PHARM - Constipation, Diarrhoea, Vomiting Flashcards
4 classes of constipation drugs
- bulk laxatives
- osmotic laxatives
- stimulant laxatives
- faecal softeners
bulk laxatives
- MOA
- A/Es
- e.g.
- contain poorly digested compounds (e.g. plant polysaccharides) which draw water into the GIT
- forms bulky, hydrated stools = pressure on gut wall detected by stretch receptors = promotes peristalsis
- bloating (bacterial digestion of plant fibres produces gas), can also decrease efficacy of other drugs b/c can’t reach site of action
- e.g. metamucil
osmotic laxatives
- MOA
- types
- uses
- A/Es and C/Is
- MOA: draw water into the gut = forms bulky, hydrated stools = pressure on gut wall detected by stretch receptors
- 4 types: Mg2+ salts, lactulose, polyethylene glycol (PEG), sorbitol
- indications: constipation, bowel prep
- A/Es: cramping, systemic effects of Mg2+ salts therefore C/I in children (there is a kid-friendly version) and Pts w/ impaired renal function
what happens when a child resists bowel movement?
- causes prolonged distension and weakening of colon wall
stimulant laxatives
- MOA
- A/Es
- e.g.
- MOA: stimulates mucosa to secrete electrolytes = water follows = stool softens = peristalsis, can also stimulate enteric nerves
- A/Es: long term use can cause ‘lazy bowel’ - Pts can rely on the drugs to have a bowel movement
- e.g. dulcolax
faecal softeners
- MOA
- indications
- e.g.
- MOA: surfactant agents that reduce the surface tension of water to soften faeces (weak laxative effect)
- indications: useful if straining should be avoided (e.g. post childbirth or surgery), good first line option for children
- e.g. coloxyl
dopamine antagonists
- MOA
- A/Es
- e.g.
- MOA: inhibits dopamine (D2) receptors = enhances smooth muscle activation including increased pressure on lower oesophageal sphincter which enhances gastric emptying
- little effect on gut motility (purgation) because there are few dopamine receptors there
- A/Es: can also block D2 receptor in chemoreceptor trigger zone
- e.g. domperidone
2 classes of anti-diarrhoeal agents
- muscarinic antagonists
- opioids
opioids
- indication
- MOA
- e.g.
- anti-diarrhoeal
- act on mu receptor in GIT = decreased ACh = decreased muscle contraction = decreased peristalsis = more time to absorb water and harden stools - doesnt cross BBB = no CNS effects, selective for GIT
- e.g. loperamide
muscarinic antagonists for anti-diarrhoeal
- MOA
- e.g.
- MOA: block M3 receptors = decreased GIT motility = more time to absorb water and harden stools - doesnt cross BBB = no CNS effects, selective for GIT
- e.g. atropine, buscapan
why is vomiting hard to treat?
- there are many pathways involved so even if you treat one pathway, vomiting can still occur thru another pathway (some non-selective drugs are quite effective)
- rescue treatment can be given IV or IM (PO not much use)
what is the main structure in mediating nausea and vomiting?
- where is it located
- does it have a BBB?
- NT input
- chemoreceptor trigger zone (CTZ)
- located in area postrema (medulla of brain stem)
- lacks effective BBB = ideal for detecting emetic triggers in CSF and systemic circulation
- dopaminergic/ tryptaminergic input (5-HT)
what is the 2nd main structure involved in vomiting?
- where does it receive inputs from?
- vomiting centre (not a discrete brain area)
- receives inputs from CTZ, GIT, CVS, limbic system (olfactory, emotional, stress, pain triggers of vomiting)
labrynths via vestibular nuclei
- which cranial nerve are they associated with
- which trigger of vomiting do they control?
- what NTs control them?
- associated w/ vestibular nerve
- cause vomiting due to motion sickness
- cholinergic + histaminergic control
which NT do mechanoreceptors and chemoreceptors in the GIT use?
- serotonin/5-HT/tryptamine
main associated symptoms of vomiting to treat
- dehydration
- alkalosis (due to expulsion of H+ ions so more are drawn out of the blood and into the gut)
- hypochloraemia
- hypokalaemia
4 main targets for anti-emetics
- ACh (antimuscarinics)
- histamine (antihistamines)
- 5-HT (serotonin - tryptaminergic)
- dopamine
antimuscarinics for vomiting
- MOA
- indication
- route of administration
- A/Es
- e.g.
- blocks M1 receptors in vestibular nuclei = X transmission to vomit centre
- mostly for motion sickness (treatment AND prophylaxis)
- PO or transdermal patch
- A/Es: non-selective = blurred vision, drowsiness, urinary retention, decreased salivation
- e.g. hyoscine
antihistamines for vomiting
- MOA
- indication
- A/Es
- e.g.
- MOA: block H1 receptors in vestibular nuclei = X transmission to vomit centre
- indication: motion or morning sickness
- A/Es: sedation due to central effects (cross BBB unlike 2nd gen antihistamines for allergies), blurred vision, urinary retention, dry mouth
- e.g. promethazine
dopamine antagonists for vomiting
- MOA
- indication re: dopamine AGONISTS
- e.g.
- inhibits D2 receptors in CTZ = X transmission to vomiting centre
(crosses BBB poorly but CTZ lacks this so can still access). also facilitates gastric emptying - can be taken a few days before a dopamine AGONIST as these cause vomiting (also increases milk lactation for breastfeeding mothers)
- e.g. domperidone
5-HT antagonists for vomiting
- MOA
- indication
- A/Es
- e.g.
- MOA: inhibits 5-HT receptors in CTZ and GIT (central and peripheral action) = X transmission to vomit centre
- indication: chemotherapy induced N/V or postop vomiting
- A/Es: constipation b/c many 5-HT receptors in GIT
- e.g. ondansetron
NK1 antagonist for vomiting
- MOA
- indication
- e.g.
- MOA: substance P (tachykinin) inhibits NK1 receptors in GIT and CTZ
- indication: in combination with 5-HT antagonists and dexamethasone for vomiting due to chemotherapy, motion sickness, alcohol (acute AND delayed vomiting)
- e.g. aprepitant
