Gastroenterology Flashcards
What epithelium lines the oesophagus ?
- Non keratanised stratified squamous epithelium
what plexus controlks the instrinsic peristaltic movement of the oesophagus ?
Enteric plexus : consists of an outer myenteric plexus and inner submucosal plexus
Explain the pathophysiology behind achalasia
- Loss of inhibitory ganglion cells of the myenteric plexus in the distal oesophagus and LOS.
- Leads to a failure of peristalsis and relaxation of the LOS
How does Achalasia present ?
- Dysphagia of BOTH liquids and solids
- Heartburn, unresponsive to Tx
- Regurgitation of undigested food
- Weight loss
- Chest pain
What is the initial Ix for achalasia ?
- Barium swallow -> will show dilated oesophagus with narrowing at LOS (birds beak)
What is the diagnostic investigation for achalasia ?
- Oesophageal manometry
What is pseuodachalasia ?
- Obstruction of the distal oesophagus by something other than destruction of myenteric plexus
- Caused by : malignancy, scleroderma, strictures.
What are the endoscopic treatment options for achalasia ?
- Pneumatic (balloon) dilation
- Intra-sphincteric injection of botulinum toxin (inhibits Ach release, preventing contraction).
- Perioral endoscopic myotomy
What is the surgical treatment options for achalasia ?
Heller cardiomyotomy
What are the medical treament options for achalasia ?
- CCB (nifedipine)
- Long acting nitrates
- They act to reduce lower oesophageal pressure
What kind of malignancy are patients with achalasia for >10yrs at an increased risk of ?
- Squamous cell carcinoma
What factors can exacerbate / worsen Sx of GORD
- Greasy and spicy foods
- Coffee and tea
- Alcohol
- NSAIDs
- Stress
- Smoking
- Obesity
- Hiatus hernia
What are the symptoms of GORD
- > Dyspepsia
- Heartburn
- Acid regurg
- Retorsternal / epigastric pain
- Bloating
- Nocturnal cough
- Hoarse voice
Red flags for 2 wk wait OGD
- Dysphagia (difficulty swallowing) at any age gets an immediate two week wait referral
- Aged over 55 (this is generally the cut-off for urgent versus routine referrals)
- Weight loss
- Upper abdominal pain
- Reflux
- Treatment-resistant dyspepsia
- Nausea and vomiting
- Upper abdominal mass on palpation
- Low haemoglobin (anaemia)
- Raised platelet count
Stepwise management of GORD
- Lifestyle changes
- Reviewing medications (e.g., stop NSAIDs)
- Antacids (e.g., Gaviscon, Pepto-Bismol and Rennie) – short term only
- Proton pump inhibitors (e.g., omeprazole and lansoprazole)
- Histamine H2-receptor antagonists (e.g., famotidine)
- Surgery
Lifestyle changes for GORD
Reduce tea, coffee and alcohol
Weight loss
Avoid smoking
Smaller, lighter meals
Avoid heavy meals before bedtime
Stay upright after meals rather than lying flat
what should be ruled out when treating GORD
- H. pylori -> gram neg aerobic bacteria
H.pylori eradication
- Triple therapy
- PPI (e.g., omeprazole)
Two antibiotics (e.g., amoxicillin and clarithromycin) for 7 days
Complication of GORD
- Barrett’s oesophagus
Epithelial changes in Barrett’s
squamous to columnar epithelium = metaplasia
Management of Barrett’s
- Endoscopic monitoring for progression to adenocarcinoma
- PPI
- Endoscopic ablation (e.g., radiofrequency ablation)
Rare condition causing severe dyspepsia, diarrhoea and peptic ulcers
- Zollinger-Ellison Syndrome
- Duodenal or pancreatic tumour secretes excessive gastrin
- Gastrin = stimulates acid secretion in the stomach
RF for peptic ulcers
-> Disrupting mucus barrier = H.pylori, NSAIDs
-> Increasing stomach acid = stress, alcohol, caffeine, smoking, spicy foods
How do peptic ulcers present ?
- Epigastric pain -> worse on eating with gastric, better after eating with duodenal
- N&V
- Dyspepsia
Signs of UGIB from a peptic ulcer (4)
- Haematemesis
- Melaena
- Hypotension
- tachycardia
Diagnosis of a peptic ulcer
- Endoscopy with a rapid urease test to check for H.pylori
Treatment of peptic ulcer
- Stopping NSAIDs
- Treating H. pylori infections
- Proton pump inhibitors (e.g., lansoprazole or omeprazole)
Repeat endoscopy 4-8 wks later to ensure healing of ulcer
Complications of a peptic ulcer
-> Bleeding
-> Perforation = acute abdominal pain and peritonitis
-> Scaring and strictures = can lead to gastric outlet obstruction = presents with early fullness / upper abdo discomfort / abdo distention and vomiting, particularly after eating
4 causes of an UGIB
- Peptic ulcers (most common)
- Mallory-Weiss tear
- Oesophageal varices
- Stomach cancers
3 presenting features of an UGIB
- Haematemesis
- Coffee ground vomit
- Meleana
What score is used to assess the risk of a pt having an UGIB based on inital presentation ?
Glasgow-Blatchford Bleeding Score
- Haemoglobin (falls in upper GI bleeding)
- Urea (rises in upper GI bleeding)
- Systolic blood pressure
- Heart rate
- Presence of melaena (black, tarry stools)
- Syncope (loss of consciousness)
- Liver disease
- Heart failure
An isolated rise in what suggest an UGIB
UREA
what score is used after endoscopy to estimate the risk of rebledding and mortality in an UGIB
-> Rockall score
- Age
- Features of shock (e.g., tachycardia or hypotension)
- Co-morbidities
- Cause of bleeding (e.g., Mallory-Weiss tear or malignancy)
- Endoscopic findings of recent bleeding (e.g., clots and visible bleeding vessels)
Initial management of UGIB
-> A – ABCDE approach to immediate resuscitation
-> B – Bloods
-> A – Access (ideally 2 x large bore cannula)
-> T – Transfusions are required
-> E – Endoscopy (within 24 hours)
-> D – Drugs (stop anticoagulants and NSAIDs)
what bloods are sent in an UGIB
- Haemoglobin (FBC)
- Urea (U&Es)
- Coagulation (INR and FBC for platelets)
- Liver disease (LFTs)
- Crossmatch 2 units of blood
what additional medications are given if an UGIB is due to suspected oesophageal varcies ?
Terlipressin
Blood spectrum Abx
Features of crohn’s disease
NESTS
-> N – No blood or mucus (PR bleeding is less common).
-> E – Entire gastrointestinal tract affected (from mouth to anus).
-> S – “Skip lesions” on endoscopy.
-> T – Terminal ileum most affected and Transmural (full thickness) inflammation.
-> S – Smoking is a risk factor (don’t set the nest on fire).
Features of ulcerative colitis
CLOSE UP
-> C – Continuous inflammation
-> L – Limited to the colon and rectum
-> O – Only superficial mucosa affected
-> S – Smoking may be protective (ulcerative colitis is less common in smokers)
-> E – Excrete blood and mucus
-> U – Use aminosalicylates
-> P – Primary sclerosing cholangitis
Bloods done in IBD
- Faecal calprotectin
Inducing remission in UC
- MILD TO MODERATE : Aminosalicylate (e.g., oral or rectal mesalazine) first-line, Corticosteroids (e.g., oral or rectal prednisolone) second-line
- SEVERE : IV hydrocortisone
Maintaining remission in UC following a mild to moderate flare
- Low maintenance dose of oral aminosalicylate
Inducing remission in crohn’s
Oral pred or IV hydrocortisone first line
Maintaining remission in crohn’s
- First line : azathioprine or mercaptopurine
3 key features of IBS
-> I – Intestinal discomfort (abdominal pain relating to the bowels)
-> B – Bowel habit abnormalities
-> S – Stool abnormalities (watery, loose, hard or associated with mucus)
Autoantibodies involved in coeliac disease
-> Anti-tissue transglutaminase antibodies (anti-TTG)
-> Anti-endomysial antibodies (anti-EMA)
-> Anti-deamidated gliadin peptide antibodies (anti-DGP)
Seen on endoscopy in coeliac disease
- Villous atrophy
- Crypt hyperplasia
- Jejunum most affected
Genotypes associated with coeliac disease
HLA-DQ2
HLA-DQ8
Presenting symptoms of coeliac disease
-> Failure to thrive in young children
-> Diarrhoea
-> Bloating
-> Fatigue
-> Weight loss
-> Mouth ulcers
Skin rash seen in coeliac disease
Dermatitis herpetiformis : itchy, blistering skin rash, typically on the abdomen
Neurological symptoms seen in coeliac disease
-> Peripheral neuropathy
-> Cerebellar ataxia
-> Epilepsy
First line blood tests for coeliac disease
- Total immunoglobulin A levels (to exclude IgA deficiency)
- Anti-tissue transglutaminase antibodies (anti-TTG)
what does coeliac disease increase the risk of
-> Enteropathy-associated T-cell lymphoma (EATL)
-> NHL
-> Small bowel adenoacarcinoma
Long term PPI use can cause disturbance in which electrolyte and what could be the presenting symptoms ?
- Hypomagnesaemia
- Muscle aches
Leading cause of c.diff
Second and third generation cephalosporins
(PPI are also RF)
Expain features of mild, moderate, severe and life threatening C. diff infection
- Mild : normal WCC
- Moderate : Raised WCC, 3-5 loose stool
- Severe : WCC (>15), creatinine >50% baseline, temp >38.5 or evidence of colitis
- Life threatening : hypotension, partial or complete ileus, toxic megacolon
Management of 1st episode of C.diff
- 1st : 10 days oral vancomycin
- 2nd : oral findaxomicin
- 3rd : oral vancomycin +/- IV metronidazole
management of recurrent c.diff infection
- Within 12 weeks of symptom resolution: oral fidaxomicin
- After 12 weeks of symptom resolution: oral vancomycin OR fidaxomicin
Management of Life threatening c.diff infection
Oral vancomycin and IV metronidazole
Mantaining remission in UC following a severe relapse or >=2 exacerbations a year
- oral azathioprine or oral mercaptopurine
Histological findings in crohn’s
- Transmural inflammation
- Increased goblet cells
- Granulomas
Histological findings in UC
- Neutrophils migrate through the walls of glands to form crypt abscesses
- Depletion of goblet cells and mucin from gland epithelium
- Granulomas are infrequent
Carcinoembryonic antigen is a tmour marker for what
colorectal cancer
Recognised complications of enteral feeding
- Diarrhoea
- Aspiration
- Metabolic : refeeding / hyperglycaemia
Alcohol excess
Severe epigastric pain
Raised amylase
Pancreatitis
Management of mild acute pancreatitis (stable vital signs)
IV fluids (v important)
Opioid analgesia
Lifestyle measures for constipation
Increase fibre
Adequate fluid
Adequate activity level
1st line management of constipation
Bulk forming laxative (isphagula husk)
Second line for constipation
Osmotic (e.g. macrogol)
Refeeding syndrome
- Metabolic abnormalities that occur following extended period of starvation
metabolic abnormalities of refeeding syndrome
Hypophosphataemia
Hypokalaemia
Hypomagnesaemia
Abnormal fluid balance
Pathophysiology of refeeding
- Long period of catabolism ends with reintorudction of carbohydrates.
- Leads to increased insulin secretion and increased cellular uptake of glucose
- This cause phosphate to move intracellularly = low phosphate serum levels.
= Cardiac dysrhythmia, resp failure, rabdomyolysis, seizures
high risk of refeeding
One or more of
- BMI < 16 kg/m2
- nintentional weight loss >15% over 3-6 months
- little nutritional intake > 10 days
4 Hypokalaemia, hypophosphataemia or hypomagnesaemia prior to feeding (unless high)
High risk of fefeeding
2 or more of
- BMI < 18.5 kg/m2
- Unintentional weight loss > 10% over 3-6 months
3.Little nutritional intake > 5 days - History of: alcohol abuse, drug therapy including insulin, chemotherapy, diuretics and antacids
4 RF for gastric cancer
- H.pylori
- Atrophic gastritis
- High salt diet
- Smokinh
5 Sx of gastric cancer
- Vague epigastric pain
- Weight loss and anorexia
- N&V
- Dysphagia
- UGIB
Lymphatic spread seen in gastric cancer
- Left supraclavicular (Virchow’s)
- Periumbilical (Sister mary joseph)
Diagnosis gastric cancer
- Oesophago-gastro-duodenoscopy with biopsy ->
signet ring cells - Staging: CT
Eradication of h.pylori
- PPI + amoxicillin + (clarithromycin OR metronidazole)
- If penicillin-allergic: a proton pump inhibitor + metronidazole + clarithromycin
Screening tes for malnutrition
MUST (Malnutrition Universal Screen Tool).
Most common oesophageal cancer
Adenocarcinoma
4 FR for oesphageal adenocarcinoma
GORD
Barrett’s oesophagus
smoking
obesity
4 features of oesophageal cancer
- dysphagia: the most common presenting symptom
- anorexia and weight loss
- vomiting
- other possible features include: odynophagia, hoarseness, melaena, cough
Diagnosis of oesophageal cancer
Upper GI endoscopy with biopsy
Plummer vinson sydnrome
Triad of:
dysphagia (secondary to oesophageal webs)
glossitis
iron-deficiency anaemia
Boerhaave syndrome
Severe vomiting → oesophageal rupture
Mallory-weiss syndrome
syndrome Severe vomiting → painful mucosal lacerations at the gastroesophageal junction resulting in haematemesis. Common in alcoholics
Most significant source of UGIB from peptic ulcer disease
gastroduodenal artery1
1st line for H.pylori test
Urea breath or stool antigen
Management of more significant diverticulitis
Nil by mouth
IV fluid
IV cephalosporin and metronidazole
Pharyngeal puch sx
- Dysphagia
- Regurgitation
- Aspiration and chronic cough.
Halitosis may occasionally be seen
Investigation of choice for GI ischaemia
CT
Acute mesenteric ischaemia presentation
- Abdominal pain is typically severe, of sudden onset and out-of-keeping with physical exam findings.
- Often embolism occluding the superior mesenteric artery or other artery supplying small bowel
- Hx of AF
- Urgent surgery needed
