upper GI drugs Flashcards

1
Q

how can peptic ulcers form (2)

A
  1. too much damage to the gastric mucoss
  2. weak mucosa (=> easily damaged)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what 3 factors is the parietal cell secretion under the control of

A
  1. vagus nerve (Ach)
  2. gastrin
  3. histamine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

6 ways to reduced gastric acid secretion and exaamples of these drugs

A
  1. H2 receptor ANTagonist - cimetidine, famotidine, nizatidine;
  2. gastrin anatagonist - none clinically available
  3. muscarinic anatgonist (have many other side effects) - atropine, pirenzepine
  4. H+ secretion mechanism blocker - PPI
  5. parietal cell inhibition physiologically - misprostol, somatostain
  6. neutralisation - antacids e.g. gaviscon
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what are antacids used for

A

symptomatic relief of GORD, dyspepsia etc -> they hv rapid onset but are only transient so generally used for symptom relief

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what metals do anatacids commonly contain and what side effect do they produce

A
  1. magnesium - constipation;
  2. calcium
  3. Sodium - HTN
  4. aluminium - diahorrea

=> give aluminium for constipationa nd magnesium for diahorrea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what is milk-alkali syndrome

A

systemic alkalosis due to high doses of antacids, characterized by a triad of elevated calcium levels, metabolic alkalosis, and acute kidney injury

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what medications can aluminium not be given alongside (2)

A
  1. levodopa
  2. tetracyclines

Al chelates to them

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

side effects of carbonate containing antacids

A

CO2 release leading to burping and stomach distension

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

H2 receptor antagonist MOA

A

reversible, competitive, inhibitors of H2 receptors -> reduced histamine release leading to reduced parietal cell activation => reduced basal and stimulated acide secretion, reduced pepsin secretion (from chief cells)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what non-GI condition might H2 antagonists be used in

A

Heart failure - has significant negative iontropic and chronotropic effects

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

H2R antagonist side effects

A

side effects are uncommon
1. diahorrea
2. headache
3. elderly confusion
4. gynaecomastia (cimetidine specifically, it binds to androgen receptors)
5. interacts with warfarin, throphylline etc. (enhances their effect as inhibits P450 - cimetidine)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

PPI MOA

A

irreversibly binding (covalently bonds to receptor) to and inhibiting the hydrogen-potassium ATPase pump that resides on the luminal surface of the parietal cell membrane

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what enatiomer of esomeprazole is used (R,S)

A

S - more potent as it is broken down slower, so acid suppression is prolonged

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

side effects of PPI

A
  1. headaches
  2. diahorrea (due to bacterial overgrowth, microscopic colitis etc.)
  3. infectious gastroenteritis
  4. hypergastrinaemia
  5. imparied Ca and Mg absorption -> increase in osteoporotic fractures
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

step up vs step down GORD mgx

A

step up - start on a lower dose and build up
step down - start on a high dose and work down to lowest dose needed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what does parenteral mean

A

administered or occurring elsewhere in the body than the mouth and alimentary canal

17
Q

indications for pareneteral therapy (5)

A
  1. prevention of aspiration during anesthesia
  2. stress ulcer prophylaxis in certain critically ill patients
  3. peptic disease and inability to take oral mgx for 5days
  4. post endoscopic mgx in selected GI haemorrhage pts
  5. non-responsive ZE syndrome
18
Q

what is the importance of CYP450 in PPI use

A

All PPIs are metabolized to varying degrees by hepatic P450 cytochromes in the liver

19
Q

what antiplatelet might PPIs interact with

A

clipidogrel - may inhibit its action

20
Q

upper GI vs lower GI bleed blood results

A

upper GI - high urea, low Hb
lower GI - low Hb, urea normal

21
Q

red flag features for dyspepsia (6)

A
  1. dysphagia
  2. anoerxia
  3. anaemia
  4. recurrent vomiting
  5. mass
  6. loss of weight
22
Q

misoprostol MOA

A
  1. a synthetic prostaglandin E1 analog that stimulates prostaglandin E1 receptors on parietal cells in the stomach to reduce gastric acid secretion
  2. EP3 agonist -> inhibitory effect on proton pump of the parietal cell

=> acid secretion inhibited, duodenal HCO3- increased, gastric mucous increase, mucosal blood flow increased

23
Q

what is the effect of misoprostol on peptic ulcers

A

helps them heal and reduces further complications from NSAID use

24
Q

misoprostol adverse effects (3)

A
  1. diarrhoea
  2. uterine contractions (induced labour/termination of pregnancy)
  3. menorrhagia/post menopausal bleeding
25
Q

sucralfate MOA

A
  1. sucralfate forms a complex that binds to protein-rich exudate found on the surface of ulcers -> barrier to H+ ions
  2. increase FGF leading to increased PGE secretion
26
Q

bismuth moa

A

bismuth subsalicylate hydrolyzes in the stomach into bismuth oxychloride, which is minimally absorbed into the bloodstream, and salicylic acid, which is almost completely absorbed -> Bismuth interacts with other anions and compounds, such as hydrochloric acid, bicarbonate, phosphate, and hydrogen sulfide, in the gastrointestinal tract to form bismuth salts -> Bismuth salts possess bactericidal and antimicrobial activity, mainly by preventing bacteria from binding and growing on the mucosal cells of the stomach (esp. H.Pylori!)

27
Q

bismuth adverse effects

A
  1. black stools
  2. black tongue
  3. minimal absoption -> could lead to accumulation, so 6-8wks is max treatment
28
Q

Mesenteric ischaemia triad

A

triad of CVD, high lactate and soft but tender abdomen