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GERR Pharmacology > Pharmacology of Upper and Lower GIT Drug Treatment > Flashcards

Pharmacology of Upper and Lower GIT Drug Treatment Flashcards

1
Q

What is the drug target in the gastric mucosa

A

Parietal cells gastric acid secretion

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2
Q

What is the physiological control of gastric acid secretion ( 4 controls)

A
  • vagal nerve works through ACH to give a positive signal by H/K ATPase proton pump to stimulate acid secretion
  • histamine stimulates acid secretion via histamine 2 receptor
  • gastrin responds to dietary intake to stimulate acid secretion
  • Prostaglandin decreases secretion
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3
Q

What is a peptic ulcer

A
  • defect in the gastric or duodenal mucosa
  • caused by imbalance in peptic acid secretion and gastroduodenal mucosal defence
  • acids higher than mucosal defines can cope with
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4
Q

Principles of PUD therapy

A

1- Relief of pain ( epigastric pain )
2- Ulcer healing
3- Prevention of relapse and complications
4- everyone at increased risk of gastric carcinoma must be investigated since treatment could mask symptoms (ex: elderly, smokers, alcoholics)

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5
Q

What is the treatment for PUD ( 5 steps )

A 
1- remove irritants : especially NSAIDS , helicobacter pylori infection 
2- Antacids : alkali based salts 
3- proton pump inhibitors 
4- H2 receptor antagonists 
5- Antibiotics for helicobactor pylori
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6
Q

How NSAIDs effect acid secretion

A
  • NSAIDs act on COX 1 &2
  • COX 1 housekeeps prostaglandin formation and the prostaglandin signal that’s used to reduce acid signal
  • COX 2 causes inflammation
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7
Q

Drugs that can cause PUD (8)

A
  • NSAIDs
  • aspirin
  • corticosteroids
  • bisphosphonates ( mucosal toxic)
  • Nicotine ( smoking )
  • alcohol
  • caffeine
  • severe physiological stress
  • Hypersecretory states ( gastronomes )
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8
Q

Describe role of antacids, and the common ones used for PUD treatment

A
  • increase gastric PH and reduce proteolytic activity
  • can’t something too alkali or too easily absorbed because will get into blood
  • aluminium and magnesium salts combinations are used
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9
Q

Why is sodium bicarbonate not used to treat PUD

A
  • easily absorbed and therefore will not stay in GIT

- will go into blood and can cause metabolic alkalosis , sodium and water retention and renal stones

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10
Q

Why is milk not good for PUD

A
  • temporary pain relief but contains a lot of fat and sugar which stimulates gastrin
  • gastrin increases acid secretion which makes situation worse
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11
Q

Why are antacids sometimes not used fo PUD treatment

A
  • parietal cells are still releasing acid so the problem is not being fixed
  • antacids just react with acids so they’re not longterm treatment
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12
Q

What is the first line treatment for significant ongoing dyspepsia or PUD , give examples

A
  • proton pump inhibitors
  • Omeprazole
  • Lansoprazole
  • Pantoprazole
  • Esomeprazole
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13
Q

What is PPIs mode of action

A
  • Targeted irreversible proton pump inhibition
  • Inhibit the H/K ATPase proton pump = decrease acid secretion
  • used for dyspepsia , PUD , GORD
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14
Q

Why to be careful of PPIs

A
  • can mask gastric cancer because effect are so good
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15
Q

Common ADRs of PPIs

A
  • causes slight change to normal GIT function

- nausea , vomiting , abdominal pain , flatulence, diarrhoea, constipation , headache

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16
Q

Important ADRs of PPIs (5)

A
  • clostridium difficile
  • Hypomagnesaemia : if magnesium is low then patient feels weak
  • Hyponatraemia : if PPI is helping with nausea it will decrease hyponatraemia risk
  • Hepatitis
  • pneumonia
17
Q

PPIs drug interactions

A
  • warfarin : omeprazole and esomeprazole are weak CYP450 enzyme inhibitor so metabolism of warfarin will decrease , warfarin effect will fo up
  • clopidogrel ( hepatic pro-drugs ) : omeprazole and esomeprazole are weak CYP450 enzyme inhibitor so anti platelet effect will not be activated
18
Q

Describe RAHS

A
  • rebound acid hypertension syndrome
  • when PPIs switch of acid secretion irreversible a reaction can occur 2-3 months after PPIs are stopped
  • recommended to only use PPIs for 8 weeks
19
Q

What is the second line treatment for PUD, give examples

A
  • Histamine 2 receptor antagonists
  • ex: cimetidine and ranitidine
  • blocks histamine 2 signal decreasing gastric acid secretion
20
Q

Cimetidine mode of action and ADRs

A
  • competitive antagonist of H2 receptor in gastric parietal cells
  • ADRs: diarrhoea , confusion , gynaecomastia
21
Q

Cimetidine drug interactions

A
  • potent inhibitor of cytochrome P450

- messes with all drugs that are hepatic ally processed by CYP450

22
Q

Why is Ranitidine better than Cimetidine

A
  • did not cause gynaecomastia and was only a mild inhibitor of CYP450
23
Q

What is Helicobacter pylori , why does it cause PUD

A
  • gram negative bacillus
  • stays in gastric mucosae secreting inflammatory proteins and toxins
  • produced urease which converted urea to ammonia and CO2
24
Q

How to find H pylori

A
  • detected by carbon 13 urea breath test

- takes urea tablet and if there is a spike of CO2 in breath after that’s urease working

25
Q

What are Helicobactor Eraditication Regimens

A
  • 2 antibiotics + PPI / H2 inhibitor for 7 days
  • PPI used for 3 more weeks if ulcer is large
  • reduces recurrence of H pylori by 90%
  • Clarithromycin and Amoxicillin usually used
26
Q

When to due an urgent upper GI endoscopy (7)

A
  • acute bleeding
  • chronic bleeding
  • iron deficiency anaemia
  • weight loss
  • dysphagia
  • persistent vomiting
  • persistent dyspepsia of patients 55+
27
Q

Constipation treatment

A
  • usually non-pharmacological
  • increase fluid intake , mobility , fibre
  • stopping constipating drugs
28
Q

Causes of Constipation ( 5)

A
  • Drugs : opioids, antimuscarinics ( antidepressants ) , diuretics , Ca salts, PPI
  • Local pain : anal fissure , anal abscess
  • benign colorectal disease : prolapse, stricture
  • Hypothyroidism , hypercalcaemia , autonomic problems
  • malignancy
29
Q

osmotic Laxatives Mode of action

A
  • highly osmotically macromolecules will pull water into gut lumen softening stool
30
Q

Stimulant laxatives mode of action

A
  • stimulate enteric nervous system
31
Q

Bulk laxatives mode of action

A
  • swells and distends colon
32
Q

Constipation management

A
  • people on opioids are put on laxatives

- promote non pharmacological treatment

33
Q

drugs used for Constipation

A
  • 1st line : Bulk laxative Fybogel
  • 2nd line : osmotic laxative Movicol
  • 3RD LINE : stimulant laxative if stool is soft
34
Q

What to avoid if someone has opioid-induced constipation

A
  • bulk laxatives

- don’t use fibre

GERR Pharmacology (9 decks)

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