GI Flashcards
gaviscon:
- drug class?
- mechanism of action?
combined alginate and antacid
antacid:
- buffering stomach acids
alginate:
- increase viscosity of stomach contents, reducing reflux into oesophagus
- reacts w acid to create a floating ‘raft’ on top of contents, protecting sphincter
nb alginates may also inhibit pepsin production
nb an antacid is basically just an alkali salt (eg sodium bicarb, calcium carbonate, magnesium or aluminium salts)
gaviscon:
- indications? 2
- contraindications? 3
- safe in pregnancy?
indications
- symptomatic relief of heartburn for people with GORD
- short term relief of dyspepsia (indigestion)
contraindications
- safe for infants but should NOT be given with thickened milk preperations as can -> increased stomach contents -> bloating + discomfort
- Na + K containing versions should be used w caution in patients w fluid overload or hyperkalaemia (eg CKD)
- some versions contain glucose -> could worsen hyperglycaemia in diabetics
well tolerated + safe in pregnancy
gavison:
- side effects? 2
- possible interactions (+ mechanism)? 8
few side effects!
- Mg salts can -> diarrhoea
- Aluminium salts can -> constipation
alginates bind to other drugs, reducing serum conc of:
- ACE inhibitors
- some Abx (cephalosporins, ciprofloxacin + tetracyclines)
- bisphosphonates
- digoxin
- levothyroxine
- PPIs
antacids increase alkilinity of urine, increasing excretion of:
- aspirin
- lithium
info for patients taking gaviscon:
- effect it should have?
- when/how to take?
- what to do if symptoms continue?
- other info?
- relieve heart burn + indigestion within 20 mins + for several hours afterwards
- nb only a temporary measure
- after meal times
- before bed
- leave a gap of at least 2 hours between gaviscon + other medicines which interact with it
- if symptoms persist, go back to Dr
- discuss lifestyle measure to reduce reflux (eg small + often meals, avoiding triggers, stop smoking, raising head of bed etc)
H2- receptor anatagonists:
- example?
- mechanism of action?
ranitidine
reduce gastric acid secretion
- proton pumps are regulated by histamine, which binds to H2-receptors on parietal cells to stimulate acid secretion
- blocking these receptors therefore reduces acid secretion
nb however as proton pump can also be stimulated by other pathways the effect is not as suppressive as PPIs, hence why PPIs are normally first line
H2 receptor antagonists:
- example?
- indications? 2
- contraindications? 2
ranitidine
indications
- 2nd line (after PPIs) for prevention + treatment of peptic ulcer disease
- relief of symptoms for GORD and dyspepsia (PPIs for more severe cases)
contraindications
- excreted by kidney so reduce dose if renal mpairment
- can disguise symptoms of gastric cancer so be vigilent
H2 receptor antagonists
- example?
- possible side effects? 3
- possible interactions?
- elimination?
ranitidine
side effects are rare
- diarrhoea (rarely constipation)
- headache
- dizziness
no major drug interactions
kidneys
patient info for taking H2-antagonists:
- effect it should have?
- other info?
- when should they go back to the Dr?
- reduce stomach acid -> reduced symptoms
- allow ulcers to heal
- side effects are uncommon
- if they have any ALARMS symptoms (eg weight loss, swallowing difficulties)
Proton pump inhibitors:
- examples? 3
- drug suffix?
- mechanism of action?
- lansoprazole
- omeprazole
- pantoprazole
-prazole
reduce gastric acid secretion by irreversibly inhibiting H+/K+-ATPase in gastric parietal cells
nb they are more effective at supressing gastric acid production than H2 receptor antagonists
PPIs:
- example?
- indications? 4
- contraindications? 2
- lansoprazole
- omeprazole
- pantoprazole
first line treatment for:
- prevention + treatment of PUD (incl NSAID induced)
- dyspepsia (symptom relief)
- GORD (symptom relief)
- erradication of H pylori infection (used w Abx)
- can mask gastric cancer
- can increase risk of fractures (patients at risk of osteoporosis should be treated for this)
PPIs:
- example?
- side effects? 4
- possible interactions?
- lansoprazole
- omeprazole
- pantoprazole
- GI disturbances
- headaches
- slight increase in infection risk (esp c diff)
- hypomagnesaemia (w. prolonged use)
- OMEPRAZOLE reduces effectiveness of CLOPIDOGREL
nb omeprazole is a mild CP450 inhibitor
Patient info for taking PPIs:
- effect they should have?
- when to take?
- how long to take for?
- red flags to look out for? 2
- reduce the amount of acid in stomach, reducing and allowing ulcers to heal/not develop
- best taken in the morning
- depends on what taking it for, but be clear with instructions
- weight loss
- swallowing difficulty
Anti-motility drugs:
- aka?
- example?
- mechanism of action?
anti-diarrhoeal drugs
- loperamide
an opioid which CANNOT enter CNS so just works to reduce gut motility (an agonist of the opiod u-receptors in the GI tract)
- it increases non-propulsive contraction of gut smooth muscle but reduces propulsive (peristaltic) contractions
anti-motility drugs:
- example?
- indications? 1
- contraindications? 3
- loperamide
symptomatic treatment for diarrhoea
- norm in context of IBS or viral gastroenteritis
- ulcerative colitis (increases risk of megacolon + perforation)
- c diff colitis
- acute bloody diarrhoea (aka dysentery, increases risk of HUS)
anti-motility drugs:
- example?
- side effects? 3
- interactions?
- loperamide
- constipation
- abdo cramping
- flatulence
none known
info for patients re anti-motility drugs:
- purpose of drug?
- when to stop taking it? 3
to help settle diarrhoea (doesn’t treat underlying cause)
- if develop constipation
- abdo pain
- need to take it for more than 5 days (in acute diarrhoea)
stimulant laxatives:
- example?
- mechanism of action?
- senna
(other egs: bisacodyl, glycerol suppositories, docusate sodium)
- increase water + electrolyte secretion from colonic mucosa -> increasing volume + stimulating peristalsis
- also acts directly to increase peristalsis (mechanism unclear)
nb there are other types of laxatives (osmotic, bulk-forming) which have slightly different mechanisms and indications
stimulant laxatives:
- example?
- indications? 2
- contrandications? 2
- senna
- constipation
- as suppositories for faecal impaction
- suspected intestinal obstruction (can induce perforation)
- rectal preparations avoided if haemorrhoids or anal fissure
stimulant laxatives:
- example?
- side effects? 2
- interactions?
- senna
- abdo pain
- cramping
(- diarrhoea, obviously!)
none known
what to tell patients re stimulant laxatives:
- what effects drug should have?
- how long will it take to work?
- what can they do to help?
- when should they stop taking it?
- anything else?
help them pass stools
- doesn’t work immediately and takes a few doses before effect occurs
- drink lots of water (6-8 glasses a day)
- stop taking if passing more than 2-3 stools a day (nb can adjust dose for comfort)
- may get side effects but these often improve with time
aminosalicylates:
- examples? 2
- suffix?
- mechanism of action?
- mesalazine
- sulfasalazine
-salazine (suffix)
has anti-inflammatory + immunosuppressive effects,especially topically in the gut
- exact mechanism is unclear
aminosalicylates:
- examples? 2
- indications? 2
mesalazine
- first line for ulcerative colitis (UC)
sulfasalazine
- used for rheumatoid arthritis (RA)
nb not effective in crohns
aminosalicylates:
- examples? 2
- contraindications? 1
- interactions? 1
- mesalazine
- sulfasalazine
- anyone allergic to aspirin (as they are also salicylates)
- combinations w pH sensitive coating may interact with drugs that effect pH of stomach (eg PPIs)
aminosalicylates:
- examples? 2
- common side effects? 2
- rare side effects? 4
- mesalazine
- sulfasalazine
common:
- GI upset
- headache
rare
- severe blood abnormalities
- renal impairment
- reversible reduction in sperm
- hypersensitivity reaction (anaphylaxis)
nb mesalazine generally has fewer side effects than sulfasalazine
info for patients taking aminosalicylates:
- method of taking for UC?
- what adverse signs should they look for? 3
foam enema is best method of administration
- helps to use a lube to get the end of the can as far up as possible
(can be taken orally but this is less effective for UC)
- unexplained bleeding
- unexplained bruising
- infective symptoms
(as these could be signs of blood count disorder)
Dopamine D2-receptor anatagonists antiemetics:
- examples? 2
- mechanisms of action? 2
- metoclopramide
- domperidone
- blocks the D2 receptors found in the chemorecpetor trigger zone (area responsible for sensing emetogenic substances in the blood - eg drugs)
- blocks the D2 receptors in the gut (dopamine norm relaxes the gut) therefore it has a prokinetic effect, promoting gastric emptying etc
Dopamine D2-receptor anatagonists antiemetics:
- examples? 2
- indications? 1
- contraindications? 3
- metoclopramide
- domperidone
prophylaxis + treatment of nausea + vomitting
- esp in context of reduced gut motility
- children + young adults (side effects more common)
- GI obstruction (dt GI effects)
- GI perforation
Dopamine D2-receptor anatagonists antiemetics:
- examples? 2
- most common side effect?
- other side effect?
- interactions? 2
- metoclopramide
- domperidone
- diarrhoea
- extra-pyramidal side effects (movement abnormalities)
- — norm in form of acute dystonic reaction (eg an oculogyric crisis*)
nb extra-pyramidal side effects are only seen in metoclopramide + interactions only apply to this
- antipsychotics (risk of extra-pyramidal side effects increased)
- dopaminergic drugs for parkinsons (antagonise each other!)
info for patients taking dopamine D2-receptor anatagonists antiemetics:
- when should they look out for?
extra-pyramidal side effects
- may be subtle, eg falling over more
