CASE 1

Question 1

what is barrett’s oesophagus?

Answer 1

change of epithelium from stratified squamous to gastric glandular columnar epithelium in the lower part of the oesophagus

Question 2

what layer of the oesophagus in barrett’s undergoes metaplasia, and then occasionally dysplasia?

Answer 2

mucosal layer

Question 3

what is barrett’s a consequence of?

Answer 3

GORD - repeated damage from gastric reflux

Question 4

barrett’s oesophagus is a major risk factor in what?

Answer 4

oesophageal adenocarcinoma

Question 5

what is the sequence in barrett’s to cancer?

Answer 5

metaplasia-dysplasia-adenocarcinoma sequence

Question 6

what are risk factors for barrett’s?

Answer 6

• GORD
• acid-bile reflux
• increasing age
• obesity
• white ethnicity
• male
• smoking (but not alcohol)

Question 7

clinical features of barrett’s

Answer 7

the change from normal to premalignant cells is asymptomatic, however patients may have symptoms of acid reflux:
• heartburn
• regurgitation
• dysphagia
• haematemesis (vomiting blood)
• unintentional weight loss
• less common : chest pain, laryngitis, cough, dyspnoea,
wheezing

Question 8

what is the main investigation in barrett’s?

Answer 8

upper GI endoscopy with biopsy

Question 9

how does the oesophagus in barrett’s visually change?

Answer 9

paler squamous epithelium is replaced with ‘salmon-coloured’ columnar epithelium above the gastro-oesophageal junction (GOJ)

Question 10

what is oral mucosa like?

Answer 10

thick stratified squamous epithelium which is resistant to abrasion, produces defensins to inhibit bacterial growth

Question 11

what are the muscles of mastication and what are they innervated by?

Answer 11

innervated by CNV3 = masseter, temporalis, medial and lateral pterygoid

Question 12

what does saliva contain?

Answer 12

water (99%), lipases and alpha-amylase, mucoproteins (lubricant), lysozyme, immunoglobulins (esp IgA), electrolytes, calcium and phosphate (dental repair)

Question 13

superior vs inferior salivatory nucleus

Answer 13

• superior salivatory nucleus = CN VII = sublingual and
submandibular glands
• inferior salivatory nucleus = CN IX = parotid

Question 14

where is Meissner’s plexus and what does it mainly control?

Answer 14

• submucosa
• controls mainly GI secretion and local blood flow

Question 15

where is the myenteric plexus and what does it control?

Answer 15

• between longitudinal and circular muscle layers
• controls motility
• also secretes vasoactive intestinal polypeptide - the resulting inhibitory signals are especially useful for inhibiting some of the intestinal sphincter muscles that impede movement of food

Question 16

what is the usual stimulus for peristalsis?

Answer 16

distention of the gut

Question 17

peristalsis requires an active what?

Answer 17

myenteric plexus

Question 18

what are the 4 swallowing stages?

Answer 18

1. cephalic
2. oral (voluntary)
3. pharyngeal (involuntary)
4. oesophageal (involuntary)

Question 19

what is the cephalic stage?

Answer 19

thinking ab having a meal

The cephalic phase of digestion is the stage in which the stomach responds to the mere sight, smell, taste, or thought of food. About 20% of total acid secretion occurs before food enters the stomach.

Question 20

what type of muscle is used in the oral and pharyngeal stages of swallowing?

Answer 20

striated

Question 21

how does the neural control differ for the different 3 main stages of swallowing?

Answer 21

1. oral = cortex/medulla
2. pharyngeal = medulla
3. oesophageal = medulla/ENS (mainly vagal nerve and ENS)

Question 22

top part of oesophagus and pharynx controlled by __________ and bottom part by __________

Answer 22

top part of oesophagus and pharynx controlled by nucleus ambiguous and bottom part by dorsal motor nucleus of vagus

Question 23

describe the chewing reflex

Answer 23

• the presence of bolus of food in the mouth initiates reflex inhibition of the muscles of mastication, which allows the lower jaw to drop
• the drop in turn initiates a stretch reflex of the jaw muscles that leads to rebound contraction
• this causes raising of the jaw to cause closure of the teeth, but it also compresses the bolus again against the linings of the mouth, which inhibits the jaw muscles once again, allowing the jaw to drop and rebound another time
• this leads to the physical breakdown of food, which is important for the digestion of many carbs

Question 24

the rate of digestion is absolutely dependent on what?

Answer 24

the total SA exposed to the digestive secretions

Question 25

upper oesophageal sphincter innervation?

Answer 25

CN X

Question 26

for the UOS to open, what must relax?

Answer 26

cricopharyngeus

Question 27

in swallowing, what happens after the tongue thrusts up and back?

Answer 27

1. tongue thrusts up and back 2. nasopharynx closed 3. larynx elevated 4. airway closed 5. upper oesophageal sphincter open 6. pharynx contracts 1 + 2 = bolus in mouth 3-6 = bolus moves through pharynx and UOS

Question 28

what sphincter fails in GORD?

Answer 28

LOS

Question 29

why is intraoesophageal pressure -ve?

Answer 29

lungs and pleura pull against oesophagus

Question 30

taste nuclei?

Answer 30

nucleus solitarius : rostral (taste anterior 2/3 = CN VII), caudal (taste posterior 1/3 = CN IX)

Question 31

what are important efferent nuclei in swallowing?

Answer 31

> nucleus ambiguous (IX, X) > dorsal vagal nucleus (X) > hypoglossal nucleus (XII)

Question 32

saliva is secreted how?

Answer 32

2 stage process = a primary secretion from the acinus is modified by duct cells to result in a hypotonic secretion

Question 33

parasympathetic vs sympathetic nerve activity effect on saliva

Answer 33

Question 34

what happens when an AP arrives at a salivary gland?

Answer 34

ACh activates M1/M3 — phospholipase C — IP3 — Ca++ — +ve effect on Cl- and K+ channels — increased ion flow rate — increased Cl- movements — increased Na+ movement — increased H20 osmotic movement

Question 35

what causes acid neutralisation in the lower oesophagus?

Answer 35

HCO3 in the saliva

Question 36

Na/H channels in the oesophageal epithelium do what?

Answer 36

remove H ions

Question 37

how do acinar cells and duct cells differ in terms of H20 permeability?

Answer 37

duct cells impermeable to water unlike acinar cells — hypotonic final saliva

Question 38

achalasia — failure of the ___ to relax and is associated with lack of ______. caused by the destruction of the ganglion cells in the ________ plexus, particularly the ___ inhibitory neurones, with the ___ stimulatory neurons relatively spared. genetically associated with _________

Answer 38

achalasia — failure of the LES to relax and is associated with lack of peristalsis. caused by the destruction of the ganglion cells in the myenteric plexus, particularly the NO inhibitory neurones, with the ACh stimulatory neurons relatively spared. associated with HLA-DQw1

Question 39

what are the 2 types of dysphagia?

Answer 39

1. oropharyngeal dysphagia - abnormal bolus transfer to the oesophagus, difficulty initiating a swallow, only one manifestation of the primary disease (eg. stroke) 2. oesophageal dysphagia - abnormal bolus transport through the oesophagus, food stops after initiation of swallow, oesophagus is location of the primary disease (eg. achalasia)

Question 40

what may endoscopy reveal in a dysphagic patient?

Answer 40

candida, dilation and debris

Question 41

what is GORD?

Answer 41

- gastro-oesophageal reflux disease - reflux of stomach contents into oesophagus due to the inappropriate relaxation of the LOS

Question 42

risk factors for GORD

Answer 42

• high BMI • smoking • genetic association • pregnancy • hiatus hernia (part of upper stomach pushes up through the diaphragm) • NSAIDs, caffeine and alcohol • alcohol • Helicobacter Pylori

Question 43

what is the cardinal symptom of GORD?

Answer 43

heartburn - classically after meals and is made worse by lying down or bending forward

Question 44

what are common GORD symptoms?

Answer 44

• dyspepsia (indigestion/heartburn) • chest pain • dysphagia • odynophagia (painful swallowing) • cough • hoarse voice • nausea and/or vomiting

Question 45

what are non-pharmalogical treatments of GORD?

Answer 45

• weight loss • smoking cessation • small regular meals • avoid meals before sleep • avoid : fizzy drinks, alcohol, coffee, citrus fruits, spicy foods • raising head of bed

Question 46

name some medications that can exacerbate GORD?

Answer 46

eg. alpha-blockers, anticholinergics, benzodiazepines, NSAIDs, Ca channel blockers, tricyclic antidepressants, theophyllines etc

Question 47

describe antacids

Answer 47

neutralise stomach acid as they are alkaline. sometimes given with simeticone to prevent the foaming effect of acid + alkaline. many antacids also include alginates - form a gel which floats on top of stomach contents to prevent stomach acid from irritating the oesophagus (protective barrier)

Question 48

describe proton pump inhibitors

Answer 48

eg. omeprazole - inhibit H+/K+ ATPase on parietal cells in the stomach — decrease gastric acid secretion

Question 49

describe H2-receptor antagonists (H2RAs)

Answer 49

inhibit the histamine receptors and thus inhibit the stimulation of parietal cells by enterochromaffin cells

Question 50

describe a nissen fundoplication

Answer 50

operation to reinforce the LOS (fundus of stomach is wrapped around the oesophagus — increase lower oesophageal pressure)

Question 51

what muscle makes up the UOS?

Answer 51

cricopharyngeus

Question 52

what is a relaxant of the LOS?

Answer 52

alcohol

Question 53

oesophageal cancer risk factors?

Answer 53

• GORD • smoking • barrett’s oesophagus • obesity • alcohol • bile reflux • achalasia • radiation treatment to upper abdomen or chest • lack of fruit and vegetables

Question 54

what cancer develops in the upper 2/3rds vs lower 1/3rd of the oesophagus?

Answer 54

• upper 2/3rds = squamous — develops squamous carcinoma • lower 1/3 = columnar — develops adenocarcinoma

Question 55

barrett’s oesophagus : _______ to _________. can then undergo dysplasia —> __________

Answer 55

barrett’s oesophagus : stratified squamous to gastric glandular columnar. can then undergo dysplasia —> adenocarcinoma

Question 56

symptoms of oesophageal cancer

Answer 56

• dysphagia • unintentional weight loss • chest pain, pressure or burning • worsening indigestion or heartburn • coughing • hoarse voice

Question 57

how is oesophageal cancer diagnosed?

Answer 57

- barium swallow - endoscopy - biopsy

Question 58

omeprazole makes you more susceptible to what?

Answer 58

c diff infection

Question 59

what can omeprazole interact with?

Answer 59

clopidogrel

Question 60

what can cause interstitial nephritis?

Answer 60

omeprazole

Question 61

what are the alarm symptoms of dyspepsia (indigestion)?

Answer 61

a - anaemia l - loss of weight a - anorexia r - recent onset of progressive symptoms (<3 months) m - melaena or haematemesis d - dysphagia

Question 62

what is melaena?

Answer 62

black colored stools that occur as a result of gastrointestinal bleeding. this bleeding usually comes from the upper gastrointestinal (GI) tract, which includes the mouth, esophagus, stomach, and the first part of the small intestine.

Question 63

what is haematemesis?

Answer 63

vomiting blood

Question 64

what is the link between cancer and anaemia?

Answer 64

• anaemia is a common side effect of cancer and cancer treatment, esp chemotherapy • chemotherapy damages bone marrow (where RBCs are made) • damage to kidney in chemotherapy — reduced production of erythropoietin (stimulates RBC production) • nausea and vomiting —> anaemia • cancer is most commonly associated with iron-deficiency anaemia • cancer growing quickly - using rbcs, iron etc

Question 65

what are the ASA gradings?

Answer 65

= assessment of physical status 1. ASA I = a normal healthy patient 2. ASA II = a patient with mild systemic disease 3. ASA III = a patient with severe systemic disease 4. ASA IV = a patient with severe systemic disease that is a constant threat to life 5. ASA V = a moribund patient who is not expected to survive without the operation 6. ASA VI = a declared brain-dead patient whose organs are being removed for donor purposes

Question 66

statement of intent?

Answer 66

confused.com google it again It means the death can be registered without automatically having to refer the death to the coroner (as was the case previously) provided the patient has been seen by a doctor within the last 28 days. This is why Statement of Intent is valid for 28 days.

Question 67

withdrawing and withholding treatment/end of life

Answer 67

Question 68

what does the self-regulatory model involve?

Answer 68

primary appraisal of a stimulus which then brings about a coping response which is then itself evaluated via a secondary appraisal

Question 69

what are some causes of oropharyngeal dysphagia?

Answer 69

- myasthenia gravis - stroke - zenker’s (oesophageal) diverticulum - MS - motor neurone disease (ALS) - Gillian Barre syndrome

Question 70

what are some causes of oesophageal dysphagia?

Answer 70

- achalasia - Chagas’ disease - GORD - carcinoma and benign tumours - eosinophilic oesophagitis - goitre - mediastinal tumours - scleroderma and other rheumatologic disorders - Schatzki ring

Question 71

what is schatzi ring? cause?

Answer 71

- a Schatzki ring is a circular membrane of mucosa and submucosa that forms at the squamocolumnar junction of the distal esophagus. Schatzki rings appear as thin membranous structures that do not contain any muscularis propria - can be due to prolonged irritation of the oesophagus due to acid reflux

Question 72

how is vasodilation achieved in saliva production?

Answer 72

salivary glands produce more kallikrein as they become more active which cleaves bradykinin causing vasodilation

Question 73

__________ stimulates the flow of bile from the liver to the gallbladder. _______ stimulates the gallbladder to contract, causing bile to be secreted into the ________

Answer 73

- secretin - CCK - duodenum

Question 74

CCK mediates digestion in the small intestine by _________ gastric emptying. It stimulates the ________ cells of the pancreas to release a juice rich in ___________. Thus, as the levels of the substances that stimulated the release of CCK drop, the concentration of the hormone drops as well. The release of CCK is also inhibited by ___________ and ______________. ________, a protease released by pancreatic acinar cells, hydrolyzes CCK-releasing peptide and monitor peptide, in effect turning off the additional signals to secrete CCK

Answer 74

- inhibiting - acinar - pancreatic digestive enzymes - somatostatin - pancreatic peptide - trypsin

Question 75

As a peptide hormone, CCK mediates satiety by acting on the CCK receptors distributed widely throughout the central nervous system. The mechanism for hunger suppression is thought to be a __________ in the rate of gastric emptying. CCK also has _________ effects on the vagus nerve, effects that can be inhibited by _________. The stimulatory effects of CCK oppose those of ________, which has been shown to inhibit the vagus nerve.

Answer 75

- decrease - stimulatory - capsaicin - ghrelin (hunger hormone)