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Stage 2 > Case 1 > Flashcards

Case 1 Flashcards

1
Q

What are some dysfunctional physiologies and disease of the mouth?

A
  • Oral ulceration: break in the oral epithelium, exposing nerve endings in underlying connective tissue
  • Stomatisis: inflammation of the lining of any of the soft tissues of the mouth
  • Leukoplakia (painless white patches in the side of the tongue/ cheek
  • Dysphagia (difficulty swallowing)
  • Mumps: infection of the salivary gland - can cause sterilisation in men
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2
Q

What are some causes of oral ulceration?

A
  • Physical or chemical injury
  • Drugs
  • Malignancy
  • Systematic diseases
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3
Q

What are some causes of stomatitis?

A
  • Poor hygiene
  • Poorly fitter dentures
  • Heat burns
  • Drugs
  • Allergy
  • Infections
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4
Q

Dysfunctional physiologies and disease of the oesophagus

A
  • GORD - can lead to Barrett’s oesophagus
  • Hiatal hernia
  • Motiloty disorders
    • Achalasia - inadéquat LOS relaxation
    • Diffuse oesophageal spasm - uncoordinated contraction
    • Hypercontraction
    • Ineffectice oesophageal motility - hypocontraction
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5
Q

Causes of GORD

A
  • Meds
  • Obesity
  • Spicy and acidic food
  • Smoking
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6
Q

What can GORD lead to?

A

Barrette’s oesophagus

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7
Q

What is a hiatal hernia?

A

When part of the stomach pokes up and gets stuck in the diaphragm - high risk of infection -> need surgery

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8
Q

What are the motility disorders of the oesophagus?

A
  • all muscular disorders
  • achalasia: inadequate LOS relaxation
  • diffuse oesophageal spasm - uncoordinated contraction
  • hyper contraction
  • ineffective oesophageal motility- hypo contraction
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9
Q

What does GORD do?

A
  • Causes exposure of ‘unprotected’ oesophageal squamous epithelium to acid
  • Have transient LOS relaxation in absence of swallowing - response of stimulation of gastric vagal mechanoreceptors and oesophageal hypomotility
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10
Q

What are the three types of dyspepsia and GORD?

A
  • non-erosive reflux disease (heart burn)
  • erosive oesophagitis (acute inflammatory response)
  • barrettes oesophagus (metaplasia of mucos) => cancer risk
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11
Q

What are the three acid secretion pathways?

A
  • Ach (M3 receptor)
  • Histamine (H2 receptor)
  • Gastrin (CKKB/CCK2 receptor) => directly and indirectly indue HCl secretion
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12
Q

What is the most powerful stimulus for HCl secretion?

A

Histamine which acts through G-coupled receptor to increase cAMP

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13
Q

How do prostaglandins regulate acid production?

A
  • PGE2 is produced by COX2/1 and increases mucus production
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14
Q

How do NSAIDs prevent mucus being produced?

A
  • Binds to COX1/2 and prevents PGE2 being produced
  • acidic so can cause gastric ulcers
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15
Q

How can prominent stress cause peptic ulcers?

A

Inhibit HCO3- production

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16
Q

How does mucus protect the stomach from HCl?

A
  • Trapping HCO3- rich fluid near apical border of epithelia
  • HCO3- stops acid damage
  • The apical cell membrane TJ limits H+ ion diffusion and locally produces PGE2 and PGI2 which increases mucus production and decreases HCl
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17
Q

Who does peptic ulcer disease affect?

A

All ages but rare in children

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18
Q

What are the two types of peptic ulcers?

A
  • Gastric
  • Duodenal
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19
Q

Who do gastric ulcers typically present in?

A

55-65 yrs old

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20
Q

Who do duodenal ulcers typically present in?

A

25-75 yrs old

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21
Q

If peptic ulcers are presenting in >45yr olds, what does that mean?

A

Possibly cancerous => investigate further

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22
Q

Who’s more at risk of getting peptic ulcers?

A
  • Males are more at risk
  • Females are more likely to get gastric rather than duodenal
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23
Q

What sort of genetic factors contributed to peptic ulcers?

A
  • increased acid production
  • weaker mucosa
  • abnormal mucus production
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24
Q

What causes peptic ulcers?

A
  • stress
  • H.pylori
  • long term NSAID use
  • caffeine and smoking
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25
Q

Which ulcer is made worse with food?

A

Gastric ulcers - associated with weight loss, anorexia and nausea

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26
Q

Which ulcers are made worse at night?

A

Duodenal as gastric juice may enter and the pH is lower due to no food and lying down

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27
Q

What is the pathophysiology of gastric ulcer?

A
  • Normally an inflammatory response of parietal cells - atrophic gastritis (less able to secrete acid and increase pH)
  • normal/ decreased acid secretion
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28
Q

What is the pathophysiology of duodenal ulcers?

A
  • Associated with an increase in H+ (due to increase gastrin) and decreased HCO3-
  • Gastric inflammation elevated in pyloric region
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29
Q

What is the pathophysiology of H.pylori?

A
  • Infects the lower part of the stomach and causes inflammation of the gastric mucosa
  • May lead to an ulcer, proliferation and bleeding
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30
Q

How do NSAIDs cause peptic ulcers?

A
  • Reduce prostaglandin formation (COX1 inhibition) and may trigger gastric ulceration and bleeding which decreases HCO3- => decreasing mucus production and blood flow
  • Aspirin causes irreversible inhibition
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31
Q

What are three neutralisation methods for gastric acid?

A
  • Antacids
  • Alginates
  • Sucralfate (mucosal protectants)
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32
Q

How to reduce acid secretion?

A
  • PPI
  • Histamine H2 receptor antagonists
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33
Q

What helps move things faster?

A

Prokinetics

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34
Q

What are antacids?

A

Formed from weak bases (mainly weak inorganic bases) and neutralise excess acid in the stomach and reduce foaming => prevents heartburn

35
Q

What are antacids often combined with?

A

Alginates and anti foaming agents => decrease surface tension which prevents bubbles as they’re trapped in an egg box

36
Q

Pros and cons of systematic antacids

A
  • Useful in short term therapy - rapid onset of action
  • Prolonged use can cause overload on the kidneys
37
Q

Pros of non systematic antacids

A
  • Most of them remain in the GIT
  • Examples: Tums (Ca), milk of magnesia (Mg)
38
Q

Disadvantage of antacids

A

-Binding of other drugs can cause reduced bioavailability and chemical inactivity
- Mg - laxative properties - not in renal failure
- Al - constipation
- Calcium carbonate- kidney stone?/ constipation
- Carbonates - generate CO2=> bloating and flatulence
- NaHCO3 - problems with hypertension and renal insufficiency and metabolic acidosis

39
Q

What are alginates?

A

Polysaccharides found in the cell walls of brown algae and it forms a protective barrier on top of gastric contents (usual combine with antacids)

40
Q

What is gavicson?

A
  • Combination of antacids and alginates
  • reacts rapidly with acid to form a raft (egg box) of alginic-acid gel (pH~7) => floats on the stomach contents => impending gastro-oesophageal reflux
41
Q

How do PPI work?

A
  • Bind to parietal cells (specific H+/k+ ATPase) so they inhibit HCl production as proton pump can’t move to the surface
  • prodrugs - activated in strongly acidic conditions
  • activated form irreversibly binds to cystein of the H+/K+ ATPase to inhibit the active proton pump
42
Q

What are the different ways that histamine is released in the stomach?

A
  • H2 receptors (expressed by parietal cells)
  • ECL cells (gastrin stimulation)
  • Mast cells (during infection)
43
Q

How is the PPI activated?

A

Activated by proton-catalysed (pH~5) formation of sulfonic acid and the drug irreversibly binds to sulphydryl groups of cysteines of H+/K+ ATPase

44
Q

Examples of H2 receptor blockers

A
  • Cimetidine (inhibits P450)
  • Ranitidine (doesn’t inhibit P450=> fewer side effects)
45
Q

Mechanism of action of histamine receptor blockers

A

Acts as a competitive antagonist of H2 receptors on the basolateral membrane of parietal cells. Completely block the histamine-mediated component of acid secretion and reduce secretions evoked by gastrin and acetulylcholine
Only effective for ~28 days

46
Q

What reduces the effects of H2 blockers?

A

Smoking

47
Q

How to prostaglandins reduce acid secretion?

A
  • Bind to EP3 receptors on parietal cells
  • Have cytoprotective effects which stimulate mucin and bicarbonate production
48
Q

What is a synthetic analog of PGE1?

A

Misoprostol - inhibits basal and stimulated secretion of acid

49
Q

What is sucralfate used for?

A

Used to treat begnign gastric and duodenal ulceration

50
Q

Why are dopamine receptor antagonists used?

A
  • Enhance prokinetics
  • rarely used due to severe side effects
51
Q

What is dyspepsia?

A

A collection of symptoms and typically presents as feeling pain/ discomfort located primarily in the upper abdominal region (not a diagnosis itself)

52
Q

What can cause dyspepsia?

A
  • Smoking
  • Stress
  • H.pylori
  • Meds (NSAIDS)
  • Diet
53
Q

When should you investigate dyspepsia?

A
  • Dysphagia is present (cancer?)
  • Haematemosis
  • > 54 yrs old with weight loss
  • Upper abdominal pain
  • Reflux
54
Q

How to test for H.pylori?

A
  • Breath test
  • Stool
  • Blood
55
Q

What should you do when testing for H.pylori?

A

Stop PPI use for two weeks (give antacids) and antibiotics for 4 weeks

56
Q

What is the risk of triple therapy?

A

C.difficile

57
Q

Issues with long term PPI use

A
  • Rebound hypersecretion
  • osteoporotic fractures
  • Hypomagnesia
  • Community and hospital acquired pneumonia
  • Drug interactions?
58
Q

How to investigate GORD?

A

Carry out an endoscope

59
Q

What to prescribe for proven GORD?

A
  • lifestyle advice
  • full-dose PPI (4-8 weeks)
  • severe? Full dose PPI
  • recurring? Low dose (half dose) PPI
  • refractory? Double dose and H2RA
60
Q

Why would you give prokinetics to those with GORD?

A

Can increase LOS pressure and stimulate the motility (include metaclopromide => fairly toxic)

61
Q

What is nausea?

A

An unpleasant sensation, vaguely referred to the epigastrium and abdomen with a tendency towards inward vomiting

62
Q

What is vomiting?

A

Vomiting is involuntary contractions of the abdomen, thoracic and GI muscles so it is therefore forceful expulsions of stomach contents from the mouth

63
Q

What is regurgitation?

A

The effortless return of oesophageal/ gastric contents in the mouth. It is unassociated with nausea or vomiting

64
Q

What complications can nausea and vomiting cause?

A
  • dehydration => tested by pinching someone’s skin
  • electrolyte imbalances
  • malnutrition
  • aspirational pneumonia => when vomiting enters the lungs
  • oesophageal tear
65
Q

What is motion sickness?

A

When there is a disagreement in the brain between visually perceived movement and the vestibular systems sense of movement. Both acetylcholine and histamine are involved
Hyoscine butylbromide => anticholinergic

66
Q

How to treat motion sickness?

A

Using anticholinergic drugs and antihistamines that cross the BBB

67
Q

Side effects of anticholinergic

A
  • drowsiness
  • blurred vision
  • dry mouth
  • constipation
  • urinary retention
  • dementia => long term use as ACh is important for Brian’s development
68
Q

What are the three different types of chemotherapy induced nausea and vomiting?

A
  • acute - within 24hrs
  • delayed - after 24 hours
  • anticipatory - conditional response
69
Q

What can affect CINV?

A
  • type of chemo routine
  • genotypic factors
  • patient based factors - motion sickness: female/ morning sickness
70
Q

What are the side effects of metoclopromide?

A

Helps with sickness but causes akathisia, tremors, dystonia, tardive dyskinesia (irreversible) => only given to >18 yrs

71
Q

Examples of selective 5HT3 receptor antagonists in CINV

A
  • ondasteron (pharmacogenetics in the future)
  • palonesteon
72
Q

Examples of neurokinin-1[NK1] receptor antagonists in CINV

A

Aprepitant

73
Q

Example for corticosteroid for CINV

A

Dexamethasone

74
Q

Example of D2 receptor antagonist in CINV

A

Metoclopromide

75
Q

PONV risk factors

A
  • female
  • non-smoker
  • post-operative opioids
  • history of PONV or motion sickness
76
Q

Complications of PONV

A
  • increased hospital stay
  • stress on surgical closure
  • aspiration pneumonia
77
Q

Management plan got PONV

A

1) zero risk factors: management is debatable => receive 0-2 antiemetics
2) one-two risk factors: give 2 antiemetics in combination
3) >2 risk factors: give 3-4 antiemetics in combination

78
Q

What are the causes is NV in palliative care?

A
  • chemicals
  • gastric stasis
  • bowel obstruction
  • raised intracranial pressure
  • psychological
79
Q

What is rumination?

A

Food that is regurgitated in the postpranidal period, re-chewed and then re-swallowed

80
Q

What are the consequences of coeliac disease?

A
  • abdominal distension
  • malabsorption
  • diarrhoea
  • anaemia
  • intestinal cabcer
81
Q

What is the cause of coeliac disease?

A
  • Gluten is identified in the body by priming of IFNy, producing CD4+ cells by antigen peptides derived from alpha-gliadin (major protein in gluten). For immune recognition, alpha-gliadin must undergo deamination by tissues transglutaminase (tTG) => glutamine => glutamic acid
  • has a genetic predisposition => major genes are on the human leukocytes antigen region (HLA) => highly polymorphic
82
Q

What is IBD?

A
  • Chronic inflammatory bowel diseases with features of autoimmune disease (Crohns and UC)
83
Q

What does Crohns do?

A
  • affects anywhere in the GIT
  • causes thickening of the wall, cobblestoning, fishes (cracks) and fat wrapping
84
Q

What does ulcerative colitis do?

A
  • mainly affects the large intestines
  • causes thinning of the vowel wall and pseudopolyps of the bowel

Stage 2 (5 decks)

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