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PBL SEM 4 > CASE 1 > Flashcards

CASE 1 Flashcards

1
Q

what is barrett’s oesophagus?

A

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

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2
Q

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

A

mucosal layer

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3
Q

what is barrett’s a consequence of?

A

GORD - repeated damage from gastric reflux

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4
Q

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

A

oesophageal adenocarcinoma

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5
Q

what is the sequence in barrett’s to cancer?

A

metaplasia-dysplasia-adenocarcinoma sequence

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6
Q

what are risk factors for barrett’s?

A

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

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7
Q

clinical features of barrett’s

A

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

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8
Q

what is the main investigation in barrett’s?

A

upper GI endoscopy with biopsy

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9
Q

how does the oesophagus in barrett’s visually change?

A

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

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10
Q

what is oral mucosa like?

A

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

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11
Q

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

A

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

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12
Q

what does saliva contain?

A

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

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13
Q

superior vs inferior salivatory nucleus

A

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

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14
Q

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

A
  • submucosa
  • controls mainly GI secretion and local blood flow
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15
Q

where is the myenteric plexus and what does it control?

A
  • 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
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16
Q

what is the usual stimulus for peristalsis?

A

distention of the gut

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17
Q

peristalsis requires an active what?

A

myenteric plexus

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18
Q

what are the 4 swallowing stages?

A
  1. cephalic
  2. oral (voluntary)
  3. pharyngeal (involuntary)
  4. oesophageal (involuntary)
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19
Q

what is the cephalic stage?

A

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.

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20
Q

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

A

striated

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21
Q

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

A
  1. oral = cortex/medulla
  2. pharyngeal = medulla
  3. oesophageal = medulla/ENS (mainly vagal nerve and ENS)
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22
Q

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

A

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

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23
Q

describe the chewing reflex

A
  • 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
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24
Q

the rate of digestion is absolutely dependent on what?

A

the total SA exposed to the digestive secretions

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25
Q

upper oesophageal sphincter innervation?

A

CN X

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26
Q

for the UOS to open, what must relax?

A

cricopharyngeus

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27
Q

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

A
  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

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28
Q

what sphincter fails in GORD?

A

LOS

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29
Q

why is intraoesophageal pressure -ve?

A

lungs and pleura pull against oesophagus

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30
Q

taste nuclei?

A

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

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31
Q

what are important efferent nuclei in swallowing?

A

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

32
Q

saliva is secreted how?

A

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

33
Q

parasympathetic vs sympathetic nerve activity effect on saliva

A
34
Q

what happens when an AP arrives at a salivary gland?

A

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

35
Q

what causes acid neutralisation in the lower oesophagus?

A

HCO3 in the saliva

36
Q

Na/H channels in the oesophageal epithelium do what?

A

remove H ions

37
Q

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

A

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

38
Q

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 _________

A

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

39
Q

what are the 2 types of dysphagia?

A
  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)
40
Q

what may endoscopy reveal in a dysphagic patient?

A

candida, dilation and debris

41
Q

what is GORD?

A
  • gastro-oesophageal reflux disease
  • reflux of stomach contents into oesophagus due to the inappropriate relaxation of the LOS
42
Q

risk factors for GORD

A

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

43
Q

what is the cardinal symptom of GORD?

A

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

44
Q

what are common GORD symptoms?

A

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

45
Q

what are non-pharmalogical treatments of GORD?

A

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

46
Q

name some medications that can exacerbate GORD?

A

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

47
Q

describe antacids

A

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)

48
Q

describe proton pump inhibitors

A

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

49
Q

describe H2-receptor antagonists (H2RAs)

A

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

50
Q

describe a nissen fundoplication

A

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

51
Q

what muscle makes up the UOS?

A

cricopharyngeus

52
Q

what is a relaxant of the LOS?

A

alcohol

53
Q

oesophageal cancer risk factors?

A

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

54
Q

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

A

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

55
Q

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

A

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

56
Q

symptoms of oesophageal cancer

A

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

57
Q

how is oesophageal cancer diagnosed?

A
  • barium swallow
  • endoscopy
  • biopsy
58
Q

omeprazole makes you more susceptible to what?

A

c diff infection

59
Q

what can omeprazole interact with?

A

clopidogrel

60
Q

what can cause interstitial nephritis?

A

omeprazole

61
Q

what are the alarm symptoms of dyspepsia (indigestion)?

A

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

62
Q

what is melaena?

A

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.

63
Q

what is haematemesis?

A

vomiting blood

64
Q

what is the link between cancer and anaemia?

A

• 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

65
Q

what are the ASA gradings?

A

= 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
66
Q

statement of intent?

A

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.

67
Q

withdrawing and withholding treatment/end of life

A
68
Q

what does the self-regulatory model involve?

A

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

69
Q

what are some causes of oropharyngeal dysphagia?

A
  • myasthenia gravis
  • stroke
  • zenker’s (oesophageal) diverticulum
  • MS
  • motor neurone disease (ALS)
  • Gillian Barre syndrome
70
Q

what are some causes of oesophageal dysphagia?

A
  • achalasia
  • Chagas’ disease
  • GORD
  • carcinoma and benign tumours
  • eosinophilic oesophagitis
  • goitre
  • mediastinal tumours
  • scleroderma and other rheumatologic disorders
  • Schatzki ring
71
Q

what is schatzi ring? cause?

A
  • 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
72
Q

how is vasodilation achieved in saliva production?

A

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

73
Q

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

A
  • secretin
  • CCK
  • duodenum
74
Q

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

A
  • inhibiting
  • acinar
  • pancreatic digestive enzymes
  • somatostatin
  • pancreatic peptide
  • trypsin
75
Q

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.

A
  • decrease
  • stimulatory
  • capsaicin
  • ghrelin (hunger hormone)

PBL SEM 4 (50 decks)

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