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104 Cards in this Set
- Front
- Back
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Definition of dysphagia
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sensation of "sticking" or obstruction of passage of food through mouth, pharynx or oesophagus
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Term for pain on swallowing
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odynophagia
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dysphagia - clinical categories
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dysphagia with the swallow - oropharyngeal cause
dysphagia after swallow - oesophageal cause |
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dysphagia - pathological categories
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*mechanical (luminal narrowing, intrinsic, extrinsic)
*motor (inco-ordination or weakness of peristalsis) |
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Give mechanical causes of dysphagia
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*Intrinsic - web and rings, oesophagitis,oesophageal carcinoma, strictures
*Extrinsic - mediastinal mass, vascular compression, diverticula, thyroid mass |
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Give motor causes of dysphagia
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*Difficulty initiating swallowing - lack of saliva (e.g. Sjogren's), upper or lower motor neuron lesions, muscular/neuromuscular disorders, paralysis of tongue
*abnormalities of smooth muscle - weakness (e.g. scleroderma), impaired relaxation (e.g. achalasia), nonperistaltic contraciton (e.g. diffuse oesophgeal spasm) |
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Causes of haematemesis
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*acute gastritis/gastric erosions
*peptic ulcers *oesophageal varices *oesophagitis *mallory-weiss tears *neoplasms *others (e.g. AV malformation) |
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Important questions to ask on presentation of haematemesis
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*alcohol consumption, use of drugs e.g. NSAIDs
*recent history of retching, signs of chronic liver disease |
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Haematemesis - moderate rate of bleeding manifests as
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thirst, syncope, postural hypotension, tachycardia
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haematemesis - severe bleeding produces...
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clinical symptoms of hypovolaemic shock
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haematemesis - slower or more distal bleeding may be associated with...
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malaena
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relevant investigations for haematemesis
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*haematological studies: FBC/coags
*oesophageal manometry - diagnosis of motility disorders *barium swallow/upper GI contrast study *CT/PET - diagnosis of tumours *endoscopy - also allows biopsy |
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Describe three layers of oesophagus
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*mucosa - non keratinising strat squamous epi; LP; muscularis mucosa
*submucosa - lymphatics, blood vessels, nerves, mucin secreting gland *musclaris propria - inner circular, outer longitudinal; also top 1/3 striated, bottom 2/3 SM |
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two functional sphincters of oesophagus
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*upper sphincter - continuous contraction of cricopharyngeus muscle
*lower sphincter - area of lower oesophagus with high resting tone |
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three points of luminal narrowing
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*at level of cricoid cartilage
*at anterior crossing of L main bronchus *at oesophageal hiatus T10 |
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describe some non neoplastic mechanical causes of dysphagia
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*oes webs - protruding mucosa
*oes rings - hypertrophied musclaris propria *oes strictures - fibrotic submucosa and atrophied muscularis propria |
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benign tumours causing dysphagia are mostly _______ in origin, e.g.?
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mesenchymal, e.g. leiomyoma, lipoma, fibrovascular polyp
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Two common malignant tumours causing dysphagia
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*SCC
*adenocarcinoma |
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RF for SCC
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*male, smoking, urban environment, FH
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SCC most commonly in which part of oesophagus; usually presents macroscopically as???
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*50% in middle 1/3 of oesophagus
*60% are poplypoid, 15% are flat and spread within oes wall, 25% ulceration and erode into surrounding structures |
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how does SCC spread?
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along lymph nodes
*upper oes SCC - cervical nodes *middle oes SCC - paratracheal, mediastinal, tracheobronchial nodes *lower oes SCC - gastric/coeliac nodes |
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clinical presentation of oes SCC
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insidious onset of progressive dysphagia (solid --> liquid); weight loss due to malnutrition, haemorrhage or sepsis due to infiltration of tumour
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RF for adenocarcinoma
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*male, Barret's mucosa, smoking, H. pylori infection
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Natural history of adenocarcinoma - how does it usually develop?
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reflux oesophagitis --> Barrett mucosa (metaplasia) --> dysplasia --> adenocarcinoma
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macroscopic appearance of oes adenocarcinoma
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*near gastro-oesophageal junction
*initially raised/flat mucosa then progress into nodular mass up to 5cm in diameter |
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microscopic appearance of oes adenocarcinoma
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*mucin-producing, intestinal-like glandular appearance with goblet cells
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clinical presentation of oes adenocarcinoma
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*progressive dysphagia, weight loss, bleeding, chest pain, vomiting
*<50% have long standing GORD |
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achalasia is characterised by three abnormalities....
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*aperistalsis
*incomplete relaxation of LOS during swallowing *increased resting tone of LOS |
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cause of achalasia
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*due to dysfunction of inhibitory neuron
*can be primary or secondary (e.g. due to infection, diabetic autonomic neuropathy, infiltrative disorders like amyloidosis) |
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macroscopic appearance of achalasia
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*progressive dilatation of oes proximal to LOS
*oes lining may be thin, thick, or normal *mucosa lining is normal |
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clinical presentation of achalasia
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*young; may drink large amounts of liquid before eating solid to increase downward pressure
*nocturnal regurg with aspiration of undigested food |
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Complications of achalasia
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*candida infection
*SCC (5%) *lower oesophageal diverticula *aspiration pneumonia |
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management of achalasia
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*gold standard - endoscopic dilatation with pneumatic bag
*endoscopic injection of botox into LOS *surgical cardiomyotomy |
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what is diffuse oesophgeal spasm
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*severe dysmotility
*causes retrosternal chest pain and dysphagia *swallowing accompanied by bizarre contractino of oesophagus without wave propagation *barium swallow shows "corkscrew" |
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management of diffuse oes spasm
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*anti reflux
*Ca-channel blocker *balloon dilatation or myotomy |
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management of diffuse oes spasm
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*anti reflux
*Ca-channel blocker *balloon dilatation or myotomy |
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effect of scleroderma on oesophagus
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*90% of patients have oes involvement
*decreased peristalsis due to replacement of SM by fibrous tissues *decreased LOS pressure --> reflux oesophagitis, strictures |
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normal anti reflux mechanism
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*LOS relaxes only transiently to allow food bolus to pass
*increased LOS tone intra-abdominal pressure increases (e.g. when lying flat) *diaphragmatic crura pinches off oes *acute gastro-oes angle |
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what mechs have been implicated in pathogenesis of GORD?
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*pregnancy and obesity --> intraabodminal pressure increased --> failure of LOS
*smoking *scleroderma *post cardiomyotomy for achalasia *hiatus hernia - acid trapped in hernial sac and large hernia impairs the pinchcock mech of diaphragm crura |
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clinical features of reflux oesophagitis
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*heartburn esp. after meals
*regurg of food and acid when lying flat or bending over *cough and nocturnal asthma due to aspiration and regurg *can mimic angina |
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complications of reflux oesophagitis
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*Barrett oes
*peptic stricture *adenocaricinoma |
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what is Barrett oes?
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intestinal metaplasia where columnar epi and goblet cells extend upwards from lower oes to replace squamous epi
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how to manage reflux oesophagitis?
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*nonpharmacological - avoid aggravating foods, eating at night and try raising head of bed
*pharmacological - antacids, H2 receptor antagonist, PPI *surgery - nissen fundoplication - gastric fundus wrapped or plicated around lower end of oes and stitched in place |
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Endoscopy vs oes manometry - role in Ix of oes disease
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*endoscopy - detect structural abnormalities. Allows biopsies, rapid urease test, balloono dilatation and band varices
*manometry - identify functional abnormalities (via catheter inserted through nose into oesophagus and measuring pressure) |
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Other Ix for oes disease
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*24 hour pH monitoring - correlate reflux episodes (pH<4) with symptoms
*barium swallow - detect obstruction |
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describe normal protective mechanisms for low pH environment in GI
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*mucus secretion - prevents H+ from diffusing back; acid exits gastric gland through "jets" hence do not come in contact with epi
*bicarb secretion by surface epi cells *tight intercellular junction *mucosal blood flow - removes backflowed acid *PG synthesis - lowers acid secretion by incresaing mucus/bicarb secretion |
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upper GI bleeding presents with... and is located...
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*haematemesis or malaena
*any lesion proximal to and including caecum |
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common causes of upper GI bleed
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*most common - 50% - gastric/duodenal ulcers
*other 50% - varices, Mallory-Weiss tears, drugs (e.g. NSAIds, corticosteroids), gastritis/erosion, malignancies |
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lower GI bleed is....
*where? *presents with? |
*after caecum
*maybe occult (if in ascending colon) or malaena of haematochezia |
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Blood mixed with stool - Dx
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carcinoma of colon
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Blood coating stool
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carcinoma of rectum
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blood after defecation - Dx?
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haemorrhoids, anal fissure
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blood and mucus - Dx?
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CD, UC, gastroenteritis, IBS
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blood alone - dx?
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diverticular disease
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GI bleed - what features will suggest severe disease?
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*old
*features of shock *features of chronic liver disease *Fe deficiency anaemia *weight loss |
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what is erosive gastritis?
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inflammation of gastric mucosa, due to failure of normal mucosal protective mechanisms
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clinical presentation of erosive gastritis
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*asymptomatic
*or presents with epigastric pain and haematemesis |
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erosive gastritis is associated with...
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*alcohol
*NSAID, cytotoxic drugs *chemical injury *smoking *ischaemia and shock *mechnical trauma from nasogastric intubation |
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erosive gastritis is associated with...
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*alcohol
*NSAID, cytotoxic drugs *chemical injury *smoking *ischaemia and shock *mechnical trauma from nasogastric intubation |
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erosive gastritis is associated with...
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*alcohol
*NSAID, cytotoxic drugs *chemical injury *smoking *ischaemia and shock *mechnical trauma from nasogastric intubation |
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ruputured gastro-oes varices are common in patients with?
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cirrhosis
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ruputured gastro-oes varices are common in patients with?
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alcoholic cirrhosis
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pathophysiology of gastro oes varices
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shunting of blood away from hypertensive portal venous system into the low pressure systemic venous system
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T/F 50% of alcoholics die from ruptured oes varices
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T
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T/F most cases of haematemesis are due to varices
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F
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Mx of oes varices
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*balloon tamponade
*sclerotherapy (endoscopic injection of prothrombotic agents) |
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What is Mallory weiss tear?
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longitudinal tears in oes at the gastro-oes junction or gastric cardia, due to severe retching or vomiting
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Mallory Weiss tear is common in patients who are also _____
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alcoholics
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what are peptic ulcers
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*breaches in the mucosa that extend through the muscularis mucosa into the submucosa or deeper!!
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ulcer vs erosions
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ulcers can extend into submucosa or deeper
erosions are epithelial disruptions but submucosa are intact |
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two most common site for peptic ulcers
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1. proximal duodenum
2. stomach antrum |
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Causes of peptic ulcer
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*most common - H. pylori infection
*Hyperacidity e.g. Zollinger-Ellison syndrome *chronic NSAID use (decrease PG synthesis) *smoking (decrease mucosal blood flow) |
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pathophys of zollinger-ellison syndrome
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excessive gastrin secretion by tumour --> increased H+ --> hyperacid environment --> development of ulcers
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T/F
aspirin is a mucosal irritant |
T
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lead toxicity treatment
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Ca-EDTA, dimercaprol, succimer, penicillamine
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clinical presentation of peptic ulcer
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*epigastric pain
*gnawing/burning/aching *worse at night and 1-3 hours after meal *better with food/alkalis *sometimes nausea + vomiting, weight loss, irony deficiency anaemia |
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antral vs pangastritis
*similarities *differences |
*both caused by exposure to H. pylori
*Antral gastritis - only involves stomach antrum --> increased H+ production and increased risk of duodenal ulcers *pangastritis - involves all parts of the stomach --> multifocal atrophy --> decreased H+ production --> increased risk of adenocarcinoma |
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how does pangastritis lead to increased risk of adenocarcinoma
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decreased H+ AND chronic mucosal inflammation --> mucosal epi cell proliferation --> increased risk of genomic mutation
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How does h. pylori cause damage to the stomach?
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*causes mucosal cells to produce proinflammatory cytokines (which then recruit neutrophils)
*produces urea enzyme which degrades urea into several toxic substances *secretes proteases and phospholipases that degrade gastric mucus *enhances gastric H+ secretion and inhibits duodenal bicarb secretion *produces platelet-activating factor --> thrombotic occlusion of mucosal surface capillaries |
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relationship between H. pylori and risk of developing tumours
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*chronic infection of H. pylori increases risk of gastric carcinoma by 5x
*h. pylori infection also associated with gastric MALT lymphoma |
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sequence of carcinogenesis for gastric carcinoma
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1. chronic gastritis
2. multifocal atrophy with decreased H+ secretion 3. intestinal metaplasia 4. dysplasia 5. carcinoma |
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complications of chronic peptic ulcer
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*bleeding - most common; can be life threatening
*perforation - accounts for most of ulcer death *obstruction |
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factors predisposing to gastric carcinoma
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*environment RF - smoking, h. pylori exposure, low SE, diet (smoked food, lack of fibre)
*host RF - chronic gastritis, partial gastrectomy (favours bilious intestinal fluid i.e. low H+), gastric adenomas, Barret's oesophagus *Genetic factors - FHx, HPNCC (autosomal dominant) |
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clinical px of gastric carcinoma
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*typical cancer things - weight loss, anorexia, nausea and vomiting
*abdo pain *change in bowel habits *less commonly - anaemia and haemorrhage |
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Mode of spread of gastric carcinoma
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*develop in mucosal layers and other deeper layers
*spread to duodenum, pancreas, retroperitoneum *lymph node spread (i.e. VIRCHOWS) *peri-umbilical region --> sister mary joseph nodule *peritoneal seeding, lungs and liver mets common at autopsy *Kruckenberg tumours = mets to ovaries |
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pattern of growth of gastric carcinoma
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*early gastric carcinoma - confined to mucosa and submucosa; may be exophytic, flat/depressed, excavated
*late gastric carcinoma - extend into muscularis propria and beyond |
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what is linitis plastica
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when broad region of gastric wall or entire stomach is infiltrated by gastric carcinoma --> rigid, thickened "leather bottle" appearance
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advantage of endoscopy in upper GI bleed
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*both diagnostic and treatment modalities (sclerotherapy, banding, diathermy)
*safe - low risk of perforation; does not need GA *identify source of haemorrhage |
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what is the treatment of choice when endoscopy fails for upper GI bleed
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balloon tamponade
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what complications can result from reflux oesophagitis
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*Barret's oesophagitis
*oes adenocarcinoma *peptic stricture *chronic cough and sore throat |
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how to treat oes adenocarcinoma
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diathermy, cauterisation, photodynamic therapy and PPI
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incidence of patients with BO developing oes adenocarcinoma
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0.5%/year
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peptic stricutre forms in ____ of people with oesophagitis
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5%
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how to treat peptic stricture
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*dilation with graduated polyvinyl catheters passed over a wire placed at the time of endoscopy
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how does scleroderma cause diarrhea and offensive stool?
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small bowel hypomotility (loss of microvillin in small bowel --> bacterial overgrowth, diarrhea, bloating, malabsorption, weight loss)
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difference between dysplasia and neoplasia
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dysplasia - can be reversed
neoplasia - cannot be reversed |
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triple therapy for h. pylori
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triple therapy for 2 weeks
*omeprazole *amoxycillin (metronidazole in penicillin allergic individual) *clarithromycin |
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which vessels to worry about for an eroding stomach ulcer?
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*lesser curvature (more common) - splenic artery
- coeliac trunk *greater curvature (less common) - right and left gastro-epiploic artery *antral region - gastroduodenal a - SMA - R gastric a * |
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DDX for epigastric tenderness
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*peptic ulcer disease
*non ulcerative dyspepsia *cholecystitis *pancreatitis *AAA dissection/rupture *peritonitis *malignancy *referred spinal pathology - MSK/infiltrative (Paget's disease, mets) |
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DDX for normocytic normochromic anaemia
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*acute blood loss
*pregnancy *anaemia of chronic disease *haemolytic anaemia |
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Increased platelet count + normocytic normochromic anaemia - most common dx?
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acute bleed
*increased platelet count due to reactive thrombocytosis |
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resuscitative measure for hypovolaemic shock
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*cannula access
*give cyrstalloid to increase BP |
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how to tell if an ulcer is benign or maligant
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benign ulcers are usually:
*pre-pyloric *smaller *sharper punched out edge *B/G of gastritis *multiple *no heaped up margin Ix by biopsy of edge epithelium |
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Complications of untreated hypovolaemic shock
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*brain - stroke and encephalopathy
*heart - MI *lungs - ARDS (no lung infarct due to dual supply) *kidneys - ARF --> ATN *GI - gut ischemia *DIC previous co-morbidities determine which happens first |
