3. Upper GI Disease Flashcards
Diff btw oropharyngeal and oesophageal dysphagia
Oropharyngeal ⇒ can’t bring food from the mouth to the oesophagus ( ENT rather than gastro), diff initiating swallowing - may have choking or aspiration
Eg. of oropharyngeal dysphagia
- Skeletal muscular disorders in context of stroke ⇒ dysphagia may be one of the early Sx, may take weeks to get better
- Neuromuscular - MND, bulbar pulsy
- Throat tumour or pharyngeal tumour would block the back of mouth ( mech obst.)
- Sjogren’s ( decreased saliva) is associated with primary BILIARY sclerosis or rheumatic diseases
- Alzheimer’s and depression
Eg. of oesophageal dysphagia
- mech obstr due to narrowing of oesophagus eg. strictures
- Motility disorders
- Autonomic neuropathy due to diabetes
- Alcohol and GOR can also disorganize oeso motility
What CN are involved if weak tongue or cheek muscles cannot move food around in the mouth for chewing?
V, VII
What CN are possibly involved if pts are not able to start swallowing reflex that allows foods to move safely through pharynx? And what can cause this?
IX, X, XI, XII
Stroke, nervous system disorder
What could progressive dysphagia suggest
Tumour getting worse?
What does intermittent dysphagia suggest?
Dysmotility syndrome or oesophagitis
If dysphagia to solids then liquids, is it likely to be obstructive or dysmotility
Obstructive, dysmotility more likely to be both
What could cause odynophagia
Severe oesophagitis associated with inflammation
Red flag as may suggest malignancy
Can benign UGI diseases cause weight loss
Yes if severe eg. severe strictures
What does hoarse voice with dysphagia suggest
Tumour pressing on recurrent laryngeal nerve (branch of vagus nerve)
What do chest pains associated with dysmotility suggest
- Oesophageal spasm ( may be caused by acid reflux)
- Referred pain ⇒ similar nerves from heart and oesophagus
What are the likely causes of dyspjagia in an elderly patient?
Elderly patient ⇒ neurological causes if intermittent/ long standing, or sinister causes like oesophageal ca if new, progressive with regurgitation and weight loss
What are the likely causes of dysphagia in an younger patients?
Oesinophillic oesophagitis ( with food bolus obstruction), or dysmotility
What are the likely causes of dysphagia in middle aged patients?
Dysmotility eg. achalasia secondary to acid reflux
Is dysphagia for liquids netter than for solids for achlasia
No, equal
Regurg of prev day’s food, bad breath
Pharyngeal pouch
Should endoscopy be done for pharyngeal pouch
No, risk of camera going into pouch and causing perforation during endoscopy
What could Inflammation, bleeding, hyperplastic process on endoscopy suggest
Stricture
Causes of struictures
- Benign :Acid reflux oesophagitis, Barrettt’s, extrinsic comppresion ( mediastinal tumour), post-radio, anastomotic from area of previous oesophagectomy, corrosive (alkali ingestion)
- Malignant stricture
What sphincter is involved in Achalasia and what happens to it
Increased tone of LOS, inability to relax and high resting pressure, when oesophagus contracts, goes through stage of hypertrophy and dilatation ( baggy oeso)
Test for achalasia
Oesophageal function test (manometry) can check for decreases motility of oesophagus- LOS is tight and fails to open completely
What is treatment for benign strictures
- Dilatation
- Endoscopic Balloon or push dilators to stretch oeso
- PPIs ( long term therapy)
- Recurrent strictures → put stent to open oesophagus
62 yo man, 3mo history of progressive dysphagia for solids- frequent choking and feeling of food stuck in middle of chest
Eventually also liquid dysphagia
longstanding smoker and drinker
lost 6 kg of weight but bmi 31
long standing gord, rennies for years
regurg even liquid and pain every time food gests into gullet
What are other more severe Sx possibly.
Possible oeso cancer
Fistulation between the oesophagus and the trachea or bronchial tree leads to coughing after swallowing, pneumonia and pleural effusion. cachexia, cervical lymphadenopathy or other evidence of metastatic spread is common.
Squamous vs adenocarcinoma oeso cancer- different pop?
Adeno- GORD, overweight, younger, typically lower 3rd oeso
Squamous- Alcohol, smoking, most common worldwide
how to establish Dx of oeso cancer
Endoscopy and biopsy
oesophager CA T staging
- T4 - beyond to nearby tissues
- T1- usually mucosa or submucosa
- T2- muscularis
- T3- border of lesion
What imaging modality to stage tumour for oeso ca
Endoscopic US- allows to see through the wall and take biopsies of LNs, determin depth of penetration into oesophageal wall and LN involvement
How to look at mets and LN and what can be done to show met spread and invasion (if tumour is malignant)
CT scan best way to look at mets and LN, CT PET can show if tumour is malignant or not
Palliative care for malignant strictures
Stenting (SEM) ,
40 YO F , 9 mo history of intermittent dysphagia for liquids and solids
Weight gone down, normal UGE
Typical dysmotility, severe as weight has gone down
DO BARIUM SWALLOW- Dx of achlasia
Treatment for achalasia
- Pneumatic dilatiation using air filled balloon to disrupt sphincter
- Risk of perforation
- Surrgical myotomy
- done laprascopially to weaken LOS
- Most common in young people
- may need PPI after
- done laprascopially to weaken LOS
- Botox injection at LOS in older people → much safer but need to repeat because last for only 1-1.5 yr
- Most common in older people
- POEM
- Open oesophagus and cut muscle
17Yo man, asthmatic, 3wks hx of dysphagia and bolus obstr.
Eosinophillic oesophagitis - FBO common presentation, pmhx of atopy of food allergies
How to make confirmation dx of Eosinophillic Oesophagitis
- esophageal biopsy - 3 in middle and 3 in lower oeso
- > 15 eosinophils per HPF
- May have white spots ( eosinophillic abscesses,) tram line (linear ulcerations)
Tx of Eosinophillic Oesophagitis
An empiric 8-week trial of high-dose PPI can be used in the first instance. Around one-third of patients will respond to this, known as PPI-responsive oesophageal eosinophilia.
In patients who do not respond, 8–12 weeks of therapy with topical glucocorticoids can be used, such as fluticasone and budesonide. Treatment with topical steroids (orodispersible budesonide )
Can liquids be swallowed when there are stirctures
Yes, until it becomes severe
What drugs can cause benign strictures
Bisphosphonates, can cause intermittent dysphagia and oesophageal ulceration
Ix algorithm for dyspepsia
If alarm features eg. unintentional weight loss, anaemia, persistent vomiting, hematemesis and/or melaena, dysphagia, palpable abdominal mass - do urgent endoscopy OR above 55 despite alarm features, then endoscopy
If not, just H pylori test if persistent Sx eg. urea breath test or stool antigen
If positive, triple therapy, if not, treat Sx
Post-eradication confirmation of H.pylori
Urea breath test
Main causes of UGIB
Peptic ulcer - NSAIDs or peptic ulcer
Varices ( liver disease or portal vein thrombosis)
Retching can cause Mallory-Weiss tear
Ca
Gastric erosions/ Gastritis due to NSAIDs and Alcohol
Oesophagitis may also cause UGIB
Can melaena be caused by LGIB
Yes, may be from right side of colon
Should antithrombotic durgs be stopped during GIB
Yes, but aspirinn can be continued in UGIB
Treatment for non-variceal UGIB
Can treat endoscopically using cautherization or clips, with adrenaline. Haemospray as rescue therapy
give PPI IV to reduce gastrin secretion and promote clot stability
Tx for variceal blead
Band ligation, balloon tamponade if BL failed
Risk factors that may exacerbate dyspepsia Sx
Obesity ( related to diet) , trigger foods like tomatoes, fatty or spciy foods, smoking and alchol. Stress, anxiety and depression may worsen Sx
Drugs that can exacerbate dyspepsia -
Aspirin and NSAIDs
alpha-blockers, anticholinergics,benzodiazepines,beta-blockers, bisphosphonates, calcium-channel blockers, corticosteroids, nitrates,theophyllines,and tricyclic antidepressants.
Tx for dyspepsia
Usually just use antacid
IF H pylori +ve
Full dose PPI for 1 mo if no H pylori
OR
If positive, then PPI and amox and clarithro or metro
If allergic to pen, then clarithro and metro
If Sx recure, switch to alternate therapy and cpnsider alternate acid supression therapy with histamine receptor antagonist eg. ranitidine
For h pylori test, what should be ensured?
Pt has not taken PPI in past 2 weeks or abx in past 4 wks
Is tone of LOS increased or decreased in GORD
Decreased
Complications of GORD
Barrett’s - pre-malignant condition due to chronic GORD
Oesophagitis ( may have stricture)
Ca
Barrett’s - what kind of cells
Columnar instead of squamous
Risk factor for Barrett’s
Age, male, obseity and smoking
Ix and Mx of Barrett’s
Endoscopy is gold standard, multiple bipsies should be taken
Mx only for Sx of reflux compl eg. stricture - endoscopic resection + RFA or oesophagectomy
Ix for GORD
Usually treat empirically in young pts, but in older pts can do endoscopy to exclude other diseases
tx for GORD
Give lifestyle advice (weight loss, avoidance of dietary items that worsen symptoms, having small mails often, elevation of the bed head in those who experience nocturnal symptoms, avoidance of late meals and cessation of smoking.)
Antacids, then empric full dose PPIs,if severe and progressive Sx despite anatacid.
if stilll poor response then consider pH monitoring and perform fundoplication if positive
Pharyngeal pouch Ix and Tx
Barium swallow - will reveal incoordination of swallowing
Treatment is indicated in symptomatic patients, and can be via a surgical approach, such as cricopharyngeus myotomy (diverticulotomy), with or without resection of the pouch. or stapling
Achalasia Sx
Dysphagia to solids and liquids, regurg to saliva and food may occur, may have chest pain due to oeso spasm, weight loss
Causes of acute gastritis, Sx and usual treatment
NSAIDs + aspirin , alcohol, antacids and PPIs,
Sx include dyspepsia, anorexia, nausea or vomiting, and haematemesis or melaena
Tx include symptomatic therapy with antacids, and acid suppression using PPIs, prokinetics like domperidone or antiemetics like metoclopramide
Where are peptic ulcers commonly located
Stomach or duodenum
BUT may also occur in lower oeso, jejunum after surgical anastomosisto stomach, or in ileum adjacent to Meckel’s diverticulum
What other non GI cancer can cause dysphagia
Lung cancer or mediastinal adenopathy can cause external compression of oesophagus
Goitre compression can cause oropharyngeal dysphagia
Ix for dysphagia -
If progressive and sever, or persistent, should do UGI endoscopy
Two largest risk factors for PUD
H pylori and Aspirin + NSAIDs
PUD sx
post prandial abd pain, localisation to epigastrium
Dyspesia, vomiting
Gastric outlet obst (persistent vomitting)
Perforation
Haemtemesis, coffee ground vomiting or malaena
Benign vs malignant ulcer
Shallow with no rolled edges vs craggy, quite deep
Red flag Sx for PUD
Epigastric pain with weight loss
Ix for PUD
Endoscopy with histologic biopsies to exclude cancer
+ H pylori testing- 1 wk triple therapy if +ve
+ 2 months high dose PPI for PUD
Requires follow up endoscopy for gastric ulcers to ensure healing and that they are not malignant
What kind of oesophagealcancer arises from Barrett’s and where else can this type be found
Adenocarcinoma, can be found lower at GO jtn
Tx for Oeso Ca
Oesophagectomy if resectable, if not then chemo +radio
Common Sx of oesophagitis
Similar to GORD- Heartburn, regurgitation (provoked by bending, straining or lying down), water or acid brash
May have dysphagia or odynophagia
Risk factors for oesophagitis
Smoking, obesity, alcohol, hiatus hernia
What is dyspepsia
Discomfort in the epifastric area, usually after a meal
What is heartburn
Burning restrostenal sensation, often due to acid reflux
What is Schatzi ring
Fibrous rink at GOJ linked to acid reflux
How may H pylori lead to duodenal ulceration?
may have hypergastrinaemia and increased acid productionby parietal cells.
Or may have gastric atrophy and hypochlorohydria, allowing proliferation of bacteria- predispose to cancer
What should be prescrobed with long term NSAIDs
PPI
Recent flu-like illness, worsening abd pain despite analgesia, nausea with dark stools (also on PR exam), non-specific tennderness, HR 92, BP 107/65
On aspirin + PPI , B blocker and statin, apixaban
Non-smoker, 0.5 bottle wine thrice a week
Likely bloods?
UGIB
Low Hb, High Urea and Creatinine normal
Risk factors for bad outcome in acute UGIB
History of malignancy or cirrhosis, haematemesis, hypovolaemia, Hb <80
Should anticoag be stopped in pts with UGIB
Stop apix ( esp if only one DVT and not recurrent), continue aspirin
What does GBS predict
Risk stratifies pts at risk of UGIB
includes the need for endoscopic intervention
Target for transfusion if have Sx
Hb>70
Timing of endoscopy for UGIB
24 hrs if haemodynamically stable, no persistent hematemesis, and can discontinue anticoag temporarily, otherwise < 12hrs
What to do if UGIB can’t be controlled endoscopically
Interventional radiology
PPI post endoscopy
IV PPI continuous infusuion for 72 hrs
Should H pylori tx be given for PUD
Yes if +ve for H pylori, if -ve and not on NSAID just treat emprically
If alcohol history in pt with melena, suspect?
Variceal blead
What does low lactate in pt with melena and jaundice suggest
Patient hypoxic
What are platelet levels likely to be like in pt with splenomegaly and cirrhosis
Decreased levels as platelts will pool in spleen due to cirrhotic level
Na and K levels in pt with severe cirrhosis
Hyponatremia and hypokalaemia
How to manage pts with increased PT
Can give Vit K IV to stimulate pdtn of clottining factors
Mx of variceal bleed, time limit
IV abx and consider IV terlipressin to reduce blood into varices
Then endoscopy and variceal ligation
Should be done < 12h if stable, earlier if not
What drug should be given for long term Mx of variceal bleeds
Carvedilol
Ix for pt with variceal bleed and liver cirrhosis
Assess Liver function, liver screen for Hep B and C, US or CT (flow in portal vein) for complications like HCC, and
Another possible cause of ulcerative esophagitis and Tx
Alcohol, PPI
