Esophageal Disorders Flashcards
What are the symptoms associated with Oropharyngeal dysphasia and what disorders is it usually seen in?
Difficulty after initiation of swallowing Nasal regurgitation Choking Aspiration Coughing
Seen in neurological disorders: Stroke, ALS, Myasthenia, Parkinson’s
What is a high esophageal lesion that can cause oropharyngeal dysphasia? And how is it diagnosed and treated?
Zenker’s Diverticulum
Diagnosed with Video Fluoroscopy or US
Treatment is Surgery if symptomatic or >1cm in size
What are the symptoms of esophageal dysphasia and things that can cause it?
Feeling of food getting stuck in the chest
Can be caused by:
Esophageal mucosal disorders: peptic stricture , esophageal rings, tumors, lye ingestion, pill esophagitis, sclerotherapy, radiation esophagitis, infectious esophagitis
Mediastinal disorders: Lung cancer, lymphoma, Granulomatous disorders
Esophageal smooth muscle disorders: Achalasia, Scleroderma, Motility
How is candida esophagitis treated?
Fluconazole for 14-21 days
If patients do not respond to Fluconazole within 48 hours then send for EGD
How long should patients be treated with PPI for GERD? And What happens if there is a recurrence?
Treat for 8 weeks
If Symptoms recur < 3 months or patient has erosive esophagitis or Barrett’s esophagus long term PPI is recommended.
If symptoms recur >3months, repeat another 8 weeks of PPI acid suppresion
Steps in Diagnosing GERD?
Treat for 8 weeks if no improvement increase to BID dosing
I
I (-)
V
EGD—->Manometry—->pH monitoring (hold PPI for 7 days)
What is the therapy of choice for refractory GERD?
Diaphragmatic breathing—reduces belching
When is anti-reflux surgery recommended in GERD?
Recommended for patients who responded to PPI but are intolerant of PPI or does not want long term PPI mgmt.
Prior to surgery Manometry is performed to rule out impaired peristalsis if that’s positive fundoplication is C/I; If patient does not have erosive esophagitis (EGD not showing any erosions) then prep ambulatory pH monitoring is needed.
Complications of PPI
Hypergastrinemia B12 deficiency Iron and Calium deficiency Hypomagnesemia C.Dif Pneumonia Acute interstitial nephritis Acute headache
According to the FDA which 2 types of PPI should not be used with Plavix?
Omeprazole
Esomeprazole
(Pantoprazole can be used)
Indications for long term PPI use?
Maintenance treatment for GERD (4-8 weeks)
Maintenance of erosive gastritis healing
BArret’s esophagus
NSAIDS high risk users approved for 12 weeks to 6 months
Antiplatelet high risk users (patients on DAT, Blood thinners)
ZES
What is the screening criteria for Barrett’s Esophagus
Men with GERD >5 years AND 2 of the following:
- Caucasian
- Age >50
- Central obesity
- Smoker or Former
- First degree relative with Barrets or esophageal adenocarcinoma
Screening is not recommended for Women
What is the surveillance criteria for Barrett’s?
Barrett’s Metaplasia and No Dysplasia= Every 3-5 years
EGD by showing Barrett’s with indefinite dysplasia= treat with PPI for 3-6 months then repeat EGD, if repeat EGD is again indefinite then repeat EGD in 12 months with biopsy every 2cm along the Barrett’s epithelium to look for dysplasia
Low-Grade dysplasia=Patient can either go for endoscopic ablative therapy or EGD every 12 months
High Grade dysplasia=Ablation
Evidence shows that Adenocarcinoma risk decreases with what management?
- Medical treat of Barretts wit PPI and Aspirin
2. Anti reflux surgery
What does Manometry show in Achalasia?
How is Achalasia Diagnosed?
- Absent Peristalsis
- Incomplete relaxation of LES with swallowing
———————————-
Barium Swallow—>EGD to r/o pseudo Achalasia which is a tumor of the plexus——->Manometry (confirmatory test)
How is Achalasia Treated?
- Pneumatic dilation, which can be repeated (complication perforation)
For Patients who can undergo Surgery:
First line is Laparoscopic Myotomy with Fundoplication to prevent GERD
Non-surgical candidates can undergo Botox injection
What does Manometry show in Esophageal Spasm
What does Manometry show in Nutcracker esophagus
What does Manometry show in Scleroderma
=Esophageal Spasm shows Simultaneous contractions with wet swallow along with intermittent normal peristalsis
- Nutcrackers shows high amplitude contractions
- Scleroderma you have no peristalsis and hypotension (decrease)LES leading to severe GERD (because of no peristalsis Reglan can be used in these patients)
What are the 2 types of esophageal cancer and their location and risk factors?
- Adenocarcinoma (MC)
Involves Distal 1/3
risk Factors: GERD, Barret’s Smoking - SCC
Involves proximal 2/3
Risk factors: Smoking, Alcohol, HPV, corrosive injury, zinc and selenium deficiency, Tylesosis (hyperkeratosis of palm and soles)
What is the typical presentation of Eosinophilic esophagitis?
WhAT DOES EGD SHOWS?
Pt with history of Atopy plus solid Dyshagia requiring disimpaction with EGD
EGD Shows: Esophageal concentric rings, white specks, friable mucosa, linear tears with minimal trauma
Bx: Eosinophilic infiltration >15 sos/her
What are 3 conditions in which we see isolated esophageal eosinophilia?
- Eosinophilic Esophagitis
- GERD (usually < 5eos/hpf)
- PPI responsive esophageal eosinophilia
So because of these disorders whenever eosinophilia is seen treatment is 8 weeks of BID dose PPI then repeat EGD if symptoms and eosinophilia resolve then the diagnosis is GERD or PPR responsive esophageal eosinophilia. If no improvement then its Eosinophilic esophagitis
How is Eosinophilic esophagitis treated?
Swallowed steroids or viscous budesonide should show response in <1 week
What is the definition of Dyspepsia?
What is the guideline for mgmt of new onset dyspepsia?
Predominantly epigastric pain lasting for at least 1 year
Age:
>60 Get EGD
<60 Test and Treat (EGD is not recommended for pure dyspepsia if < 60, pure dyspepsia mean no dysphasia,weight loss, epigastric pain radiating to the back)
- H.Pylori positive—> treat
- H.Pylori negative—->or treatment of h.pylori doesn’t relive symptoms treat with PPI for 8 weeks
IF no relief after 8 weeks give Reglan for no more than 12 weeks or Amitriptylene
If still no improvement psychotherapy
When is EGD recommended for Patients <60 with dyspepsia
> 1 Alarm Symptoms
Or
Severe Alarm symptoms
OR
Family history of gastric cancer
Diagnosing H.Pylori
- Stools antigen test can be used for both initial diagnosis and confirming eradication (Patients taking PPI or bisthmuth cant be treated for stool antigen)
- Urea breath test= same as above plus antibiotic
If patients on PPI, Bistmuth, Antibiotic then initial test is Serology but that should not be used to confirm eradication
Treatment of H.Pylori
- Clarithromycin + Amoxiciliin (Flagyl if allergic)+ PPI
- Tetracycline+ Flagyl + PPI + Bistmuth
- Clarithromycin + Amox + Flagyl + PPI
14 day treatment is recommended
Choose a different antibiotic if previous macro life exposure or >15% macro life resistance)
Once the treatment regimen is concluded the next step is Ulcer healing Therapy:
For Duodenal ulcers: PPI for 4 weeks or H2 for 8 Weeks
For Gastric Ulcers: PPI for 8 weeks or H2 for 12 weeks
What are the reasons for failure to heal of PUD?
- Noncompliance
- Smoking
- NSAID use
- Acid hypersecretion: ZES, Cancer
What is the indication for maintenance (half dose H2 or PPI)for ulcers
- H. Pylori positive PUD with unsuccessful eradication
- H. Pylori negative ulcers with >3 recurrences per year
- Complications such as bleeding or perforation
How is Gastric MALT lymphoma treated?
Stage I disease can have complete remission with antibiotics
Patients with ulcers, mass, submucosal or serosal disease or LN involvement need to be treated with traditional gastric lymphoma chemotherapy.
What are the risk factors for NSAID induced Ulcer?
Does Celecoxib plus NSAID GI Protective?
Should patients be tested for h.pylori before starting NSAIDS
Age > 60 Prior Ulcer High dose NSAIDs NSAID+steroid NSAID + anticoagulant
these patients can be placed on prophylactic treatment
Combining Cox 2 inhibitor Celecoxib with NSAID removes its GI protectiveness and confer the same risk
Patients should be tested for h.pylori prior to starting NSAIDS if they have prior history of PUD
How do we manage NSAID induced PUD?
What is the gold standard NSAID induced ulcer prophylaxis?
- Stop NSAID
- Test and treat for H. Pylori
- Ulcer healing therapy with PPI or H2 blocker
- if NSAIDS must be continued then only use PPI and not H2 blocker
Prophylaxis gold standard is Misoprostol (but not well tolerated because of diarrhea) and now Esomeprazole and Lansoprazole are approved for prophylaxis
What are the recommendations to prevent NSAID induced ulcers?
Based on GI and CV risk
Low risk GI and Low risk CV= NSAID only
Low GI/ High CV= Naproxen plus PPI/Misoprostol
Moderate GI/ Low CV=NSAID plus PPI/Misoprostol
Moderate GI/ High CV= Naproxen plus PPI/Misoprostol
High GI risk/Low CV risk= Cox 2 plus PPI/Misoprostol
High and High= Avoid NSAIDs and Cox 2
When should we suspect ZES?
PUD + Diarrhea PUD + Hypercalcemia PUD unrelated to NSAID or H.Pylori REcurrent ulcers Postbulbar duodenal ulcer Nonhealing ulcers Multiple ulcers Fhx of PUD Fhx MEN1 Enlarged rural fold of stomach with dilated duodenum (acid hypersecretion)
How is ZES diagnosed? And Treated?
First check Gastrin level (>1000 picograms)plus evidence of acid hypersecretion (define as >15 mEq/hour or low gastric pH)because normally high acid should suppress gastrin
If gastrin is <1000 with evidence of acid hypersecretion the next step is secretin stimulation test
Once diagnosed next thing is imaging with octreotide scan
If surgical candidate then surgery if unresectable then high dose PPI and chemo
What are the risk factors for stress ulcer prophylaxis?
Coagulopathy Mechanical ventilation for 48 hours or more CNS Trauma Burn Organ transplant Patients with history of PUD
Aim is to keep gastric pH >4
What is the Gold standard for diagnosing Gastroparesis?
How is it treated?
Solid Phase Gastric Emptying
EGD is performed to rule out obstruction
Note: EGD showing residual food in stomach after overnight fast might suggests gastroparesis.
Treatment is Small, frequent, low residue meals
medical is Reglan
GI bleed endoscopic findings?
- Actively bleeding= 55% chance of rebleed
- Non-Bleeding visible vessel= 43% chance or rebleed
- Visible clot=22%
- Flat pigmented spot=10%
- Clean base ulcer=patient can be discharged have <5% chance of rebleed
What are the causes of nonvariceal upper GI bleed
- PUD
- Gastritis/esophagitis
- Mallory-Weiss
- Watermelon stomach- gastric vascular ectasia as seen in scleroderma
- AV malformation
- Dieulafoy lesion
- Cancer
- Aorta-enteric fistula
- Cameron’s lesions (Linear erosion in patients with hiatal hernia at the diaphragm level, that may be missed on EGD leading to occult GI bleed)
What is the antibiotic of choice for variceal bleeding
IV Ceftriaxone for 7 days
What are the 2 types of GI bleed?
Upper (Proximal to ligament of Treitz)
- Melena
- Hematemesis
- Hematochezia IF the bleed is severe and patient presents with shock
(NG tube not needed for UGIB)
Lower GI Bleed (distal to ligament of Treitz)
- Hematochezia
- if proximal lower GI bleed it can present as melena
What are the causes of Lower GI bleed?
Diverticulosis
AV malformation
Hemorrhoid especially in a young patient
Colon Cancer
How is GI bleed worked up?
Perform EGD (if negative or LGIB is suspected) Perform Colonoscopy
If Bleeding stop and Colonoscopy is negative small bowel bleeding must be ruled out with capsule endoscopy or CT enteropathy (more sensitive)
If Bleeding continues and colonoscopy is negative or cannot control bleeding send patient for RBC scan with arteriogram for embolization and surgical consult
(Note angiography can detect bleeding rate >1 ml/min)
If patient has severe bleed and colonoscopy is not possible then first step is arteriogram for emergent embolization
If patient has ongoing bleed and tagged RBC, Arteriogram are negative then rule out small bowel bleed with capsule endoscopy and consult surgery
