GI System Flashcards

1
Q

What is the drug class for Gaviscon and Peptac?

A

Alginates and Antacids

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2
Q

how does Gaviscon work?

A

Alginates - forms a raft (increase liquid viscosity) to prevent any reflux and mucosal damage

Antacids - buffers acids

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3
Q

Indications for Gaviscon and Peptac?

A

GORD and dyspepsia

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4
Q

Contra-indication for Gaviscon and Peptac?

A

Do not give with thickened milk as this can cause stomach discomfit, bloating etc.

Preparation with Na+/K+ for pt with fluid overload/hyperkalaemia

Sucrose - for diabetes pts

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5
Q

What are the main component of Gaviscon?

A

Aluminium hydroxide and magnesium trisilicate

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6
Q

Side effect for alginate and antacid?

A

Aluminium - cause constipation

Magnesium - cause diarrhoea

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7
Q

interaction of alginate and antacids?

A

alginates - lower drug absorption
antacids - lower drug serum conc. (cause urine to become more alkaline - more aspirin/lithium excretion)
possible interact with ACEi, cephalosporins, ciprofloxacin, tetracyclines, bisphsphonates, digoxin, levothyroxine, PPis

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8
Q

where is alginates and antacids eliminated

A

kidney

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9
Q

what advice can you give pts who are taking gaviscon

A
  • take after meals, before bed and following symptoms

- leave 2 hrs before taking any other drugs

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10
Q

What is the drug class for Ranitidine

A

H2-receptor antagonists

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11
Q

What is the MOA of Ranitidine?

A

antagonist of H2 receptors (limit the numbers of H2 receptors which can be bind by histamine)

Histamine –> H2 receptors –> Proton Pump –> H+

so eventually stops the production of gastric acid

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12
Q

Where is histamine produced in the stomach

A

paracine cells

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13
Q

Where is H2 receptors located in the stomach?

A

parietal cells

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14
Q

Main indication for H2 receptor antagonist

A

GORD, Dyspepsia, peptic ulcer

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15
Q

What is the contra-indication for Ranitidine

A

renal pts (eliminated in kidney), disguise symptoms of stomach cancer

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16
Q

What is some of the side effect of Ranitidine

A

Diarrhoea, headache, dizziness

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17
Q

What is the possible interaction of Ranitidine

A

N/A

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18
Q

Where is Ranitidine eliminated?

A

kidneys

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19
Q

What are some drugs of the family of Proton Pump Inhibitors

A

Lansoprazole, Omeprazole, pantoprazole

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20
Q

What is the MOA of PPI

A

Inhibits the proton pump (H+/K+ ATPase) presnet in the parietal cells of the stomach and almost permanently stops the production of stomach acids (unlike Ranitidine)

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21
Q

What is the downfall of Ranitidine

A

not complete stop to the production of stomach acids as there are other ways to stimulate proton pumps (unlike PPI eg Lansoprazole, Omeprazole, Pantoprazole)

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22
Q

What are the main indication for PPI?

A

peptic ulcer disease (mostly NSAID associated)
H.pylori infection (used in combination with other antibiotics)
GORD
Dyspepsia

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23
Q

Contraindication for PPI?

A
Disguise stomach cancer 
Osteoporotic pts (increase risk of fracture)
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24
Q

Side effect for PPI?

A

Gi disturbance ( diarrhoea, constipation, nausea)
headache
Increase C.diff infection (as stomach acidity is reduced)
Hypomagnesaemia ( can lead to tetany and ventricular arrhythmia)

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25
Interaction of PPIs with other drugs
reduce the anti-platelet effect of Clopidogrel (Heparin) - as PPI reduces the activation of P450.
26
Where is PPI eliminated?
in the liver
27
What are some pt info for PPI?
- Take on empty stomach | - 7-day course for H.pylori in combination if used for H.pylori infection
28
What is the class name for Loperamide and Codeine phosphate
Anti mobility or diarrhoeal agents
29
What is the MOA of antimobility/diarrhoeal agents?
Opioid-μ agonist - which reduces the peristaltic action of the bowl and increase sphincter/muscle tone and slow the movement allowing more water to be absorbed and hence less watery diarrhoea.
30
main indication for Loperamide?
Diarrhoea (eg IBD, viral gastroenteritis
31
contraindication for Loperamide
- acute UC, C.diff colitis - might lead to megacolon or perforation) - dysentery (acute blooding diarrhoea) which is caused by E.coli and can lead to haemolytic uraemic syndrome
32
What are the side-effect of Loperamide
GI Disturbance (contispation, cramping, flatuence) Opioid toxicity - if cross blood-brain barrier (eg Pethidine) Paralytic ileus (lack of movement of the intestine) drowsiness
33
What are the interaction of Loperamide?
no major interaction
34
Where is the elimination of Loperamide taken place?
Kidney
35
What are the main type of laxatives?
Bulk-forming, osmotic, stimulant, stool softener, lubricant
36
What are some of the examples for different types of laxative?
Bulk-forming - Ispaghula husk, methylcellulose, sterculia Osmotic - lactulose, macrogol, phosphate enema Stimulant - Senna, bisacodyl, glycerol suppositories Stool Softener - Sodium docusate Lubricant - oil
37
What is MOA for bulking forming laxative?
This type of laxative contain some sort of hydrophilic substance such as cellulose which attracts water into the stools giving it the form (same as the MOA for fibres) and this stimulate the peristalsis mechanism of the bowel
38
What is the MOA for osmotic laxative?
this type of laxative contain osmotic active substance (eg sugar and alcohol) which holds water in stool giving it the form and stimulating peristalsis
39
What is the MOA for stimulant laxative?
this type of laxative causes secretion of the water and electrolyte from the colon mucosa which increase the content in the bowl and so stimulating peristalsis also has a direct stimulating pro-peristalsis effect eg senna - bacterial metabolism produces metabolites which stimulate the entire nervous system stimulating peristalsis.
40
Indication for Laxatives?
constipations, faecal impaction bulk forming - mild chronic diarrhoea osmotic - pre-surgery/endoscopy bowl prep, liver encephalopathy
41
How does osmotive laxative help with liver encephalopathy
Lactulose (one of the osmotic laxative) reduces the absorption of ammonia which is excreted in the liver and so useful in liver failure and liver encephalopathy
42
What are some of the contra-indication of laxatives
pt with intestinal obstruction (which can lead to perfusion risk), haemorrhoids and anal fissures (especially applied to anal prep) Bulk-forming - ileus (stoped movement of bowl and so if more bulk forming then more stool will get stuck in the intestinal track) Osmotic - phosphate enemas (which works by pulling fluid into the bowls and can cause significant fluid shift, use with caution in heart failure, ascites and electrolyte imbalanced pts)
43
What are some of the side effect of laxatives
abdominal cramping/pain, diarrhoea, melanosis coli (dark stool due to deposited pigmentation of the intestine), flatulence,
44
What are the possible interaction of laxatives
osmotic - might slightly increase the effect of warfarin
45
what are some advices which you can give to pts who are taking laxatives?
drink plenty of water as laxative draws water into stool to form bulks, maintain bulk and to stimulate by secreting water into the bowls.
46
What are some examples for aminosalicylates?
Mesalazine, sulfasalazine (oral, enema)
47
What is the MOA for aminosalicylates?
Mesalazine - release 5-aminosalicylates (5-ASA) which is an anti-inflammatory substance which is only really absorb in the large intestine and has topical effecy but rarely any systemic effects Sulfasalazine - similar to mesalazine and release 5-ASA but it also has sulfapyridine which acts as an immunosuppressant but no anti-inflammatory effect.
48
What are the main indications for aminosalicylates?
mesalazine - for ulcerative colitis | Sulfasalazine - for UC and RA (due to sulfapyridine's immunosuppressive effect)
49
Contra-indication for aminosalicylates?
Aspirin hypersensitivity(allergy?) - salicylates have simialr structure to aspirin
50
side effect for aminosalicylates?
GI upset (nausea, dyspepsia), headache rare - lecuopenia, thrombocytopenia, renal impariment, sulfasalazine - cause oligospermia ( decrease in sperm production)
51
potential interaction of aminosalicylates?
PPI - as PPI inc stomach pH and promote early drug breakdown - no delivery to the colon Lactulose - as lactulose lower stool pH and no 5-ASA release
52
What is the special prescription detail for aminosalicylates?
if UC occurs distally ie rectal, rectosigmoid, then use enema as more tropical but otherwise oral.
53
Where is aminosalicylates eliminated?
Kidney, liver (need to monitor kidney function)
54
What are the different types of antiemetics
Dopamin D2 antagonist Histamine H1 antagonist Phenothiazines Serotonin 5-HT3-receptor antagonist
55
Examples of each class of antiemetics
Dopamine D2 antagonist - Metocloperamide, domperidone Histamine H1 receptor antagonist - cyclizine Phenothiazines - Prochlorperazine Sertotonin 5-HT3-receptor antagonist - Ondansetron
56
how does dopamine d2 antagonist work
Stimuli for vomiting converts into information and travel to the the 'vomiting' centre of the medulla through the chemoreceptor trigger zone, the solitary tract nucleus, the vestibular system. dopamine (important neurotransmitter in the gut - promote relaxation of stomach and lower oesophageal sphincter and inhibits gastroduduoenal coordination) acting through D2 receptors (which is the main receptor in the chemoreceptor trigger zone) to promote anti-vomiting. metocloperamide then inhibits the D2 receptors and so have a prokinetic effect (promoting gastric emptying) which contribute to the main antiemetic action. Mainly effect in the nausea and vomiting due to CTZ trigger and reduced gut motility (eg opioids etc) metocloperamide --> inhibits D2 receptor and so more dopamine to work on guts
57
main indication for dopamine D2 receptor antagonist
N&V (esp in the case of reduced gut motility)
58
contra-indication for dopamine D2 receptor antagonist
Children and young adults(extrapyramidal side effect common) Gi obstruction (pro-kinetic effect on gut) and can lead to perforation
59
Side effect for dopamine D2 receptor antagonist
diarrhoea metocloperamide - promote extrapyramidal symptoms (movement disabilities) through the same action of antipsychotic in short term treatment - more likely to present extrapyramidal symptoms as acute dystonic reaction (oculogyric crisis - prolonged involuntary upward deviation of the eyes) extrapyramidal syndromes - tremor, bradykinesia, rigidity
60
Interaction of dopamine D2 receptor antagonist
Metocloperamide antipsychotic, dopaminergic agents antagonist (Parkinson Treatment, cancel effect of treatment - must not be given together) Domperidone
61
how does histamine H2 receptor antagonist work
histamine (H1) and ACh (muscarinic) receptors predominate in the vomiting centre and in its communications with the vestibular system cyclizine block both of the receptors and work in a wide range of causes - drug induced, post-operative, radiotherapy, motion sickness and vertigo)
62
main indication for Histamine H1 receptor antagonist
Nausea and vomiting - esp motion sickness or vertigo
63
contra-indication for histamine H1 receptor antagonist
pt at risk of hepatic encephalopathy - due to sedating effect prostatic hypertrophy - anticholingeric and might cause urinary retention
64
side-effect of cyclizine
drowsiness (sedating drug although the least effective one) dry throat and mouth - anticholingeric effect tachycardia - noticed as palpation if used in IV form
65
main interaction of cyclizine
sedation maybe greater effect in combine with other sedating drugs (benzodiazepines, opioids) anticholinergism - ipratropium (used to treat COPD)
66
how does phenothiazine work
block a wide range of receptors - D2 receptors - in CTZ and gut - H1 receptors and ACh receptors in vomiting centre and vestibular system
67
main indication for phenothiazines
N&V - esp vertigo Pyschotic drug - for schizophrenia
68
special information about phenothiazines
usually not first line for N&V due to side-effect profile
69
contra-indication for phenothiazines
sedating effect - avoid using in severe liver disease anticholingeric effect - prostatic hypertrophy does should be reduced in elderly
70
interaction with Prochlorperazine
drowsiness and postural hypotension extrapyramidal syndrome - acute dystonic reaction (same as dopamine D2 receptor antagonist) QT-interval prolongation (like other psychotic drugs)
71
how does serotonin 5-HT3-receptor antagonist work
high density of 5-HT3 receptors present in the CTZ serotonin - key neurotransmitter released by the gut in response to emetic substances stimulation of 5-HT3 receptor will stimulate vagus nerve which then activate the vomiting centre via solitary nucleus so serotonin 5-HT3 receptors antagnoist works on CTZ only not other system
72
main indication for serotonin 5-HT3- receptor antagonist
N&V - particular in general anaesthesia and chemotherapy
73
contra-indication for ondansetron
small risk of QT interval prolongation (but only in high dose) - so avoid use with pt with a prolonged QT interval
74
side-effect of ondansetron
rare - diarrhoea, constipation and headache might occur
75
interaction with serotonin 5-HT3 receptors antagnoist
avoid with other drugs which prolong QT interval too - antipsychotic, quinine, SSRI
76
where are all the antiemetic drugs eliminated
in the liver