Clinical Gastroenterology Flashcards
List features you would look for on general inspection of a patient with a GIT disorder.
Mental status Obvious distress or pain Rolling around in pain vs. lying still in pain Body habitus - obesity, cachexia Jaundice Vomiting, presence of a vomit bag In and out - drains, IV fluids, catheter
What do you look for in the hands in a GIT examination?
NAILS:
- Leukonychia (opacification of the nail bed due to hypoalbuminemia)
- Clubbing (GIT causes are cirrhosis, IBD and coeliac disease)
PALMS:
- Palmar erythema (GIT causes are cirrhosis)
- Palmar crease pallor (anaemia)
- Dupuytren’s contracture (visible and palpable thickening of the palmar fascia, often associated with excess alcohol consumption)
ASTERIXIS (Patient stretches out arms in front, with wrists extended and fingers separated for 15 seconds. Jerking can be a sign of liver failure.)
What would you look for on inspection of the arms in a GIT examination?
Bruising Bleeding - petechiae, ecchymoses Spider naevi Jaundice Scratch marks Muscle wasting Acanthosis nigricans at the axilla
List what features you would examine for in the face during a GIT examination.
EYES:
- Xanthelasma
- Scleral icterus
- Conjunctival pallor
- Kayser-Fleischer rings (excess copper deposition in Wilson’s disease)
- Iritis (extra-GIT manifestation of IBD)
SALIVARY GLANDS:
- Palpate for the parotid. It is normally impalpable.
MOUTH:
- Breath: hepatic fetor
- Lips - angular stomatitis, pigmentation
- Oral mucosa - ulceration, leukoplakia, candidiasis
- Gums - hypertrophy, pigmentation
- Tongue - glossitis, leukoplakia
Describe your approach to inspection of the abdomen in a GIT examination.
- General inspection of the abdomen to note:
- Pain: patient in obvious pain, lying very still in pain or rolling around in pain
- Scars
- Stoma
- Striae
- Swellings/distention/lumps - generalised, localised
- Prominent veins, caput medusae
- Bruising - Cullen’s sign (peri-umbilical), Grey-Turner (flanks)
- Movements - visible pulsations, visible peristalsis
Then squat down by the side of the bed so that the patient’s abdomen is at eye level. Ask them to take deep breaths in and out through the mouth. Watch the abdomen move and note any asymmetry.
Where are the constrictions of the oesophagus?
- Junction of the oesophagus and pharynx (the upper oesophageal sphincter)
- Where it is crossed by the left main bronchus and arch of aorta
- At the hiatus of the diaphragm
Describe the venous drainage of the oesophagus.
The oesophagus drains into both the systemic venous system and the portal venous system.
Via the azygos and hemiazygos vein blood enters the systemic system. Via the left gastric vein blood drains into the portal system.
When there is an increase in portal venous pressure, anastomoses can form between these two systems, causing the development of oesophageal varices.
Name the 4 histological layers of the GIT.
- Mucosa - the GIT is lined by an epithelial layer, which is surrounded by the lamina propria and then the muscularis propria.
- Submucosa - dense connective tissue, contains the submucosal plexus aka Meissner’s plexus.
- Muscularis externa - smooth muscle generally composed of 2 layers (inner circular layer and outer longitudinal layer). Between these two layers myenteric plexus aka Auerbach’s plexus.
- Adventitia/serosa - adventitia is connective tissue that covers retroperitoneal organs; serosa has a mesothelium and covers intraperitoneal organs.
What type of epithelium lines the oesophgus?
Stratified squamous nonkeratinized epithelium
Briefly outline the physiology of swallowing.
Swallowing can be divided into 3 phases:
1. VOLUNTARY STAGE - food is rolled posteriorly by the tongue moving backwards against the palate.
2. Involuntary stages -
First involuntary stage = PHARYNGEAL STAGE.
- the bolus enters the pharynx and this stimulates receptors
- the message is sent to the brain, and this initiates: (1) soft palate pulled upwards to prevent food entering nose; (2) vocal cords approximated and larynx pulled upwards so that the epiglottis covers the larynx to prevent food passing into the lungs; (3) relaxation of upper oesophageal sphincter; (4) contraction of pharynx, peristalsis transfers the bolus into the oesophagus.
Secondary involuntary stage = OESOPHAGEAL STAGE.
- The peristaltic wave carries the bolus through the oesophagus to the stomach. The peristaltic wave is generated by CN IX and X in the upper oesophagus (striated muscle), and the ENS in the lower oesophagus (smooth muscle).
- Relaxation of the lower oesophageal sphincter
- Food enters stomach
List DDX for dysphagia.
ORAL, PHARYNGEAL AND OESOPHAGEAL DYSPHAGIA:
1. Dysmotility - achalasia, diffuse oesophageal spasm, nutcracker oesophagus
2. Infection/inflammation - GORD, pharyngitis, epiglottitis, oesophageal candidiasis, eosinophilic oesophagitis
3. Cancer
4. Drugs/toxins - pill-induced oesophageal injury, caustic ingestion
5. Iatrogenic - radiation therapy
6. Anatomical abnormality - Hiatus hernia, foreign body, diverticulum (e.g. Zenker), rings, webs
7. Extrinsic compression - neck abscess, cervical lymphadenopathy, goiter
8. Autoimmune disease - scleroderma, Sjogren’s syndrome
NEUROLOGICAL CAUSES:
1. Stroke
2. Motor neurone disease
3. Multiple sclerosis
4. Muscular dystrophy
List 4 common DDX for upper GIT bleeding.
Peptic ulcer disease
Oesophageal varices
Oesophagitis
Mallory-Weiss tear
What is the ligament of Treitz? Where is it located? What is its relevance in upper GI bleeding?
The ligament of Treitz is also known as the suspensory ligament of the duodenum. It is located at the DJ flexure, and supports the flexure.
Hematemesis suggests that the bleeding is occurring from proximal to the ligament of Treitz.
Most melena originates proximal to the ligament of Treitz.
Hematochezia is more common in lower GI bleeding, but it could potentially come from an upper GI source if the bleeding is massive.
Define orthostatic hypotension.
Orthostatic hypotension is a decrease in systolic BP of > 20 mmHg or diastolic BP of > 10 mmHg when the patient moves from lying to standing.
Define achalasia.
Achalasia is a motility disorder of the oesophagus that is characterised by: (1) failure of peristalsis and (2) insufficient relaxation of the lower oesophageal sphincter in response to swallowing.
Explain the pathogenesis of primary achalasia.
Achalasia is caused by progressive degeneration of cells in the myenteric plexus. The degeneration is mainly of NO-producing inhibitory neurons that cause relaxation of the lower oesophageal sphincter smooth muscle. The cholinergic neurons are relatively spared.
The cause of primary achalasia is unknown.
What are the typical features of achalasia on history? (6)
- Dysphagia is to both solids and liquids from the onset
- Regurgitation occurs, which may cause coughing or choking
- Gradual mild weight loss
- Retrosternal pressure or pain
- Certain postures/manoeuvres may assist - e.g. eat walking around
- May have heartburn, frequently resistant to PPI
How would you confirm achalasia?
- Upper endoscopy, which shows:
- retained food in oesophagus
- resistance to passing the scope through the LOS - Manometry, which shows:
- elevated resting pressure in LOS
- incomplete relaxation of LOS during swallowing
- abnormal peristalsis/aperistalsis in distal 2/3 of the oesophagus - If the diagnosis is still equivocal, manometry can also be performed, which shows:
- ‘bird beak’ appearance, caused by a narrow oesophagogastric junction
- dilated, tortuous oesophagus
- aperistalsis
- delayed emptying of barium from oesophagus into the stomach
What is the major cause of secondary achalasia?
Chagas disease, caused by Trypanosoma cruzi infection
What factors contribute to GORD?
INCOMPETENCE OF LOWER OESOPHAGEAL SPHINCTER
The sphincter normally prevents reflux on gastric contents into the oesophagus, but its ability to do this is affected by:
1. Increased transient relaxations
2. Hypotensive sphincter, which can be caused by: smoking, foods (peppermint, chocolate, caffeine, alcohol), medications (calcium channel blockers, nitrates)
3. Anatomic disruption - hiatus hernia
REDUCED CLEARANCE OF REFLUXED MATERIAL
If material is refluxed into the oesophagus, it is usually rapidly cleared. If this does not occur, the oesophagus has increased exposure to the acidic stomach contents, which is damaging. Factors that impair the clearance are:
1. Motility disorders - achalasia
2. Decreased salivation (would normally act as a buffer)
IMPAIRED MUCOSAL DEFENCES
The oesophageal mucosa contains tight junctions that are resistant to the passage of H+.
List 5 common causes of GORD.
- Hiatus hernia
- Obesity
- Pregnancy
- Foods - chocolate, caffeine, peppermint, alcohol
- Medications - calcium channel blockers, nitrates
What are the symptoms of GORD? (7)
- Heartburn (retrosternal burning pain)
- Acid regurgitation into the back of the mouth
- Waterbrash (sudden, brisk stimulation of salivation)
- Odynophagia
- Chronic cough
- Hoarse voice
- Dysphagia can result from reflux oesophagitis and stricture formation.
List red flags of dysphagia that would require further investigation.
- New onset of dyspepsia in a patient aged 60+ years.
- GI bleeding: hematemesis, melena, hematochezia, positive FOBT, iron deficiency anaemia
- Anorexia, unexplained weight loss
- Dyspepsia with dysphagia
- Persistent vomiting
- Family history of GI cancer
What is the first thing you would try in a patient with symptoms of GORD and no red flags?
Trial of PPI
What is the first line investigation in patients with symptoms of GORD?
Upper endoscopy
Besides upper endoscopy, what investigations might be useful in GORD. Why?
You may consider ordering:
- MANOMETRY - this can be used to diagnose or exclude a motility disorder
- AMBULATORY OESOPHAGEAL PH MONITORING. This is useful if there are persistent symptoms/failure of PPI therapy.
What lifestyle modifications could be useful in GORD?
Eat smaller meals. Avoid lying down after eating; Avoid eating/drinking before bed. Elevate the head of the bed. Stop smoking. Weight loss if overweight.
What are the complications of GORD? (5)
Oesophageal ULCER – can lead to HAEMORRHAGE or PERFORATION
Oesophageal STRICTURE
BARRETT’S OESOPHAGUS
ADENOCARCINOMA of the oesophagus
What are the risks of long term PPI therapy? (5)
Long term PPI therapy places the patient at increased risk of:
- Osteoporosis and fracture
- C difficile infection and diarrhoea
- Bacterial gastroenteritis
- Community acquired pneumonia
- Interstitial nephritis
Define Barrett’s oesophagus.
Barrett’s oesophagus is metaplasia of the oesophagus, in which the cells change from the normal stratified squamous nonkeratinized epithelium to columnar epithelial cells normally found in the intestines.
What is the main causative factor for Barrett’s oesophagus?
GORD
Patients with Barrett’s oesophagus are at increased risk of which condition?
Adenocarcinoma of the oesophagus
Define the 4 types of hiatus hernia.
Type 1 = sliding hiatus hernia (gastro-oesophageal junction displaced above the diaphragm)
Type 2 = para-oesophageal aka rolling (gastro-oesophageal junction remains below the diaphragm, but part of the stomach herniates into the thorax)
Type 3 = Mixed, with elements of both type 1 & 2
Type 4 = giant hiatus hernia, where organ/s other than the stomach are herniated
Discuss differences in clinical features of a type 1 and type 2 hiatus hernia.
Type 1 is a sliding hernia. This involves displacement of the gastro-oesophageal junction above the diaphragm, and decreases the pressure at the LOS. As a result, the main symptom is reflux/heartburn.
Type 2 is a rolling/para-oesophageal hernia. The LOS remains within the abdomen, but part of the stomach herniates into the thorax. This part can rotate and twist, causing strangulation/obstruction/ischemia. This causes pain, vomiting and possibly necrosis.
What would you look for on CXR to confirm a hiatus hernia?
Opacity behind the heart with an air-fluid level
Define a Mallory-Weiss tear.
A MW tears are longitudinal mucosal lacerations in the distal oesophagus and proximal stomach typically caused by forceful retching/vomiting.
How do Mallory-Weiss tears typically present?
- History of retching/vomiting
- History of recent alcohol binge
- Self-limited and usually small episode of hematemesis
- Varies from flecks, streaks of blood, bright red or coffee ground vomitus
- No severe pain (this occurs with Boerhaave syndrome)
Define portal hypertension.
Portal hypertension = hydrostatic pressure of > 5mmHg in the portal system
What is the most common cause of portal hypertension?
Liver cirrhosis
How does cirrhosis cause portal hypertension?
Portal pressure is determined by the volume of blood flowing through the portal system, and the resistance to outflow from the portal vein.
Both are increased in cirrhosis.
- Sinusoidal obstruction occurs due to the disease.
- Hepatic stellate cells are activated, further contributing to obstruction of blood flow.
- Splanchnic vasodilatation causes increased portal blood flow
Why do varices develop in portal hypertension? Where do they usually occur?
In portal hypertension, collaterals open between the portal circulation and the systemic circulation so that blood can be bypassed around the liver.
As these collaterals increase in size they form varices.
These occur at:
1. Oesophagus/stomach - left gastric vein (portal) anastomosis with tributaries of the azygos vein (systemic)
2. Anus - superior rectal vein (portal) anastomosis with middle and inferior rectal veins (systemic)
3. Anterior abdominal wall around umbilicus - para-umbilical veins (portal) anastomoses with anterior abdominal wall veins (systemic) - causes caput medusae
Give DDX for portal hypertension.
Portal hypertension can be caused by:
- PRE-HEPATIC: portal vein occlusion
- HEPATIC: cirrhosis
- POST-HEPATIC: Budd-Chiari syndrome, restrictive cardiomyopathy
What 2 approaches can be used for primary prophylaxis of oesophageal varices?
- Non-selective B blocker to block adrenergic dilatation of arterioles in the mesentery to decrease the amount of blood flowing into the portal system
- Endoscopic ligation of varices
