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CPT > L18 GI Pharmocology > Flashcards

L18 GI Pharmocology Flashcards

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1
Q

GORD symptoms, complications and risk factors

A

Symptoms:

  • heart burn
  • cough
  • laryngitis
  • asthma
  • dental erosion

Complications:

  • Barrett’s oesophagus
  • oesophagitis
  • ulceration
  • haemorrhage
  • stricture formation

Risk factors:

  • older age
  • hiatus hernia
  • obesity
  • pregnancy
  • smoking
  • alcohol
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2
Q

Medication that causes GORD

A 
Alpha blockers
Anticholinergics
Benzodiazepines 
Beta blockers 
CCBs 
Corticosteroids 
NSAIDs 
Nitrates 
Theophylline
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3
Q

GORD management medication

A

PPIs:

  • omeprazole
  • lansoprazole
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4
Q

Gastritis symptoms, complications and risk factors

A

Symptoms:

  • burning epiblast tic pain
  • nausea and vomiting
  • food may increase or decrease pain

Complications:
- GI bleeding

Risk factors:

  • H. Pylori
  • chronic NSAIDs
  • bile reflux
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5
Q

Erosive causes of gastritis

A

NSAIDs
Alcohol
Bile

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6
Q

Non erosive causes of gastritis

A

H. Pylori

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7
Q

Treatment of erosive gastritis

A

Stop or reduce use of NSAIDs or alcohol

Give PPI or a H2 receptor antagonist

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8
Q

Treatment of non erosive gastritis

A

Triple therapy
- PPI + 2x antibiotic (amoxicillin + clarythromycin or metronidazole)

Quadruple therapy - given if resistant to clarythromycin
- PPI + bismuth + 2x antibiotics

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9
Q

Autoimmune cause of gastritis

A

Antibodies produced against parietal cells

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10
Q

Treatment for autoimmune gastritis

A

Cyanocobalamin

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11
Q

Peptic ulcer disorder symptoms, complications and risk factors

A

Symptoms:
- epigastric pain before (gastric) or after (duodenal) meals

Complications:
- perforation causing peritonitis

Risk factors:

  • H pylori
  • NSAIDs
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12
Q

Treatment for H pylori negative peptic ulcer disease

A

Stop NSAIDs
COX 2 inhibitor - celecoxib
PPI
H2 receptor antagonist - IGF unresponsive to PPI

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13
Q

Why is COX2 inhibitors used

A

Doesn’t effect COX 1 mediated prostaglandin synthesis

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14
Q

Treatment of peptic ulcer disease when NSAIDs need to be taken or elderly

A 
Consider misoprostol (prostaglandin analogue) 
- inhibits adenylate cyclase decreased cAMP - decreases PPI activity
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15
Q

Treatment of H. Pylori positive peptic ulcer disease

A

Test for H. Pylori using a urea breath test or stool antigen test

Triple therapy:
- PPI + amoxicillin and clarythromycin or metronidazole

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16
Q

NSAID effect on COX

A

NSAIDs inhibit COX enzymes therefore less prostaglandins are synthesised from arachidonic acid

17
Q

COX 1 abundance and regulation

A

High concentration in:

  • platelets
  • vascular endothelial cells
  • kidney
  • stomach

Regulates:

  • prostaglandins - decreases platelet aggregation, vasodilation and mucosal protection
  • thromboxane - platelet aggregation and vasoconstriction
18
Q

COX 2 abundance and effects

A

High concentration:

  • at sites of tissue damage
  • brain
  • kidney
  • bones

Regulates:
Prostaglandins - can cause inflammation and fever

19
Q

Roles of prostaglandins

A

Vasodilation
Decrease gastric release
Stimulates mucus and bicarbonate release in stomach
Reduce permeability of epithelium to acid back flow
Reduce release of inflammatory mediators
Promotes ulcer healing

20
Q

Parietal cell non secreting state

A

Non secreting state:

  • proton pump (H+, K+ ATPase) are located in tubulovesicles
  • lack K+ permeability therefore no activity
  • apical membrane of parietal cells have K+ channels and involutions (canaliculi) and microvilli
21
Q

Parietal cell secreting state

A

Tubulovesicles fuse with canalicular membrane forming canaliculi
More proton pumps where K+ exchange can occur
Elongation of microvilli

22
Q

PPI activation

A

PPIs are activated by acidic condition of the parietal canaliculus
PPIs are weak bases therefore accumulate in the canaliculi in high concentration

23
Q

Enteric coating of PPI

A

Prevents premature activation in stomach
Absorbed in the small intestine and transported to parietal cells
Activated in canaliculi

24
Q

PPI mechanism of action

A

Bind covalently to proton pumps irreversibly and block function

  • short half life
  • long term effect
  • requires de novo synthesis of pump enzyme to produce more acid
25
Q

Interactions of PPIs

A

Metabolised by CYP 450

  • liver failure - decreased dose
  • decrease effectiveness of clopidogrel

Excreted by kidneys

Increased levels of gastric

  • as increased pH
  • no somatostatin release
26
Q

Side effects of PPIs

A

Generally well tolerated

  • headache
  • nausea
  • Abdominal Pain
  • increase gastric carcinoid tumours (rare)
  • increased risk of hip fracture - increases stomach pH reduces gastric absorption of calcium and non haem iron
27
Q

H2 receptor antagonist mechanism of action

A

Competitively and reversibly inhibits H2 receptors therefore less histamine binds

  • blocks gastric and Ach effects on parietal cells
  • decreased protein kinase A synthesis therefore parietal cells do not form canaliculi for proton pump activity
  • decreased proton pump activity
28
Q

Common side effects of H2 receptor antagonists

A

Diarrhoea
Constipation
Muscle aches
Fatigue

29
Q

H2 receptor antagonist interactions

A

Decreased Ketoconazole absorption
Inhibits CYP450
- decreased metabolism of lidocaine, phenytoin, theophylline and warfarin

30
Q

Prostaglandin analogues use

A

Treatment of NSAID induced ulcers

31
Q

Mechanism of action of prostaglandin analogues

A

Acts on PGE2

Decreases protein kinase A therefore less parietal cell canaliculi therefore decreased activity of proton pump

32
Q

Side effects of prostaglandin analogues

A

Diarrhoea

Abdominal pain

33
Q

Contraindication of prostaglandin analogues

A

Pregnant women - causes uterine contractions

34
Q

Antacids use

A

Symptom relief for dyspepsia

35
Q

Antacid mechanism of action

A

Neutralise HCL

Reacts with acid to form water and salt

36
Q

Common forms of antacids and side effects

A

Slow/moderate:

Aluminium hydroxide

  • constipation
  • weakness and malaise
  • neurotoxicity in renal failure

Magnesium hydroxide

  • diarrhoea
  • avoid in renal clearance as increased magnesium

Fast:
Sodium bicarbonate
- reacts with HCL to form water and salt
- avoid in hypertension and fluid overload

Calcium carbonate
- reacts with water to from calcium chloride and CO2

37
Q

Step up therapy GORD

A
  1. PPI, H2 receptor antagonist or antacid on demand
  2. full dose H2 receptor antagonist
  3. half dose PPI
  4. full dose PPI
  5. Double dose PPI
  6. Double dose PPI + H2 receptor antagonist at night
38
Q

How does H pylori damage gastric epithelium

A

Promotes strong immune response
Ammonium hydroxide is toxic to gastric epithelia
Endotoxins
Hypertrophy of parietal cells - increased gastric and decreased somatostatin

Metaplasia of duodenum:

  • due to increased acid
  • duodenal ulceration

Colonisation in stomach body:

  • parietal cell atrophy
  • dysplasia
  • increased risk of gastric cancer

CPT (23 decks)

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