 Cards in this Set

  • Front
  • Back
What GI disease causes 1/3rd of all cases of dyspepsia?
Peptic Ulcer Disease
Peptic ulcer disease includes both _____ and ____ ulcers
gastric and duodenal

90% are duodenal ulcers located in the first portion of duodenum
Peptic ulcers are primarily associated with ______ and ________
NSAIDS and H PYLORI

although it can occur with or without h pylori infections
Gastric ulcer: Definition
chronic ulceration in the lining of the stomach, frequently in the lesser curvature of the antrum near the pre-pyloric area
What is the peak age range for PUD?
Peak ages: 55-65 years, rare before age 40
PUD: Etiology
Familial tendency for gastric ulcer

Causes of gastric ulcer are multifactoral

>60% have positive H. pylori
Whereas >80% of pts with duodenal ulcers have H. pylori

NSAIDs – ulcerogenic drugs

Cocaine use: may increase stomach imbalance

Imbalance between aggressive factors
Gastric acid, pepsin
..and protective factors
Mucous, blood flow, cell turnover
H pylori and cancer risk
2 – 6 x higher risk for gastric cancer in presence of H. pylori

90% adenocarcinoma of stomach have pos H. pylori
H pylori and ulcer formation
More than 50% of adults have chronic H pylori infection, but only 5-10% develop ulcers (Peters, 2010)
People at higher risk for H pylori infection
Hispanic
African American
Older adults
Lower socioeconomic level of income
PUD: PRIMARY PREVENTION
Avoid/decrease use NSAIDs

Quit cigarette smoking

Associated with corticosteroid use – minimize overuse if possible

Stress reduction (questionable if effective)

May not be related to etoh, caffeine, dietary spices, Tylenol

If anything irritates stomach, best to avoid but … bland diet DOES NOT promote healing!
PUD and bland diet
If anything irritates stomach, best to avoid but … bland diet DOES NOT promote healing!
Primary prevention if caused by NSAIDs
Secondary Prevention: PUD
NONE!

Early diagnosis facilitated by high level of suspicion in:
1. pts taking NSAIDs to facilitate early diagnosis
2. H pylori levels in symptomatic pts (some resources suggest only doing in face of positive ulcer finding e.g. positive fecal blood)
3. Fecal blood – requires follow-up studies to determine site of bleed
NB: Hg may be normal unless hemorrhage
***GASTRIC ULCERS AND EFFECT ON HEMOGLOBIN
NB: Hg may be normal unless hemorrhage!
What are classic symptoms (relieving and exacerbating factors) of gastric ulcers?
Pain decreased or absent with fasting (CLASSIC)

Pain occurs almost immediately after eating (CLASSIC)

Food avoidance, weight loss common
Duodenal Ulcer Symptoms
Gnawing or burning epigastric pain 1-3 hours after meals

Nocturnal pain causing early morning awakening

Pains relieved by: food, antacids, antisecretory agents
NSAID INDUCED ULCERS: SYMPTOMS
NSAID induced ulcers may be asymptomatic – perforation may be first overt sign of disease (medical emergency!)
PUD: DIFFERENTIAL DIAGNOSIS
Non-ulcer dyspepsia

Zollinger-Ellison syndrome (gastrinoma)

Usually tumors in head of pancreas or sm intestine are cause – they secrete gastrin that increases gaastric acid. About ½ of these are malignant, and many of the patients have MENS (Multiple Endocrine Neoplasia), which also effects the pitutitary and parathyroid.

NB: Gastric carcinoma – symptoms of this are vague and it is rare to diagnose this in early stage!

H pylori induced gastritis

GERD

Cholecystitis

Crohn’s disease (gastroduodenal)

Variant angina pectoris
****GASTRIC CARCINOMA: SYMPTOMS
NB: Gastric carcinoma – symptoms of this are vague and it is rare to diagnose this in early stage!
PUD: Assessment: GENERAL
Overall appearance including Weight and Affect

Skin: including Hydration

Abd exam: esp. epigastric tenderness
PUD: ASSESSMENT: IMAGING
Endoscopy more accurate than radiology, and Endoscopy is considered less expensive
PUD: ASSESSMENT: LABS
H. pylori (Peters, 2010)

Serum antibody –
cheapest non-invasive test-remains positive for years
after eradication
Only useful if negative as a positive needs to be
confirmed with one of other two tests

Stool antigen – highest sensitivity and specificity – can
test for resolution

Carbon-labeled urea breath testing – most accurate
non-invasive test and resolution

Accurate 4 weeks after treatment for
eradication

Fecal occult blood

Would you draw a Hg?

Consider serum gastrin (seen in Zollinger-Ellison syndrome)
H Pylori Serum Antibody
cheapest non-invasive test-remains positive for years
after eradication
Only useful if negative as a positive needs to be
confirmed with one of other two tests
What h pylori test has the highest sensitivity and specificity?
Stool antigen – highest sensitivity and specificity – can test for resolution
most accurate non-invasive test and resolution for h pylori
Carbon-labeled urea breath testing – most accurate non-invasive test and resolution

Accurate 4 weeks after treatment for eradication
Zollinger-Ellison syndrome: Definition
Extensive ulcerations in stomach and duodenum due to excess secretion of acids
PUD: Management: Guidelines
In young, healthy, person with dyspepsia and without weight loss, or persistent vomiting; AND <45 years (American College Gastroenterology, 2010; Chey, 2007)

Empiric treatment initially is considered reasonable

All others:

Endoscopy

Emergency endoscopy and hospitalization if suspected ulcer bleeding
IF NEGATIVE FOR H pylori treat: RULE OF THUMB
just with acid suppression:
If negative for H PYLORI how long do you treat a gastric ulcer
12 weeks
If negative for H PYLORI how long do you treat a duodenal ulcer
8 weeks
PUD therapy: H2 receptor antagonists (H2RA)
No longer considered first line, but much cheaper and otc when compared to PPIs

Examples:
Ranitidine or Nizatidine 150 bid or 300 mg HS
Cimetidine 400 bid or 800 HS (very inexpensive)
PUD Therapy: Proton pump inhibitor
Treat for 4 – 8 weeks e.g.
First line drug choice usually
Promote healing of ulcer

Examples:
Omeprazole 20 mg qd (may be curative of PUD in 8 weeks)
What is the first line treatment for PUD?
PPI

treat for 4-8 weeks (may be curative in 8 weeks)

promotes healing of ulcer
H pylori eradication protocols
Multiple “triple therapy” regimen

Example for two weeks (first line treatment 2013)
Omeprazole 20 mg bid
Clarithromycin 500 bid
Amoxicillin 1 gm bid
PUD from NSAIDS
PUD: Follow up
Return visit in 2 weeks (or sooner) to evaluate
Weight
Symptom relief
Adherence to plan
Ensure quit smoking plan

If no improvement or if any high suspicion symptoms occur, refer to gastroenterologist for endoscopy
PUD: Economic, ethical, legal psychosocial, cultural, and family considerations
During treatment, symptoms usually mild enough to allow essentially normal activities for work/school/family/social

Dietary restrictions no longer required within reason.
PUD: Health policy implications
There have been proposals to increase health insurance in those who smoke – this is another example, including those of respiratory origin, indicating an increased health risk and subsequent health care cost from those who smoke. Should insurance costs be based on risks?
GERD: definition
the reflux of stomach contents into the esophagus – a ‘mobility disorder’
GERD: causes
usually related to dysfunctional relaxation of the lower esophageal sphincter

Other causes: pregnancy, scleroderma, delayed gastric emptying, acid hypersecretion, some surgeries e.g. colon resection
GERD: Primary Prevention
Avoid smoke, ETOH, and caffeine – coffee
Weight management
Avoid meds that lower esophageal sphincter tone:
Theophylline, anticholinergics, progesterone, calcium
channel blockers, alpha adrenergic agents, diazepam,
meperidine
Avoid foods that lower esophageal sphincter tone:
High-fat foods, yellow onions, chocolate, peppermint
Avoid foods that irritate esophagus:
Citric fruits and juices, spicy food and drinks
GERD: SECONDARY PREVENTION
NONE!

Testing for H pylori in high risk population is controversial. Use if no improvement with treatments – then is diagnostic NOT screener.
GERD: Tertiary prevention
Step therapy:
Elevate HOB, avoid laying supine after meals, avoid
valsalva maneuver, low fat diet, smaller more freq
meals

Wt loss if needed

OTC antacids or H2 antagonists

Stool antigen test for H pylori eradication following
treatment

Vitamin B 12 levels in patients with atrophic gastritis

Hct
GERD: Symptomatology and assessment
Heartburn (most pts have esophageal mucosal pathology, though not usually ulcers are present)

Regurgitation – almost all patients have heartburn and regurg – other symptoms are less often (Fisichella, 2010)

Dysphagia

Angina CP

Bronchospasms

Laryngitis

Chronic cough

Globus sensation

Loss of dental enamel
GERD: ASSESSMENT: DIAGNOSTICS
Consider

Barium swallow (finds ulcers and strictures, but not mucosal injury) – INSENSITIVE TO GASTRITIS

Useful if patient also has dysphagia

Esophagoscopy with biopsy ( preferred choice for outcome, cost, finding of Barrett’s esophagus, and pt preference)

Esophageal pH monitoring and/or gastric analysis (use if atypical GERD)

Esophageal manometry if surgery considered
What is the preferred choice for GERD DIAGNOSTICS?
Esophagoscopy with biopsy ( preferred choice for outcome, cost, finding of Barrett’s esophagus, and pt preference)
Barrett’s esophagus
Strong links between prolonged unresolved GERD, Barrett’s esophagus, and esophageal cancer (Ferri, 2013)
GERD: Differential diagnosis
Infectious esophagitis candida, herpes, HIV, CMV

Chemical esophagitis

Radiation injury

Chron’s disease of esophagus

Angina pectoris

Esophageal/gastric carcinoma

Medication related

Achalasia

PUD
GERD: Management and Interventions
Step therapy includes dietary/lifestyle changes listed earlier for all individuals

Step treatment

Mild symptoms: OTC H2 receptor antagonists (H2RA), antacids

American Gastroenterology Assn most recent guidelines at guidelines.gov (2008): “Antisecretory drugs for the treatment of patients with esophageal GERD syndromes (healing esophagitis and symptomatic relief). In these uses, proton pump inhibitors (PPIs) are more effective than histamine2 receptor antagonists (H2RAs). ….Twice-daily PPI therapy for patients with an esophageal syndrome with an inadequate symptom response to once-daily PPI therapy.”

Moderate - severe symptoms: proton pump inhibitors (PPIs) or prescription strength H2RAs

Ulcerated esophagus: surgery

H2RAs: Cimetidine (Tagamet) 800mg bid is least expensive option

Many patients may have tried this otc already

Heartburn history has a positive predictive value >80% warranting empiric initial care in absence of worrisome symptoms

Empiric trial of proton pump inhibitor compares well to pH monitoring as diagnostic tool for GERD

NB: Complications more likely in elderly
GERD: National protocols
Agency for Healthcare Research and Quality (AHRQ)
PPIs are superior to histamine H2-receptor antagonists
for the resolution of GERD symptoms at 4 weeks and
healing of esophagitis at 8 weeks.
Typical GERD symptoms treatable with acid suppression therapy for 6-8 weeks
If cont symptoms, or if not typical from onset, endoscopy
Risk factors exist for stricture and Barrett’s esophagus – evaluation needed if unresolved GERD
GERD: Resistant cases
Patients who do not respond to usual treatment after 4-8 weeks acid suppression therapy, should:
undergo is upper endoscopy to exclude a diagnosis of peptic ulcer disease or cancer and identify the presence of esophagitis (Richter, 2007)

Refractory reflux syndromes associated with normal endoscopy findings are more problematic
testing may include 48 h pH testing, impedance measurements (for nonacid reflux), esophageal manometry and gastric function tests.

May need fundoplication surgery if not resolved with medications (90% effective; Cooper, 2007)
Nissen fundoplication
GERD: Case management: economic, psychologic considerations
Common disorder in adults

May limit socializing due to regurgitation, pain, cough, food limitation

OTC medications ease access to treatment but don’t assist in identification of those with serious underlying disease
Cholecystitis: definition
acute or chronic inflammation of the gallbladder, usually related to previously asymptomatic gallstones
Cholecystitis: what race is at higher risk?
Native Americans (Pima) and Scandanavian descent with greatest incidence
Cholecystitis: Risk factors
Women
Older adults (>40 years)
Obese
Fasting Low LDL, Elevated triglycerides
Pregnancy
Hyperalimentation
Oral contraceptive pills
Cirrhosis
Cholecystitis: Primary prevention
Most risk factors not malleable
Avoid obesity
Avoid rapid weight loss
Consider alternate BC than OCP in Native Americans
Low fat diet? Adequate fluid intake?
Exercise may increase bile duct motility
What ever happened to the undergraduate neumonic: fair, female, fat, forty, fertile?
Only partly correct
Cholecystitis: secondary prevention
NONE
Cholecystitis: Symptomatology
Intermittent pain, typically RUQ immediately following classically a meal of high fats

Pain is intense with radiation to epigastrum, R shoulder or back

Classic ‘biliary colic’ is pain rising over 2-3 minutes to plateau of intensity maintained for >20 minutes

Any suspicion that pain origin is cardiac warrants an emergent referral for cardiac workup

Usual symptoms
Anorexia, Abd bloating, Belching
Nausea , Vomiting
Cholecystitis: acute presentation
Acute presentation – emergent surgical referral:

May appear acutely ill
Temp may be mildly to moderately elevated
Abdominal distension
Local epigastric/RUQ tenderness – rarely diffuse
Jaundice
Loose, light-colored stools

Physical assessment special tests:
Inspiratory arrest when palpating RUQ and pt taking deep inspiration (also with tenderness)
Ortner’s sign: tenderness when hand taps the R edge of costal arch.
Georgievskiy - Myussi's sign (phrenic nerve sign) - pain when press between edges of sternocleidomastoid muscle
Boas' sign – Tenderness inferior to R scapula (also can be seen with phrenic nerve irritation)
Murphy's sign
Inspiratory arrest when palpating RUQ and pt taking deep inspiration (also with tenderness)
Ortner’s sign
tenderness when hand taps the R edge of costal arch.
Georgievskiy - Myussi's sign
(phrenic nerve sign) - pain when press between edges of sternocleidomastoid muscle
Boas' sign
Tenderness inferior to R scapula (also can be seen with phrenic nerve irritation)
Cholecystitis: Symptomatology and assessment - chronic
Chronic presentation –
Usually only pain and nausea as with acute presentation, other symptoms absent

Consider laparoscopic cholecystectomy as outcomes poorer if acute presentation for surgery (Ferri, 2007)

Consider referral to gastroenterologist for dissolution agent, shock-wave lithotripsy or possible removal by endoscopic retrograde cholangiopancretography (ERCP)
Diagnose acute cholecystitis: The diagnosis of acute cholecystitis is based on the presence of at least two of three factors;
• acute right upper quadrant tenderness

• fever higher than 99-5° F (37.5° C) or leukocytosis
greater than 10,000/mm-

• ultrasound evidence such as a thickened and edematous gallbladder wall, the presence of maximal tenderness elicited over the gallbladder, and pericholecystic fluid collection.
Cholecystitis: differential diagnosis
PUD
Hepatitis
Diverticulitis
Dypsepsia
Neoplasms
Pancreatitis
Perforated duodenal ulcer
MI
Pneumonia
Nephroliasis
Cholecystitis: Diagnostics: Labs
HCG in women of childbearing age

Amylase – if elevated >500U – consider pancreatitis

ALT/AST (elevated)

Alkaline phosphatase (elevated)

Bilirubin (elevated)

U/A

CBC – expect leukocytosis in >70% patients
GBUS: Cholecystitis
Highly sensitive and specific for GB disease – before ordering if symptoms suggest PUD, or gastritis would consider trial of PPIs for 2 weeks

Ultrasound can accurately detect cholecystitis in 95% of patients.
Cholecystitis: management and interventions
Referral to surgeon if require narcotics

Acute cases remain NPO while transport to hospital

Chronic presentations advise on low fat diets

Consider watchful waiting in cases without biliary colic

But in those cases with biliary colic (constant acute pain R
shoulder or abd, with onset and resolution sudden, typically at HS, often with N/V), incidence of recurrence 50% annually and pt may likely benefit from surgery.
When do you use non surgical options for cholecystitis?
Used for patients who are asymptomatic or poor surgical candidates
What are the non surgical options for cholecystitis?
Oral medications:

Drugs made from bile acid—including ursodiol (Actigall) (8-10mg/kg/day po divided qd-tid) used to dissolve the stones. These drugs work best on small (less than 20mm) cholesterol stones, and months or years of treatment may be necessary before all the stones are dissolved.

Extracorporeal shockwave lithotripsy (ESWL):

This treatment uses shock waves to break up stones into smaller pieces that can pass more easily through bile ducts and avoid blockages. However, intense pain can follow treatment, and the long-term success rate is not known.
Cholecystitis: Economic, ethical, legal psychosocial, cultural, and family considerations
Post op course may limit family/social/work/school responsibilities for several weeks