Week 1 Flashcards
(179 cards)
1
Q
What are the layers of the GI tract wall, from innermost to outermost?
A
Mucosa (epithelium, lamina propria, muscularis mucosa)
Submucosa (submucosal plexus)
Muscularis propria (circular muscle, myenteric plexus, longitudinal muscle)
Serosa/adventitia
2
Q
What type of contraction is circular muscle responsible for?
A
Constriction
3
Q
What type of contraction is longitudinal muscle responsible for?
A
Shortening
4
Q
What are the 3 salivary glands?
A
Parotid, submandibular and sublingual
5
Q
How much saliva is produced in a day?
A
0.5 litres
6
Q
What are the components of saliva and their functions?
A
Mucus (lubrication), amylase (starch digestion), bicarbonate (acid neutralisation), thiocyanate/lysosome (bactericidal agents)
7
Q
Describe the mechanism of swallowing
A
Soft palate is pushed upwards and the epiglottis is pushed downwards
8
Q
What types of muscle are found in the oesophagus?
A
Upper 1/3 striated, middle 1/3 transition, lower 1/3 smooth
9
Q
What controls motility of the oesophagus?
A
Sympathetic and parasympathetic (vagus) nerves and myenteric plexus
10
Q
What is achalasia?
A
Neurogenic oesophageal motility disorder characterised by impaired peristalsis and lack of LOS relaxation during swallowing causing dysphagia and regurgitation
11
Q
What is the arterial supply to the oesophagus?
A
Superior and inferior thyroid arteries
Branches of bronchial, intercostal and descending aorta
Branches of left gastric, left inferior phrenic and splenic arteries
Dense anastomosis within submucosa
12
Q
What is the venous drainage of the oesophagus?
A
Oesophageal veins drain into left gastric (drains into portal vein) and short gastric veins and azygous and hemiazygous veins
13
Q
What are oesophageal varices and how do they occur?
A
Extremely dilated sub-mucosal veins prone to bleeding caused by an increased pressure in the left gastric vein due to portal hypertension
14
Q
What are the functions of the stomach?
A
Reservoir to store ingested food
Initiation of digestion
Acid secretion
Controlled release of contents into duodenum
15
Q
What are the 3 muscle layers of the stomach, from innermost to outermost?
A
Oblique, circular and longitudinal
16
Q
Outline the gross anatomy of the stomach
A
LOS, cardia, fundus, body, pyloric antrum, pyloric canal, pyloric sphincter
Stomach walls are covered by rugae
Lesser and greater curvatures
17
Q
What controls the motility of the stomach?
A
Constricted at rest - BER of 3 min
Vago-vagal reflex - mechanoreceptors sense presence of food and send afferents to the brainstem which sends efferents back
Cholinergic vagal activity must reach threshold to initiate peristalsis
Negative feedback by secretin
18
Q
What are the components of gastric secretions and what cell type produces them?
A
Hydrochloric acid/H+ ions (parietal cells)
Pepsin (pepsinogen precursor produced by peptic/chief cells)
Intrinsic factor (parietal cells)
Mucus (prostaglandins)
Water
19
Q
What is the role of intrinsic factor?
A
Forms a complex with vitamin B12 to allow its absorption
20
Q
What is the pH of gastric acid?
A
1
21
Q
Describe the mechanism of gastric acid secretion via 3 main transporters
A
- Na+/K+ ATPase pumps K+ into the parietal cell from the blood and Na+ into the blood from the parietal cell
- H+ ions are actively pumped into the gastric lumen from the parietal cell and K+ into the parietal cell from the gastric lumen by H+/K+ ATPase (proton pump)
- Cl-/HCO3- transporter pumps Cl- into the parietal cell from the blood and HCO3- into the blood from the parietal cell
22
Q
What substances stimulate gastric acid secretion, where are they released from and which receptors do they bind to?
A
Histamine from ECL cells binds to H2 receptor
Gastrin from G cells binds to CCK2 receptor
Acetylcholine from vagus nerve binds to muscarinic acetylcholine receptor
23
Q
How is gastric acid secretion inhibited naturally?
A
Decrease in stomach pH on exit of food causes inhibition of gastrin and stimulation of inhibitory somatostatin
24
Q
How is movement of food into the duodenum slowed down?
A
Release of enterogastrones - GIP, secretin and CCK
25
How can gastric acid secretion be blocked?
Vagotomy, antihistamines and proton pump inhibitors
26
What are the 3 phases of gastric secretion and what happens during each?
1. Cephalic (see/smell/taste food) - vagal activation of parietal and G cells → moderate stimulation of HCl and pepsinogen
2. Gastric (food enters stomach) - stomach distention and presence of protein in antrum → vago-vagal reflex, gastrin and histamine → strong stimulation of HCl and pepsinogen
3. Intestinal (food enters duodenum) - protein → gastrin (excitatory); HCl → secretin (inhibitory); lipids → peptide YY (inhibitory)
27
What are the functions of the small intestine?
Mix food with digestive enzymes
Circulate intestinal contents to facilitate contact with mucosa
Propel intestinal contents towards terminal ileum
28
What are the 4 parts of the duodenum?
Superior, descending, inferior and ascending
29
Where are Brunner's glands found and what do they do?
Duodenum
| Secrete bicarbonate to neutralise gastric secretions
30
What are Peyer's patches and where are they found?
Lymph follicles
| Ileum
31
What controls the motility of the small intestine?
At rest - migrating motility complex (MMC)
| During digestion - various contractions
32
What is the MMC?
Migrating motility complex
Distinct pattern of electromechanical activity observed in GI smooth muscle between meals; housekeeping role in sweeping residual undigested material
33
What types of contractions occur in the small intestine and what components are responsible for each?
Segmentation - non-synchronised, circular muscle
Pendular - longitudinal muscle
Villus - muscularis mucosae
Peristalsis - waves from duodenal bulb
34
What secretions occur from the crypts and villus tips within the small intestine and what purpose do they serve?
Crypts - NaCl/NaHCO3- (gastric HCl neutralisation), amylase (starch digestion), enteropeptidase (trypsinogen activation)
Villus tips - brush border enzymes
35
What is absorbed in the small intestine and by which mechanisms?
Protein - trypsin and other pancreatic proteases
Fat - emulsification by bile salts, lipase activation, micelle formation
Carbohydrate - amylase, maltase, sucrase, lactase
Vitamins - passive diffusion
Water - 7-8 L/day, diffusion down osmotic gradient
36
What are the functions of the pancreas?
Endocrine - islets of Langerhans; β cells produce insulin, α cells produce glucagon, δ cells produce somatostatin
Exocrine - aqueous/bicarbonate (duct cells) and enzymatic/NaCl components (acinar cells)
37
What are the main risk factors for duodenal ulcers?
Being male, smoking and stress
38
What are the complications of duodenal ulcers?
Haemorrhage (superficial) and acute peritonitis (deep)
39
Describe the surgical and pharmacological management of duodenal ulcers
Surgical - vagotomy or excision of part of the stomach
| Pharmacological - antihistamines, proton pump inhibitors
40
Describe how gastric acid secretion is stimulated
Gastrin (from G cells in response to food) and the vagus nerve → parietal cells release acid
41
Describe how gastric acid secretion is inhibited
Increased acid levels → D cells (antral glands only) release somatostatin → G cells stop release of gastrin → parietal cells inhibited
42
Where are D cells of the stomach located?
Glands of the antrum only
43
Define Helicobacter pylori
Gram negative microaerophilic bacterium found in the stomach which can colonise the mucosa to cause ulceration
44
How do H.pylori cause infection?
Colonise surface of stomach mucosa and release urease which converts urea to ammonium and CO2 - subsequent ammonium bicarbonate alkaline cloud increases pH locally to stimulate acid secretion (gastrin released → parietal cells release acid)
45
Describe the epidemiology of H.pylori infection
Present in much of the population without causing disease
Infection occurs at a young age and persists
Increased prevalence associated with lower socioeconomic status
46
How is H.pylori infection treated?
Proton pump inhibitor (e.g. omeprazole)
| Antibiotics (e.g. metronidazole and amoxycillin/clarithromycin)
47
What are the 3 components of duodenal ulcer pathophysiology?
Increased gastrin, acid secretion and duodenal acid load
48
In respect to H.pylori, what is CAG?
Pathogenicity/genomic island acquired by bacteria from horizontal gene transfer allowing evolution; strains carrying this cause more inflammation and are more likely to lead to duodenal ulcers
49
What are the main signs/symptoms of gastric cancer?
Weight loss and anaemia
50
What relation does H.pylori infection have to gastric cancer?
Attributable to 95% of gastric cancers - necessary but insufficient factor
51
How does gastric cancer develop from H.pylori infection?
Infection → superficial gastritis → atrophic gastritis (decreased parietal and chief cell density) → dysplasia and cancer
Host genetics, bacterial strain, diet, smoking and male gender are major influences
52
What is the relationship between peptic ulcer disease and gastric cancer?
Those who develop peptic ulcers appear to be protected from developing gastric cancer
53
How can H.pylori infection be prevented?
Test patients with dyspepsia for H.pylori and improve living conditions
54
What is the relationship between gastric cancer and gastro-oesophageal junction cancer?
Decreasing the incidence of gastric cancer appears to increase incidence of gastro-oesophageal junction cancer
55
What defences does the body have against reflux?
Intrinsic sphincter tone
Flap valve (angle at which the oesophagus enters the stomach)
Overlap of the sphincter with the diaphragm
Length of the oesophagus
Bicarbonate secretion (saliva)
56
How can the body's defences against reflux fail?
Decreased sphincter pressure
Hiatus hernia
Oesophageal motility disorder
Smoking decreasing saliva and bicarbonate
Obesity (increased intra-abdominal pressure)
57
What is hiatus hernia?
A condition in which part of the stomach protrudes superiorly through the hiatus of the hernia into the chest region; classified as sliding (in and out) or rolling (stays in, rare)
58
What is the main cause of mild reflux?
TLOSR - transient lower oesophageal sphincter relaxation
59
What is the main cause of moderate reflux?
Decreased sphincter pressure
60
What is the main cause of severe reflux?
Sliding hiatus hernia
61
What is GORD?
Gatro-oesophageal reflux disease; symptoms caused by acid reflux which are sufficient to impair quality of life and/or cause complications
62
What epithelium is found in the oesophageal mucosa and how is it adapted for its function?
Stratified squamous epithelium; resistant to shear stress
63
What epithelium is found in the stomach and how is it adapted for its function?
Columnar epithelium; contains mucous-producing cells for protection
64
What clinical conditions can affect the oesophagus?
Oesophagitis - inflammation of mucosa causing strictures
Barrett's oesophagus - replacement of squamous epithelium with columnar due to reflux, increasing cancer risk
Oesophageal cancer - cell dysplasia
Oesophageal ulcreation - can be caused by bisphosphonates
65
How can oesophageal disease be diagnosed and treated?
Endoscopy - incision or radio frequency ablation (burning) of affected areas
pH monitoring - catheter over 24 hours, abnormal if pH < 4 is sustained
Manometry - pressure/function measurement at 36 points (1cm apart) down the length of the oesophagus
66
What is the most important sign of upper GI bleeding?
Melena - black diarrhoea due to partially digested blood
67
How might an actively bleeding ulcer be treated?
Local adrenaline injection to cause vasoconstriction and improve field of view in order to clip or ablate the area
68
Where are pyloric glands found and what cell types are they composed of?
Antrum of the stomach; enterochromaffin-like and D cells
| NO PARIETAL CELLS
69
Where are oxyntic glands found and what cell types are they composed of?
Fundus and body of the stomach; parietal cells
70
What are the 2 main causes of peptic ulcers?
NSAIDs (inhibit COX1 which decreases stomach mucus protection) and H.pylori
71
What is Zollinger-Ellison syndrome?
A rare condition characterised by development of benign gastrin-secreting tumours in the pancreas or duodenum which can cause ulceration
72
How is H.pylori infection tested for?
Breath test - measures urease activity by ingestion of urea with labelled C 13/14; detection of C alone indicates breakdown by bacteria
Stool test - bacterial antigen; present infection, less acceptable to public
Endoscopic biopsy - histology/culture/rapid urease test (ammonia measurement)
Blood test - antibodies (IgG); less reliable, persist after cleared infection
73
What are alarm symptoms which would indicate endoscopy?
```
Dysphagia
Epigastric pain with unintentional weight loss
Persistent vomiting
Haematemesis
Abdominal mass
Iron deficiency anaemia
Dyspepsia in male >55 years old
```
74
What is the mechanism of action of proton pump inhibitors?
Drug becomes ionised when ingested to allow concentration to build-up inside parietal cells and block pump action
75
Why is dose timing important when taking proton pump inhibitors?
Only active pumps are blocked and only 20% of pumps are active at rest; drug must be taken 30 minutes before a meal so that 80% of pumps will be active due to digestion
76
What side-effect can occur from stopping proton pump inhibitor therapy?
Rebound hypersecretion of acid as gastrin takes up to 3 months to rise to normal levels; must not be prescribed for general dyspepsia
77
Outline how to take a basic history
```
Introduction
Presenting complaint
History of presenting complaint
Past medical history
Family history
Social history
Drug history
Lifestyle history
Systematic enquiry
Summary
```
78
Define professionalism
A set of values, behaviours and relationships which underpins the trust the public has in doctors
79
What are the main values doctors should possess?
Integrity, compassion, altruism, continuous improvement, excellence, working in partnership
80
Define professional development planning
A structured and supported process undertaken by an individual to reflect on their own learning, performance and achievement and to plan for personal, educational and career development
81
Outline Gibbs reflection cycle
```
Description
Thoughts/feelings
Evaluation
Analysis
Conclusion
Action plan
```
82
How long is the oesophagus?
25cm
83
Where is the oesophagus located anatomically?
Midline in the posterior mediastinum
84
What part of the diaphragm does the oesophagus pierce and how is this different to the inferior vena cava?
Oesophagus pierces muscle - contraction holds it shut during inspiration
IVC pierces tendon - contraction holds it open during inspiration
85
What is anatomically significant about the fundus of the stomach?
Protrudes above the level of oesophageal entry; defence against reflux
86
Which areas of the stomach contain mucus-producing and acid-producing glands?
Mucus - pyloric glands
| Acid - fundic and body glands
87
Describe the pyloric sphincter
Anatomical; distinct thickening of smooth muscle which controls gastric emptying and lies in the transpyloric plane
88
Describe the cardiac/lower oesophageal sphincter
Physiological; no distinct thickening of muscle but helps to prevent reflux
89
What is the function of the oblique muscle in the stomach?
Pulls at an angle to prevent regurgitation
90
What major arterial network supplies the stomach?
Coeliac trunk, from the aorta
91
What arteries supply the lesser curvature of the stomach?
Right and left gastric arteries (anastomosis)
92
What arteries supply the greater curvature of the stomach?
Right and left gastroepiploic arteries (anastomosis)
93
Where is the angular notch of the stomach located?
Bottom of the lesser curvature; boundary between the pylorus and body
94
What does the inferior border of the liver line up with?
Costal margin
95
Why does the liver need additional protection via the ribcage?
Lack of fibrous tissue
96
What is the falciform ligament of the liver?
Fold of peritoneum which splits the left and right subphrenic spaces
97
What is the ligamentum teres/round ligament of the liver?
Fibrous cord at the free inferior edge of the falciform ligament; remnant of umbilical vein
98
What is the greater omentum?
Peritoneal fold which hangs off the greater curvature of the stomach and serves as the 'policeman' of the abdominal cavity (contains infection, inflammation, hernia); transverse colon is attached to the posterior surface
99
What is the intracolic compartment?
Part of the greater sac under the transverse colon; faecal matter from trauma to the small intestine can collect here
100
What is the lesser omentum?
Fold of peritoneum between the lesser curvature of the stomach and the liver; bile duct located at the free edge
101
What is the lesser sac/omental bursa and what is its importance?
Recess of peritoneal cavity behind the stomach reached via the epiploic foramen; slippery to prevent friction and allow the stomach to move freely
102
Where is the gallbladder located in the abdominal cavity in relation to surface anatomy?
Where the right edge of the rectus abdominus muscle meets the costal margin
103
What are the subdiaphragmatic/subphrenic spaces and what is their significance?
Spaces between the liver and diaphragm; duodenal ulcer perforation will cause intestinal contents to fill these areas
104
What are the areas on either side of the colon called?
Right and left paracolic gutters
105
Where are the supracolic and infracolic compartments located?
Superior and inferior to the transverse colon
106
What is the epiploic foramen?
An opening in the lesser sac which connects the lesser and greater sacs
107
What arteries supply the fundus of the stomach?
Short gastric arteries
108
What are the main vessels involved in venous drainage of the stomach?
Superior mesenteric and hepatic portal veins
109
What is the lymphatic drainage of the stomach?
Lymph nodes named similarly to the blood vessels drain into the coeliac lymph node
110
What are the main functions of the liver?
Metabolism of amino acids/carbohydrates/lipids
Synthesis of plasma proteins and enzymes
Production of bile
Detoxification
Storage of proteins/glycogen/vitamins/metals
Immunity
111
What major blood vessels enter the liver and what fraction of oxygen do they supply?
Hepatic artery (30-40% of blood, 2/3rds of oxygen) and portal vein (60-70% of blood, 1/3rd of oxygen)
112
What organs are drained by the portal vein?
Small and large intestine, stomach and spleen
113
What is the portal triad made up of?
Hepatic artery, portal vein and bile duct
114
What is the portahepatis?
'Gateway to the liver'; point where the hepatic artery and portal vein enter and bile duct exits
115
Describe the characteristics of the portal vein blood
Low pressure deoxygenated blood which has already passed through the capillary bed of the gut
116
Describe hepatocytes
```
Most abundant cell type in the liver
Sinusoidal (fenestrated), intercellular and canalicular surfaces
Lie in plates and cords
Exchange material with blood
Microvilli
```
117
What cell types are present in the liver?
```
Hepatocytes
Endothelial cells
Kupffer cells
Perisinusoidal/fat-storing cells
Lymphocytes
```
118
What collagen types are found in the capsule of the liver?
Type I and III
119
What transport mechanism is used in bile canaliculi?
Active transport
120
How does the liver ensure all blood comes into contact with its tissue?
Incoming blood needs to pass through parenchyma to leave
121
What are the 3 requirements for cirrhosis?
Diffuse, fibrosis, nodules
122
What is cirrhosis?
End-stage liver disease which results from chronic inflammation due to persistence of an injury-causing agent
123
Describe the pathogenesis of cirrhosis
Hepatocyte injury → progressive liver cell loss → chronic inflammation leading to fibrosis and hepatocyte regeneration leading to hyperplastic nodules
124
What are the causes of cirrhosis?
```
Acquired or inherited
Alcohol - 60-70%
Unknown - 10-15%
Hepatitis - 10%
Biliary disease - 5%
Haemochromatosis - 5%
```
125
What complications are associated with cirrhosis?
Portal hypertension (causing portal-systemic shunts, varices, ascites and splenomegaly)
Liver failure
Hepatocellular/liver cancer
126
What is an acinus?
Micro-circulatory physiological unit of the liver composed of zones 1-3 in which different metabolic processes are carried out
127
What processes occur in zone 1 of the acinus?
Periportal zone, closest to afferent arteriole; aerobic/oxidative functions
Respiratory chain, citric acid cycle, fatty acid oxidation, gluconeogenesis, urea synthesis, cholesterol synthesis, amino acid utilisation, production/excretion of bile
128
What processes occur in zone 2 of the acinus?
Ill-defined intermediate area
129
What processes occur in zone 3 of the acinus?
Perivenular zone, closest to terminal hepatic veins; anaerobic functions
Glutamine synthesis, xenobiotic metabolism, glycolysis, lipolysis, ketogenesis
130
How is the liver involved in carbohydrate metabolism?
Storage and release of glycogen
Synthesis of glucose from lactate/pyruvate/glycerol/alanine
Conversion of fructose and galactose to glucose phosphates
131
How is the liver involved in lipid metabolism?
Mitochondrial β oxidation of short chain fatty acids
| Synthesis of fatty acids, triglycerides, cholesterol, phospholipids and lipoproteins
132
How is the liver involved in protein metabolism?
Most circulating proteins are produced by the liver
Albumin can be used to measure hepatic function
Metabolism of amino acids and disposal of urea - nitrogen is converted to urea in the liver, ammonia is produced and cleared
133
How is the liver involved in biotransformation and excretion?
Phase 1 reactions - in smooth endoplasmic reticulum, mediated by cytochrome P450 to produce hydroxylated/carboxylated compounds
Phase 2 reactions - subsequent conjugation with glucuronic acid, acetyl/methyl radials or glycine/taurine/sulphate
134
What volume of bile is produced and excreted per day?
3L produced, 1L excreted
135
What is bile composed of?
Water, electrolytes, phospholipids, bile salts/acids, bile pigments, cholesterol, haeme waste products, other blood substances
136
What is the function of bile?
Emulsification of fats to allow absorption
| Mechanism to remove cholesterol and waste
137
What 3 components is haemoglobin broken down to and what becomes of them?
Haem - converted to bilirubin
Globins - broken down into amino acids and recycled
Iron - bound by transferrin and returned to iron stores in the liver/bone marrow
138
Once intestinal bacteria have degraded bilirubin to urobilinogen, where does it end up?
80% is oxidised to stercobilin and excreted in faeces
20% is absorbed by extra-hepatic circulation, recycled by the liver, excreted into the systemic circulation and filtered by the kidney for excretion in urine
139
Outline the 4 main stages of bilirubin metabolism
1. Unconjugated bilirubin is bound by albumin and transported to the liver
2. UB is released from albumin in sinusoidal tissue of the liver
3. Ligandin presents UB to glucuronic acid
4. UDP-glucuronyl transferase conjugates UB (water soluble, expelled into intestines)
140
Approximately how much urobilinogen is excreted in faeces per day?
50-250 mg
141
Approximately how much urobilinogen is excreted in urine per day?
1-4 mg
142
What can metabolic functions be disturbed by?
Enzyme deficiency
Nutritional deficiency/excess
Toxic/chemical damage
Hypoxia
143
What are the 3 types of inherited metabolic liver disease (give examples)?
```
Essential product deficit (G-6-P deficiency)
Precursor accumulation (hyperammonaemia)
Alternative pathway activation (amino-acidopathy)
```
144
In liver metabolic disease, what is the effect of inhibition of β oxygenation of fatty acids?
Microvesicular steatosis
145
In liver metabolic disease, what is the effect of interfering with oxidative phosphorylation?
Insufficient ATP production
146
In liver metabolic disease, what is the effect of impairment of the respiratory chain?
Excess ROS with lipid peroxidation
147
What toxic substances can cause mitochondrial damage in the liver?
Drugs - antivirals, tetracycline
| Toxins - hypoglycin
148
What toxic substances can cause endothelial damage to hepatic veins in the liver?
Drugs - cytotoxic drugs
| Toxins - aflatoxin
149
What toxic substances can cause glutathione depletion and cell death in the liver?
Drugs - paracetamol
| Hypoxic ischaemia
150
What causes centrilobular necrosis of the liver and how might these effects be worsened?
Sepsis, shock induced ischaemia, congestive heart failure, toxicity from drugs and poisons
Exacerbated by malnutrition, infection, fasting, exercise
151
What is the pathogenesis of metabolic disease of the liver?
Severe functional disturbance
Hepatocyte injury/death/cirrhosis
Hepatomegaly due to storage of lipids
152
What are the clinical indications of metabolic disease of the liver?
Acute metabolic crisis (newborns), severe vomiting, failure to thrive, encephalopathy with acidosis, progressive retardation, seizures, hepatomegaly, jaundice
153
Describe Reye-like inherited metabolic liver disease presenting with acute onset liver failure
Age - neonatal to 3 years
History - vomiting, failure to thrive, family
Clinical features - progressive enchephalopathy, multisystem failure, acidosis
Biochemistry - hypoglycaemia, metabolic acidosis, transaminases elevated
Functional - mitochondrial dysfunction
Pathological - microvesicular steatosis
Treatment - supportive for liver failure, treat clinical features
154
What percentage of acid production in the stomach is reduced by PPIs?
90%
155
What is tachyphylaxis?
A rapid decrease in the response to a drug due to previous (long term) exposure to that drug
156
What is the role of secretin?
Promotion of alkalinisation of the small intestinal contents
157
Where is the major site of bile salt reabsorption?
Ileum
158
What brain nuclei are responsible for control of swallowing?
Non-vagal nuclei
Nucleus ambiguus
Dorsal motor nucleus
159
What are the pharmacological agents used in GORD?
```
Antacids
Alginates
Mucosal agents
H2 receptor antagonists
PPIs
Prokinetics
```
160
What are antacids?
Salts (alumunium and magnesium) which neutralise acid in the stomach and are useful in mild GORD
161
What are the actions of antacids?
Raise pH of gastic secretions
Decrease pepsin activity
May bind bile acids
162
What are the disadvantages of antacids?
Constipation (aluminium)
Diarrhoea (magnesium)
Cardiac/renal problems (some high in sodium)
Interactions - tetracyclines, digoxin, iron, prednisolone
163
What are alginates?
```
Sodium alginate (mix of polyurionic acids) used to treat GORD
Algin extracted from giant Pacific kelp (macrocystis pyrifera)
```
164
How are alginates used?
Added to antacids as foaming agents - layer of foam on stomach contents provides mechanical barrier to reflux
165
What prokinetics are used for GORD and how do they work?
Metoclopramide/domperidone Increase gastric emptying and LOS pressure
Meto increases acetylcholine release
166
What are the advantages and disadvantages of prokinetics in GORD?
GORD and dyspepsia treatment
| Drowsiness, diarrhoea, hyperprolactinaemia, renal problems
167
What is sucralfate?
Complex sucrose polymer/cytoprotective agent used for GORD
168
How does sucralfate work?
Anionic sulphate binds to positive glycoproteins in the ulcer and forms a past which blocks and buffers acid for 6-8 hours
169
What are the side effects of H2 receptor antagonists?
```
Diarrhoea
Deranged LFTs
Headache
Dizziness
Fatigue
Rash
Tachyphylaxis
```
170
What are the side effects and interactions of cimetidine?
Gynaecomastia and constipation
| Interacts with warfarin, phenytoin, theophylline (cytochrome P450)
171
What is the mechanism by which PPIs work?
Cationic sulfenamide binds irreversibly with sulphydryl groups on the proton pump causing inhibition
172
What are the side effects of PPIs?
```
Diarrhoea
Rash
Headache
Hip fracture
C.difficile infection
Cytochrome P450 interaction
```
173
What is hypochlorrhydria?
Reduced acid secretion
174
How can GORD be managed surgically?
Nissen fundoplication - fundus of stomach wrapped around lower oesophagus and sutured in place
175
What are the limitations of antacids and alginates?
Produce symptomatic relief but are relatively ineffective at producing healing of
oesophageal erosions and ulceration
176
By what percentage do H2 receptor antagonists reduce acid secretion?
60%
177
Why does stopping PPIs cause hypersecretion of gastrin?
Hyperplasia of ECL cells
178
What is triple therapy for H.pylori infection?
PPI + 2 antibiotics for a week
179
How can mucosal ulceraton by NSAIDs be reduced?
Prostaglandin analogues taken alongside (e.g. misoprostil)
