PBL Topic 4 Case 2 Flashcards
1
Q
Identify three motor functions of the stomach
A
- Storage of food until it can be processed
- Mixing of food with gastric secretions to form chyme
- Emptying chyme into small intestine at a suitable rate
2
Q
What are the orad and caudad portions of the stomach?
A
- Orad: First third of stomach
- Caudad: Second two thirds of stomach
3
Q
What is the role of the vagovagal reflex?
A
- Reduction of muscle tone in the stomach wall
- To accommodate greater quantities of food
4
Q
What is the maximum quantity of the stomach in litres?
A
- 1.5 L
5
Q
Which nucleus in the brain is responsible for the vagovagal reflex and where is this nucleus located?
A
- Dorsal vagal nucleus
- Medulla oblongata
6
Q
Which region of the stomach possesses the fewest gastric glands
A
- Lesser curvature
7
Q
What are mixing waves and what causes them?
A
- Weak peristaltic constrictor waves
- Caused by gut wall basic electrical rhythm from slow waves
8
Q
How do mixing waves change throughout the stomach? What is the effect of this on the antral contents?
A
- They become progressively more powerful towards the antrum
- Forcing antral contents under increasing pressure towards the pylorus
9
Q
What is retropulsion? What is its cause and function?
A
- Contraction of pyloric muscle impedes emptying through the pylorus
- Causing antral contents to be squeezed upstream towards the body
- Increased mixing of contents with gastric juices
10
Q
What is chyme?
A
- Mixture of food, stomach secretions and water following mixing
11
Q
What are hunger contractions?
A
- Intense stomach contraction when the stomach has been empty for several hours
- Which may result in mild pain in the stomach (pangs)
12
Q
What are hunger pangs? When do they occur and when are they most intense?
A
- Mild pain in the stomach from hunger contractions
- Which big 12-24 hours after the last ingestion of food
- Reaching their greatest intensity in 3-4 days
13
Q
Outline the process of stomach emptying
A
- Caused by ringlike constrictions
- That begin progressively farther up the stomach as it empties
- Food passes through the pyloric sphincter when it been thoroughly mixing
14
Q
Outline the nervous regulation of stomach emptying
A
- Increased food volume in the stomach causes stretching of the stomach
- Which elicits local myenteric reflexes resulting in increased activity of the pyloric pump and inhibition of the pylorus
15
Q
Outline the hormonal regulation of stomach emptying
A
- Increased volume in the stomach causing stretching fo the stomach
- Which elicits release of gastrin from G cells of the pyloric antrum
- Which secreted highly acidic gastric juice, and enhances activity of the pyloric pump
16
Q
Identify the two duodenal mechanisms to inhibit stomach emptying
A
- Inhibit the pyloric pump
- Increase the tone of the pyloric sphincter
17
Q
Identify five factors that are continually monitored that can cause enterogastric inhibitory reflexes
A
- Degree of distension
- Irritation of the mucosa
- Acidity (pH<4.0)
- Osmolality (hypotonic or hypertonic)
- Presence of breakdown products (breakdown products of protein)
18
Q
Identify 3 nervous pathways from the duodenum to the stomach that result in reflex inhibition of the stomach
A
- From duodenum to stomach via local myenteric nerves
- Extrinsic nerves from duodenum to prevertebral ganglia and then to stomach through inhibitory sympathetic nerves
- Vagus nerves to the brainstem where they inhibit excitatory signals via the vagus nerve
19
Q
Identify the role of CCK in gastric emptying
A
- Fat extracts bind to receptors on duodenal epithelium
- Which causes release of CCK
- Which inhibit the pyloric pump and increase the tone of the pyloric sphincter (reverse of gastrin)
20
Q
What are secretin and gastric inhibitory peptide (GIP) in response to?
A
- Secretin is released from duodenum in response to gastric acid
- GIP is release in upper intestine in response to fat
21
Q
Identify two functions of secretory glands in the GI tract
A
- Release of digestive enzymes
- Release of mucus for lubrication and protection
22
Q
Identify two types of nervous stimulation to GI Tract glands
A
- Enteric nervous stimulation
- Parasympathetic stimulation
23
Q
Outline how the material for secretion is formed?
A
- Nutrients diffuse into glandular cell from blood
- ATP from mitochondria combines with nutrients to synthesise product
- Which is transported through endoplasmic reticulum to Golgi complex for modification and storage in vesicles
- Release of vesicles in response to nervous or hormonal stimulation
24
Q
Outline the role of calcium ions in glandular secretions
A
- Causes vesicles to fuse with apical cell membrane
- Allowing apical cell to break open and empty vesicle by exocytosis
25
What is the importance of water and electrolytes in relation to glandular cells
- Causes cell to swell
| - Resulting in minute openings of the secretory border of the cell
26
Outline the process by which water and electrolytes enter the glandular cell
- Active transport of chloride ions into cell
- Resulting electronegativity causes inward diffusion of sodium ions
- Increased osmotic force (hypotonic solution) causes inward osmosis of water
27
What is mucus composed of?
- Glycoproteins e.g. mucin
- Water
- Electrolytes
28
Identify 5 characteristics of mucus that make it an excellent lubricant and protectant
- Adheres to food
- Coats gut wall
- Slides along epithelium with ease
- Causes adherence of faecal particles to form faeces
- Resists digestion
- Buffer acids and alkali due to mucin (amphoteric properties ) bicarbonate ions neutralise acids
29
Outline the effect of prostaglandins on mucus production
- PGE2 and PGI2
| - Act on EP4 receptors on mucus secreting cells to increase mucus production
30
Outline the effect of prostaglandins on bicarbonate production
- PGE2 and PGI2
| - Act on EP1/2 receptors on foveolar cells to increase bicarbonate production
31
What do oxyntic glands secrete and where are they located?
- Secrete HCl, pepsinogen, intrinsic factor and mucus
| - Proximal 80% of stomach (body and fundus)
32
What do pyloric glands secrete and where are they located?
- Secrete mucus and gastrin
| - Distal 20% of stomach (antral portion)
33
Identify 3 cell types of oxyntic glands and what each type secretes
- Neck cells: mucus
- Chief cells: pepsinogen
- Parietal cells: HCl + intrinsic factor
34
How many millimoles / L of HCl is secreted by oxyntic parietal cells and what is the pH?
- 160 mmol / L
| - pH = 0.8
35
What are canaliculi? Which cell type possesses them and what is their function?
- Extensive branching network
- Found in parietal cells
- Through which HCl is conducted to secretory end of cell
36
Outline the initial step of HCl formation that results in an electronegativity of -55 mV
- Active transport of chloride ions into canaliculi from cytoplasm
- Active transport of sodium ions into cytoplasm from canaliculi
37
Outline the step of HCl secretion that occurs in response to the electronegativity of -55 mV
- Negativity causes diffusion of potassium and sodium ions into canaliculi from cytoplasm
38
Outline the initial step of HCl formation that involves the proton pump and osmosis
- Water dissociates into hydrogen and hydroxyl ions
- Hydrogen is actively secreted into canaliculus in exchange for potassium ions
- Catalysed by H+K+ATPase
- Resulting in osmosis of water
- Sodium is reabsorbed into extracellular fluid through a separate pump
39
Identify 3 hormones that stimulates secretion by the proton pump and one that inhibits it
- Stimulate: Gastrin, ACh, histamine (secretagogue)
| - Inhibit: Somatostatin
40
Outline the initial step of HCl formation that involves carbon dioxide
- Metabolism of parietal produces CO2
- Which reacts with hydroxyl ion to form bicarbonate ion
- This reaction is catalysed by carbonic anhydrase
- Bicarbonate diffuses into extracellular fluid in exchange for chloride ions (and cycle repeats itself)
41
Outline the process of secretion and activation of pepsinogen.
- Secreted by chief cells of oxyntic glands
| - Activated by HCl to form pepsin
42
What is the optimum pH range for pepsin?
- pH = 1.8 - 3.5
43
What is the role of intrinsic factor?
- Absorption of B12 in the ileum
44
Identify a condition that results in achlorhydria and pernicious anaemia?
- Gastritis
45
How does the cellular composition of pyloric glands differ to that of oxyntic glands?
- Contains few chief and parietal cells
- Possesses large amounts of mucus cells
- Which are involved in lubrication of food and protecting stomach wall from gastric enzymes
46
Identify two characteristics of the mucus secreted by foveolar / surface mucus cells
- Viscid: Thick gel layer of mucus provides a shell of protection for stomach wall
- Alkaline: Neutralises any acid that comes into contact with stomach wall
47
Where are enterochromaffin-like cells (ECL cells) located and what do they secrete?
- Deep recesses of oxyntic glands
| - Secrete histamine in direct contact with the parietal cells of the gland
48
Identify the biochemical effect of ECL cell release
- Histamine acts in a paracrine fashion on H2 receptors on parietal cells
- Which elevates cAMP and activates secretion of H+ ions
49
Identify two ways in which histamine release from ECL cells can be increased
- Hormonal secretion of gastrin
| - Neural stimulation from ACh
50
Which cells secrete gastrin and where are they located?
- G cells
| - Located in pyloric glands in anturm
51
Identify the two forms of gastrin and which is most abundant
- G34 and G17 (most abundant)
52
Identify the biochemical effect of gastrin on ECL cells
- Acts on CCK2 receptors on ECL cells
| - Which increases histamine release
53
Identify a drug that inhibits gastrin action
- Proglumide
54
Identify two factors that regulate pepsinogen secretion
- Stimulation of peptic cells by ACh from vagus nerves or from enteric nervous plexus
- Stimulation of peptic cells in response to stomach acid
55
Outline the cephalic stage of gastric secretion and what percentage of gastric secretion it accounts for
- Sight, smell, thought or taste of food
- Increases activity in appetite centres of hypothalamus (e.g. lateral hypothalamic feeding centre)
- Signals are transmitted through dorsal motor nuclei and through vagus nerves to stomach
- 20%
56
Outline the gastric stage of gastric secretion and what percentage of gastric secretion it accounts for
- Food enters stomach
- Excites long vagovagal reflex, local enteric reflexes and the gastric mechanism
- All of which increase gastric juice secretion
- 70%
57
Outline the intestinal stage of gastric secretion and what percentage of gastric secretion it accounts for
- Presence of food in duodenum
- Causes stomach to secrete gastric juice
- In response to gastrin released by duodenal mucosa
- 10%
58
What is the purpose of the reverse enterogastric reflex?
- Slow passage of chyme from stomach
| - When small intestine is filled / overactive
59
Outline the reverse enterogastric reflex
- Signals transmitted through myenteric plexus, extrinsic sympathetic fibres and vagus nerves
- To inhibit stomach secretion
60
Identify three causes of the reverse enterogastric reflex
- Distension of small intestine
- Presence of protein and fat breakdown products
- Irritation of mucosa
- Acid
- Hypertonic/hypotonic fluids
61
Outline the effect of somatostatin on gastric secretion
- Paracrine inhibitory actions on gastrin release from G cells, histamine release from ECL cells
- By acting on its SST2 receptor
62
Outline the effect of ACh on somatostatin release and the subsequent effect of this
- Acts on D cells
- To inhibit somatostatin release
- To increase parietal cell acid secretion
63
Outline the effect of PGE2 and PGI2 on gastric output
- Reduces gastric output
- By acting on EP2/3 receptors on ECL cells
- To reduce histamine release which in turns reduces H+ secretion
64
Outline the gastric secretions that occurs during the interdigestive phase
- Mainly mucus secretion
| - Emotional stimuli can also increase peptic and acidic secretion
65
Outline the chemical composition of gastrin
- Molecular weight of 2400
| - Functional activity resides in terminal four amino acids
66
What is pentagastrin and its clinical uses
- Synthetic gastrin
- Composed of terminal four amino acids plus the amino acid alanine
- Given parenterally as a diagnostic aid of gastric acid function (e.g. achlorhydria, pernicious anaemia. gastric carcinoma)
67
Identify the process of carbohydrate hydrolysis
- Hydrolysis
- Splitting of the glycosidic covalent bond of a disaccharide molecule
- To form two separate monosaccharides
68
Identify the process of protein hydrolysis
- Hydrolysis reaction
- Splitting a peptide link of a proteins
- To its constituent amino acids
69
What is the optimum pH range of pepsin?
- pH: 2.0 - 3.0
70
What is the importance of collagen in protein digestion?
- Collagen is an albuminoid type protein that is affected little by other digestive enzymes
- Major constituent of intracellular connective tissue of meats
71
Identify the process of fat hydrolysis
- Hydrolysis
- Splitting of ester bonds of a triglyceride
- Into fatty acids and glycerol
72
What is the role of lingual lipase?
- Responsible for small amount of fat digestion in stomach (10%)
- Secreted by lingual glands in mouth and swallowed
73
What is dyspepsia?
- Inexact term used to describe a number of abdominal symptoms such as heartburn, nausea, or belching
74
Identify three features of dyspepsia of serious disease such as cancer
- Dysphagia
- Anorexia and weight loss
- Vomiting, haematemesis, melaena
75
Identify 3 upper GI disorders that can result in dyspepsia
- Peptic ulcer disease
- Acute gastritis
- Gallstones
76
Identify 3 other GI disorders that can result in dyspepsia (excluding upper GI disorders)
- Pancreatic disease (pancreatitis, cancer)
- Hepatic disease (hepatitis, cancer)
- Colonic carcinoma
77
Identify four drugs that can cause dyspepsia
- Bisphosphonates
- NSAIDS
- Corticosteroids
- Iron and potassium supplements
- Digoxin
78
Identify two systemic diseases that can cause dyspepsia
- Renal failure
| - Hypercalcaemia
79
What is the difference between gastritis and gastropathy?
- Gastritis is inflammation associated with mucosal injury
| - Gastropathy indicates epithelial cell damage and regeneration without inflammation
80
Identify 3 causes of acute gastritis
- H.pylori
- NSAIDS
- Alcohol
81
Identify 3 causes of chronic gastritis
- H.pylori
- Pernicious anaemia
- Post-gastrectomy
82
Outline the pathology and complications of autoimmune gastritis
- Pangastritis
- Leading to atrophic gastritis and loss of parietal cells with metaplasia
- With achlorhydria and intrinsic factor deficiency
- Resulting in pernicious anaemia
83
Outline the epidemiology of GORD
- Affects 30% of people
- Higher prevalence in older age
- Asthma patients have a higher risk of developing GORD
84
Outline 6 factors involved in the development of GORD
- Reduce LOS tone and increased number of LOS relaxations
- Hiatus hernia
- Delayed gastric emptying results in increased pressure against LOS
- Pregnancy
- Obesity
- Dietary fat, chocolate, alcohol
85
Outline the clinical features of GORD
- Heartburn and regurgitation provoked by bending, straining and lying down
- Chest pain
86
How is the chest pain or GORD distinguished from angina?
- Does not radiate down arm
- Relieved by antacids
- Worse with hot drinks and alcohol
87
How does the diagnosis of GORD differ between young and old patients
- Young patients: Diagnosed with history if no alarm signs
| - Older patients: pH monitoring at gastro-oesophageal junction if warning signs
88
Identify the treatments used in GORD
- Antacids
- Proton pump inhibitors
- H2 antagonists
- Dopamine antagonists
- Surgery: Gastroplication or fundoplication
89
Identify two complications of GORD
- Barrett's oesophagus (metaplastic columnar mucosa, risk factor for adenocarcinoma)
- Oesophagitis (redness, ulceration, iron-deficiency anaemia)
90
Outline the mechanism of action of antacids
- Neutralise acid
| - Which inhibits peptic enzymes
91
What are alginates and what are they combined with?
- Increase viscosity and adherence of mucus to oesophageal mucosa, forming a protective barrier
- Combined with an antacids
92
Identify adverse effects of antacids and how these are overcome
- Magnesium salts cause diarrhoea
- Aluminium salts cause constipation
- Overcome using combined treatment to preserve bowel function
93
Outline the mechanism of action of H2 receptor antagonists
- Inhibit histamine- and gastrin-stimulated acid secretion and pepsin secretion
94
Identify 2 H2 receptor antagonists
- Cimetidine
| - Ranitidine
95
Identify adverse effects of H2 receptor antagonists
- Gynaecomastia
| - Interacts with oral anticoagulants and TCAs due to inhibition of cytochrome P450
96
Outline the mechanism of action of proton pump inhibitors
- Enters parietal cells from bloodstream
- Irreversibly inhibits H+K+ATPase
- Preventing active secretion of hydrogen ions into canaliculus
- And thus reducing HCl production for up to 3 days
97
Identify 3 proton pump inhibitors
- Omeprazole
- Esomeprazole
- Lansoprazole
98
Direct vagal stimulation provokes acid secretion by released ACh which acts on which parietal cell receptors?
- M3
99
Identify adverse effects of proton pump inhibitors
- Dizziness
- Somnolence
- Mental confusion
100
What is non-erosive reflux disease? (NERD)
- Normal endoscopy
- Oesophagus may be hypersensitive
- Patients do not respond to proton pump inhibitors
101
What type of drug is metoclopramide and how can it be used to treat GORD?
- Anti emetic drug
- D2 receptor antagonist on vomiting centres
- Increases motility of oesophagus, stomach and duodenum
- Increasing gastric emptying
- And reduces pressure against LOS
102
Identify 3 adverse effects of metoclopramide
- Torticollis (involuntary twisting of neck)
- Occulogyric crisis (involuntary upward eye movement)
- Galactorrhea
103
What is peptic ulcer disease?
- Break in GI epithelium down to muscularis mucosa
- That occur mainly in lower oesophagus, stomach and duodenum
- Caused by H.pylori infection, NSAIDs and smoking
104
When may peptic ulcer disease occur in jejunum and ileum
- Jejunum: after surgical anastomosis to stomach
| - Ileum: Meckel's diverticulum
105
What type of bacteria is H.pylori?
- Spiral Gram-negative
106
Identify the adaptations of H.pylori that allow it to survive in the GI system
- Multiple flagella for motility to allow it to burrow deep in gastric pits
- Adhesion molecule (BabA) that allows it to adhere to Lewis b antigen
107
What are the effects of the cagA gene of H.pylori on chronic gastritis? Which form of this gene is more strongly associated with disease?
- Gene product injected into epithelial cells
- Binds to MHC-II and interferes with cell replication and apoptosis pathways
- cagA+
108
What are the effects of the vacA gene of H.pylori on chronic gastritis? Which form of this gene is more strongly associated with disease?
- Causes large vacuoles in cells
- Resulting in increased permeability, efflux of micronutrients, induction of apoptosis
- s1/ml
109
Both vacA and cagA induce which potent mediator of gastric inflammation?
- IL-8
110
Identify a genetic variation in the host in H.pylori infections
- Increased levels of IL-1 beta
| - Which is more strongly associated with gastric atrophy and subsequent carcinoma
111
Why does H.pylori cause duodenal ulceration
- Depletion of somatostatin from D cells
- Resulting in increased gastrin from G cells (hypergastrinaemia)
- Resulting in increased acid production by parietal cells
112
How does pangastritis caused by H.pylori predispose to the development of gastric cancer?
- Pangastritis results in atrophy and achlorhydria
- Allowing bacteria to proliferate
- Which may produce mutagenic nitrates from dietary nitrates
113
Identify 3 non-invasive tests for diagnosing H.pylori infection
- Serological tests (IgG)
- 13C-Urea breath test
- Stool antigen test
114
Identify 3 invasive tests for diagnosing H.pylori infection
- Biopsy urease test
- Histological examination
- Microbiological culture
115
Outline how NSAIDs can result in peptic ulceration
- PGE2 and PGI2 have cytoprotective effects
- Including increased bicarbonate and mucin, reduced gastric acid output
- NSAIDSs deplete PGE2 and PGI2 by inhibiting COX-1
- Resulting in damage to gastric mucosal barriers
116
Identify the clinical features of peptic ulcer disease
- Burning epigastric pain which can be pointed to with one finger
- Is worse at night and when hungry
- Nausea and vomiting (which may relive pain)
- Anorexia and weight loss
117
Identify the investigations in peptic ulcer disease
- Investigations for H.pylori
| - Endoscopic diagnosis to rule out cancer in older patients
118
Identify the management of peptic ulcer disease
- Smoking cessation, avoidance of NSAIDs or switching to COX-2 inhibitors . or those without low GI-side effects
- Second endoscopy after 6 weeks to rule out cancer
- Eradication therapy with a PPI and 2 antibiotics
119
Identify an example of a regimen used in eradication therapy. What additional drug would be added if this regimen failed?
- Omeprazole + clarithromycin + amoxicillin
| - Bismuth chelate
120
Identify two complications of peptic ulceration
- Perforation (leading to peritonitis)
| - Gastric outlet obstruction
121
Identify the clinical features of perforation leading to peritonitis
- Sudden, severe pain that follows the spread of gastric contents
- Shoulder tip pain via C3-C5
- Shallow breathing due to limitation of diaphragmatic movements
- Generalised rigidity of abdomen
- Absent bowel sounds and reduced liver percussion
- CXR shows free air beneath diaphragm
122
Identify the treatments involved in perforation
- Acute perforation: simple closure (partial mastectomy may be required)
- Conservative management in elderly very sick patients: nasogastric suction, IV fluids and antibiotics
123
Outline the pathology of gastric outlet obsturction
- Obstruction in the pre-pyloric, pyloric or duodenal regions
- Due to an active ulcer with surrounding oedema or healing form an ulcer followed by scarring
- Stomach becomes full of gastric juice and ingested fluid and food
- Resulting in projectile vomit that is large in volume and dehydration
124
Outline the treatment involved in gastric outlet obstruction
- Nasogastric suction
- IV correction of dehydration
- For ulcers: PPI, endoscopic balloon dilatation, gastrectomy
125
What is dumping?
- Complication of gastric bypass
- Resulting in distension of proximal small intestine as the hypertonic contrast draws fluid into the lumen
- Resulting in nausea, sweating, faintness and palpitations
126
Outline the mechanism of action of bismuth chelate as well as two side effects
- Toxic effects on H.pylori
- Prevents its adherence to mucosa and inhibition of its enzymes
- Nausea and vomiting
- Blackening of tongue and faeces
127
Outline the mechanism of action of misoprostol
- Analogue on PGE1
- Direct action on EP2/3 receptor on ECL
- Inhibiting basal secretion of gastric acid and augments secretion of mucus and bicarbonate
- Promotes healing of ulcers and prevents gastric damage that occurs with NSAIDs
128
Outline two adverse effects of misoprostol
- Diarrhoea
- Abdominal cramps
- Uterine constrictions
129
Outline the mechanism of action of clarithromycin
- Macrolide
- Inhibition of protein synthesis by interfering with translocation
- Binds to P site on 50S subunit on bacterial ribosome
- Preventing addition of incoming tRNA and its attached amino acid
130
Outline the mechanism of action of amoxicillin
- Penicillin
- Interferes synthesis of bacterial cell wall peptidoglycan
- Attaches to penicillin binding proteins
- Inhibits transpeptidation enzyme that crosslinks the peptide chains attached to the backbone of peptidoglycan
131
Outline the mechanism of action of metronidazole
- Amoebicidal
- It is reduced of its nitro-groups in anionic radicals
- It inhibits nucleic acid synthesis by disrupting DNA of microbial cells
132
Outline the epidemiology of gastric cancer
- Fourth most common cancer worldwide
- Peak incidence 50-70
- Highest incidence in Eastern Asia, Europe and South America
133
Outline the pathogenesis of gastric cancer
- H.pylori is a group1 gastric carcinogen
- Dietary nitrates can be converted to nitrosamines by bacteria (also present in patients with achlorhydria)
- Smoking and diets high in salt increase risk
- Loss of p53 and APC, mutations in E-cadherin gene CDH-1
134
Outline the intestinal type (type 1) of gastric cancer
- Well formed glandular structures (differentiated)
- More likely to involve distal stomach, with intestinal metaplasia often with H.pylori
- Strong environmental association
135
Outline the diffuse type (type 2) of gastric cancer
- Poorly cohesive cells (undifferentiated)
- More likely to involve cardia (loss of expression of E-cadherin is key event for carcinogenesis)
- Similar frequencies in geographic areas
- Accounts for 50% of gastric cancers and carries poorer prognosis
136
Outline the clinical features of gastric cancer
- Symptoms are associated with advanced disease
- Epigastric pain (relieved by food and antacids)
- Nausea and vomiting
- Anorexia and weight loss
- Dysphagia
137
Outline 5 signs of metastatic spread of gastric cancer
- Jaundice and ascites if liver involvement
- Virchow's node (Troisier's sign) is lymph node involvement
- Sister Mary Josephs nodule in epigastric region
- Krukenburg tumour in ovaries
- Dermatomyositis and acanthosis nigricans
138
Outline the diagnostic procedures involved in gastric cancer
- Gastroscopy to obtain biopsies for histological assessment
- CT of chest and abdomen demonstrates gastric wall thickening, lymphadenopathy and secondaries
- Endoscopic ultrasound demonstrates depth of penetration
139
What is TNM staging?
- Classifies tumour according to depth of tumour invasion (T) presence of lymph nodes (N) and metastasis (M)
- TNM classification is combined into stage categories
- Which can be used to determine 5 year survival rate
140
Outline the survival rates for each stage of gastric cancer
- Stage 1: 99%
- Stage 2: 65%
- Stage 3: 35%
- Stage 4: 5%
141
Outline the treatment options for gastric cancer
- Early gastric cancer: Endoscopic mucosal resection
| - Advanced disease: Gastrectomy with lymphadenectomy
142
Outine palliative measures involved in gastric cancer
- Chemotherapy can alleviate symptoms
- Laser ablation for control of dysphagia and bleeding
- Dilation and stents for dysphagia or vomiting
- Nasogastric tube for relief of vomiting from gastric outlet obstruction
143
Outline the causes, symptoms and treatment of primary gastric lymphoma
- Causes include H.pylori and chromosomal abnormalities (t(11:18))
- Diagnosed in 60s with stage 1/2
- Symptoms include stomach pain, ulcers, fatigue or fever
- Treatment involved eradication of H.pylori and chemotherapy
144
Outine the pathology of pernicious anaemia
- Atrophic gastritis
- Chief cells replaced by mucin-secreting cells
- Achlorhydria and absent intrinsic factor production with B12 malabsorption
- Blocking antibody prevents binding of B12 to intrinsic factor
- Precipitating antibody which inhibits B12 / intrinsic factor complex binding to receptor site in ileum
145
Outline the clinical features of pernicious anaemia
- Polyneuropathy (tingling)
- Lemon-yellow colour owing to jaundice and pallor
- Glossitis and angular stomatitis
146
Outline the investigations and findings in pernicious anaemia
- Haematological findings show features of megaloblastic anaemia (MCV>96 fL) with leukopenia / thrombocytopenia
- Schilling test shows low B12 levels
- Raised bilirubin due to ineffective erythropoiesis
147
Outline the treatment for pernicious anaemia
- Intramuscular hydroxocobalamin
| - Oral B12
148
What is meant by referred pain?
- Visceral pain is referred to skin areas
- That are innervated by the same segments of spinal cord
- Since brain misinterprets source of obnoxious stimulation
- Due to common spinothalamic neurons (convergence projection theory)
149
Where is referred pain from stomach felt? Identify the nerve roots involved
- Lower chest and abdominal wall
| - T5-T9
150
Where is referred pain from appendix felt?
- Umbilicus (T10)
| - Spreads to right iliac fossa ( (T12-L1)
151
Where is referred pain from gallbladder felt?
- Lower chest and abdominal wall (T5-T9)
| - Tip of shoulder due to involvement of diaphragmatic parietal peritoneum (C3-C5)
152
What is shared decision making?
- Process in which clinicians and patients work together
- To select tests, treatments, management or support packages
- Based on both clinical evidence and the patients informed preference
153
What is the importance of shared decision making?
- Ethical imperative by professional regulatory bodies
| - Patients want to be more involved than they currently are in making decisions about their own health and health care
154
What does patient driven decision making involve?
- Physician presents all options
- Physician makes no recommendation
- Patient makes their own choice
155
What does physician recommendation decision making involve?
- Physician presents all options
- Physician makes a recommendation
- Based on patient's values and perspective
156
What is meant by equal partners decision making involve?
- Physician presents all options
- Physicians and patients work together to reach a mutual decision
- Based on patients values and perspectives
157
What is meant by informed non-dissent decision making?
- Physician determines best course of action
- Based on patients values and perspectives
- Patient has a right to veto a decision
- Silent is construed as tacit consent
158
What is meant by physician driven decision making
- Only applies to value neutral decisions
- Care must be taken as they do not necessarily know what a patient deems as value neutral
- Physicians should be aware of possible patient perspectives
159
What should be taken into account in an occupational history?
- All jobs done
- What each job involved
- Specifically any chemical or dust exposure
160
What information from a history might suggest an occupational disorder?
- Symptoms improve over the weekend or during holidays
161
Identify factors of a job that may cause stress
- Work overload
- Poor work relationships
- Poor control over work
- Role ambiguity
162
Outline the demand-job control model of stress
- Two aspects of job strain
- Job demands which reflect conditions that affect performance
- Job autonomy which reflects control over the speed or nature of decisions made within the job
- High job demands and low job autonomy predict coronary heart disease
163
How has the demand-job control model of stress been made to include social support?
- Emotional support involving trust between colleagues and social cohesion
- Instrumental social supporting involving provision of extra resources and assistance
- High levels of social support correlate with fewer CHD symptoms
164
What are zymogens?
- Enzyme precursors requiring some change to become active
| - Such as pepsinogen, trypsinogen
165
What is the clinical use of pirenzepine? Outline its mechanism of action
- M1 antagonist
- Inhibits gastric secretion by action on ganglion cells
- Peptic ulcers
