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
What type of hormone is gastrin
Peptide
26
Types of gastrin
G-17 in gastric antrum G17 and G-34 in duodenum
27
What is gastrin
Main physiological stimulant of gastric acid secretion
28
What can gastrin be directly stimulated by
Ca2+ Amines
29
When is gastrin release inhibited
pH <3 (-ve feedback) Too much acid, turns off antral G cell Less gastrin produced Less HCl produced
30
Examples of spp gastric receptors
CCK2 CCKB
31
Main stimulants of acid secretion
ACh Gastrin Histamine Activation of multiple pathways is synergistic
32
Where is ACh released from
Vagus nerve
33
Role of ACh in acid secretion
Stimulates release of gastrin and histamine Directly activates parietal cell Binds to muscarinic M3 receptor - elevates Ca2+
34
Role of gastrin in acid secretion
Stimulates histamine release Directly stimulates parietal cells Binds to CCK2 receptor - stimulates Ca2+
35
Role of histamine in acid secretion
Directly stimulates parietal cell Binds to histamine H2 receptors - stimulates cAMP
36
Main inhibitors of acid secretion
Somatostatin PGE2
37
Role of somatostatin in inhibition of acid secretion
Inhibits gastrin and histamine secretion Inhibits parietal cell directly
38
Role of PGE2 in inhibition of acid secretion
Inhibits parietal cell directly
39
Gastrin effects on ECL cells
A/c - histamine release Intermediate - histamine synthesis C/c - hyperplasia of ECL cells
40
Parietal-ECL-D cell unit
Functional cellular unit of acid secretion
41
Where is the parietal-ECL-D cell unit located
Gastric body
42
Activation by the parietal-ECL-D cell unit
Direct activation of parietal cell Indirect activation by ECL-cell secreted histamine
43
Inhibition of parietal-ECL-D cell unit
Paracrine inhibition by somatostatin
44
How does somatostatin secretion restrain gastrin
Immunoneutralisation Receptor inhibition
45
At which pH does somatostatin secretion decline
pH >3
46
How can diseases w/ abnormal acid secretion be classified
Infl +/- atrophy of the gastric body e.g. AI gastritis, H. pylori gastritis Iatrogenic..g drugs, vagotomy
47
Vagotomy
Surgical procedure to remove part of vagus nerve, typically to reduce rate of gastric secretion
48
What are diseases w/ too little acid secretion associated w/
Infectious diarrhoea Gastric adenocarcinoma
49
Which spinal levels does the oesphagus run from
C5/6 to T10
50
Important muscles in the oesophagus
Cricopharyngeal/ upper oesophageal sphincter Oesophagus Lower oesophageal sphincter
51
Role of cricopharyngeus
Part of swallowing and preventing aspiration
52
Control of sphincters in oesophagus
Voluntary control - cricopharynxgeus Involuntary - lower oesophageal sphincter
53
Layers of oepshageal wall
Mucosa Submucosa Muscualris - circular layer and longtudinal layer Adventitia NO serosa, unlike rest of intestinal tract
54
What is muscularis in the oesophagus involved in
Peristalsis
55
Role of squamous mucosa in oesophagus
Barrier, protective effect
56
Circular vs longitudinal layer in muscularis
Circular muscle - contraction cause an increase in luminal pressure Longitudinal muscle - contraction causes shortening
57
Control of muscle in oeophagus
Largely under parasympathetic control via vagus nerve
58
How does food travel down the oesphagus
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
59
Definition of peristalsis
Coordinated contraction and relaxation of muscles in oesphagus
60
Components of lower oesophageal sphincter components
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
61
LOS function after swallowing
Inhibitory signals generated by peristalsis cause a reflex relaxation of the LOS for ~5secs The diaphragmatic crura also relax
62
Transient LOS relaxation
TLESR Gastric distension causes both the LOS and diaphragmatic crura to relax, allowing release of excess gas (burping)
63
Foods that increase LOS pressure
Protein Carbs (Refluxed) acids
64
Foods that decrease LOS pressure
Chocolate Fat Caffeine Citrus Garlic Tomato Decreased pressure causes acid reflux
65
Drugs that increase LOS pressure
Alpha-agoints Beta-blockers Cholinergics Metoclopramide Domperidone
66
Drugs that decrease LOS pressure
Alcohol Anticholinergics Beta-agonits Calcium channel blockers Dopamine (D2 receptors) Nicotine Nitrates TCAs
67
Stomach as a provider of storage capacity
Small amounts can be fed into small intestine where it is broken down more efficiently Pylorus opens 3x/min to allow small amounts through
68
How is the grinding motion of the stomach caused
By 3 muscle layers: longitudinal, circular & oblique causes food to be broken down physically
69
Function of stomach rugae
Make acid These folds increase SA of stomach
70
Where is stomach rugae found
Body of stomach, not antrum
71
Processes involved in gastric acid secretion
Neural Endocrine (gastrin) Paracrine (histamine and SST)
72
Which cells are found in the gastric body
Parietal cell ECL cell
73
Examples of diseases w/ too much acid
Zollinger-Ellison syndrome
74
What substances does the gastric gland secrete
Gastric acid Proteolytic pepsin(ogen)
75
When does pepsinogen --> pepsin
Once pepsinogen meets an acidic environment
76
Why is the canalicular membrane of the PC partially internalised
Increase SA for secretion
77
Where do the contents of PC secretions go
Into canaliculi --> gastric gland --> lumen
78
Features of proton pump in canalicular membrane
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
79
Stimulation of protein pump
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)
80
Cephalic phase of acid secretion
Thought, taste, smell, sight, swallowing Vagus nerve sends signal to stomach to prepare for food Done through release of ACh
81
What is gastrin secreted in response to
Gastric distention - stomach stretched by a meal AA/ peptides - foods high in this increase gastric production Low acidity (i.e buffering by food)
82
Feedback loop in gastric phase of gastric acid secretion
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
83
Intestinal phase of gastric acid secretion
Least important (5-10%) Stimulation via duodenal distension (neural) and chyme (gastrin) Inhibition via enetroendocrine cells secreting various gastric inhibitory peptides
84
In which fashion does SST work
Paracrine
85
Main gastric acid treatment
Antacids - simplest way (neutralise) Surgery Anti-secretory drugs
86
Surgery to help with gastric acid treatment
Vagotomy - inhibits cephalic phase Antrectomy - inhibits gastric phase
87
Main anti-secretory drugs used in gastric acid treatment
Anticholinergics H2 receptor antagonise PPIs Potassium- competitive acid blockers
88
Pyloric stenosis
Narrowing of the pylorus leading to intestinal obstruction in infants Usually 2-8 weeks
89
Cause of pyloric stenosis
Hypertrophy and hyperplasia of pylorus Mechanical obstruction to outflow of gastric contents into duodenum
90
Px of pyloric stenosis
Non-bilious vomiting Regurg
91
O/E seen in pyloric stenosis
Visible peristalsis Palapable mass after feeding in RUQ/ epigastrium
92
How is diagnosis of pyloric stenosis made
Abdominal ultrasound
93
Mx of pyloric stenosis
Appropriate fluid rests and correction of electrolyte abnormalities Ramstedt pyloromyotomy
94
Pyloromyotomy
Open procedure that involves cutting thickened muscle to release stenosis
95
Complications of pyloromytomy
Mucosal perforation Haematoma Wound infection
96
Risk factors for pyloric stenosis
Fhx Maternal smoking Bottle feeding Macrolide use in first 2/52 of life?
97
Causes of acquired pyloric stenosis
Ulcer Antral tumour Pancreatic tumour (head)
98
Causes of a/c gastritis
Irritants Drugs Severe stress Radiation Chemo
99
Irritants as a cause of a/c gastritis
Smoking Alcohol
100
Drugs as a cause of a/c gastritis
Aspirin NSAIDs Oral steroids
101
Severe stress as a cause of a/c gastritis
Burns Trauma Surgery Shock Sepsis
102
Complications of a/c gastritis
Erosions A/c stress ulcers
103
Erosions as a result of a/c gastritis
Small ulcers in which depth is limited to Lamina propria Tend to bleed
104
A/c stress ulcers as a complication of a/c gastritis
Penetrate muscular mucosa Particularly associated w/ stress - Curling's ulcers and Cushing's ulcers Associated w/ drinking and smoking Tend to bleed
105
Curling ulcer's
Occurs following severe burns Reduced plasma volume --> iscahemia and necrosis of stomach
106
Cushing ulcers
Occur secondary to raised ICP e.g. intracranial tumour, trauma etc
107
HP associated c/c gastritis
Spirochetes found at surface of gastric epithelium causing infl C/c infl is host immune repose to HP but improves after eradication of bacteria
108
What is HP associated gastritis associated w/
DU GU Gastric MALT lymphoma and cancer
109
Features of chemical/ relative c/c gastritis
Due to bile reflux Usually HP -ve Hx is important Reactive change in surface epithelium w/out significant a/c infl
110
Features of AI c/c gastritis
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
111
What can loss of PCs in AI gastritis cause
Achlorhydria
112
Achlorhydria
Loss of HCl in stomach
113
What can loss of IF in AI gastritis lead to
B12 deficiency and pernicious anaemia
114
Natural protective factors against ulcers
Surface ,luscious secretion Bicarb secretion into mucous Mucosal blood flow Epithelial barrier function Epithelial regenerative capacity
115
Examples of injury to mucosa that can cause peptic ulcers
HP infection NSAID tobacco Alcohol Gastric hyperacidity Duodenal-gastric reflux Ischaemia NSAIDs
116
Peptic ulcer disease
Umbrella term for development of gastric ulcers and duodenal ulcers
117
Epidemiology of gastric ulcers
Incidence increases w/ age Gender distribution is closer to equal (1:1 to 2:1)
118
Epidemiology of duodenal ulcers
Mean ages 30-40 M > F 4:1
119
A/c stress ulcers vs c/c peptic ulcers - penetration
A/c doesn't penetrate musuclaris propria C/c does
120
A/c stress ulcers vs c/c peptic ulcers - scarring
A/c has no scarring ulder ulcer C/c does
121
A/c stress ulcers vs c/c peptic ulcers - endarteritis obliterates
A/c has no endarteritis obliterans C/c does
122
Endarteritis obliterans
Infl of intimacy which proliferates and ultimately plugs lumen of artery
123
A/c stress ulcers vs c/c peptic ulcers - healing
A/c heals w/ regeneration C/c heals by repair w/ fibrous scar
124
A/c stress ulcers vs c/c peptic ulcers - number & location
A/c is multiple and can be anywhere C/c is single and usually antral
125
Aetiology of peptic ulcer disease
H. pyloric* - 95% of DU and 75% of GU Medication Zollinger-Ellison A/c stress Malignancy Infl e..g Crohn's
126
Medication causing peptic ulcer disease
NSAIDS* Corticosteroids Alcohol
127
Symptoms of peptic ulcer disease
Epigastric pain Dyspepsia (e.g. distension, bloating) Heartburn
128
Signs of peptic ulcer disease
Mild epigastric tenderness
129
DU vs GU - pathophys
DU - high acid eroding a normal mucous membrane GU - low or normal acid eroding mucous membrane w/ reduced resistance
130
DU vs GU - pain
DU - ulcer pain relived by eating GU - ulcer pain worsens by eating
131
DU vs GU - genetic factors
DU - important genetic component GU - no genetic component
132
How is dx of peptic ulcer disease made
Endoscopic examination
133
Genetic factors in c/c DUs
2x increase in 1st deg relatives 37% increase in blood group O HLA B5
134
DU disease associations
H pylori c/c gastritis Hyperparathyroidism (increased serum Ca stimulates gastric --> acid ++) Alcoholic cirrhosis C/c renal failure
135
Where do DUs typically px
90% in 1st part Ant > post
136
Where do GUs typically px
Lesser curve, antrum/ upper body
137
What does heaping up of a peptic ulcer suggest
Malignancy
138
Histology of peptic ulcers - 4 zones
Surface layer of necrotic debris Cellular infl layer rich in neutrophll polymorphs Granulation tissue layer Layer of fibrosis - vessel walls in this zone
139
H. pylori testing
Invasive - urease test (CLO), histology, culture Non-invasive - breath test, serological test, stool antigen test
140
HP breath test
Pts must be off PPIs Can be used for both dx and testing for eradication
141
Mx of PUD
Lifestyle modification Abx PPIs
142
Lifestyle modifcation for PUD
Avoid triggers Obesity Smoking and alcohol
143
Treating PUD associated w/ HP
No association w/ NSAIDs - 1st line eradication Association w/ NSAIDS - 2/12 full dose PPIs then 1st line eradication
144
Treating PUD w/ no association to HP
4-8 wk full dose PPIs
145
Follow up in PUD
Gastric ulcers require bx in 6-8 weeks due to possibility of malignancy
146
1st line eradication of HP
7/7 course of PPIs, amoxicillin, clarithromycin if no penicillin allergy If penicllin allergy - PPIs, clarithromycin, metronidazole
147
Complications of PUD
Penetration Perforation Haemorrhage Gastric outlet obstruction (pyloric stenosis)
148
Perforation as a complication of PUD
Pts px w/ signs of infection and severe abdominal pain Mx is supportive care, abx and laparoscopic repair
149
Possible perforation zone in PUD
Posterior ulcers ---> pancreas Anterior DU --> peritoneal cavity GU in lesser curve ---> lesser sac Less common is common bile duct and transverse colon
150
Haemorrhage as a complication of PUD
Can cause UGIB Typically posterior DU eroding into gasproduodenal artery Bleeding can be mild and c/c infl --> IDA
151
Gastric outlet obstruction as a compciaton of PUD
Pts px w/ nausea and vomiting, abdominal pain and distension
152
Zollinger Ellison syndorme
Occurs secondary to increased gastrin secretion by hyper-secreting gastrinoma in pancreas
153
Features of ZE syndrome
Recurrent DUs - multiple ad in atypicla sites 1/3 have diarrhoea due to increased gastric acid Ulceration/ eriosn of stomach rare
154
ZE syndrome and MEN
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
MEN
Multiple endocrine neoplasia
156
Examples of primary gastric neoplasia
Adenocarcinomas Malignant gastrointestinal stromal Lymphoma (MALT lymphomas associated w/ HP may resolve w/ HP eradication)
157
Polyp
Any lesion raised above mucosa
158
Epidemiology of gastric adenocarcinomas
4th most common malignancy Age - 50+ Sex - M > F 2:1 Geography - Japan/ Central & S america
159
Anatomical classification of gastric adenocarcinoma
Epicentre of the tumour <2cm from the GOJ - oespheageal Epicentre of the tumour >2cm from the GOJ - gastric
160
Histological classification of gastric cancer
Intestinal - most common, gland-forming Diffuse - less common, formed of discohesive cells
161
Intestinal gastric cancer features
More commonly seen in males Affects older ages Better prognosis
162
Diffuse gastric cancer features
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
Genetic predisposing factors for gastric adenocarcinomas
Fhx Increased risk w/ blood group A
164
Predisposing factors for gastric adenocarcinomas - diet
Carcinogens Polycyclic hydrocarbons in smoked food Increased starch - decreased fat, fresh fruit, green, leafy veg
165
Predisposing factors for gastric adenocarcinomas - premalignant condns
Pernicious anaemia Operated stomach Atrophic gastritis (dysplasia) Adenomas (dysplasia)
166
Gastric cancer types
Type 1 - polypoid Type 2 - fungating Type 3 - ulcerated Type 4 - infiltrative
167
What % of gastric malignancies is made up by gastric lymphoma
15% Commonest site of GIT lymphoma
168
Causes of a/c epigastric pain
A/c pancreatitis Perforated peptic ulcer Peptic ulcer A/c cholecystitis Biliary colic Mesenteric vascular disease Perihepatitis Supradiaphragmatic
169
Causes of dyspepsia
Functional GORD Pepetic ulcer Oesophageal cancer Gastric cancer Other causes incl colon cancer, c /c pancreatitis, pancreatic cancer etc
170
Associated features of dyspepsia that may help w/ dx
Dysphagia Wt loss Physical signs Anaemia/ thrombocytois
171
Assumptions based on risk factors for dyspepsia
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
Investigations for dyspepsia
Endoscopy Barium swallow/ meal H. pylori tests Oesophageal pH/ pH-impedance Anti-tag Ab/ Ig Gastric emptying
173
Pain modulators given for dyspepsia
Amitriptyline Mirtazipin Buspirone
174
Mx of GORD
Lifestyle measures Lowest dose required to control sx - PPI/ H2RA/ antacid (except Barrett's) Surgical intervention
175
Surgical intervention for GORD
Laparoscopic fundoplication Magnetic sphincter augmentation (Bariatric surgery: Roux-en-Y)
176
Other terms for functional dyspepsia
Post-prandial distress syndrome Epigastric pain syndrome
177
Rx for functional dyspepsia
HP eradication PPI Prokinetics Amitriptyline/ imipramine Buspirone Mirtazipine Sulpiride Behavioural intevrenyions e.g. diaphragmatic breathing, psych rx
178
Theoretical ways to reduce acid secretion
H2 antagonist Gastrin antagonist - none clinically available Muscarinic antagonist - atropine, pirenzepine Block H+ secretion - PPIs Inhibits PC secretion physiologically - misoprostol, SST Neutrralisation - antacids
179
Onset of antacids
Rapid but transient
180
What can large, regular doses of antacids heal
Duodenal ulcers
181
What do antacids provide symptomatic relief for
GORD Indigestion
182
What are examples of compounds found in antacids
Mg, Ca, Na or Al Al --> constipation Mg ---> diarrhoea
183
Adverse effects of antacids
Systemic alkalosis in v high doses Carbonate containing compounds release CO2 --> belching
184
Adverse effects of antacids - Al
Osteodystrophy and encephalopathy in c/c renal failure Al chelates tetracyclines and levodopa
185
Adverse effects of antacids - Ca
Calcium stimulates gastrin --> counterproductive
186
Examples of H2 receptor antagonists
Cimetidine Ranitidine Nizatidine Famotidine
187
Where do H2RAs act
PCs Cardiac atria
188
Actions of H2RAs
Reduce basal and stimulated acid secretion Reduce pepsin secretion by about 60%
189
What is the rate of peptic ulcer healing dependent on
Degree of acid suppression
190
Time frame for healing ulcers using H2RAs
DU: 4/52 - 6-52 GU: 6/52 - 8/52
191
H2RAs for GORD
Provides symptomatic relief Healing requires much higher doses
192
Metabolism of H2RAs
Cimetidine and ranitidine rapidly absorbed Short half lives Cimetidine excreted renally but other renal and liver
193
Adverse effects of H2RAs - uncommon
Diarrhoea Headache Confusion in elderly Cimetidine - anti androgen (gynaecomastia) Cimetidine - inhibits P450 (enhances warfarin, theophylline, tolbutamide)
194
Examples of PPIs
Omeprazole Lansoprazole Rabeprazole Esomeprazole
195
Actions of PPIs
Inhibits acid secretion by 90% Covalently inhibit PP Some PPIs may inhibit clopidogrel activation
196
Metabolism of PPIs
All via P450 system Mild inhibition of P450 isoforms
197
Adverse effects of PPIs
Diarrhoea Headache Infectious gastroenteritis Hypergastrinaemia and acid rebound Impaired Ca and Mg - osteoporotic fractures
198
Adverse effects of PPIs
Diarrhoea Headache Infectious gastroenteritis Hypergastrinaemia and acid rebound Impaired Ca and Mg - osteoporotic fractures
199
Why is infectious gastroenteritis an adverse effect of PPIs
Reduces bacterial killing
200
Why is diarrhoea an adverse effect of PPIs
Idiosyncratic Bacteria overgrowth Microscopic colitis
201
Uses of acid suppression
GORD Prevention of NSAID-induced peptic ulcer Helaing of peptic ulcer HP eradication Stress ulcer and aspiration prevention
202
Indications for parenteral therapy for acid suppression
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
Alarm features of dyspepsia
Anorexia Loss of weight Anaemia Recurent vomiting Dysphagia
204
Acid suppression in peptic ulcer
Remove etiological factors Use PPIs to help prevent Maintenance high doses fr ZES
205
Cytoprotective agents used in GIT
Misoprostol Sucralafte Bismuth
206
Misoprostal as 'gastroprotection'
PGE1 analogue Inhibits acid secretion Increases duodenal bicarb secretion, gastric mucous production, mucosal blood flow
207
Misoprotsol features
Heals peptic ulcers Reduces NSAID-induced ulcers AND complications Rapidly absorbed from gut - extensive 1st pass metabolism
208
Adverse features of misoprostol
Diarrhoea - 30% Uterine contractions - avoid in pregnancy and young women Menorrhagia and pots-menopausal bleeding
209
Features of sucralfate
Coats ulcer base Increases prostaglandins secretion Prevents diffusion of acid
210
What can sucralfate be used to prevent
Sclerotherapy-induced oesophageal ulcers Stress ulceration in critically ill pts
211
Features of bismuth
Bind to base of ulcers Enhances locals protective mechanism Anti H pylori action
212
Adverse effects of bismuth
Black stool Black tongue Can produce encephalopathy in renal failure
213
Adverse effects of sucralfate
Constipation
214
Bismuth uses
Commonly used in 2nd and 3rd line HP eradication regimens Widely used OTC - pepto-bismol, indigestion, diarrhoea
215
Barrett's oesphagus
Normal distal oesophageal squamous epithelial lining replaced w/ metaplastic columnar epithelium
216
Transformation to cancer from Barrett's
Non dysplasie Barrett's oesophagus Low-grade dysplasia High grade dysplasia Oesophageal adenocarcinoma
217
Clinical px of oesophageal cancer - alarm sx
Progressive dysphagia Change to liquid diet Wt loss Regurg Persistent reflux NOT responding to PPI Others e.g.g food bolus obstruction
218
Dx of oesophageal cancer
Upper GI endoscopy and biopsies is the ix of choice Mucosal visualisation Biopsies x8 Other modalities incl CT and barium swallow (obsolete)
219
Barium swallow to dx oesophagela cancer
Only for v frail pts who ca tolerate OGD
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OGD
Oesophagogastro dudodenoscopy
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Staging pathways for oesophageal carcinoma
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
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Treatment pathways for oeosphageal carcionma
Curative treatment = chemo +/- surgery Palliative treatment = chemo +/- stent
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Ideal curative pathway for oesophageal xcarcinoma
3 cycles of chemo - eradicate systemic disease, prevent disease progression surgery Adjuvant chemo = 3 further cycles (75% doses)
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Surgery for oesophageal cancer
Ivor Lewis oesophagectomy Oesophagus joined to stomach
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How may gastric cancer px as
IDA Early satiety Wt loss Abdominal pain/ mass Reflux Non-healing gastric ulcer
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How may gastric cancer px as
IDA Early satiety Wt loss Abdominal pain/ mass Reflux Non-healing gastric ulcer
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How can gastric cancer px as an emergency
Haematemesis/ melaena Gastric outlet obstruction Perofrated gastric ulcer Disseminated disease e.g. ascites
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Treatment for gastric cancer
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
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Curative intent for gastric cancer
Period chemo then gastrectomy Straight to gastrectomy (age > 80, co-morbidities ++)
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Palliative intent for gatsric cnacer
Palliative care Stents e..g pyloric stent for obstruction Best supportive care Drain e.g. ascites etc Palliative chemo +/- Herceptin
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Total gastrectomy for proximal cancer
Oesphagus joined to jejunum Functionally v debilitating Causes wt loss and nutritional deficiencies NEVER as a palliative option
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Obesity stigma
Highly stigmatised disease Amongst the public, medical professionals, and healthcare commissioners Obesity is 'self-inflicted'
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Consequences of pts' experiences of obesity
Depression gets worse Anxiety Suicidal thoughts Disordered eating Decreased self esteem Avoidance of physical activity Shaming themselves Decreased QoL
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Obesity - surgery vs non-surgical
Surgery produces sustained wt loss Ultimately, improved long-erm survival compared to those w/out surgery
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Effects of bariatric surgery
Acts through restrictive or malabsprptive effect Acting centrally within the hypothalamus to control appetite , hunger and satiety Gut hormonal changes Alterations in bile acids
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Bariatric MDT
Core members incl Obesity physician Specialist surgeon Dietitian Psychologist Anaesthetists
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Tired structure of obesity mx in the NHS
Tier 1 - universal interventions Tier 2 - lifestyle interventions, diets, pharmacology Tier 3 - specialist services Tier 4 - surgery
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Main bariatric surgery operations
Sleeve gastrectomy Roux en Y bypass Laparoscopic Adjustable Gastric Band (LAGB)
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Features of sleeve gastrectomy
One of the most common procedures Majority of stomach excised Faster, less technically demanding, fewer post-op complications
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In which pts is a sleeve gastrectomy contraindicate din
Pts who suffer from GORD
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Mechanism of sleeve gastrectomy
Produces neurohormonal changes in GLP-1 and PYY as well as reduced gherkin production due to removal of gastric fundus
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Features of Roux en Y gastric bypass
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
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Gastrojejunostomy
Anastomosis between stomach and jejunum
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Jejunojejunostomy
Anastomosis between two parts of jejunum
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Complications of Roux en Y bypass
Anastomotic leaks - can be life threatening Internal herniation - can be life threatening
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What does a Roux en Y bypass allow for in the future
Access to gastric remnant for gastric cancer Access to duodenum for ERCP
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Laparoscopic Adjustable Gastric Band
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
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Example of an bariatric emergency
Slipped band
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Sliped band as a bariatric emergency
Distal stomach herniates upward through the band, causing proximal pouch dilatation Left untreated, this can result in ischaemia and necrosis
249
Px of slipped gastric band
Upper abdominal or chest pain, dysphagia and regurg of all fluid
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Mx of slipped band
Urgent deflation of band Can be deflated on the ward via an abdominal port w/ a Huber needle
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How may regurg px in children
FTT
252
GORD
Gastro-oesophageal reflux disease Reflux of stomach contents in oesophagus
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Pathophys of GORD
Lower Oesophageal Sphincter (LOS) relaxes inappropriately
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Risk factors for GORD
High BMI Smoking Genetic associations Pregnancy NSAIDs, alcohol
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Sx of GORD
Heartburn - postprandial and worse lying down Chest pain Regurg Acid brash Hoarse voice Dysphagia
256
Atypical sx of GORD
'Laryngopharyngeal reflux' Cough Throat clearing Dental issues
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Oesophageal syndromes of GORD
Reflux (erosive) oesophagitis Reflux stricture Barrett's oesphagus Oesophageal adenocarcinoma
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Things to ask in hx of GORD
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
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Red flags for GORD - ALARM
Gastroscopy is required Anaemia Loss of wt Anorexia Refarctoru to med Maelena & haemetesis Swallowing difficulties New onset dyspepsia (>55 yrs)
260
Ddx of GORD
Functional heartburn Achalasia (failed relaxation of LOS) Eosinophilic oesophagitis Cardiac causes of chest pain Malignancy
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Ix in GORD
pH monitoring - when dx is uncertain. 24hr pH monitoring can be combined w/ high res manometry Gastroscopy
262
Manometry
Assesses motor abnormlaities of the oesophagus
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Gatsroscopy for GORD
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
Steps in mx of GORD
Lifestyle changes Pharmacological treatment
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Conservative mx of GORD
Wt loss Smoking cessation Reducing stress Reducing caffeine (lowers LOS pressure) Elevating head of bed Stop eating within 2hrs of bed
266
Pharmacological mx of GORD
PPis (2/52 trial) - best for treating erosive disease Ranitidine Over counter meds e.g.g gaaviscon Prokinetics e.g. domperidone Baclofen Amitriptyline
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Anti-reflux surgery
NIssen fundoplication - wrapping fundus around lower oesophagus Constructs new anti-reflux barrier
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Who is anti-reflux surgery reserved for
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
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Endoscopic treatment for reflux
Stretta radio frequency Endoscopic suturing Endoscopic fundoplication
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Complications of GORD
Erosive oesophagitis Stricture Barrett's oesophagus
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Erosive oesophagitis
Infl of oesophagus --> ulcers, bleeding, peptic stricture formation
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Stricture
Scarring and narrowing of oesophagus due to repeated damage
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Barrett's oesophagus
Premalignant condn due to columnar metaplasia (seen in stomach) of the normal squamous mucosa of oesophagus
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Oral ulcers 'stomatitis'
AKA apthous ulcers Caused by HSV (aciclovir) or candida (fluconazole)
275
Bacterial causes of pharyngitis
Strep tonsillitis (peritonsillar abscess) Diphtheria Vincent's angina Ludwig's angina Chlamydia HIV
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Viral causes of pharyngitis
Common cold Enteroviral pharyngitis Herpangina Infectious mononucleosis
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Epidemiology of diphtheria
Common disease in 19th century 10,00 death/ yrs Seen in children < 5 (immunisation introduced in 1942)
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Dipheriae definition
URTI characterised by sore throat, low grade fever, adherent membrane of tonsils, pharynx, nose
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Causative organism of diphtheria
Corynebacterium diphtheria
280
Local px of diphtheria
Tough pseudomembrane Grey, semitransparent necrotic area Pain, bleeding if scraped
281
Systemic effect of diphtheria
Eraly, cardiac damage - myocraditis, heart failure, heart block Late, neuro damage - demtylination, palate palsies Late, nephritis
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Mx of diphtheria
Abx - benzylpenicillin, erythromycin Antitoxin Tracheostomy if oedema threatens airway Prevention/ control - vaccine
283
Causative organisms of oesphagitis
Candida CMV HSV VZV
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Sx of oepshagitis
Difficulty swallowing Odynophagia Retrosternal discomfort Anorexia Fever
285
Common risk factors for oesophagitis
Abx use - candida spp AIDS - CMV, HSV, candida Leukaemia, lymphoma - candida, HSV Corticosteroids - candida
286
Dx of oesphagitis
Flexible endoscopy, X-ray (barium) Swab or brushings Tissue bx (histology culture)
287
Features of oesophageal candiasis
Typical white plaques, nodules Causes severe odynophagia Seen in pts w/ MM and HIV
288
Features of Herpes simplex oesophagitis
Usually seen in immunocompromised pts Numerous small ulcerations Fever and odynophagia
289
Treatment for herpes simplex oesophagitis
Candida spp - azoles (fluconozaole, intraconozole), amphotericin B HSV, ZVZ - aciclovir, foscarnet if resistant to acyclovir CMV - ganciclovir, foscarnet
290
How can we prevent acid rebound in pts on PPIs
Step down before stopping
291
Mx of achalasia
Botox injections/ dilation CCBs Nitrates
292
Can you give omeprazole to patients on clopi
No
293
Surveillance for Barrett's oesophagus
Every 3-5 yrs
294
Mx of high grade Barrett's
Oesophagectomy
295
Mx low grade Barrett's
Ablation to encourage new normal cell growth
296
Risk of oesophagectomy
Issues w/ aperistalsis and bloating Worse when combined w/ fundoplication
297
Side effects of PPIs
Nausea Abdo pain Rash Dizziness Constipation
298
Types of dysphagia
Low vs high Oropharyngeal - can't initiate swallow Oesophageal - blockage or irritation
299
Key gastro ddx of difficulty swallowing
Adenocarcinoma SCC Pharyngeal pouch Epiglottitis Hiatus hernia Rare - achalasia, corkscrew oesophagus
300
Drugs as risk factor for GORD
Nitrates CCBs TCAs Anticholinergics
301
Presentation of gastritis
Dyspepsia Anorexia Nausea and vomiting Haematemesis or maleana Many cases resolve spontaneously
302
Ix for gastritis
Endoscopy Bx H pylori test
303
Risk factors for oesphageal cancer
Older age, M gender GORD, Barrett's Smoking and chewing tobacco Obesity and Poor diets Alcohol Previous head and neck cancer or RT
304
Classification of oesophageal cancer
Adenocarcinomas tend to arise in distal third oesipahgus SCC in upper or middle, more prevalent WW
305
Clinical px of oesophageal cancer
Sx tend to arise when lumen < 2cm Progressive, painless dysphagia Dyspepisa, regurg - reistant to PPI Lymphadenoathy Mediastinal inasion - chest pain
306
Ix for oesophageal cancer
Upper Gi endoscopy w/ 8 separate bx Barium swallow for pts who can't tolerate gastroscopy
307
Hiatus hernia definition
Herniation of part of stomach through diaphragmatic oesophageal hiatus
308
Risk factors for hiatus hernia
Older age Male sex Obesity Increased intra-ab pressure
309
Classification of HH
Type I - sliding Type II to IV - para-oesophageal
310
Type I HH
Displacement of GOJ above diaphragm Usually asymptomatic
311
Type II HH
Dislocation of fundus GOJ unchanged
312
Type III HH
Dislocatiom of BOTH HH and fundus Most common para-oesophagela type
313
Type IV HH
Presence of other organs within hernia sac May lead to gastric volvulus
314
Sx of HH
Mainly asymptomatic Heartburn Regurg Dysphagia Bowel sounds in L chest If volvulus - post-pradial pain and distension
315
Ix for HH
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
Mx of HH
Usually nothing PPIs for symptomatic Type I
317
Complications of HH
Gastric volvulus Strangulated hernias Uncontrolled bleeding Gastric outlet obstruction