Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

CP1 Therapeutics > Gastrointestinal and hepatic disorders > Flashcards

Gastrointestinal and hepatic disorders Flashcards

1
Q

Antacids: MoA, indications, contraindications, side effects

A

MoA:

  • Bicarbonate: CO2 released as burps so not appropriate for patients reporting fullness
  • Magnesium and aluminium hydroxide
    • Used in combination to avoid their respective side effects of diarrhoea and constipation
  • Gavison: Aliginates (form a raft when in contact with salivia) combined with antacids

Indications:

  • Dyspepsia
  • Provides instant relief but is not curative

Contraindications:

Side effects:

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

H2 receptor antagonists: MoA, indication, contraindications, side effects

Ranitidine, cimetidine, famotidine

A

MoA: Antagonise the binding of histamine to its receptor, preventing stimulation of gastric acid release.

  • Prevents production of cAMP, which normally acts to activate the proton pump, allowing for gastric acid production
  • ↓ cAMP, ↓ ATPase activity, ↓ gastric acid production

Indication:

  • Low dose OTC for short term relief, high dose POM
  • Allows for the repair of gastric ulcers
    • Reduce the need for surgery
  • Best given at night (H2 mediated secretion is highest)

Contraindication:

  • Cimetidine inhibits CytP450 and hence has interactions with many other medications (oral anticoagulants, phenyotin, carbamazepine, TCAs)

Side effects:

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

Proton pump inhibitors: MoA, indications, contraindications, side effects

Omeprazole, lansoprazole, pantoprozole

A

MoA: Irreversibly inhibit the proton pump, leading to decreased gastric acid production

  • As they target a common component of the pathway they are the most effective
  • Activated by acidic pH, meaning their action is limited to parietal cells

Indications:

  • Alongside NSAID use

Contraindications:

Side effects:

  • Decrease gastric acid so much that achlorhydria and increased risk of food poisoning may occur (C. diff)
  • Long term use at high doses is associated with osteoporosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Misoprostol: MoA, indications, contraindications, side effects

A

MoA: A synthetic prostaglandin analogue that has antisecretory properties. Decreasing gastric acid secretion and promoting ulcer healing.

Indications:

  • For the promotion of gastric ulcer healing
  • Prophylaxis of NSAID induced gastric ulcer

Contraindications:

  • Conditions in which hypotension may cause severe complications (e.g. CVD)
  • Conditions in which predispose to diarrhoea (e.g. IBD)

Side effects:

  • Potent uterine stimulant (used in abortion)
  • Diarrhoea (via cAMP)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Prokinetic drugs: MoA, indications, contraindications, side effects

A

MoA: Promote the movement of gastric contents from the stomach to the duodenum

Indications:

  • GORD (of benefit in the condition - reduces gastric acid secretion)
  • Doperimide: D2 receptor antagonist. Promotes closure of the oesophageal sphincter and opening of the lower sphincter
  • Metocloperamide: Promotes gastric motility and emptying

Contraindications:

Side effects:

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

Triple therapy: Medications utilised, indication, contraindications, side effects

A

Medications:

Any 2 of the following antibiotics

  1. Metronidazole
  2. Clarithromycin
  3. Amoxicillin

PLUS PPI/H2 antagonist

PPI/H2 antagonist is continued for 2-4 weeks following treatment to allow for ulcer healing

Indications:

  • H. Pylori eradication
  • H.Pylori ulceration

Contraindications:

Side effects:

  • Must avoid alcohol if taking metronidazole
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Describe the management of: Non-ulcer dyspepsia

A

Step wise approach to treatment:

Antacid or alginate + antacid → H2 antagonist → omeprazole

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

Describe the management of: Peptic ulceration associated with H.Pylori infection

A

Triple therapy for 1 week:

  • PPI or H2 antagonist
  • Clarithromycin and 1 of the following:
  1. Clarithromycin
  2. Amoxicillin OR
  3. Metronidazole

PPI/H2 antagonist continued for a further 2/4 weeks to allow for ulcer healing

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

Describe the managment of: Peptic ulceration not associated with H.Pylori infection

A

General changes such as smoking cessation, taking antacids and antisecretory therapy.

CHECK

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

Describe the management of: Peptic ulceration associated with NSAID use

A
  • Cease NSAID use (if possible)
  • PPI produces the most rapid healing effect
  • H2 antagonist or misoprostol may be used as an alternative
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Describe the management of: GORD

A

Lifestyle advice: Smoking cessation, weight reduction, raising the head of the bed

Mild symptoms:

Antacid or antacid + alginate → H2 antagonist → PPI

Severe symptoms:

PPI

Titrated down once symptoms are under control and substituted to H2 antagonist

GORD symptoms: Heartburn, acid regurgitation

Sometimes: Dysphagia, oesophagitis, ulceration and stricture formation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q
A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Outline the mechanism by which NSAIDs and steroids cause gastric damage

A

Inhibition of the conversion of arachidonic acid to prostaglandins and leukotrienes by COX is the MoA of NSAIDs.

The inhibition of COX 1 leads to the production of gastro-protective prostaglandins being decreased. This leads to increased susceptibilty of the gastric mucosa to damage and possible ulceration.

Steroids prevent the conversion of membrane lipids to arachidonic acid, again preventing the production of prostaglandins.

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

Outline the mechanism by which gastric acid secretion is regulated

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Describe the management of: Constipation

A

Magnesium:

  • Has an osmotic effect
  • Causes CCK release, which increases GI motility
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Describe the management of: Diarrhoea

A

Diarrhoea: Abnormal passing of loose or liquid stools with increased frequency and/or volume. Acute diarrhoea lasts for less than 14 days.

May be resultant of infection or secondary to medication use (antibiotics, orlistat, digoxin, metformin, misoprostol)

Treatment of diarrhoea:

Oral dehydration therapy: Replaces electrolytes and glucose

• Must be isotonic

Antimotility agents:

Loperamide: Acts on μ opioid receptors to reduce the release of ACh, which subsequently reduces gastric motility.

  • Provides symptomatic relief
  • Does not cross the BBB and therefore does not have opioid side effects
  • May prolong infection as the infecting organisms are not cleared
  • Not recommended in bloody or inflammatory diarrhoea, or in the presence of significant abdominal pain (suggests inflammatory cause).

Codeine: Analgesic. Constipation may be a side effect via the same MoA as loperamide.

Antimuscarinics: Act on the ACh receptor to prevent NT binding and reduce GI motility

TCAs: Constipation may occur as a side effect of their action upon muscarinic receptors

Ciprofloxacin can be used for prophylaxis against traveller’s diarrhoea but routine use is not recommended.

NOTE: Bloody diarrhoea following treatment with clindamycin could indicate pseudomembraneous colitis (swelling/inflammation of the intestine due to overgrowth of C. Diff. This is commonly seen following antibiotic use). A complication of C. Diff infection is toxic megacolon.

17
Q

Describe the management of: Irritable bowel syndrome

A

Irritable bowel syndrome: A common, chronic, relapsing and often life-long condition often affecting women aged 20-30.

Symptoms: Abdominal pain, disordered stool defaecation, passage of mucus and bloating, diarrhoea/constipation

Treatment of diarrhoea/constipation

Lactulose (osmotic laxative) or loperamide (anti-diarrhoea drug (opioid)) for respective symptoms.

Antispasmodics

Antimuscarinics: Inhibit parasympathetic activity and therefore GI motility.

Mebeverine: Direct relaxant of GI smooth muscle

Amytriptyline (TCA)

  • Low doses are widely used, and are effective
  • Provide some pain relief
  • Some antimuscarinic effects
  • May alter the sensitvity of nerves within the lower GI tract
18
Q

Describe the management of: Inflammatory bowel disease

A
19
Q

State the medications which may be responsible for secondary diarrhoea

A
  • Antibiotics
    • Increase infection risk BUT ciprofloxacin may be used empirically for travellers diarrhoea
    • Bloody diarrhoea following treatment with clindamycin - indicates pseudomembranous colitis
  • Orlistat
    • Steatorrhoea
  • Prostaglandins
    • via cAMP
  • PPIs
    • Predispose to C. diff infection due to decreased stomach pH
  • Metformin
  • Digoxin toxicity
  • Iron salts
  • Acarbose

CP1 Therapeutics (7 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions