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Semester 4: Nutrition and Metabolism > PBL Topic 4 Case 2 > Flashcards

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
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2
Q

What are the orad and caudad portions of the stomach?

A
  • Orad: First third of stomach

- Caudad: Second two thirds of stomach

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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

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4
Q

What is the maximum quantity of the stomach in litres?

A
  • 1.5 L
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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

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6
Q

Which region of the stomach possesses the fewest gastric glands

A
  • Lesser curvature
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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

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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

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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
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10
Q

What is chyme?

A
  • Mixture of food, stomach secretions and water following mixing
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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)
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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
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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
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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
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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
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16
Q

Identify the two duodenal mechanisms to inhibit stomach emptying

A
  • Inhibit the pyloric pump

- Increase the tone of the pyloric sphincter

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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)
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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
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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)
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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
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21
Q

Identify two functions of secretory glands in the GI tract

A
  • Release of digestive enzymes

- Release of mucus for lubrication and protection

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22
Q

Identify two types of nervous stimulation to GI Tract glands

A
  • Enteric nervous stimulation

- Parasympathetic stimulation

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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
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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

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25
Q

What is the importance of water and electrolytes in relation to glandular cells

A
  • Causes cell to swell

- Resulting in minute openings of the secretory border of the cell

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26
Q

Outline the process by which water and electrolytes enter the glandular cell

A
  • 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
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27
Q

What is mucus composed of?

A
  • Glycoproteins e.g. mucin
  • Water
  • Electrolytes
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28
Q

Identify 5 characteristics of mucus that make it an excellent lubricant and protectant

A
  • 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
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29
Q

Outline the effect of prostaglandins on mucus production

A
  • PGE2 and PGI2

- Act on EP4 receptors on mucus secreting cells to increase mucus production

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30
Q

Outline the effect of prostaglandins on bicarbonate production

A
  • PGE2 and PGI2

- Act on EP1/2 receptors on foveolar cells to increase bicarbonate production

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31
Q

What do oxyntic glands secrete and where are they located?

A
  • Secrete HCl, pepsinogen, intrinsic factor and mucus

- Proximal 80% of stomach (body and fundus)

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32
Q

What do pyloric glands secrete and where are they located?

A
  • Secrete mucus and gastrin

- Distal 20% of stomach (antral portion)

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33
Q

Identify 3 cell types of oxyntic glands and what each type secretes

A
  • Neck cells: mucus
  • Chief cells: pepsinogen
  • Parietal cells: HCl + intrinsic factor
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34
Q

How many millimoles / L of HCl is secreted by oxyntic parietal cells and what is the pH?

A
  • 160 mmol / L

- pH = 0.8

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35
Q

What are canaliculi? Which cell type possesses them and what is their function?

A
  • Extensive branching network
  • Found in parietal cells
  • Through which HCl is conducted to secretory end of cell
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36
Q

Outline the initial step of HCl formation that results in an electronegativity of -55 mV

A
  • Active transport of chloride ions into canaliculi from cytoplasm
  • Active transport of sodium ions into cytoplasm from canaliculi
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37
Q

Outline the step of HCl secretion that occurs in response to the electronegativity of -55 mV

A
  • Negativity causes diffusion of potassium and sodium ions into canaliculi from cytoplasm
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38
Q

Outline the initial step of HCl formation that involves the proton pump and osmosis

A
  • 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
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39
Q

Identify 3 hormones that stimulates secretion by the proton pump and one that inhibits it

A
  • Stimulate: Gastrin, ACh, histamine (secretagogue)

- Inhibit: Somatostatin

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40
Q

Outline the initial step of HCl formation that involves carbon dioxide

A
  • 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)
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41
Q

Outline the process of secretion and activation of pepsinogen.

A
  • Secreted by chief cells of oxyntic glands

- Activated by HCl to form pepsin

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42
Q

What is the optimum pH range for pepsin?

A
  • pH = 1.8 - 3.5
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43
Q

What is the role of intrinsic factor?

A
  • Absorption of B12 in the ileum
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44
Q

Identify a condition that results in achlorhydria and pernicious anaemia?

A
  • Gastritis
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45
Q

How does the cellular composition of pyloric glands differ to that of oxyntic glands?

A
  • 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
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46
Q

Identify two characteristics of the mucus secreted by foveolar / surface mucus cells

A
  • 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
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47
Q

Where are enterochromaffin-like cells (ECL cells) located and what do they secrete?

A
  • Deep recesses of oxyntic glands

- Secrete histamine in direct contact with the parietal cells of the gland

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48
Q

Identify the biochemical effect of ECL cell release

A
  • Histamine acts in a paracrine fashion on H2 receptors on parietal cells
  • Which elevates cAMP and activates secretion of H+ ions
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49
Q

Identify two ways in which histamine release from ECL cells can be increased

A
  • Hormonal secretion of gastrin

- Neural stimulation from ACh

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50
Q

Which cells secrete gastrin and where are they located?

A
  • G cells

- Located in pyloric glands in anturm

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51
Q

Identify the two forms of gastrin and which is most abundant

A
  • G34 and G17 (most abundant)
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52
Q

Identify the biochemical effect of gastrin on ECL cells

A
  • Acts on CCK2 receptors on ECL cells

- Which increases histamine release

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53
Q

Identify a drug that inhibits gastrin action

A
  • Proglumide
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54
Q

Identify two factors that regulate pepsinogen secretion

A
  • Stimulation of peptic cells by ACh from vagus nerves or from enteric nervous plexus
  • Stimulation of peptic cells in response to stomach acid
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55
Q

Outline the cephalic stage of gastric secretion and what percentage of gastric secretion it accounts for

A
  • 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%
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56
Q

Outline the gastric stage of gastric secretion and what percentage of gastric secretion it accounts for

A
  • Food enters stomach
  • Excites long vagovagal reflex, local enteric reflexes and the gastric mechanism
  • All of which increase gastric juice secretion
  • 70%
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57
Q

Outline the intestinal stage of gastric secretion and what percentage of gastric secretion it accounts for

A
  • Presence of food in duodenum
  • Causes stomach to secrete gastric juice
  • In response to gastrin released by duodenal mucosa
  • 10%
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58
Q

What is the purpose of the reverse enterogastric reflex?

A
  • Slow passage of chyme from stomach

- When small intestine is filled / overactive

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59
Q

Outline the reverse enterogastric reflex

A
  • Signals transmitted through myenteric plexus, extrinsic sympathetic fibres and vagus nerves
  • To inhibit stomach secretion
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60
Q

Identify three causes of the reverse enterogastric reflex

A
  • Distension of small intestine
  • Presence of protein and fat breakdown products
  • Irritation of mucosa
  • Acid
  • Hypertonic/hypotonic fluids
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61
Q

Outline the effect of somatostatin on gastric secretion

A
  • Paracrine inhibitory actions on gastrin release from G cells, histamine release from ECL cells
  • By acting on its SST2 receptor
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62
Q

Outline the effect of ACh on somatostatin release and the subsequent effect of this

A
  • Acts on D cells
  • To inhibit somatostatin release
  • To increase parietal cell acid secretion
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63
Q

Outline the effect of PGE2 and PGI2 on gastric output

A
  • Reduces gastric output
  • By acting on EP2/3 receptors on ECL cells
  • To reduce histamine release which in turns reduces H+ secretion
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64
Q

Outline the gastric secretions that occurs during the interdigestive phase

A
  • Mainly mucus secretion

- Emotional stimuli can also increase peptic and acidic secretion

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65
Q

Outline the chemical composition of gastrin

A
  • Molecular weight of 2400

- Functional activity resides in terminal four amino acids

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66
Q

What is pentagastrin and its clinical uses

A
  • 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)
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67
Q

Identify the process of carbohydrate hydrolysis

A
  • Hydrolysis
  • Splitting of the glycosidic covalent bond of a disaccharide molecule
  • To form two separate monosaccharides
68
Q

Identify the process of protein hydrolysis

A
  • Hydrolysis reaction
  • Splitting a peptide link of a proteins
  • To its constituent amino acids
69
Q

What is the optimum pH range of pepsin?

A
  • pH: 2.0 - 3.0
70
Q

What is the importance of collagen in protein digestion?

A
  • Collagen is an albuminoid type protein that is affected little by other digestive enzymes
  • Major constituent of intracellular connective tissue of meats
71
Q

Identify the process of fat hydrolysis

A
  • Hydrolysis
  • Splitting of ester bonds of a triglyceride
  • Into fatty acids and glycerol
72
Q

What is the role of lingual lipase?

A
  • Responsible for small amount of fat digestion in stomach (10%)
  • Secreted by lingual glands in mouth and swallowed
73
Q

What is dyspepsia?

A
  • Inexact term used to describe a number of abdominal symptoms such as heartburn, nausea, or belching
74
Q

Identify three features of dyspepsia of serious disease such as cancer

A
  • Dysphagia
  • Anorexia and weight loss
  • Vomiting, haematemesis, melaena
75
Q

Identify 3 upper GI disorders that can result in dyspepsia

A
  • Peptic ulcer disease
  • Acute gastritis
  • Gallstones
76
Q

Identify 3 other GI disorders that can result in dyspepsia (excluding upper GI disorders)

A
  • Pancreatic disease (pancreatitis, cancer)
  • Hepatic disease (hepatitis, cancer)
  • Colonic carcinoma
77
Q

Identify four drugs that can cause dyspepsia

A
  • Bisphosphonates
  • NSAIDS
  • Corticosteroids
  • Iron and potassium supplements
  • Digoxin
78
Q

Identify two systemic diseases that can cause dyspepsia

A
  • Renal failure

- Hypercalcaemia

79
Q

What is the difference between gastritis and gastropathy?

A
  • Gastritis is inflammation associated with mucosal injury

- Gastropathy indicates epithelial cell damage and regeneration without inflammation

80
Q

Identify 3 causes of acute gastritis

A
  • H.pylori
  • NSAIDS
  • Alcohol
81
Q

Identify 3 causes of chronic gastritis

A
  • H.pylori
  • Pernicious anaemia
  • Post-gastrectomy
82
Q

Outline the pathology and complications of autoimmune gastritis

A
  • Pangastritis
  • Leading to atrophic gastritis and loss of parietal cells with metaplasia
  • With achlorhydria and intrinsic factor deficiency
  • Resulting in pernicious anaemia
83
Q

Outline the epidemiology of GORD

A
  • Affects 30% of people
  • Higher prevalence in older age
  • Asthma patients have a higher risk of developing GORD
84
Q

Outline 6 factors involved in the development of GORD

A
  • 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
Q

Outline the clinical features of GORD

A
  • Heartburn and regurgitation provoked by bending, straining and lying down
  • Chest pain
86
Q

How is the chest pain or GORD distinguished from angina?

A
  • Does not radiate down arm
  • Relieved by antacids
  • Worse with hot drinks and alcohol
87
Q

How does the diagnosis of GORD differ between young and old patients

A
  • Young patients: Diagnosed with history if no alarm signs

- Older patients: pH monitoring at gastro-oesophageal junction if warning signs

88
Q

Identify the treatments used in GORD

A
  • Antacids
  • Proton pump inhibitors
  • H2 antagonists
  • Dopamine antagonists
  • Surgery: Gastroplication or fundoplication
89
Q

Identify two complications of GORD

A
  • Barrett’s oesophagus (metaplastic columnar mucosa, risk factor for adenocarcinoma)
  • Oesophagitis (redness, ulceration, iron-deficiency anaemia)
90
Q

Outline the mechanism of action of antacids

A
  • Neutralise acid

- Which inhibits peptic enzymes

91
Q

What are alginates and what are they combined with?

A
  • Increase viscosity and adherence of mucus to oesophageal mucosa, forming a protective barrier
  • Combined with an antacids
92
Q

Identify adverse effects of antacids and how these are overcome

A
  • Magnesium salts cause diarrhoea
  • Aluminium salts cause constipation
  • Overcome using combined treatment to preserve bowel function
93
Q

Outline the mechanism of action of H2 receptor antagonists

A
  • Inhibit histamine- and gastrin-stimulated acid secretion and pepsin secretion
94
Q

Identify 2 H2 receptor antagonists

A
  • Cimetidine

- Ranitidine

95
Q

Identify adverse effects of H2 receptor antagonists

A
  • Gynaecomastia

- Interacts with oral anticoagulants and TCAs due to inhibition of cytochrome P450

96
Q

Outline the mechanism of action of proton pump inhibitors

A
  • 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
Q

Identify 3 proton pump inhibitors

A
  • Omeprazole
  • Esomeprazole
  • Lansoprazole
98
Q

Direct vagal stimulation provokes acid secretion by released ACh which acts on which parietal cell receptors?

99
Q

Identify adverse effects of proton pump inhibitors

A
  • Dizziness
  • Somnolence
  • Mental confusion
100
Q

What is non-erosive reflux disease? (NERD)

A
  • Normal endoscopy
  • Oesophagus may be hypersensitive
  • Patients do not respond to proton pump inhibitors
101
Q

What type of drug is metoclopramide and how can it be used to treat GORD?

A
  • 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
Q

Identify 3 adverse effects of metoclopramide

A
  • Torticollis (involuntary twisting of neck)
  • Occulogyric crisis (involuntary upward eye movement)
  • Galactorrhea
103
Q

What is peptic ulcer disease?

A
  • 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
Q

When may peptic ulcer disease occur in jejunum and ileum

A
  • Jejunum: after surgical anastomosis to stomach

- Ileum: Meckel’s diverticulum

105
Q

What type of bacteria is H.pylori?

A
  • Spiral Gram-negative
106
Q

Identify the adaptations of H.pylori that allow it to survive in the GI system

A
  • 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
Q

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?

A
  • Gene product injected into epithelial cells
  • Binds to MHC-II and interferes with cell replication and apoptosis pathways
  • cagA+
108
Q

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?

A
  • Causes large vacuoles in cells
  • Resulting in increased permeability, efflux of micronutrients, induction of apoptosis
  • s1/ml
109
Q

Both vacA and cagA induce which potent mediator of gastric inflammation?

110
Q

Identify a genetic variation in the host in H.pylori infections

A
  • Increased levels of IL-1 beta

- Which is more strongly associated with gastric atrophy and subsequent carcinoma

111
Q

Why does H.pylori cause duodenal ulceration

A
  • Depletion of somatostatin from D cells
  • Resulting in increased gastrin from G cells (hypergastrinaemia)
  • Resulting in increased acid production by parietal cells
112
Q

How does pangastritis caused by H.pylori predispose to the development of gastric cancer?

A
  • Pangastritis results in atrophy and achlorhydria
  • Allowing bacteria to proliferate
  • Which may produce mutagenic nitrates from dietary nitrates
113
Q

Identify 3 non-invasive tests for diagnosing H.pylori infection

A
  • Serological tests (IgG)
  • 13C-Urea breath test
  • Stool antigen test
114
Q

Identify 3 invasive tests for diagnosing H.pylori infection

A
  • Biopsy urease test
  • Histological examination
  • Microbiological culture
115
Q

Outline how NSAIDs can result in peptic ulceration

A
  • 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
Q

Identify the clinical features of peptic ulcer disease

A
  • 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
Q

Identify the investigations in peptic ulcer disease

A
  • Investigations for H.pylori

- Endoscopic diagnosis to rule out cancer in older patients

118
Q

Identify the management of peptic ulcer disease

A
  • 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
Q

Identify an example of a regimen used in eradication therapy. What additional drug would be added if this regimen failed?

A
  • Omeprazole + clarithromycin + amoxicillin

- Bismuth chelate

120
Q

Identify two complications of peptic ulceration

A
  • Perforation (leading to peritonitis)

- Gastric outlet obstruction

121
Q

Identify the clinical features of perforation leading to peritonitis

A
  • 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
Q

Identify the treatments involved in perforation

A
  • Acute perforation: simple closure (partial mastectomy may be required)
  • Conservative management in elderly very sick patients: nasogastric suction, IV fluids and antibiotics
123
Q

Outline the pathology of gastric outlet obsturction

A
  • 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
Q

Outline the treatment involved in gastric outlet obstruction

A
  • Nasogastric suction
  • IV correction of dehydration
  • For ulcers: PPI, endoscopic balloon dilatation, gastrectomy
125
Q

What is dumping?

A
  • 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
Q

Outline the mechanism of action of bismuth chelate as well as two side effects

A
  • Toxic effects on H.pylori
  • Prevents its adherence to mucosa and inhibition of its enzymes
  • Nausea and vomiting
  • Blackening of tongue and faeces
127
Q

Outline the mechanism of action of misoprostol

A
  • 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
Q

Outline two adverse effects of misoprostol

A
  • Diarrhoea
  • Abdominal cramps
  • Uterine constrictions
129
Q

Outline the mechanism of action of clarithromycin

A
  • 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
Q

Outline the mechanism of action of amoxicillin

A
  • 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
Q

Outline the mechanism of action of metronidazole

A
  • Amoebicidal
  • It is reduced of its nitro-groups in anionic radicals
  • It inhibits nucleic acid synthesis by disrupting DNA of microbial cells
132
Q

Outline the epidemiology of gastric cancer

A
  • Fourth most common cancer worldwide
  • Peak incidence 50-70
  • Highest incidence in Eastern Asia, Europe and South America
133
Q

Outline the pathogenesis of gastric cancer

A
  • 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
Q

Outline the intestinal type (type 1) of gastric cancer

A
  • Well formed glandular structures (differentiated)
  • More likely to involve distal stomach, with intestinal metaplasia often with H.pylori
  • Strong environmental association
135
Q

Outline the diffuse type (type 2) of gastric cancer

A
  • 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
Q

Outline the clinical features of gastric cancer

A
  • Symptoms are associated with advanced disease
  • Epigastric pain (relieved by food and antacids)
  • Nausea and vomiting
  • Anorexia and weight loss
  • Dysphagia
137
Q

Outline 5 signs of metastatic spread of gastric cancer

A
  • 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
Q

Outline the diagnostic procedures involved in gastric cancer

A
  • 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
Q

What is TNM staging?

A
  • 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
Q

Outline the survival rates for each stage of gastric cancer

A
  • Stage 1: 99%
  • Stage 2: 65%
  • Stage 3: 35%
  • Stage 4: 5%
141
Q

Outline the treatment options for gastric cancer

A
  • Early gastric cancer: Endoscopic mucosal resection

- Advanced disease: Gastrectomy with lymphadenectomy

142
Q

Outine palliative measures involved in gastric cancer

A
  • 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
Q

Outline the causes, symptoms and treatment of primary gastric lymphoma

A
  • 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
Q

Outine the pathology of pernicious anaemia

A
  • 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
Q

Outline the clinical features of pernicious anaemia

A
  • Polyneuropathy (tingling)
  • Lemon-yellow colour owing to jaundice and pallor
  • Glossitis and angular stomatitis
146
Q

Outline the investigations and findings in pernicious anaemia

A
  • 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
Q

Outline the treatment for pernicious anaemia

A
  • Intramuscular hydroxocobalamin

- Oral B12

148
Q

What is meant by referred pain?

A
  • 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
Q

Where is referred pain from stomach felt? Identify the nerve roots involved

A
  • Lower chest and abdominal wall

- T5-T9

150
Q

Where is referred pain from appendix felt?

A
  • Umbilicus (T10)

- Spreads to right iliac fossa ( (T12-L1)

151
Q

Where is referred pain from gallbladder felt?

A
  • Lower chest and abdominal wall (T5-T9)

- Tip of shoulder due to involvement of diaphragmatic parietal peritoneum (C3-C5)

152
Q

What is shared decision making?

A
  • 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
Q

What is the importance of shared decision making?

A
  • 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
Q

What does patient driven decision making involve?

A
  • Physician presents all options
  • Physician makes no recommendation
  • Patient makes their own choice
155
Q

What does physician recommendation decision making involve?

A
  • Physician presents all options
  • Physician makes a recommendation
  • Based on patient’s values and perspective
156
Q

What is meant by equal partners decision making involve?

A
  • Physician presents all options
  • Physicians and patients work together to reach a mutual decision
  • Based on patients values and perspectives
157
Q

What is meant by informed non-dissent decision making?

A
  • 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
Q

What is meant by physician driven decision making

A
  • 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
Q

What should be taken into account in an occupational history?

A
  • All jobs done
  • What each job involved
  • Specifically any chemical or dust exposure
160
Q

What information from a history might suggest an occupational disorder?

A
  • Symptoms improve over the weekend or during holidays
161
Q

Identify factors of a job that may cause stress

A
  • Work overload
  • Poor work relationships
  • Poor control over work
  • Role ambiguity
162
Q

Outline the demand-job control model of stress

A
  • 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
Q

How has the demand-job control model of stress been made to include social support?

A
  • 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
Q

What are zymogens?

A
  • Enzyme precursors requiring some change to become active

- Such as pepsinogen, trypsinogen

165
Q

What is the clinical use of pirenzepine? Outline its mechanism of action

A
  • M1 antagonist
  • Inhibits gastric secretion by action on ganglion cells
  • Peptic ulcers

Semester 4: Nutrition and Metabolism (17 decks)

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