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CP3 Medicine > Gastro > Flashcards

Gastro Flashcards

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
Q

What is oesophageal dysphagia?

A 
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

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26
Q

What is Plummer-Vinson syndrome?

A

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

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27
Q

What are the symptoms of oesophageal malignancy?

A

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

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28
Q

what kind of cancers are most oesophageal malignancies?

A 
Mainly adenocarcinomas (lower 1/3)
some SCC (upper 2/3)
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29
Q

What are the risk factors for adenocarcinoma?

A 
GORD
Barrett's oesophagus
smoking
achalasia
obesity
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30
Q

Who tends to get oesophageal SCC?

A

Heavy smoking and drinking males

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31
Q

What is the prognosis like for adenocarcinoma / SCC?

A

Poor
SCC has a slightly better prognosis as it is more responsive to radiotherapy
mets are common at diagnosis: in the liver/lungs/bone

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32
Q

How is staging of oesophageal malignancy done?

A

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

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33
Q

What is the management of oesophageal malignancy

A

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

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34
Q

What is the presentation of achalasia?

A

Dysphagia, regurgitation, substernal cramps, nocturnal cough and weight loss, often in the third decade

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35
Q

Describe why achalasia occurs

A

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
Q

How is diagnosis of achalasia done?

A

Barium swallow
OGD shows dilated oesophagus with a pond of stagnant food/fluid and finally oesophageal manometry to show increased lower oesophageal sphincter

37
Q

What is the management of achalasia?

A

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
Q

Describe the aetiology of peptic ulcer disease

A

Helicobacter pylori infection (90% duodenal/70% gastric ulcers)
NSAIDs
Zollinger-Ellison syndrome

Other: smoking, coffee consumption and hepatic/renal failure

39
Q

What are the symptoms of peptic ulcer disease?

A

Epigastric pain, related to food intake, relieved by antacids

Nausea
anorexia and weight loss
Haematemesis / meleana

40
Q

What are the investigations for peptic ulcer disease?

A

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
Q

How are patients investigated for H.Pylori?

A

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
Q

Which are more common , gastric or duodenal ulcers?

A

Duodenal (4x commoner)

43
Q

Where do duodenal ulcers tend to occur?

When does pain occur?

A

90% within 2cm of the pylorus

Pain at night and before meals, relieved by eating

44
Q

Where do gastric ulcers occur?

When does pain occur?

A

Mainly on the lesser curve of the stomach

Pain worse on eating and relieved by antacids

45
Q

How does HPylori cause peptic ulceration?

A

Produces gastritis + activation of inflammatory infiltrate

Increased acid secretion in the presence of H.Pylori and abnormal mucus production - leading to epithelial damage

46
Q

How does smoking cause peptic ulceration?

A

Impairs gastric mucosal healing

Nicotine increases acid secretion

47
Q

How do NSAIDs cause peptic ulceration?

A

NSAIDs inhibit COX which have anti-inflammatory properties as COX-2 isoform normally causes inflammatory prostaglandin synthesis

48
Q

What is the management for peptic ulceration?

A

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
Q

How is H.Pylori treated?

A

TRIPLE THERAPY:
PPI + antibiotics for 7 days:
Omeprazole + clarithromycin + amoxicillin
Metronidazole can be used in penicillin allergic patients

50
Q

What surgery is done for peptic ulceration?

A

Vagotomy - severing of vagus nerve to reduce acid production

Vagotomy + pyloroplasty

Gastrectomy: may be required

51
Q

What are the causes of upper GI bleeding?

A 
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
Q

What are the symptoms of upper GI bleeds?

A

Haematemesis
Meleaena
Haematochezia
Abdominal pain

Chronic GI blood loss –> signs of iron-deficient anaemia

53
Q

What is the management of GI haemorrhage?

A

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
Q

How should haemorrhagic shock be scored?

A

Glasgow Blatchford:
SBP, pulse, Hb, blood urea
Scores >6 = mortality 50% so urgent intervention

55
Q

What are the risk factors of gastric cancer?

A

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
Q

What are the symptoms of gastric cancer?

A

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
Q

What are the signs of gastric cancer?

A

Palpable epigastric mass (50%)
Large left supraclavicular node (Virchow’s)
Hepatomegaly, jaundice and ascites
Acanthosis nigricans

58
Q

What investigations can be done for gastric cancer?

A

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
Q

Who does gastric cancer tend to affect?

A

50-70 y/o

Especially in Japanese populations

60
Q

What kind of cancers are most gastric cancers?

A

Adenocarcinomas, occurring in the antrum

61
Q

What are the appearances of gastric cancer?

A

Polypoids / ulcerating lesions with rolled edges

Leather bottle stomach

62
Q

How do mets of gastric cancers occur?

A

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
Q

What are the more rare types of gastric cancers?

A 
Stromal tumours (leiomyomas / leiomyosarcomas) 
Arise from interstitial cells of Cajal 
usually slow growing/benign
64
Q

What are the management options for gastric cancers?

A

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
Q

What are the complications of gastrectomy?

A 
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
Q

What is the prognosis for gastric cancer?

A

<10% 5 year survival

<20% for those undergoing radical surgery

67
Q

What is diarrhoea?

A

3 loose/watery stools per day
Acute: <14 days
Chronic >14 days

68
Q

What are the causes of diarrhoea?

A

Gastroenteritis
Diverticulitis
Antibiotic therapy
Constipation causing overflow

69
Q

What defines traveller’s diarrhoea?

A 
At least 3+ watery stools per day plus 1 of: 
Abdominal cramps
Fever
N+V
Bloody stool
70
Q

What is the usual cause of traveller’s diarrhoea?

A

E.coli

71
Q

What are the causes of food poisoning?

A

Staph A or Clostridium perfringens

72
Q

What are the features of C diff infection?

A

Diarrhoea
Abdo pain
Increased WBC count

73
Q

What are the risk factors for C diff?

A

Clindamycin
2nd/3rd gen cephalosporins
PPI’s

74
Q

What is the treatment for C diff?

A

1st line: oral metronidazole 10-14 days

2nd line: oral vancomycin

Life threatening: Oral Vanc and IV metronidazole

75
Q

What is the presentation of malabsorption

A

Diarrhoea
decreased weight
lethargy

Anaemia, bleeding disorders, oedema, osteomalacia, neuropathy

76
Q

What are the causes of malabsorption?

A

Common:
Coeliac
Chronic pancreatitis
Chron’s

rare: BILE: obstruction
pancreatic insufficiency (CF or cancer)
Bacterial overgrowth
infection

77
Q

What investigations can be done for malabsorption?

A 
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
Q

Why does coeliac disease occur?

A

Inflammation of jejunal mucosa in response to gluten
Biopsy will show flattened mucosa due to decreased villi

Crypt hyperplasia
increased intraepithelial lymphocytes

79
Q

What is the presentation of coeliac disease?

A

Asymptomatic
IDA, decreased weight, fatigue

Diarrhoea, abdo pain, bloating, vomiting

Dermatitis herpetiformis

80
Q

What investigations are done for coeliac?

A

FBC, clotting, bone profile

Antibodies: EMA and TTG
Duodenal biopsy = gold standard

81
Q

What is the management for coeliac disease?

A

Lifelong gluten free diet

82
Q

What are the symptoms of IBS?

A

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
Q

What red flags should be excluded in IBS?

A

weight loss
rectal bleeding
FH of bowel cancer
>60 years

84
Q

What investigations can be done for IBS?

A

Examination - anaemia or mass

Coeliac screen - CRP/ESR/TTG/EMA aabs

85
Q

What is the management of IBS?

A

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
Q

What is the management of bleeding oesophageal varices?

A 
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
Q

What is the prophylactic management of variceal haemorrhage?

A

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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