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GI > Dyspepsia - oesophageal disease, peptic ulcer, pancreatitis > Flashcards

Dyspepsia - oesophageal disease, peptic ulcer, pancreatitis Flashcards

1
Q

What is Benign Oesophageal stricture?

A

Narrowing of the oesophagus due to corrosives, surgery or radiotherapy. Highly associated to GORD, oesophagitis, achalasia or a hiatus hernia.

Underlying cause needs to be treated or stricture needs to be opened by an endoscopic balloon
dilatation.

Symptoms: dysphagia, food regurgitation, dyspepsia, heartburn, frequent burps and hiccups

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2
Q

What are the symptoms of malignant oesophageal stricture?

A

Dysphagia,
Haematemesis,
Unintentional weight loss,
Same symptoms as benign oesophageal stricture.

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3
Q

What is Zenker’s diverticulum?

What are the symptoms?

A

The oesophageal wall herniates through the point of
least resistance; the Killian’s triangle. It is a pseudodiverticulum, as not all layers of the oesophageal
wall herniate.
Also called pharyngeal pouch

Symptoms: cough, regurgitation, halitosis (bad breath) and dysphagia

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4
Q

What is achalasia?

What is the pathophys?

A

Oesophageal motility disorder involving the smooth muscle layer of the oesophagus and
the lower oesophageal sphincter.

Degeneration of the myenteric (auerbach’s) plexus Causing an imbalance in excitatory and
inhibitory neurotransmitters, resulting in a hypertensive, non-relaxed oesophageal sphincter.

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5
Q

What are the symptoms of Achalasia?

A

Symptoms: dysphagia BOTH SOLIDS AND LIQUIDS, regurgitation, weight loss, coughing when lying down, heartburn

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6
Q

What is peptic ulcer disease?

A
  • Ulcer of stomach or duodenal mucosa for e.g. due to NSAID use (COX-1 inhibition in stomach) and H. pylori infection
  • duodenal ulcers 4 times more common than gastric and common in women
  • Symptoms: gastric ulcer - pain soon after meals, duadenal ulcers - pain 2-3 hours after meal and might wake pt at night. Abdo tenderness, fullness after meals, heartburn symptoms

Ix: Serology. Stool antigen, CLO test or urea breath test (H. pylori tests), endoscopy (can then classify by forest classification), FBC (microcytic anaemia from active bleeding), stool haem test (occult blood)

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7
Q

What is the urea breath test?

A
  • Rapid diagnostic procedure used to identify infections by Helicobacter pylori.
  • It is based upon the ability of H. pylori to convert urea to ammonia and carbon dioxide.
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8
Q

What are the risk factors for GORD?

A 
Obesity 
Pregnancy
Systemic sclerosis 
Drugs- nitrates
Smoking
Hiatus hernia (sliding hernia)/ delayed gastric emptying
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9
Q

Complications of GORD:

A

Oesophagitis
Oesophageal strictures
Barrett’s oesophagus

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10
Q

Why does GORD occur?

Symptoms?

A

Due to failure of lower oesophageal sphincter causing the angle of His to be larger and then gastric substances are more likely to travel back into oesophagus

Symptoms: Heartburn (aggravated by lying down or bending), cough and nocturnal asthma

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11
Q

What are the investigations for GORD?

A
  • PPI’s - 8-week treatment to check for improvement
  • Oesophagogastroduodenoscopy to visualise for ulcerations, erosions, oesophagitis, strictures or Barrett’s
  • Ambulatory 24h pH monitoring to demonstrate abnormal acid exposure
  • Oesophageal Manometry can be used to evaluate oesophageal contractions and sphincter function (for achalasia or spasms)
  • Barium swallow or oesophageal capsule endoscopy
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12
Q

What is functional dyspepsia?

Symptoms
Treatment

A

~ Chronic disorder of sensation and movement (peristalsis) in upper GI tract. Also non-ulcer dyspepsia. Pathophys unknown.
~ Usually due to H.pylori causing non-erosive reflux disease with epigastric symptoms only

~ Symptoms: bloating, nausea, vomiting, heartburn, indigestion
~ Sporadic, poorly localised, without consistent aggrevating or relieving factor.
~ Hb and FBC seen to assess for anaemia due to GI haemorrhage (complication of functional dyspepsia)
~ Dietary and lifestyle mods, PPIs and H2 antagonists

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13
Q

What is the management for active bleeding peptic ulcer disease?

A
  • FBC, BP, O2, Blatchford score
  • IV fluids (0.9% SODIUM 500ML IN 15 MINS) for immediate resuscitation
  • blood transfusion
  • endoscopy dual therapy (injection of adrenaline)
  • Mechanical clips or cauterization of perforation
  • PPI (72 hour infusion then oral for 4-8 weeks)
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14
Q

What is given to PPI patients who can’t stop NSAIDS?

A

Misoprostol

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15
Q

Management for non-active bleeding ulcer:

A
  • Treat underlying cause e.g. discontinuation of NSAIDS
  • Lifestyle changes and OTC antacids
  • Test for H. pylori
  • PPIs (can cause diarrhoea)
  • H2 antagonists (Ranitidine)
  • misoprostol given if NSAIDS cant be stopped
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16
Q

Management of H. pylori ulcer if no penicillin allergy:

A

For 7 days give
[FIRST LINE] PPI (twice daily) + Clarithromycin/ Metronidazole + amoxicillin

[SECOND LINE] PPI + amoxicillin + second antibiotic not used in first line

[ongoing symptoms] PPI + Amoxicillin + Tetracycline hydrochloride/Levofloxacin

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17
Q

How do PPIs work?

A

Act directly on H/K-ATPase responsible for pumping H+ out of parietal cell (which would then go on to form HCL)
It irreversibly inhibits the enzyme, therefore acid secretion only resumes on synthesis of new enzymes

PPI’s include Omeprazole, Lansoprazole + Pantoprazole

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18
Q

How do NSAIDS cause ulcers?

A

NSAIDS inhibit COX-1 which inhibits prostaglandin secretion.

Prostaglandins stimulate mucus secretion that protects GI, maintain gastric blood flow and promote platelet aggravation

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19
Q

What is the CLO test?

A

Rapid urease test for checking H. pylori

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20
Q

Management of H. pylori in patients with Penicillin allergy

A

For 7 days give
[FIRST LINE] PPI (twice daily) + Clarithromycin + metronidazole

[SECOND LINE] PPI + Bismuth subsalicylate + tetracycline hydrochloride/metronidazole

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21
Q

Gastric physiology on acid secretion:

A

Parietal cells secrete acid into the stomach via H+/K+-ATPase

Secretion is stimulated via
Acetylcholine from parasympathetic fibres or Gastrin, hormone released from G-cells into the bloodstream

Both Gastrin + Acetylcholine may act directly on Parietal cells but may also act indirectly via paracrine cells which release histamine that acts locally on parietal cells to stimulate the H+/K+-ATPase

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22
Q

Gastric physiology on mucus secretion:

A

Forms a physical barrier over surface of stomach and consists of a gel rich in HCO3 (bicarbonate)

This bicarbonate helps neutralise the acid creating a pH gradient

Prostaglandins are synthesized by gastric mucosa + are thought to protect the mucosa by stimulating secretion of mucus/bicarbonate

NSAIDs can inhibit the production of this mucosal protective prostaglandin with detrimental effects!

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23
Q

How do Histamine-2 receptor antagonists work on gastric physiology?

A

Block the action of histamine from paracrine cells acting via receptors on parietal cells which has an inhibiting effect on the H/K-ATPase channel
Examples include Cimetidine + Ranitidine

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24
Q

How do antacids work on gastric physiology?

A

Raise luminal pH of stomach
Can cause an acid rebound
Usually given between meals +at bedtime
Normally contain aluminium/magnesium compounds

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25
Q

How do Alginates work on gastric physiology?

A

Increase the viscosity of stomach contents + protect the oesophageal mucosa from reflux
Include Peptac +Gaviscon

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26
Q

Management for GORD:

A

Antacids/Alginates: OTC meds
PPIs (if symptoms persist at H2 antagonist or double dose)
Prokinetics - metoclopromide/domperidone

Surgery - Nissen Fundoplication (fundus sutured around lower oesophagus)

Endoscopic Gastroplication

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27
Q

What is H. pylori?

Transmission,
linked with what diseases,
where in the body is it mostly found
how does it cause infection?

A

Spiral shaped, gram negative, urease producing bacterium

Found in the gastric antrum predominantly

Linked with gastritis, ulcers, gastric cancer, gastric lymphoma.

Oral-oral or faecal-oral transmission

Physiologically, infection causes gastritis which reduces acid output, result in a rebound hypergastrinaemia.

28
Q

What can stool antigen testing be used for?

A

Can be used for diagnosis of H. pylori infection

My need to be delayed for several months after therapy to confirm eradication but not routinely used for this!

29
Q

Are biopsies taken for ulcers?

A

Duodenal ulcers:

  • don’t routinely require biopsy though sample maybe taken for H. Pylori status
  • Follow-up endoscopy only required if complicated ulcer ie. Bleed

Gastric ulcers:

  • 6 biopsies from the edge of ulcer + biopsy remote from ulcer looking for H.Pylori
  • Follow-up not always required if ulcer clearly benign on histology, although always be suspicious for underlying malignancy + follow-up endoscopy in 6-8 weeks time. Default is repeat scope
30
Q

What medications can cause dyspepsia?

A 
Calcium antagonists
Nitrates
NSAIDS
Oral steroids
Bisphosphonates
31
Q

When asking a patient with dyspepsia, what symptoms would cause for urgent specialist referral for endoscopic investigation

A 
[ALARMMD]:
Anaemia
Loss of weight
Anorexia
Recent onset of progressive symptoms (<3 months)
Melaena or haematemesis
Mass
Dysphagia

Patients over the age of 55 years, who have unexplained and persistent dyspepsia or recent onset alone

32
Q

Treatment for dyspepsia if no further investigation warranted?

A
  • Stopping offending medications if possible
  • Lifestyle advice
  • Healthy eating
  • Weight reduction
  • Smoking cessation
  • Avoid known precipitants – alcohol, coffee, chocolate, fatty foods
  • Raising head of the bed
  • Early main meal before going to bed
  • Trial of over the counter medications – antacids or alginates
  • Empirical treatment with PPI (full dose for 1-2 months) or testing and treating for H. Pylori (normally breath test or stool antigen)
  • Offer a low-dose PPI with a limited number of repeat prescriptions
33
Q

Epidemiology of Gastric Cancers:

A
  • Sixth most common fatal cancer in the UK
  • Incidence increases with age
  • More common in men
  • Large geographical variation – highest incidence in Far East
  • > 90% are adenocarcinomas (others include gastric lymphoma, carcinoid, gastroinestinal stromal tumour GIST)
  • 40% found in antrum, 35% in body, 15% fundus + 10% diffuse
34
Q

What are the risk factors for Gastric cancer?

A

Genetics - 10% of cancers show familial clustering [CDH1 gene]
H. Pylori infection (secondary to inducing atrophic gastritis)
Excessive intake of salted food
Smoking
Pernicious anaemia
Menetrier’s disease (massive overgrowth of mucous cells (foveola) in the lining the stomach)
Gastric polyps
NITROSAMINE EXPOSURE IS A RISK FACTOR, these are found in beer, fish, meat and
cheese.
Male, aged 50-70

35
Q

What are the symptoms and signs on gastric cancer?

A 
Late symptoms of dyspepsia
Anaemia/Upper GI bleed
Weight loss, Anorexia, nausea
Virchow's node 
Sister Mary Joseph node -- palpable lymph node in umbilical
Evidence of metastasis 
Outflow obstruction if tumour near pylorus
Palpable epigastric mass
36
Q

What investigations would you do for gastric cancer?

A

Blood tests - FBC, LFT (evidence of metastasis)
OGD - Allows visualisation + biopsy
CT - Staging CT can determine is metastasis is present. Staging determined by TNM system
PET Scan - not commonly used. Able to detect lymph node metastasis.

37
Q

Management for gastric cancer and survival rate?

A

Overall 5-year survival 5%. With curative options 50%

For early cancers confined to mucosa - EMR (Endoscopic mucosal resection)

For locally advance cancer:
Gastrectomy (total or subtotal) with LN resection

38
Q

What is Barrett’s Oesophagus?

Diagnosis and management

A

METAPLASIA from squamous -> columnar epithelium
Long-standing acid reflux.
Premalignant condition for oesophageal ADENOCARCINOMA (30x increased risk)
Asymptomatic or GORD symptoms
Diagnosis via endoscopy and biopsy

Treatment: Endoscopic photodynamic therapy to help ablate dysplastic Barrett’s
Surveillance: Recommended if length is >3cm + if there is intestinal metaplasia on biopsy

39
Q

What is Cholelithiasis?

Symptoms, investigations

A

~ Gallstones
~ Formed from cholesterol, bilirubin or mixed substances from bile,
~ Symptoms: Colicky pain in RU hypochondrium, N&V, indigestion, bloating, heartburn. although 80% patients are asymptomatic
~ symptoms/complications occur when stone obstructs cystic or bile ducts leading to cholecystitis or even pancreatitis. This can lead to increased pancreatic ductal pressure and reflux of pancreaticobiliary secretions
~ Ix: FBC, LFT, Serum lipase and amylase, abdo ultrasound

40
Q

Acute pancreatitis

A

Symptoms: Pain (radiating to back), N&V, Anorexia, tachycardia, Grey-turner’s sign or Cullen’s sign

Ix: (serum lipase, amylase), LFTs, FBCs (CRP), ABGs, abdominal plain
x-ray and transabdominal ultrasound. An ERCP may be performed to identify any pancreatic stones
and identify any enlargement of the pancreatic biliary tree.

41
Q

TNM cancer staging:

A

TX: Main tumor cannot be measured.
T0: Main tumor cannot be found.
T1, T2, T3, T4: Refers to the size and/or extent of the main tumor

NX: Cancer in nearby lymph nodes cannot be measured.
N0: There is no cancer in nearby lymph nodes.
N1, N2, N3: Refers to the number and location of lymph nodes that contain cancer.

MX: Metastasis cannot be measured.
M0: Cancer has not spread to other parts of the body.
M1: Cancer has spread to other parts of the body.

42
Q

Choledocholithiases

A

Gallstones in bile ducts
This can cause biliary colic, obstruction, acute pancreatitis and cholangitis.
Can present with Jaundice
Ix: Ultrasonography, FBC (raised bilirubin, ALK, ALT, GGT)

43
Q

What is an ascending cholangitis?

A

After choledocolithiasis, bile secretions accumulate and become stagnant, a good medium for bacteria
Bacteria enters biliary tree through portal vein or through Ampulla of Vater in duodenum. As pressure in bile duct increases the bacteria can move into bloodstream causing sepsis.

44
Q

Investigations for ascending cholangitis?

A

 FBC (raised white cell count, raised CRP, platelets decreased),
 Serum urea and creatinine (raised),
 ABG (metabolic acidosis in severe disease),
 Serum LFTs (hyperbilirubinemia, raised transaminase and ALP),
 Blood cultures (identification of bacterial species),
 Coagulation panel (prothrombin time may be raised with sepsis),
 ERCP and transabdominal ultrasound.

45
Q

What is primary sclerosing cholangitis?

risk factors?

A

Skin inflammatory lesions along biliary tree, mainly large bile ducts/
Inflammation causes fibrosis and multi-focal strictures forming diffusely thickened, fibrotic duct wall.
This can lead to ductopenia and bile stasis.

Risk factors: male gender and IBD

46
Q

Primary biliary cholangitis?

Symptoms?

Risk factors?

A

Chronic autoimmune granulomatous inflammation damaging interlobular bile ducts
Resulting cholestasis causes fibrosis, cirrhosis and portal hypertension/

Symptoms: Pruritus, fatigue, dry eyes and mouth, syncope, hepatomegaly.

Risk factors: Female, age 45-60 and history of autoimmune diseases

47
Q

What are Grey-turner’s sign or Cullen’s sign?

A

Grey-turner’ sign (bilateral flank blue discolouration)
Cullen’s sign (peri-umbilical
discolouration).

48
Q

Treatment of acute pancreatitis:

A

Resus: IV crystalloids, blood transfusion (if haemorrhagic pancreatitis). Opioids (fentanyl, morphine), antiemetics, calcium/magnesium replacement, insulin (damage to islets of langerhans prevents insulin release). antibiotic therapy, ERCP

49
Q

Chronic pancreatitis symptoms

A 
 Epigastric abdominal pain radiating to the back,
 Steatorrhea,
 Obstructive jaundice,
 Weight loss,
 Nausea and vomiting.
50
Q

Ix for chronic pancreatitis?

A 
Blood glucose (more likely to develop diabetes and have raised blood glucose
due to reduced insulin production),
CT scan 
abdominal ultrasound 
abdominal x-ray.
51
Q

Management for chronic pancreatitis?

A

More conservative than acute, involving alcohol and smoking
cessation with lifestyle modifications.
Frequent review of pain management with paracetamol,
tramadol and potentially octreotide (somatostatin analogue).
Dietary modifications are advised,
with potential for enteral feeding to reduce stimulation of pancreatic enzyme activity.
Pancreatic enzymes may be given as a supplement with PPIs to improve fat absorption.

52
Q

Why would we take away ramipril in a GI bleed?

A

Ramipril is a ace inhibitor so it will reduce blood pressure more which we don’t want as BP is already low due to the bleed.

53
Q

Can simvastatin and clarithromycin be prescribed together?

A

Significant interaction between Simvastatin and Clarithromycin as CM is a strong inhibitor of CP450 whereas sinvastatin needs it to metabolise.

Stop simvastatin during the course of the antibiotic.

Risk of side effects such as liver damage and a rare but serious condition called rhabdomyolysis

54
Q

What kind of diarrhoea is seen with a campylobacter infection?

A

Bloody stools

Abdominal pain

55
Q

When is diarrhoea caused by C diff seen?

A

Typically follows hospital stay or use of antibiotics

Profuse diarrhoea

56
Q

When is diarrhoea caused by E Coli seen?

A

Usually in travelers

Stomach cramps and nausea

57
Q

Symptoms of systemic sclerosis:

A

CREST syndrome - calcinosis, Raynaud’s phenomenon, esophageal dysmotility, sclerodactyly, and telangiectasia

Lower oesophageal sphincter pressure is reduced, unlike achalasia

58
Q

What is the treatment for achalasia:

A

Treatment: endoscopic balloon dilatation, cardiomyotomy, verapamil or nitrates used. Injection of Botulinum toxin A can be given to paralyse smooth muscle. Gastrostomy (last resort)

59
Q

Investigations when suspecting achalasia

A

manometry: excessive LOS tone which doesn’t relax on swallowing - considered most important diagnostic test
barium swallow shows grossly expanded oesophagus, fluid level, ‘bird’s beak’ appearance
CXR: wide mediastinum, fluid level

60
Q

What is the best investigation to assess for mural invasion with an oesophageal stricture?

A

Endoscopic ultrasound

61
Q

A combination or liver and neurological disease will point towards which diagnosis?

How to reveal diagnosis?

A

Wilson’s disease

Copper studies

62
Q

What does H pylori REDUCE the risk of?

A

Barrett’s oesophagus

63
Q

Causes of hypercalcaemia

A
  1. Hyperparathyroidism
  2. Drugs - thiazides, Vit D analogues
  3. Cancer - osteoclastic, PTH, metastasis
  4. Granulomatous - sarcoidosis, TB
  5. Familial
  6. Endorcrine - addison’s, thyrotoxicosis
  7. CKD
64
Q

H pylori can increase risk of what haematological malignancy?

A

Gastric lymphoma (MALT)

65
Q

What test is the best method for checking H pylori eradication?

A

Urea breath test

66
Q

Urea breath test should not be performed within how many with of PPI or antibiotic treatment?

A

4 weeks

GI (10 decks)

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