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MBBS - Year 3 > The Digestive System - Upper GI > Flashcards

The Digestive System - Upper GI Flashcards

1
Q

Foregut

A

Mouth to 2nd part of duodenum

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2
Q

Midgut

A

2nd part of duodenum to distal 1/3 of transverse colon

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3
Q

Hindgut

A

Distal 1/3rd of transverse colon to halfway down anal canal

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4
Q

Radiological modalities used in upper GI

A

Endoscopy*
Fluroscopy - barium swallow
CT
Nuclear med
Angiography
Plain radiographs
MRI

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5
Q

Parts of the stomach

A

Cardia
Fundus
Lesser curve
Greater curve
Incisura angularis
Antrum
Pyloris
Rugae

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6
Q

Hiatus hernia

A

Abnormal bulging of a portion of the stomach through the diaphragm

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7
Q

Achalasia

A

Failure of lower oesophageal sphincter to open in response to swallowing

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8
Q

Odynophagia

A

Painful swallow w/ or w/out difficulty

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9
Q

Indications for plain film

A

Dental/ trauma/ TMJ
Foreign body
Obstruction
Suspected perforation
Calculi?

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10
Q

Indications for contrast swallow/ meal

A

Dysphagia and normal endoscopy
Not fit for endoscopy
Assess pharyngeal pouch
Clarify endoscopic findings
Perforation/ leak esp post-oesophagectomy

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11
Q

Indication for CT

A

Staging malignancy
Surgical abdomen
Clarify anatomy e.g. extrinsic compression
Trauma
Unexplained sx

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12
Q

Examples of gastric secretions

A

Gastric (hydrochloric) acid
Pepsinogen
Intrinsic factor
Gastrin
Leptin
Ghrelin
Somatostatin
Histamine

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13
Q

What does the body of the stomach secrete

A

Mucus
Pepsinogen
HCl

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14
Q

What does the antrum secrete

A

Mucus
Pepsinogen
Gastrin

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15
Q

What is secreted by parietal cells

A

Acid
IF

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16
Q

What is secreted by Chief cells

A

Pepsinogen
Leptin

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17
Q

Which stomach cell secretes histamine

A

Enterochromaffin-like cell (ECL)

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18
Q

Which cell secretes gastrin

A

G- cell

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19
Q

Which cell secretes somatostatin

A

D-cell

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20
Q

Specific stomach cells

A

Parietal cell
Chief cell
ECL cell
G-cell
D-cell
Epithelial cell
Progenitor cell

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21
Q

Conventional phases of gastric secretion

A

Cephalic - stimulation
Gastric - stimulation
Intestinal - initial stimulation, later inhibition

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22
Q

Overall integrators of cephalic phase of gastric secretion

A

Vagus nerve

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23
Q

Overall integrators of gastric phase of gastric secretion

A

Neural - long vagus nerve
Gastrin

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24
Q

Overall integrators of intestinal phase of gastric secretion

A

Hormones - gastrin, enteric inhibitors (enterogastrones)

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25
Q

What type of hormone is gastrin

A

Peptide

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26
Q

Types of gastrin

A

G-17 in gastric antrum
G17 and G-34 in duodenum

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27
Q

What is gastrin

A

Main physiological stimulant of gastric acid secretion

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28
Q

What can gastrin be directly stimulated by

A

Ca2+
Amines

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29
Q

When is gastrin release inhibited

A

pH <3 (-ve feedback)
Too much acid, turns off antral G cell
Less gastrin produced
Less HCl produced

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30
Q

Examples of spp gastric receptors

A

CCK2
CCKB

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31
Q

Main stimulants of acid secretion

A

ACh
Gastrin
Histamine
Activation of multiple pathways is synergistic

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32
Q

Where is ACh released from

A

Vagus nerve

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33
Q

Role of ACh in acid secretion

A

Stimulates release of gastrin and histamine
Directly activates parietal cell
Binds to muscarinic M3 receptor - elevates Ca2+

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34
Q

Role of gastrin in acid secretion

A

Stimulates histamine release
Directly stimulates parietal cells
Binds to CCK2 receptor - stimulates Ca2+

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35
Q

Role of histamine in acid secretion

A

Directly stimulates parietal cell
Binds to histamine H2 receptors - stimulates cAMP

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36
Q

Main inhibitors of acid secretion

A

Somatostatin
PGE2

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37
Q

Role of somatostatin in inhibition of acid secretion

A

Inhibits gastrin and histamine secretion
Inhibits parietal cell directly

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38
Q

Role of PGE2 in inhibition of acid secretion

A

Inhibits parietal cell directly

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39
Q

Gastrin effects on ECL cells

A

A/c - histamine release
Intermediate - histamine synthesis
C/c - hyperplasia of ECL cells

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40
Q

Parietal-ECL-D cell unit

A

Functional cellular unit of acid secretion

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41
Q

Where is the parietal-ECL-D cell unit located

A

Gastric body

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42
Q

Activation by the parietal-ECL-D cell unit

A

Direct activation of parietal cell
Indirect activation by ECL-cell secreted histamine

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43
Q

Inhibition of parietal-ECL-D cell unit

A

Paracrine inhibition by somatostatin

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44
Q

How does somatostatin secretion restrain gastrin

A

Immunoneutralisation
Receptor inhibition

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45
Q

At which pH does somatostatin secretion decline

A

pH >3

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46
Q

How can diseases w/ abnormal acid secretion be classified

A

Infl +/- atrophy of the gastric body e.g. AI gastritis, H. pylori gastritis
Iatrogenic..g drugs, vagotomy

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47
Q

Vagotomy

A

Surgical procedure to remove part of vagus nerve, typically to reduce rate of gastric secretion

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48
Q

What are diseases w/ too little acid secretion associated w/

A

Infectious diarrhoea
Gastric adenocarcinoma

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49
Q

Which spinal levels does the oesphagus run from

A

C5/6 to T10

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50
Q

Important muscles in the oesophagus

A

Cricopharyngeal/ upper oesophageal sphincter
Oesophagus
Lower oesophageal sphincter

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51
Q

Role of cricopharyngeus

A

Part of swallowing and preventing aspiration

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52
Q

Control of sphincters in oesophagus

A

Voluntary control - cricopharynxgeus
Involuntary - lower oesophageal sphincter

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53
Q

Layers of oepshageal wall

A

Mucosa
Submucosa
Muscualris - circular layer and longtudinal layer
Adventitia

NO serosa, unlike rest of intestinal tract

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54
Q

What is muscularis in the oesophagus involved in

A

Peristalsis

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55
Q

Role of squamous mucosa in oesophagus

A

Barrier, protective effect

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56
Q

Circular vs longitudinal layer in muscularis

A

Circular muscle - contraction cause an increase in luminal pressure
Longitudinal muscle - contraction causes shortening

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57
Q

Control of muscle in oeophagus

A

Largely under parasympathetic control via vagus nerve

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58
Q

How does food travel down the oesphagus

A

As soon as food is past the cricopharyngeus its squeezed into a bolus and pushed down via peristalsis
Bolus pushed down in wave to LOS
LOS must relax to allow food into stomach then contract to prevent food coming up

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59
Q

Definition of peristalsis

A

Coordinated contraction and relaxation of muscles in oesphagus

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60
Q

Components of lower oesophageal sphincter components

A

These must all work together, neither on their own is effective
Internal - circular oepshageal muscle fibres, sling like oblique gastric muscle fibres
External - diaphragmatic crura
Angulation - angle of his between fundus and oesophagus

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61
Q

LOS function after swallowing

A

Inhibitory signals generated by peristalsis cause a reflex relaxation of the LOS for ~5secs
The diaphragmatic crura also relax

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62
Q

Transient LOS relaxation

A

TLESR
Gastric distension causes both the LOS and diaphragmatic crura to relax, allowing release of excess gas (burping)

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63
Q

Foods that increase LOS pressure

A

Protein
Carbs
(Refluxed) acids

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64
Q

Foods that decrease LOS pressure

A

Chocolate
Fat
Caffeine
Citrus
Garlic
Tomato

Decreased pressure causes acid reflux

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65
Q

Drugs that increase LOS pressure

A

Alpha-agoints
Beta-blockers
Cholinergics
Metoclopramide
Domperidone

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66
Q

Drugs that decrease LOS pressure

A

Alcohol
Anticholinergics
Beta-agonits
Calcium channel blockers
Dopamine (D2 receptors)
Nicotine
Nitrates
TCAs

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67
Q

Stomach as a provider of storage capacity

A

Small amounts can be fed into small intestine where it is broken down more efficiently
Pylorus opens 3x/min to allow small amounts through

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68
Q

How is the grinding motion of the stomach caused

A

By 3 muscle layers: longitudinal, circular & oblique causes food to be broken down physically

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69
Q

Function of stomach rugae

A

Make acid
These folds increase SA of stomach

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70
Q

Where is stomach rugae found

A

Body of stomach, not antrum

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71
Q

Processes involved in gastric acid secretion

A

Neural
Endocrine (gastrin)
Paracrine (histamine and SST)

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72
Q

Which cells are found in the gastric body

A

Parietal cell
ECL cell

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73
Q

Examples of diseases w/ too much acid

A

Zollinger-Ellison syndrome

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74
Q

What substances does the gastric gland secrete

A

Gastric acid
Proteolytic pepsin(ogen)

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75
Q

When does pepsinogen –> pepsin

A

Once pepsinogen meets an acidic environment

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76
Q

Why is the canalicular membrane of the PC partially internalised

A

Increase SA for secretion

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77
Q

Where do the contents of PC secretions go

A

Into canaliculi –> gastric gland –> lumen

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78
Q

Features of proton pump in canalicular membrane

A

Active pump - pumps H+ OUT and K+ IN PC
Requires a lot of ATP
Cl- diffuse across membrane and combines w/ H+ to form HCl

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79
Q

Stimulation of protein pump

A

3 receptors on basolateral membrane of PC - one ACh, one histamine (H2) and one gastrin
ACh is neurotransitter - stimulates proton pump
Gastrin travels in blood (endocrine effect)
Histamine travels directly to PC (paracrine effect)

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80
Q

Cephalic phase of acid secretion

A

Thought, taste, smell, sight, swallowing
Vagus nerve sends signal to stomach to prepare for food
Done through release of ACh

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81
Q

What is gastrin secreted in response to

A

Gastric distention - stomach stretched by a meal
AA/ peptides - foods high in this increase gastric production
Low acidity (i.e buffering by food)

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82
Q

Feedback loop in gastric phase of gastric acid secretion

A

Low acidity causes astral G cell to make gastrin
PC produces acid
High acidity switches on D cell to create SST
Switches OFF antral G cell

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83
Q

Intestinal phase of gastric acid secretion

A

Least important (5-10%)
Stimulation via duodenal distension (neural) and chyme (gastrin)
Inhibition via enetroendocrine cells secreting various gastric inhibitory peptides

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84
Q

In which fashion does SST work

A

Paracrine

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85
Q

Main gastric acid treatment

A

Antacids - simplest way (neutralise)
Surgery
Anti-secretory drugs

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86
Q

Surgery to help with gastric acid treatment

A

Vagotomy - inhibits cephalic phase
Antrectomy - inhibits gastric phase

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87
Q

Main anti-secretory drugs used in gastric acid treatment

A

Anticholinergics
H2 receptor antagonise
PPIs
Potassium- competitive acid blockers

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88
Q

Pyloric stenosis

A

Narrowing of the pylorus leading to intestinal obstruction in infants
Usually 2-8 weeks

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89
Q

Cause of pyloric stenosis

A

Hypertrophy and hyperplasia of pylorus
Mechanical obstruction to outflow of gastric contents into duodenum

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90
Q

Px of pyloric stenosis

A

Non-bilious vomiting
Regurg

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91
Q

O/E seen in pyloric stenosis

A

Visible peristalsis
Palapable mass after feeding in RUQ/ epigastrium

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92
Q

How is diagnosis of pyloric stenosis made

A

Abdominal ultrasound

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93
Q

Mx of pyloric stenosis

A

Appropriate fluid rests and correction of electrolyte abnormalities
Ramstedt pyloromyotomy

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94
Q

Pyloromyotomy

A

Open procedure that involves cutting thickened muscle to release stenosis

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95
Q

Complications of pyloromytomy

A

Mucosal perforation
Haematoma
Wound infection

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96
Q

Risk factors for pyloric stenosis

A

Fhx
Maternal smoking
Bottle feeding
Macrolide use in first 2/52 of life?

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97
Q

Causes of acquired pyloric stenosis

A

Ulcer
Antral tumour
Pancreatic tumour (head)

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98
Q

Causes of a/c gastritis

A

Irritants
Drugs
Severe stress
Radiation
Chemo

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99
Q

Irritants as a cause of a/c gastritis

A

Smoking
Alcohol

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100
Q

Drugs as a cause of a/c gastritis

A

Aspirin
NSAIDs
Oral steroids

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101
Q

Severe stress as a cause of a/c gastritis

A

Burns
Trauma
Surgery
Shock
Sepsis

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102
Q

Complications of a/c gastritis

A

Erosions
A/c stress ulcers

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103
Q

Erosions as a result of a/c gastritis

A

Small ulcers in which depth is limited to Lamina propria
Tend to bleed

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104
Q

A/c stress ulcers as a complication of a/c gastritis

A

Penetrate muscular mucosa
Particularly associated w/ stress - Curling’s ulcers and Cushing’s ulcers
Associated w/ drinking and smoking
Tend to bleed

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105
Q

Curling ulcer’s

A

Occurs following severe burns
Reduced plasma volume –> iscahemia and necrosis of stomach

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106
Q

Cushing ulcers

A

Occur secondary to raised ICP e.g. intracranial tumour, trauma etc

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107
Q

HP associated c/c gastritis

A

Spirochetes found at surface of gastric epithelium causing infl
C/c infl is host immune repose to HP but improves after eradication of bacteria

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108
Q

What is HP associated gastritis associated w/

A

DU
GU
Gastric MALT lymphoma and cancer

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109
Q

Features of chemical/ relative c/c gastritis

A

Due to bile reflux
Usually HP -ve
Hx is important
Reactive change in surface epithelium w/out significant a/c infl

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110
Q

Features of AI c/c gastritis

A

AI destruction of specialised glands of the body mucosa
Autoantibodies to IF and PCs
HP rare
A/c and c/c infl of body mucosa
Dysplasia –> increased risk of cancer

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111
Q

What can loss of PCs in AI gastritis cause

A

Achlorhydria

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112
Q

Achlorhydria

A

Loss of HCl in stomach

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Perfectly
113
Q

What can loss of IF in AI gastritis lead to

A

B12 deficiency and pernicious anaemia

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114
Q

Natural protective factors against ulcers

A

Surface ,luscious secretion
Bicarb secretion into mucous
Mucosal blood flow
Epithelial barrier function
Epithelial regenerative capacity

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115
Q

Examples of injury to mucosa that can cause peptic ulcers

A

HP infection
NSAID
tobacco
Alcohol
Gastric hyperacidity
Duodenal-gastric reflux
Ischaemia
NSAIDs

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116
Q

Peptic ulcer disease

A

Umbrella term for development of gastric ulcers and duodenal ulcers

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117
Q

Epidemiology of gastric ulcers

A

Incidence increases w/ age
Gender distribution is closer to equal (1:1 to 2:1)

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118
Q

Epidemiology of duodenal ulcers

A

Mean ages 30-40
M > F 4:1

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119
Q

A/c stress ulcers vs c/c peptic ulcers - penetration

A

A/c doesn’t penetrate musuclaris propria
C/c does

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120
Q

A/c stress ulcers vs c/c peptic ulcers - scarring

A

A/c has no scarring ulder ulcer
C/c does

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121
Q

A/c stress ulcers vs c/c peptic ulcers - endarteritis obliterates

A

A/c has no endarteritis obliterans
C/c does

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122
Q

Endarteritis obliterans

A

Infl of intimacy which proliferates and ultimately plugs lumen of artery

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123
Q

A/c stress ulcers vs c/c peptic ulcers - healing

A

A/c heals w/ regeneration
C/c heals by repair w/ fibrous scar

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124
Q

A/c stress ulcers vs c/c peptic ulcers - number & location

A

A/c is multiple and can be anywhere
C/c is single and usually antral

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125
Q

Aetiology of peptic ulcer disease

A

H. pyloric* - 95% of DU and 75% of GU
Medication
Zollinger-Ellison
A/c stress
Malignancy
Infl e..g Crohn’s

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126
Q

Medication causing peptic ulcer disease

A

NSAIDS*
Corticosteroids
Alcohol

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127
Q

Symptoms of peptic ulcer disease

A

Epigastric pain
Dyspepsia (e.g. distension, bloating)
Heartburn

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128
Q

Signs of peptic ulcer disease

A

Mild epigastric tenderness

129
Q

DU vs GU - pathophys

A

DU - high acid eroding a normal mucous membrane
GU - low or normal acid eroding mucous membrane w/ reduced resistance

130
Q

DU vs GU - pain

A

DU - ulcer pain relived by eating
GU - ulcer pain worsens by eating

131
Q

DU vs GU - genetic factors

A

DU - important genetic component
GU - no genetic component

132
Q

How is dx of peptic ulcer disease made

A

Endoscopic examination

133
Q

Genetic factors in c/c DUs

A

2x increase in 1st deg relatives
37% increase in blood group O
HLA B5

134
Q

DU disease associations

A

H pylori c/c gastritis
Hyperparathyroidism (increased serum Ca stimulates gastric –> acid ++)
Alcoholic cirrhosis
C/c renal failure

135
Q

Where do DUs typically px

A

90% in 1st part
Ant > post

136
Q

Where do GUs typically px

A

Lesser curve, antrum/ upper body

137
Q

What does heaping up of a peptic ulcer suggest

A

Malignancy

138
Q

Histology of peptic ulcers - 4 zones

A

Surface layer of necrotic debris
Cellular infl layer rich in neutrophll polymorphs
Granulation tissue layer
Layer of fibrosis - vessel walls in this zone

139
Q

H. pylori testing

A

Invasive - urease test (CLO), histology, culture
Non-invasive - breath test, serological test, stool antigen test

140
Q

HP breath test

A

Pts must be off PPIs
Can be used for both dx and testing for eradication

141
Q

Mx of PUD

A

Lifestyle modification
Abx
PPIs

142
Q

Lifestyle modifcation for PUD

A

Avoid triggers
Obesity
Smoking and alcohol

143
Q

Treating PUD associated w/ HP

A

No association w/ NSAIDs - 1st line eradication
Association w/ NSAIDS - 2/12 full dose PPIs then 1st line eradication

144
Q

Treating PUD w/ no association to HP

A

4-8 wk full dose PPIs

145
Q

Follow up in PUD

A

Gastric ulcers require bx in 6-8 weeks due to possibility of malignancy

146
Q

1st line eradication of HP

A

7/7 course of PPIs, amoxicillin, clarithromycin if no penicillin allergy
If penicllin allergy - PPIs, clarithromycin, metronidazole

147
Q

Complications of PUD

A

Penetration
Perforation
Haemorrhage
Gastric outlet obstruction (pyloric stenosis)

148
Q

Perforation as a complication of PUD

A

Pts px w/ signs of infection and severe abdominal pain
Mx is supportive care, abx and laparoscopic repair

149
Q

Possible perforation zone in PUD

A

Posterior ulcers —> pancreas
Anterior DU –> peritoneal cavity
GU in lesser curve —> lesser sac
Less common is common bile duct and transverse colon

150
Q

Haemorrhage as a complication of PUD

A

Can cause UGIB
Typically posterior DU eroding into gasproduodenal artery
Bleeding can be mild and c/c infl –> IDA

151
Q

Gastric outlet obstruction as a compciaton of PUD

A

Pts px w/ nausea and vomiting, abdominal pain and distension

152
Q

Zollinger Ellison syndorme

A

Occurs secondary to increased gastrin secretion by hyper-secreting gastrinoma in pancreas

153
Q

Features of ZE syndrome

A

Recurrent DUs - multiple ad in atypicla sites
1/3 have diarrhoea due to increased gastric acid
Ulceration/ eriosn of stomach rare

154
Q

ZE syndrome and MEN

A

1/3 of gastronomes in ZE are associated w/ MEN/ Werner’s synd
Gene located on chromosome 11
Hyperplasia/ neoplasia of 1+ endocrine gland
50% of pts w/ MEN have ZES

155
Q

MEN

A

Multiple endocrine neoplasia

156
Q

Examples of primary gastric neoplasia

A

Adenocarcinomas
Malignant gastrointestinal stromal
Lymphoma (MALT lymphomas associated w/ HP may resolve w/ HP eradication)

157
Q

Polyp

A

Any lesion raised above mucosa

158
Q

Epidemiology of gastric adenocarcinomas

A

4th most common malignancy
Age - 50+
Sex - M > F 2:1
Geography - Japan/ Central & S america

159
Q

Anatomical classification of gastric adenocarcinoma

A

Epicentre of the tumour <2cm from the GOJ - oespheageal
Epicentre of the tumour >2cm from the GOJ - gastric

160
Q

Histological classification of gastric cancer

A

Intestinal - most common, gland-forming
Diffuse - less common, formed of discohesive cells

161
Q

Intestinal gastric cancer features

A

More commonly seen in males
Affects older ages
Better prognosis

162
Q

Diffuse gastric cancer features

A

Equal sex prevalence
Seen in younger pts
Worse prognosis

If involves major portion of stomach may be referred to as ‘linitus plastica’ - leather bottle stomcah
Stomach unable to inflate properly

163
Q

Genetic predisposing factors for gastric adenocarcinomas

A

Fhx
Increased risk w/ blood group A

164
Q

Predisposing factors for gastric adenocarcinomas - diet

A

Carcinogens
Polycyclic hydrocarbons in smoked food
Increased starch - decreased fat, fresh fruit, green, leafy veg

165
Q

Predisposing factors for gastric adenocarcinomas - premalignant condns

A

Pernicious anaemia
Operated stomach
Atrophic gastritis (dysplasia)
Adenomas (dysplasia)

166
Q

Gastric cancer types

A

Type 1 - polypoid
Type 2 - fungating
Type 3 - ulcerated
Type 4 - infiltrative

167
Q

What % of gastric malignancies is made up by gastric lymphoma

A

15%
Commonest site of GIT lymphoma

168
Q

Causes of a/c epigastric pain

A

A/c pancreatitis
Perforated peptic ulcer
Peptic ulcer
A/c cholecystitis
Biliary colic
Mesenteric vascular disease
Perihepatitis
Supradiaphragmatic

169
Q

Causes of dyspepsia

A

Functional
GORD
Pepetic ulcer
Oesophageal cancer
Gastric cancer
Other causes incl colon cancer, c /c pancreatitis, pancreatic cancer etc

170
Q

Associated features of dyspepsia that may help w/ dx

A

Dysphagia
Wt loss
Physical signs
Anaemia/ thrombocytois

171
Q

Assumptions based on risk factors for dyspepsia

A

Young pts w/out dysphagia, NSAIDs or H.pylori are v unlikely to have organic pathology
Young pts w/ NSAIDs or HP MIGHT have PUD
Older pts (esp w/ alarm sx) are at higher risk of cancer

172
Q

Investigations for dyspepsia

A

Endoscopy
Barium swallow/ meal
H. pylori tests
Oesophageal pH/ pH-impedance
Anti-tag Ab/ Ig
Gastric emptying

173
Q

Pain modulators given for dyspepsia

A

Amitriptyline
Mirtazipin
Buspirone

174
Q

Mx of GORD

A

Lifestyle measures
Lowest dose required to control sx - PPI/ H2RA/ antacid (except Barrett’s)
Surgical intervention

175
Q

Surgical intervention for GORD

A

Laparoscopic fundoplication
Magnetic sphincter augmentation
(Bariatric surgery: Roux-en-Y)

176
Q

Other terms for functional dyspepsia

A

Post-prandial distress syndrome
Epigastric pain syndrome

177
Q

Rx for functional dyspepsia

A

HP eradication
PPI
Prokinetics
Amitriptyline/ imipramine
Buspirone
Mirtazipine
Sulpiride
Behavioural intevrenyions e.g. diaphragmatic breathing, psych rx

178
Q

Theoretical ways to reduce acid secretion

A

H2 antagonist
Gastrin antagonist - none clinically available
Muscarinic antagonist - atropine, pirenzepine
Block H+ secretion - PPIs
Inhibits PC secretion physiologically - misoprostol, SST
Neutrralisation - antacids

179
Q

Onset of antacids

A

Rapid but transient

180
Q

What can large, regular doses of antacids heal

A

Duodenal ulcers

181
Q

What do antacids provide symptomatic relief for

A

GORD
Indigestion

182
Q

What are examples of compounds found in antacids

A

Mg, Ca, Na or Al
Al –> constipation
Mg —> diarrhoea

183
Q

Adverse effects of antacids

A

Systemic alkalosis in v high doses
Carbonate containing compounds release CO2 –> belching

184
Q

Adverse effects of antacids - Al

A

Osteodystrophy and encephalopathy in c/c renal failure
Al chelates tetracyclines and levodopa

185
Q

Adverse effects of antacids - Ca

A

Calcium stimulates gastrin –> counterproductive

186
Q

Examples of H2 receptor antagonists

A

Cimetidine
Ranitidine
Nizatidine
Famotidine

187
Q

Where do H2RAs act

A

PCs
Cardiac atria

188
Q

Actions of H2RAs

A

Reduce basal and stimulated acid secretion
Reduce pepsin secretion by about 60%

189
Q

What is the rate of peptic ulcer healing dependent on

A

Degree of acid suppression

190
Q

Time frame for healing ulcers using H2RAs

A

DU: 4/52 - 6-52
GU: 6/52 - 8/52

191
Q

H2RAs for GORD

A

Provides symptomatic relief
Healing requires much higher doses

192
Q

Metabolism of H2RAs

A

Cimetidine and ranitidine rapidly absorbed
Short half lives
Cimetidine excreted renally but other renal and liver

193
Q

Adverse effects of H2RAs - uncommon

A

Diarrhoea
Headache
Confusion in elderly
Cimetidine - anti androgen (gynaecomastia)
Cimetidine - inhibits P450 (enhances warfarin, theophylline, tolbutamide)

194
Q

Examples of PPIs

A

Omeprazole
Lansoprazole
Rabeprazole
Esomeprazole

195
Q

Actions of PPIs

A

Inhibits acid secretion by 90%
Covalently inhibit PP
Some PPIs may inhibit clopidogrel activation

196
Q

Metabolism of PPIs

A

All via P450 system
Mild inhibition of P450 isoforms

197
Q

Adverse effects of PPIs

A

Diarrhoea
Headache
Infectious gastroenteritis
Hypergastrinaemia and acid rebound
Impaired Ca and Mg - osteoporotic fractures

198
Q

Adverse effects of PPIs

A

Diarrhoea
Headache
Infectious gastroenteritis
Hypergastrinaemia and acid rebound
Impaired Ca and Mg - osteoporotic fractures

199
Q

Why is infectious gastroenteritis an adverse effect of PPIs

A

Reduces bacterial killing

200
Q

Why is diarrhoea an adverse effect of PPIs

A

Idiosyncratic
Bacteria overgrowth Microscopic colitis

201
Q

Uses of acid suppression

A

GORD
Prevention of NSAID-induced peptic ulcer
Helaing of peptic ulcer
HP eradication
Stress ulcer and aspiration prevention

202
Q

Indications for parenteral therapy for acid suppression

A

Prevntion of aspiration during anaesthesia
Stress ulcer prophylaxis in certain critical ill pts
Peptic disease and inability to take oral ex for 5/7
Post-endoscopic rx in selected GI haemorrhage pts
Non-responsive ZE syndrome

203
Q

Alarm features of dyspepsia

A

Anorexia
Loss of weight
Anaemia
Recurent vomiting
Dysphagia

204
Q

Acid suppression in peptic ulcer

A

Remove etiological factors
Use PPIs to help prevent
Maintenance high doses fr ZES

205
Q

Cytoprotective agents used in GIT

A

Misoprostol
Sucralafte
Bismuth

206
Q

Misoprostal as ‘gastroprotection’

A

PGE1 analogue
Inhibits acid secretion
Increases duodenal bicarb secretion, gastric mucous production, mucosal blood flow

207
Q

Misoprotsol features

A

Heals peptic ulcers
Reduces NSAID-induced ulcers AND complications
Rapidly absorbed from gut - extensive 1st pass metabolism

208
Q

Adverse features of misoprostol

A

Diarrhoea - 30%
Uterine contractions - avoid in pregnancy and young women
Menorrhagia and pots-menopausal bleeding

209
Q

Features of sucralfate

A

Coats ulcer base
Increases prostaglandins secretion
Prevents diffusion of acid

210
Q

What can sucralfate be used to prevent

A

Sclerotherapy-induced oesophageal ulcers
Stress ulceration in critically ill pts

211
Q

Features of bismuth

A

Bind to base of ulcers
Enhances locals protective mechanism
Anti H pylori action

212
Q

Adverse effects of bismuth

A

Black stool
Black tongue
Can produce encephalopathy in renal failure

213
Q

Adverse effects of sucralfate

A

Constipation

214
Q

Bismuth uses

A

Commonly used in 2nd and 3rd line HP eradication regimens
Widely used OTC - pepto-bismol, indigestion, diarrhoea

215
Q

Barrett’s oesphagus

A

Normal distal oesophageal squamous epithelial lining replaced w/ metaplastic columnar epithelium

216
Q

Transformation to cancer from Barrett’s

A

Non dysplasie Barrett’s oesophagus
Low-grade dysplasia
High grade dysplasia
Oesophageal adenocarcinoma

217
Q

Clinical px of oesophageal cancer - alarm sx

A

Progressive dysphagia
Change to liquid diet
Wt loss
Regurg
Persistent reflux NOT responding to PPI
Others e.g.g food bolus obstruction

218
Q

Dx of oesophageal cancer

A

Upper GI endoscopy and biopsies is the ix of choice
Mucosal visualisation
Biopsies x8
Other modalities incl CT and barium swallow (obsolete)

219
Q

Barium swallow to dx oesophagela cancer

A

Only for v frail pts who ca tolerate OGD

220
Q

OGD

A

Oesophagogastro dudodenoscopy

221
Q

Staging pathways for oesophageal carcinoma

A

Staging is assessment of the extent of disease of a cancer
CT and PET scan to excl distant mets
Other specialised tests e.g. endosocpic ultrasound

222
Q

Treatment pathways for oeosphageal carcionma

A

Curative treatment = chemo +/- surgery
Palliative treatment = chemo +/- stent

223
Q

Ideal curative pathway for oesophageal xcarcinoma

A

3 cycles of chemo - eradicate systemic disease, prevent disease progression
surgery
Adjuvant chemo = 3 further cycles (75% doses)

224
Q

Surgery for oesophageal cancer

A

Ivor Lewis oesophagectomy
Oesophagus joined to stomach

225
Q

How may gastric cancer px as

A

IDA
Early satiety
Wt loss
Abdominal pain/ mass
Reflux
Non-healing gastric ulcer

225
Q

How may gastric cancer px as

A

IDA
Early satiety
Wt loss
Abdominal pain/ mass
Reflux
Non-healing gastric ulcer

226
Q

How can gastric cancer px as an emergency

A

Haematemesis/ melaena
Gastric outlet obstruction
Perofrated gastric ulcer
Disseminated disease e.g. ascites

227
Q

Treatment for gastric cancer

A

Endoscopy
Biopsies/ histology
Urgent CT san (chest/ abdo/ pelvis)
Book for oesophagogastric MDT
Inform pt - need CNS
Discuss in MDT
Decide if curative or pallitive

228
Q

Curative intent for gastric cancer

A

Period chemo then gastrectomy
Straight to gastrectomy (age > 80, co-morbidities ++)

229
Q

Palliative intent for gatsric cnacer

A

Palliative care
Stents e..g pyloric stent for obstruction
Best supportive care
Drain e.g. ascites etc
Palliative chemo +/- Herceptin

230
Q

Total gastrectomy for proximal cancer

A

Oesphagus joined to jejunum
Functionally v debilitating
Causes wt loss and nutritional deficiencies
NEVER as a palliative option

231
Q

Obesity stigma

A

Highly stigmatised disease
Amongst the public, medical professionals, and healthcare commissioners
Obesity is ‘self-inflicted’

232
Q

Consequences of pts’ experiences of obesity

A

Depression gets worse
Anxiety
Suicidal thoughts
Disordered eating
Decreased self esteem
Avoidance of physical activity
Shaming themselves
Decreased QoL

233
Q

Obesity - surgery vs non-surgical

A

Surgery produces sustained wt loss
Ultimately, improved long-erm survival compared to those w/out surgery

234
Q

Effects of bariatric surgery

A

Acts through restrictive or malabsprptive effect
Acting centrally within the hypothalamus to control appetite , hunger and satiety
Gut hormonal changes
Alterations in bile acids

235
Q

Bariatric MDT

A

Core members incl
Obesity physician
Specialist surgeon
Dietitian
Psychologist
Anaesthetists

236
Q

Tired structure of obesity mx in the NHS

A

Tier 1 - universal interventions
Tier 2 - lifestyle interventions, diets, pharmacology
Tier 3 - specialist services
Tier 4 - surgery

237
Q

Main bariatric surgery operations

A

Sleeve gastrectomy
Roux en Y bypass
Laparoscopic Adjustable Gastric Band (LAGB)

238
Q

Features of sleeve gastrectomy

A

One of the most common procedures
Majority of stomach excised
Faster, less technically demanding, fewer post-op complications

239
Q

In which pts is a sleeve gastrectomy contraindicate din

A

Pts who suffer from GORD

240
Q

Mechanism of sleeve gastrectomy

A

Produces neurohormonal changes in GLP-1 and PYY as well as reduced gherkin production due to removal of gastric fundus

241
Q

Features of Roux en Y gastric bypass

A

A loop of jejunum is brought up and anastomosed to the gastric pouch to form the Roux limb, allowing the passage of ingested food bypass the duodenum, preventing it form mixing w/ binary secretions
2nd anastomosis is created 100-120cm down Roux line, joining the biliary limb to allow mixing of food w/ bile within common channel

242
Q

Gastrojejunostomy

A

Anastomosis between stomach and jejunum

243
Q

Jejunojejunostomy

A

Anastomosis between two parts of jejunum

244
Q

Complications of Roux en Y bypass

A

Anastomotic leaks - can be life threatening
Internal herniation - can be life threatening

245
Q

What does a Roux en Y bypass allow for in the future

A

Access to gastric remnant for gastric cancer
Access to duodenum for ERCP

246
Q

Laparoscopic Adjustable Gastric Band

A

Gastric band placed over small portion of stomach and is attached to a port
The band can be adjusted by inserting fluid in a balloon around the band - this is controlled by the port

247
Q

Example of an bariatric emergency

A

Slipped band

248
Q

Sliped band as a bariatric emergency

A

Distal stomach herniates upward through the band, causing proximal pouch dilatation
Left untreated, this can result in ischaemia and necrosis

249
Q

Px of slipped gastric band

A

Upper abdominal or chest pain, dysphagia and regurg of all fluid

250
Q

Mx of slipped band

A

Urgent deflation of band
Can be deflated on the ward via an abdominal port w/ a Huber needle

251
Q

How may regurg px in children

A

FTT

252
Q

GORD

A

Gastro-oesophageal reflux disease
Reflux of stomach contents in oesophagus

253
Q

Pathophys of GORD

A

Lower Oesophageal Sphincter (LOS) relaxes inappropriately

254
Q

Risk factors for GORD

A

High BMI
Smoking
Genetic associations
Pregnancy
NSAIDs, alcohol

255
Q

Sx of GORD

A

Heartburn - postprandial and worse lying down
Chest pain
Regurg
Acid brash
Hoarse voice
Dysphagia

256
Q

Atypical sx of GORD

A

‘Laryngopharyngeal reflux’

Cough
Throat clearing
Dental issues

257
Q

Oesophageal syndromes of GORD

A

Reflux (erosive) oesophagitis
Reflux stricture
Barrett’s oesphagus
Oesophageal adenocarcinoma

258
Q

Things to ask in hx of GORD

A

Sensitivity to PPIs
How they are using PPIs
How do they sleep
Do they eat a heavy meal within few hrs of going to sleep

259
Q

Red flags for GORD - ALARM

A

Gastroscopy is required

Anaemia
Loss of wt
Anorexia
Refarctoru to med
Maelena & haemetesis
Swallowing difficulties
New onset dyspepsia (>55 yrs)

260
Q

Ddx of GORD

A

Functional heartburn
Achalasia (failed relaxation of LOS)
Eosinophilic oesophagitis
Cardiac causes of chest pain
Malignancy

261
Q

Ix in GORD

A

pH monitoring - when dx is uncertain. 24hr pH monitoring can be combined w/ high res manometry
Gastroscopy

262
Q

Manometry

A

Assesses motor abnormlaities of the oesophagus

263
Q

Gatsroscopy for GORD

A

Done for pts w/ red flag sx, suspected complications and being considered for surgery
Up to 50% of pts w/ GORD have normal gastroscopy

264
Q

Steps in mx of GORD

A

Lifestyle changes
Pharmacological treatment

265
Q

Conservative mx of GORD

A

Wt loss
Smoking cessation
Reducing stress
Reducing caffeine (lowers LOS pressure)
Elevating head of bed
Stop eating within 2hrs of bed

266
Q

Pharmacological mx of GORD

A

PPis (2/52 trial) - best for treating erosive disease
Ranitidine
Over counter meds e.g.g gaaviscon
Prokinetics e.g. domperidone
Baclofen
Amitriptyline

267
Q

Anti-reflux surgery

A

NIssen fundoplication - wrapping fundus around lower oesophagus
Constructs new anti-reflux barrier

268
Q

Who is anti-reflux surgery reserved for

A

Pts who fail to respond to medical tx
Pts who cannot tolerate med due to side effects
Pts who wish not to be on meds lifelong

269
Q

Endoscopic treatment for reflux

A

Stretta radio frequency
Endoscopic suturing
Endoscopic fundoplication

270
Q

Complications of GORD

A

Erosive oesophagitis
Stricture
Barrett’s oesophagus

271
Q

Erosive oesophagitis

A

Infl of oesophagus –> ulcers, bleeding, peptic stricture formation

272
Q

Stricture

A

Scarring and narrowing of oesophagus due to repeated damage

273
Q

Barrett’s oesophagus

A

Premalignant condn due to columnar metaplasia (seen in stomach) of the normal squamous mucosa of oesophagus

274
Q

Oral ulcers ‘stomatitis’

A

AKA apthous ulcers
Caused by HSV (aciclovir) or candida (fluconazole)

275
Q

Bacterial causes of pharyngitis

A

Strep tonsillitis (peritonsillar abscess)
Diphtheria
Vincent’s angina
Ludwig’s angina
Chlamydia
HIV

276
Q

Viral causes of pharyngitis

A

Common cold
Enteroviral pharyngitis
Herpangina
Infectious mononucleosis

277
Q

Epidemiology of diphtheria

A

Common disease in 19th century
10,00 death/ yrs
Seen in children < 5 (immunisation introduced in 1942)

278
Q

Dipheriae definition

A

URTI characterised by sore throat, low grade fever, adherent membrane of tonsils, pharynx, nose

279
Q

Causative organism of diphtheria

A

Corynebacterium diphtheria

280
Q

Local px of diphtheria

A

Tough pseudomembrane
Grey, semitransparent necrotic area
Pain, bleeding if scraped

281
Q

Systemic effect of diphtheria

A

Eraly, cardiac damage - myocraditis, heart failure, heart block
Late, neuro damage - demtylination, palate palsies
Late, nephritis

282
Q

Mx of diphtheria

A

Abx - benzylpenicillin, erythromycin
Antitoxin
Tracheostomy if oedema threatens airway
Prevention/ control - vaccine

283
Q

Causative organisms of oesphagitis

A

Candida
CMV
HSV
VZV

284
Q

Sx of oepshagitis

A

Difficulty swallowing
Odynophagia
Retrosternal discomfort
Anorexia
Fever

285
Q

Common risk factors for oesophagitis

A

Abx use - candida spp
AIDS - CMV, HSV, candida
Leukaemia, lymphoma - candida, HSV
Corticosteroids - candida

286
Q

Dx of oesphagitis

A

Flexible endoscopy, X-ray (barium)
Swab or brushings
Tissue bx (histology culture)

287
Q

Features of oesophageal candiasis

A

Typical white plaques, nodules
Causes severe odynophagia
Seen in pts w/ MM and HIV

288
Q

Features of Herpes simplex oesophagitis

A

Usually seen in immunocompromised pts
Numerous small ulcerations
Fever and odynophagia

289
Q

Treatment for herpes simplex oesophagitis

A

Candida spp - azoles (fluconozaole, intraconozole), amphotericin B
HSV, ZVZ - aciclovir, foscarnet if resistant to acyclovir
CMV - ganciclovir, foscarnet

290
Q

How can we prevent acid rebound in pts on PPIs

A

Step down before stopping

291
Q

Mx of achalasia

A

Botox injections/ dilation
CCBs
Nitrates

292
Q

Can you give omeprazole to patients on clopi

A

No

293
Q

Surveillance for Barrett’s oesophagus

A

Every 3-5 yrs

294
Q

Mx of high grade Barrett’s

A

Oesophagectomy

295
Q

Mx low grade Barrett’s

A

Ablation to encourage new normal cell growth

296
Q

Risk of oesophagectomy

A

Issues w/ aperistalsis and bloating
Worse when combined w/ fundoplication

297
Q

Side effects of PPIs

A

Nausea
Abdo pain
Rash
Dizziness
Constipation

298
Q

Types of dysphagia

A

Low vs high
Oropharyngeal - can’t initiate swallow
Oesophageal - blockage or irritation

299
Q

Key gastro ddx of difficulty swallowing

A

Adenocarcinoma
SCC
Pharyngeal pouch
Epiglottitis
Hiatus hernia
Rare - achalasia, corkscrew oesophagus

300
Q

Drugs as risk factor for GORD

A

Nitrates
CCBs
TCAs
Anticholinergics

301
Q

Presentation of gastritis

A

Dyspepsia
Anorexia
Nausea and vomiting
Haematemesis or maleana

Many cases resolve spontaneously

302
Q

Ix for gastritis

A

Endoscopy
Bx
H pylori test

303
Q

Risk factors for oesphageal cancer

A

Older age, M gender
GORD, Barrett’s
Smoking and chewing tobacco
Obesity and Poor diets
Alcohol
Previous head and neck cancer or RT

304
Q

Classification of oesophageal cancer

A

Adenocarcinomas tend to arise in distal third oesipahgus
SCC in upper or middle, more prevalent WW

305
Q

Clinical px of oesophageal cancer

A

Sx tend to arise when lumen < 2cm
Progressive, painless dysphagia
Dyspepisa, regurg - reistant to PPI
Lymphadenoathy
Mediastinal inasion - chest pain

306
Q

Ix for oesophageal cancer

A

Upper Gi endoscopy w/ 8 separate bx
Barium swallow for pts who can’t tolerate gastroscopy

307
Q

Hiatus hernia definition

A

Herniation of part of stomach through diaphragmatic oesophageal hiatus

308
Q

Risk factors for hiatus hernia

A

Older age
Male sex
Obesity
Increased intra-ab pressure

309
Q

Classification of HH

A

Type I - sliding
Type II to IV - para-oesophageal

310
Q

Type I HH

A

Displacement of GOJ above diaphragm
Usually asymptomatic

311
Q

Type II HH

A

Dislocation of fundus
GOJ unchanged

312
Q

Type III HH

A

Dislocatiom of BOTH HH and fundus
Most common para-oesophagela type

313
Q

Type IV HH

A

Presence of other organs within hernia sac
May lead to gastric volvulus

314
Q

Sx of HH

A

Mainly asymptomatic
Heartburn
Regurg
Dysphagia
Bowel sounds in L chest
If volvulus - post-pradial pain and distension

315
Q

Ix for HH

A

Usually incidental finding
Upper GI endoscopy >2cm separation form z-line
Barium swallow
CT may be used for gastric volvulus
CXR - small air fluid levels

316
Q

Mx of HH

A

Usually nothing
PPIs for symptomatic Type I

317
Q

Complications of HH

A

Gastric volvulus
Strangulated hernias
Uncontrolled bleeding
Gastric outlet obstruction

MBBS - Year 3 (9 decks)

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