Gastro Theory Flashcards
Define GORD.
Prolonged or recurrent reflux of gastric contents –> oesophagus.
How does GORD clinically present?
- Heartburn (related to lying down and meals)
- Odynophagia
- Regurgitation
What is the pathophysiology of GORD?
- Tone of the LOS (lower esophageal sphincter) is reduced
- Frequent transient relaxations of the LOS
- Increased mucosal sensitivity to gastric acids
- Hiatus hernia can cause increased reflux (but reflux can occur without hernia)
What are possible risk factors for GORD?
- Smoking
- Alcohol
- Pregnancy
- Obesity
- Big meals
- Complication of hiatus hernia
- Any LOS dysfunction
Which patient group is more affected by GORD?
Mostly in men.
25% of adults experience heartburn.
Give a diagnostic test for GORD.
Endoscopy
Barium swallow
What is the treatment for GORD?
C: weight loss, avoid excess alcohol, stop smoking
M: Antacids if mild. If severe, PPI (omeprazole) or H2RA (cimetidine)
Give 2 possible complications of GORD?
Oesophageal stricture (worsening dysphagia)
Barrett’s Oesophagus (abnormal columnar epithelium replaces squamous epithelium of distal oesophagus) - irreversible and can develop into oesophageal cancer.
Which cell type changes to which in Barret’s Oesophagus?
Squamous epithelium -> Columnar epithelium (with goblet cells)
What are 3 possible causes of Upper GI bleeding?
- Mallory Weiss Tear
- Oesophago-gastric varices
- Peptic ulcer
What is a Mallory-Weiss tear?
Mucosal laceration in the Upper GI tract —> leads to bleeding
How does a Mallory-Weiss tear clinically present?
Bout of retching or vomiting -> haemetesis
Blood volume loss:
Syncope
Light-headedness
Dizziness
What is the pathophysiology behind a Mallory-Weiss tear?
Sudden increased intragastric pressure within rigid LOS can cause tearing of the mucosa.
This then causes blood to leak out into the oesophagus and be vomited out.
What are risk factors/causes of Mallory-Weiss tears?
Trauma from frequent cough
Vomit
Retching
Hiccuping
RF: excess ETOH
In which groups of patients are Mallory-Weiss tears common in?
- Bulimics
- Alcoholics
*Comprises 4-8% of all UGIB
What is the diagnostic test for a Mallory-Weiss tear?
Endoscopy
What is the treatment for a Mallory-Weiss tear?
ABCDE (resuscitation)
Maintain airway
High flow oxygen
Correct fluid losses
Identify comorbidities
Tear tends to heal rapidly on its own
What are complications of a Mallory-Weiss tear?
Hypovolaemic shock
Re-bleeding
MI
Death
What are oesophago-gastric varices?
Dilated veins at the junction between the portal and systemic venous systems -> leading to variceal haemorrhage.
What is the clinical presentation of someone with oesophago-gastric varices?
Haematemesis
Liver disease
Pallor
Shock (low BP, high heart rate)
What is the pathophysiology behind oesophago-gastric varices?
Liver disease leads to high pressure in the portal vein –>
–>Veins at the junction with the systemic venous system distend (varices)
–> This causes damage and can lead to bleeding from the varices into the oesophagus, leading to haematemesis.
What is the main cause of oesophago-gastric varices?
Portal hypertension
majority of pt’s have chronic liver disease
What is the diagnostic test for oesophago-gastric varices?
Endoscopy
What are the treatments for oesophago-gastric varices?
C: ABCDE
Maintain airway
Treat shock
M: Vasoactive drugs, antibiotic prophylaxis
S: obturate with glue-like substances, endoscopic band ligation.
What are complications of oesophago-gastric variceal tears?
70% chance of re-bleeding
Death (high risk)
What is a peptic ulcer? What are the two types?
Break in the GI mucosa in or adjacent to acid bearing area
2 types:
- Gastric
- Duodenal
What is the clinical presentation of peptic ulcers?
How does the presentation vary between gastric and duodenal ulcers?
- Burning epigastric pain
- Nausea
- Heartburn
- Flatulence
- Occasionally painless haemorrhage
Differences:
- Duodenal gives more pain when patient is hungry + at night
Which peptic ulcer type is more associated with H. pylori infection?
Duodenal (95% of cases)
*Gastric is 80% of cases
What is the pathophysiology behind peptic ulcers?
Reduction in protective prostaglandins or increase in gastric acid secretions
–> causes acidic contents of stomach/duodenum to break down the mucosa
Pain varies with acid level of area affecting the ulcer
H. pylori can then come and infect mucosa following this pH-induced damage –> further inflammation via proteases.
What are the 2 main causes of peptic ulcers?
H. pylori (increased gastric acid secretions, disruption of mucous protective layer, reduced duodenal bicarbonate production)
NSAIDs (reduced production of prostaglandins which provide mucosal protection in the upper GI)
Which type of peptic ulcer is more common?
Duodenal is more common than gastric
What is the most common cause (50%) of Upper GI bleeds?
Peptic ulcers
What are diagnostic tests for peptic ulcers?
List 3.
H. pylori tests
- (carbon-13 urea breath test)
- (stool antigen test)
Endoscopy also possible
What is the treatment for peptic ulcers?
C: avoid NSAIDs, stop smoking
M: Eradicate H.pylori via antibiotics and PPI (triple therapy*)
*COM (clarithromycin, omeprazole, metronidazole)
What drugs are used in triple therapy when treating peptic ulcers?
Remember COM (abx and PPI)
Clarithromycin
Omeprazole
Metronidazole
What is a possible complication of a peptic ulcer?
Upper GI bleed
What is the definition of gastritis?
Inflammation of the gastric mucosa
Which WBCs are involved in ACUTE gastritis?
Neutrophils (infiltrate into gastric mucosa)
Which WBCs are involved in CHRONIC gastritis?
Mononuclear cells (lymphocytes, plasma cells, macrophages)
What is the clinical presentation of gastritis?
Usually asymptomatic
Sometimes functional dyspepsia (aka. non-ulcer dyspepsia) - indigestion!
What is the pathophysiology behind gastritis?
Local inflammatory response to H. pylori infection
Can cause increase in gastric acid secretion (due to H. pylori presence)
What is the most common cause of gastritis?
Give 2 other less common causes
Most common: H. pylori infection
Less common: autoimmune gastritis (abs to parietal cells and IF)
- viruses
- duodeno-gastric reflux
What is the diagnostic investigation for gastritis?
Endoscopy +/- biopsy
(appears reddened or normal on endoscopy) - can detect histological change with biopsy sample
What is the main treatment for gastritis?
Triple therapy (COM) to eradicate H. pylori
Clarithromycin
Omeprazole
Metronidazole
What is a complication of gastritis?
Develops into peptic ulcer.
also pernicious anaemia if due to autoimmune gastritis attack on IF
What is the definition of gastropathy?
Injury to the gastric mucosa with epithelial cell damage and regeneration.
LITTLE TO NO INFLAMMATION! (unlike gastritis)
What is the clinical presentation of gastropathy?
Indigestion (dyspepsia)
Vomiting
Haemorrhage
What is the pathophysiology of gastropathy?
Reduction in protective prostaglandins by NSAID use causes the acidic contents of the stomach/duodenum to break down the mucosa.
What is the most common cause of gastropathy?
Give 2 other less common causes.
Most common: NSAID use
Less common: severe stress
- ETOH excess
- CMV infection
- HSV infection
What is the diagnostic investigation for gastropathy and what would be seen?
Endoscopy
-> shows erosions and sub-epithelial haemorrhage
What is the treatment for gastropathy?
Remove causative agent (e.g. stop NSAID, quit ETOH, CMV, HSV)
Give PPI
What is a complication of gastropathy?
Develops into peptic ulcer.
What is cholangitis?
Infection of the biliary tree
What is the clinical presentation of cholangitis?
Charcot’s triad (fever, RUQ pain, jaundice) in most patients
What is Charcot’s triad composed of?
Fever (with chills)
RUQ pain
Jaundice (pale stools, dark urine, pruritus)
What is the pathophysiology of cholangitis?
If CBD obstruction cause, then duct obstruction -> inflammation + susceptibility to infection
If infective cause, infection ascends from junction with duodenum. Infection from GI flora causes inflammation and pain.
What is the most common cause of cholangitis?
List 2 other less common causes.
Most common: gallstones
Less common: infection (Klebsiella, E. coli)
- Benign strictures
- Malignancy of head of pancreas
In which patient group is cholangitis most commonly found?
History of gallstones
Aged 50-60
Which bloods should you take for cholangitis (and what would they show)?
FBC (raised CRP)
LFT (raised ALP, AST, ALT)
What is the definitive investigation for cholangitis?
ERCP (reveals gallstones and can remove the blockage too)
What are investigations for cholangitis?
Bloods (CRP, LFT)
Abdo USS
Blood cultures (if septic)
ERCP *gold-standard
Culturing of ERCP-collected specimens
How is cholangitis treated?
C: fluid resuscitation
M: Antibiotic therapy
S: ERCP to clear obstruction
What is the most dangerous complication of cholangitis?
Sepsis
What is the definition of primary sclerosing cholangitis?
Chronic inflammation + fibrosis of the bile ducts
What is the clinical presentation of primary sclerosis cholangitis?
- May be asymptomatic (incidentially found after LFTs)
- Charcot’s triad (fever, RUQ pain, jaundice)
- Hepatomegaly
Which form of IBD is primary sclerosis cholangitis usually associated with?
Ulcerative colitis
What is the pathophysiology behind primary sclerosing cholangitis?
Progressing fibrosis in intra/extra-hepatic ducts –> ducts become strictured –> cholestatic jaundice + RUQ pain
Eventually –> CIRRHOSIS
What are causes of primary sclerosing cholangitis?
?Unknown generally Genetic Lymphocyte recruitment Portal bacteraemia Bile salt toxicity
(can also be secondary to infection, thrombosis or iatrogenic/trauma)
Which gender and age group is primary sclerosing cholangitis most common in?
Males
30-40s
What investigations are needed to diagnose primary sclerosing cholangitis?
USS (may show bile duct dilatation)
ERCP
LFTs (elevated ALP or GGT)
AST/ALT can be normal to several times above normal. Serum albumin drops with progression of disease.
How is primary sclerosing cholangitis managed?
C: Manage symptoms of liver failure
M: High dose ursodeoxycholic acid can slow progression.
S: ERCP can dilate some extra-hepatic structures to slow progression. Eventual liver transplant needed.
What is the final outcome of primary sclerosing cholangitis?
Eventual liver failure
also 15% can get cholangiocarcinoma - cancer of bile ducts
Define achalsia
Lack of peristalsis in the oesophagus and failure of LOS to relax impairs oesophageal emptying
What is the clinical presentation of achalsia?
- Onset at any age
- Long history of dysphagia for solids and liquids
- Retrosternal chest pain (non-cardiac)
- Weight loss
What is the pathophysiology of achalasia?
Decrease in the ganglionic cells in the nerve plexus of the oesophageal wall + degeneration in the vagus nerve
Is achalasia common in children?
No.
Give 2 diagnostic investigations for achalasia?
What would these show?
Barium swallow: aperistalsis + beak deformity (oesophagus tapers to a point)
Oesophageal manometry: aperistalsis and failure of LOS to relax on swallowing.
What is the treatment of achalasia?
No cure
C: Treat symptoms.
M: Nitrates (if surgery is contraindicated. Can also use botox for elderly where surgery is not an option.)
S: Surgical division of LOS and endoscopic balloon dilatation.
What is a dangerous complication of achalasia?
If untreated, asphyxiation of material in oesophagus —> choking.
Can also result in oesophageal cancer.
What is systemic sclerosis scleroderma? (SSc)
It is a multi-system autoimmune disease.
Caused by increased fibroblast activity —> abnormal growth of connective tissue.
What are the 2 types of Systemic Sclerosis Scleroderma?
Limited cutaneous (CREST syndrome)
Diffuse cutaneous
What does CREST syndrome stand for? (in systemic sclerosis)
Calcinosis Raynaud’s phenomenon Esophageal dysmotility Sclerodactyly Telangiectasia
What is the clinical presentation of Diffuse Cutaneous subtype of systemic scleroderma?
Same as CREST syndrome but with more RAPID and WIDESPREAD onset
GI: indigestion, reflux, oesophagitis. Delayed gastric emptying
Resp: pulmonary fibrosis, pulmonary artery hypertension
What proportion of people with SSC do the following affect?
a) Limited cutaneous (CREST)
b) Diffuse cutaneous
a) Limited cutaneous affects 70% of SSc
b) Diffuse cutaneous affects 30% of SSc
Which parts of the body does limited cutaneous SSc usually affect?
Face
Forearms
Lower legs (up to knee)
Which part of the body does Diffuse cutaneous SSc usually affect?
Widespread
Face
Entire arm
Thighs + Legs
Trunk
What is the pathophysiology behind systemic scleroderma?
Excessive collagen produced and deposited —> vascular damage and inflammation then results.
What is the prevalence of systemic scleroderma in the UK?
More common in which gender?
88 in 1 million (very rare) in UK
More common in women
(Rare in children)
What is the definition of ulcerative colitis?
Continuous chronic inflammation of only the colon
How does ulcerative colitis usually present?
- Recurrent diarrhoea - blood/mucus
- Extra-gastrointestinal symptoms - arthralgia, fatty liver and gall stones
In which form of IBD is smoking protective?
Ulcerative colitis
What is the pathophysiology behind ulcerative colitis?
Mucosal inflammation that starts in the anus and continues proximally, affecting only the large colon.
No granulomata.
Goblet cell depletion and crypt abcesses.
How does Crohn’s usually present?
Symptoms depend on region affected.
Small bowel:
What are the 4 types of laxatives?
Bulk-forming
Stimulants
Osmotics
Stool softeners