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Gastro Flashcards

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1
Q

What are the anatomical factors predisposing to GORD?

A

Hiatus hernia

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2
Q

What are the physiological factors pre-disposing to GORD?

A 
Raised IAP (pregnancy/obesity)
Large meals, eaten late at night 
Smoking
High caffeinated drink intake 
High fatty food intake
Drugs (anticholinergics, nitrates, tricyclics, calcium channel inhibitors)
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3
Q

What is an oesophageal hiatus?

A

An oval aperture in the right crus of the diaphragm at T10

The oesophagus, vagal nerve trunks, oesophageal branches of the left gastric vessels and lymphatics pass through it

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4
Q

What are hiatus hernia?

A

hernia allowing Allow part of the stomach into the thoracic cavity

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5
Q

What are the two types of hiatus herniae?

A

Sliding hiatus hernia

Para-oesophageal / rolling hernia

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6
Q

What happens in a sliding hiatus hernia?

A

The gastro-oesophageal junction slides through the hiatus to lie above the diaphragm

This occurs in 30% adults >50 and is usually of no significance, however symptoms may occur due to associated reflux

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7
Q

What is a para-oesophageal / rolling hernia?

A

A small part of the fundus rolls up through the hernia alongside the oesophagus, but the sphincter remains competent below the diaphragm

Very occasionally tis can present with severe pain, requiring surgical intervention for gastric volvulus / strangulation

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8
Q

What is dyspepsia?

A

Chronic upper abdominal pain / discomfort

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9
Q

What are the three different types of dyspepsia?

A 
Reflux type (heartburn and regurgitation aka GORD)
Ulcer type (epigastric pain)
Dysmotility type (bloating and nausea)
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10
Q

What are the major features of dyspepsia?

A

Heartburn / indigestion
worse on bending/lying down, when drinking hot liquids or alcohol
Relieved by antacids

Regurgitation of food/acid
Passive process, more common when ending/lying. Can aspirate

Waterbrash

Odynophagia

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11
Q

How is GORD diagnosed?

A

Clinically

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12
Q

What are the red flag symptoms for GORD?

A 
ALARM 55 
Anaemia
Loss of weight 
Anorexia
Recent onset, progressive symptoms
Melaena or haematemesis 
Swallowing difficulties 
>55 years of age
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13
Q

What further investigations can be done for GORD?

A 
Treat empirically with PPI but: 
Barium swallow (if suspecting hiatus hernia)
24 hours luminal pH monitoring and manometry to diagnose GORD if endoscopy is normal
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14
Q

What is the management for GORD?

A

Lifestyle:
Encourage weight loss and smoking cessation
Eat small/regular meals >3h before bed and avoid hot drinks/alcohol

Raise the head of the bed at night
Avoid drugs that exacerbate the condition (above) or those that damage the mucosa (NSAIDs, potassium salts)

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15
Q

What medications can be used for GORD?

A

Antacids = mgOH2 +/- alginates = gaviscon

H2RAs (ranitidine) and then PPIs are used in a stepwise approach if antacids/alginates do not provide relief

Prokinetic drugs: metoclopramide/domperidone to promote gastric emptying

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16
Q

What is the surgical management of GORD?

A

Surgery should never be performed for hiatus hernia alone - only if symptoms are severe, refractory to medical management and there is pH monitoring evidence of acid reflux

Nissen fundoplication: gastric fundus wrapped around the oesophagus and stitched in place, so that when teh fundus contracts it creates a sphincter

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17
Q

What are the possible long term complications of GORD?

A

Oesophagitis/ulcers
Benign strictures
Barratt’s oesophagus / oesophageal adenocarcinoma

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18
Q

How does Barrett’s oesophagus occur?

A

In patients with long standing reflux, the normal stratified squamous epithelium of the oesophagus undergoes metaplasia to glandular columnar epithelium

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19
Q

How is Barrett’s oesophagus diagnosed?

A

Upper GI endoscopy, where if present it will be visible and biopsies taken

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20
Q

What is the management of Barrett’s oesophagus?

A

Regular endoscopic surveillance with biopsies to look for dysplasia / carcinoma in situ, which can be treated with endoscopic resection

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21
Q

What is dysphagia?

Odynophagia?

A

Dysphagia = difficulty swallowing

Odynophagia = pain upon swallowing

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22
Q

What are the common causes of dysphagia?

A

Diseases of the mouth / tongue: e.g. tonsillitis
Neuromuscular disorders: MG, MND, bulbar palsy
Oesophageal motility disorders: achalasia, scleroderma, DM
Extrinsic pressure: goitre, lymph nodes, enlarged left atrium

Intrinsic lesions: FB, benign/malignant stricture, pharyngeal pouch, oesophageal web (Plummer vinson syndrome

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23
Q

What are the two types of dysphagia?

A

Orophayngeal

Oesophageal

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24
Q

What is oropharyngeal dysphagia

What is it caused by?

A

Orophayngeal: difficulty initiating swallowing +/- choking / aspiration
Caused by neurological disease
Ix with neurological examination and video fluoroscopic swallowing assessment

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25
What is oesophageal dysphagia?
``` Food sticks after swallowing +/- regurgitation Causes: Dysmotility e.g. achalasia Stricture: benign or malignant Oesophagitis (reflux, candidiasis) Pharyngeal pouch ``` Investigate with barium swallow, endoscopy and biopsy
26
What is Plummer-Vinson syndrome?
Triad of dysphagia + koilonychia + glossitis (IDA signs) Pre-malignant condition due to hyperkeratinisation of the oesophagus causing an oesophageal web Treatment is with iron and dilation of the web via OGD
27
What are the symptoms of oesophageal malignancy?
Progressive dysphagia, starting with solids and progressing to liquids and eventually difficulty swallowing saliva Weight loss and anorexia Retrosternal chest pain Coughing/aspiration Occasional lymphadenopathy
28
what kind of cancers are most oesophageal malignancies?
``` Mainly adenocarcinomas (lower 1/3) some SCC (upper 2/3) ```
29
What are the risk factors for adenocarcinoma?
``` GORD Barrett's oesophagus smoking achalasia obesity ```
30
Who tends to get oesophageal SCC?
Heavy smoking and drinking males
31
What is the prognosis like for adenocarcinoma / SCC?
Poor SCC has a slightly better prognosis as it is more responsive to radiotherapy mets are common at diagnosis: in the liver/lungs/bone
32
How is staging of oesophageal malignancy done?
Staging/Grading: OGD including trans-oesophageal USS and biopsy CT of the thorax/abdomen PET to assess for metastatic disease Laparoscopy to exclude peritoneal mets prior to resection
33
What is the management of oesophageal malignancy
Operable disease is best managed by surgical resection. In addition to surgical resection many patients will be treated with adjuvant chemotherapy. Palliation: can involve oesophageal stunting to restore swallowing
34
What is the presentation of achalasia?
Dysphagia, regurgitation, substernal cramps, nocturnal cough and weight loss, often in the third decade
35
Describe why achalasia occurs
Lack of co-ordinated muscle contraction and relaxation at the lower end of the oesophagus, leading to retention of the food bolus bird beak appearance on barium studies
36
How is diagnosis of achalasia done?
Barium swallow OGD shows dilated oesophagus with a pond of stagnant food/fluid and finally oesophageal manometry to show increased lower oesophageal sphincter
37
What is the management of achalasia?
Conservative/lifestyle: chew food well, always eat upright, drink lots with meals etc BOTOX: temporary relief Endoscopic balloon dilation Heller's cardiomyotomy - muscles of the cardia are divided
38
Describe the aetiology of peptic ulcer disease
Helicobacter pylori infection (90% duodenal/70% gastric ulcers) NSAIDs Zollinger-Ellison syndrome Other: smoking, coffee consumption and hepatic/renal failure
39
What are the symptoms of peptic ulcer disease?
Epigastric pain, related to food intake, relieved by antacids Nausea anorexia and weight loss Haematemesis / meleana
40
What are the investigations for peptic ulcer disease?
Urgent oesophago-gastro-duodenoscopy (OGD) if fit ALARM 55 If resolves on antacid / GORD no investigations If persist, investigate for H pylori If previous ulcer, assume H.Pylori infection and eradicate
41
How are patients investigated for H.Pylori?
C13 urea breath test --> 13Co2 Stool test Patient should not take antibiotic drugs for 4 weeks and PPIs for 2 weeks before testing as these can cause a false negatives
42
Which are more common , gastric or duodenal ulcers?
Duodenal (4x commoner)
43
Where do duodenal ulcers tend to occur? | When does pain occur?
90% within 2cm of the pylorus | Pain at night and before meals, relieved by eating
44
Where do gastric ulcers occur? | When does pain occur?
Mainly on the lesser curve of the stomach | Pain worse on eating and relieved by antacids
45
How does HPylori cause peptic ulceration?
Produces gastritis + activation of inflammatory infiltrate Increased acid secretion in the presence of H.Pylori and abnormal mucus production - leading to epithelial damage
46
How does smoking cause peptic ulceration?
Impairs gastric mucosal healing | Nicotine increases acid secretion
47
How do NSAIDs cause peptic ulceration?
NSAIDs inhibit COX which have anti-inflammatory properties as COX-2 isoform normally causes inflammatory prostaglandin synthesis
48
What is the management for peptic ulceration?
If no ALARM55 Stop smoking and avoid food that worsen symptoms Medications: PPI/H2RA to reduce acid secretion Stop NSAIDs if possible Check H pylori and eradicate if present
49
How is H.Pylori treated?
TRIPLE THERAPY: PPI + antibiotics for 7 days: Omeprazole + clarithromycin + amoxicillin Metronidazole can be used in penicillin allergic patients
50
What surgery is done for peptic ulceration?
Vagotomy - severing of vagus nerve to reduce acid production Vagotomy + pyloroplasty Gastrectomy: may be required
51
What are the causes of upper GI bleeding?
``` Peptic ulceration (40%) Gastroduodenal erosions (15%) Oesophagitis (15%) Mallory-Weiss syndrome (tears at GO junction due to violent vomiting 15%) Varices (10%) Upper GI malignancy (1%) ```
52
What are the symptoms of upper GI bleeds?
Haematemesis Meleaena Haematochezia Abdominal pain Chronic GI blood loss --> signs of iron-deficient anaemia
53
What is the management of GI haemorrhage?
Manage as per haemorrhagic shock Transfuse to keep Hb >8 Endoscopy within 4 hours IV omeprazole to reduce risk of rebleed: 80mg stat then 8mg/hr Definitive surgery or angiographic embolisation if: bleeding recurs after endoscopy persistent despite endoscopic treatment bleeding is torrential Angiographic embolisation if unfit for laparotomy
54
How should haemorrhagic shock be scored?
Glasgow Blatchford: SBP, pulse, Hb, blood urea Scores >6 = mortality 50% so urgent intervention
55
What are the risk factors of gastric cancer?
H.Pylori infection leading to metaplasia High salt/nitrate diet Smoking Genetic: blood group A / HNPCC / Japanese heritage Pernicious anaemia Adenomatous polyps Low S/E status
56
What are the symptoms of gastric cancer?
Epigastric pain as with gastric peptic ulcer Nausea and vomiting (vomiting is frequent if the tumour is near the fundus) Dysphagia (if tumour is near fundus) Anorexia/weight loss
57
What are the signs of gastric cancer?
Palpable epigastric mass (50%) Large left supraclavicular node (Virchow's) Hepatomegaly, jaundice and ascites Acanthosis nigricans
58
What investigations can be done for gastric cancer?
OGD and multiple ulcer edge biopsy Endoscopic USS and CT for staging Staging laparoscopy for locally advanced tumours if no other metastases are detected
59
Who does gastric cancer tend to affect?
50-70 y/o | Especially in Japanese populations
60
What kind of cancers are most gastric cancers?
Adenocarcinomas, occurring in the antrum
61
What are the appearances of gastric cancer?
Polypoids / ulcerating lesions with rolled edges | Leather bottle stomach
62
How do mets of gastric cancers occur?
Direct invasion of abdominal viscera, lymphatic and then to the liver by portal dissemination Transcoelomic spread may cause peritoneal seedings, including bilateral ovarian Krunkenberg tumours
63
What are the more rare types of gastric cancers?
``` Stromal tumours (leiomyomas / leiomyosarcomas) Arise from interstitial cells of Cajal usually slow growing/benign ```
64
What are the management options for gastric cancers?
Partial gastrectomy for tumours in the distal 2/3rd of stomach, or total gastrectomy, with extensive lymphatic clearance Combination chemotherapy can increase survival in advanced disease Endoscopic mucosal resection can be used for tumours confined to the mucosa Stenting of pylorus can be palliative to relieve gastric outlet obstruction in patients with pyloric tumours Wide local excision for stomal tumours
65
What are the complications of gastrectomy?
``` Chronic diarrhoea/vomiting Dumping syndrome (third space fluid shifts due to foods with high osmotic potential being dumped in jej) ``` Bacterial overgrowth with malabsorption Anaemia (Iron / B12 deficiency) Osteomalacia
66
What is the prognosis for gastric cancer?
<10% 5 year survival | <20% for those undergoing radical surgery
67
What is diarrhoea?
3 loose/watery stools per day Acute: <14 days Chronic >14 days
68
What are the causes of diarrhoea?
Gastroenteritis Diverticulitis Antibiotic therapy Constipation causing overflow
69
What defines traveller's diarrhoea?
``` At least 3+ watery stools per day plus 1 of: Abdominal cramps Fever N+V Bloody stool ```
70
What is the usual cause of traveller's diarrhoea?
E.coli
71
What are the causes of food poisoning?
Staph A or Clostridium perfringens
72
What are the features of C diff infection?
Diarrhoea Abdo pain Increased WBC count
73
What are the risk factors for C diff?
Clindamycin 2nd/3rd gen cephalosporins PPI’s
74
What is the treatment for C diff?
1st line: oral metronidazole 10-14 days 2nd line: oral vancomycin Life threatening: Oral Vanc and IV metronidazole
75
What is the presentation of malabsorption
Diarrhoea decreased weight lethargy Anaemia, bleeding disorders, oedema, osteomalacia, neuropathy
76
What are the causes of malabsorption?
Common: Coeliac Chronic pancreatitis Chron's rare: BILE: obstruction pancreatic insufficiency (CF or cancer) Bacterial overgrowth infection
77
What investigations can be done for malabsorption?
``` Bloods: FBC, U+E, LFT, CRP Iron, B12/folate Ca, Mg, Phosphate Lipids TFT ``` Coeliac Serology Stool studies: MC&S, OCP, C.diff toxin, elastase (pancreatitis), calprotectin Endoscopy: OGD+duodenal biopsy - coeliac Colonoscopy + biopsy - Chron's ERCP - pancreatitis/biliary obstruction
78
Why does coeliac disease occur?
Inflammation of jejunal mucosa in response to gluten Biopsy will show flattened mucosa due to decreased villi Crypt hyperplasia increased intraepithelial lymphocytes
79
What is the presentation of coeliac disease?
Asymptomatic IDA, decreased weight, fatigue Diarrhoea, abdo pain, bloating, vomiting Dermatitis herpetiformis
80
What investigations are done for coeliac?
FBC, clotting, bone profile Antibodies: EMA and TTG Duodenal biopsy = gold standard
81
What is the management for coeliac disease?
Lifelong gluten free diet
82
What are the symptoms of IBS?
6 months of: Abdominal pain Bloating Change in bowel habit +ve diagnosis made if: abdo pain - relieved by defecation, associated with change in bowel habit other symptoms: altered stool passage - straining, urgerny, mucus
83
What red flags should be excluded in IBS?
weight loss rectal bleeding FH of bowel cancer >60 years
84
What investigations can be done for IBS?
Examination - anaemia or mass | Coeliac screen - CRP/ESR/TTG/EMA aabs
85
What is the management of IBS?
Lifestyle Exercise Diet - FODMAP Regular mealtimes, water, decreased caffeine and alcohol Diarrhoea: loperamide Constipation: laxatives 1st line - antispasmodic for pain Mebeverine +/- diarrhoea/constipation meds 2nd line - low dose/TCA
86
What is the management of bleeding oesophageal varices?
``` A-E correct clotting: FFP, vitamin K vasoactive agents: terlipressin prophylactic antibiotics: Quinolones are typically used ``` endoscopy: endoscopic variceal band ligation is superior to endoscopic sclerotherapy. NICE recommend band ligation Sengstaken-Blakemore tube if uncontrolled haemorrhage Transjugular Intrahepatic Portosystemic Shunt (TIPSS) if above measures fail connects the hepatic vein to the portal vein
87
What is the prophylactic management of variceal haemorrhage?
propranolol endoscopic variceal band ligation (EVL) is superior to endoscopic sclerotherapy. Proton pump inhibitor cover is given to prevent EVL-induced ulceration.

CP3 Medicine (19 decks)

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