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GI > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

What are someof the therapeutic uses of antacids?

A
  • Treat ruminal acidosis
  • Gastritis
  • Oesophagitis
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2
Q

Describe how antacids work

A
  • Bicarbbonate used to neutralise acids
  • Mucus protects stomach wall
  • Nutralisation by magnesium hydroxide and trisilicate, aluminium hydroxide gel, alginates and simeticone
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3
Q

Describe the mechanisms of action of alginates and simeticone in the stomach

A
  • Antacids
  • Adsorbents
  • Coating action, bind bacteria adn toxins, mop up HCl
  • Can be used to treat ruminal acidosis, gastritis and oesophagitis
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4
Q

Describe the mechanism of action of sucralfate

A
  • Disaccharide
  • Sticks to stomach lining
  • protects against acids
  • Can prevent uptake of other drugs
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5
Q

What is the effect of H2 antagonists in the stomach?

A
  • Prevent binding of histamine receptor, reduces action of cAMP on ion pums and so reduces proton production
  • Inhibits gastrin, histmaine and ACh stimulated secretion of HCl
  • Pepsin secretion falls (less volume of fluid)
  • Rebound increase on withdrawal
  • E.g. ranitidine
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6
Q

Why should cimetidine not be used?

A
  • H2 antagonist
  • Inhibits cytochrome P450, slows metabolism
  • can lead to toxic build up of other drugs
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7
Q

What is the effect of proton pump inhibitors in the stomach?

A
  • Prevent action of proton pump, reduce acidity of lumen of stomach
  • Highly effective
  • last around 24 hours
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8
Q

Describe the mechanism of action of proton pump inhibitors in the stomach

A
  • Bind irreversibly and competitively to enzyme that catalyses proton pump, shuts down process
  • Immature cells mature within 24 hours, ATP ase available again
  • Shut down pump for 24 hours
  • Irreversible binding to ATPase
  • Basal and stimulated release of HCl inhibited
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9
Q

What is the effect of prostaglandin analogues on the stomach?

A
  • Increase mucus and bicarbonate secretion (prostaglandin E2)
  • Inhibit acid secretion
  • Increase mucosal blood flow
  • (Increase uterine contraction so contra-indicated in late gestation)
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10
Q

Describe the mechanism of action of prostaglandin analogues in the stomach

A
  • NSAIDs inhibit COX1 and COX1 and so reduce production of prostaglandin 2, so increase acid production = increased risk of ulcers
  • Artificial prostaglandins (mesoprostol) bind to receptors, reduce acid production, increase bicarbonate and mucus production
  • Mesoprostol is stable analogue of PGE1
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11
Q

What are the 2 centres controlling vomiting?

A
  • CRTZ - chemoreceptor trigger zone

- Vomiting centre in brainstem

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12
Q

Briefly outline the chemoreceptor trigger zone in vomiting

A
  • Not protected by BBB so drugs can interact here
  • Responds to chemical stimuli
  • Also for motion sickness
  • Input from vestibular apparatus
  • Impulses pass to vomiting centre in brainstem
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13
Q

What is the function of the vomiting centre inthe brainstem?

A

Coordinates and integrates vomiting

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14
Q

Describe the process of vomiting

A
  • Controlled by emetic centre
  • Nerve impulses reach emetic centre from 2 pathways
  • Central and peripheral
  • Motion sickes input from vestibular apparatus
  • Substance P key NT in vomiting
  • Binds to NK-1 receptors, found in highest concentration in emetic centre
  • NK-1 receptors on cell membrane
  • Binding of correct ligand on external side, conformational change, triggers series of reactions
  • Stimulation of NK-1 by substance P in nucelsu tractus solitarus of emetic centre = vomiting reflex
  • Output via dorsal vagal complex
  • Fibres from DVC go first to gut
  • Close pylorus, reduce gastric tone, open cardiac sphincter, increase tone in duodenum and jejunum
  • Motor vagal fibres infor via resp muscles to contract diaphragm, contract abdo muscles to expel contents from upper GI tract
    = vomiting
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15
Q

What are drugs and compounds called that induce vomiting and give examples

A
  • Emetics
  • Apomorphine
  • Alpha-2-agonists (xylazine)
  • Syrup of Ipecac
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16
Q

Describe the mechanism of action of apomorphine

A
  • Dopamine agonsit
  • Applied via IV or mucosa
  • Rapid effect
  • Contra-indicated in cats
  • Central pathway
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17
Q

Describe the mechanism of action of Syrup of Ipecac

A
  • Direct irritant

- Cardiotoxic in high doses

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18
Q

What are the key receptors used by anti-emetics?

A
  • H1 (histamine receptor)
  • 5-HT3 (serotonin receptor)
  • Muscarinic receptors
  • Dopamine antagonists
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19
Q

What action does an anti-emetic have on the H1 receptors?

A
  • Antagonistic
  • Reduces vomiting
  • most drugs are H1 antagonists*
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20
Q

What action does an anti-emetic have on 5-HT3 receptors?

A
  • Antagonistic

- Reduces vomiting

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21
Q

What action does an anti-emetic have on muscarinic receptors?

A
  • Antagonistic
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22
Q

Describe the mechanism of action of phenothiazine derivatives and give an example

A
  • Dopamine antagonists

- Chlorpromazine

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23
Q

Where can dopamine antagonists exert their action?

A
  • CRTZ
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24
Q

Where can H1 receptor antagonists exert their action?

A
  • Vestibular nuclei

- Nucleus of solitary tract (tractus solitarus)

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25
Q

Where can 5-HT3 antagonists exert their action?

A
  • Visceral afferents

- CRTZ

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26
Q

Where can muscarinic antagonists exert their action?

A
  • Vestibular nuclei
  • Nucleus of solitary tract (tractus solitarus)
  • Vomiting centre
27
Q

Describe the mechanism of action of metaclopramide

A
  • Local anaesthetic derivative
  • Short action (need to infuse IV)
  • Central and peripheral effects
  • Central anti-dopamine effects at CRTZ
  • Increases gastric emptying and increases motility
  • Contra-indicated if vomiting due to obstruction
28
Q

Describe the effects of metaclopramide and domperidone

A
  • Increase gastric emptying
  • Increase motility
  • (Contra-indicated if vomiting due to obstruction)
29
Q

Describe the mechanism of action of cerenia (maropitant)

A
  • NK-1 antagonist
  • Competes with substance P
  • Specifically designed for dogs, also used in cats
  • Shuts down last step of vomiting initiation
30
Q

Described how the motility of the stomach can be altered

A
  • Prokinetics
  • Serotenergic H-HT4 receptor agonist (cisapride)
  • Antidiarrhoeal agents - narcotic analgesics (codeine), anticholinergics, act peripherally to reduce GI spasm, nausea, vomiting, diarrhoea, reduce gastric emptuing and may increase vomiting
31
Q

When would antifoaming agents be used?

A
  • treat frothy bloat in ruminants

- Cause bubble to break down

32
Q

Describe the pharamcological management of diarrhoea

A
  • Maintenance of fluid balance
  • Maintenance of electrolytes and acid base status
  • Use of anti-infectives
  • Altered (reduce) motility - reduce pain, increase transit time and reabsorption window
  • Oral fluids (containing citrate)
  • adsorbets (not proven)
33
Q

Why is citrate added to oral fluids in the treatment of diarrhoea?

A
  • Preservative
  • Buffer
  • Generates production of bicarbonate
34
Q

What are the 2 types of intestine motility?

A
  • Digestive and non-propulsive
35
Q

Describe digestive motility

A
  • Propulsive
  • Peristalsis
  • Short segments only
  • Longitudinal muscle relaxes behind chyme, circular muscle contracts behind chyme
  • Longitudinal muscle contracts infront of chyme, circular relaxes in front of chyme
36
Q

Describe non-propulsive motilty

A
  • Segmentation
  • Circular muscle constricts lumen
  • Used for mixing and distributing chyme for absorption
37
Q

Describe the pharmacological management of constipation

A
  • Liquid paraffin
  • Laxatives
  • Osmotics
38
Q

Explain how liquid paraffin aids the treatment of constipation

A
  • Lubriates and eases passing of faeces
39
Q

Explain how laxatives aid the treatment of constipation

A
  • Bulk e.g. methylcellulose or agar bran
  • Polysaccharide polymers not easily didgested
  • Form hydrated bulk in gut
  • Holds water
  • Promotes peristalsis (stretch)
  • aids gut motility
40
Q

Explain how osmotics aid the treatment of constipation

A
  • Poorly absorbed solutes
  • Lactulose (semi-synthetic dissacharide of fructose and galactose)
  • Broken down in lower gut, alters oH to more acid, traps ammonia and therefore more water
  • Aids movement
41
Q

What are the classes of compounds used in the treatment of diarrhoea that do not act by direct effect on intestinal motility or secretion?

A
  • Opiates
  • Muscarinic antagonists
  • Both are antimotility drugs
42
Q

Describe the mechanisms of action of opiates in the treatment of diarrhoea

A
  • Codeine or loperamide
  • IMorphine increases contractions but decreases propulsion
  • Increased large intestinal tone, overall leads to constipation
  • More chomping, less secretion
  • loperamide does not cross BBB but when combined with cerapamil can cross BBB and cause psychotropic effects
43
Q

Describe the mechanism of action of muscarinic antagonists in the reatment of diarrhoea

A
  • Neuronal control via parasympathetic from vagus (cholinergic and excitatory)
  • Stimulates GIT motility
  • Atropine not used - affects too many other systems
  • Hyoscine (buscopan) used more frequently
  • Can be used to treat colic
  • Does not cross BBB, effects are outside CNS
44
Q

What are the pathophysiogical mechanisms that can result in diarrhoea?

A
  • Secretory
  • Osmotic
  • Motlity-related
  • Inflammatory
45
Q

Explain how secretory diarrhoea can occur

A
  • Increase in active secretion OR
  • Inhibition of absorption
  • Little to no structural damage
46
Q

Explain how osmotic diarrhoea can occur

A

Too much water drawn into bowels

47
Q

Explain how motility related diarrhoea can occur

A
  • Rapid movement of food thorugh intestines

- Hypermotility

48
Q

Explain how inflammatory related diarrhoea can occur

A
  • Damage to mucosal lining or brush border

- Loss of protein-rich fluids and decreased ability to absorb lost fluids

49
Q

How do hydrophilic and hydrophobic drugs interacct with the body?

A
  • Hydrophilic do not interact, are excreted
    immediately
  • Have to be hydrophobic to interact
50
Q

Why do drugs need to be hydrophobic to interact with the body?

A

Need to be hydrophic to cross cell membrane to interact with cells

51
Q

How are drugs excreted?

A
  • Hydrophilic excreted without modification
  • Excretion via kidneys, hepatobiloary system, lungs
  • Secondary routes via milk and sweat
  • Not a ficed process, in renal failure get faecal excretion
52
Q

Compare excretion of hydrophilic drugs and lipophilic drugs

A
  • Hydrophilic excreted without modification

- Lipophilic metabolised into hydrophilic compounds using CYP450 enzymes

53
Q

Explain the fundamental role of CYP450 enzymes and how they function

A
  • Break down lipophilic drugs into parts that will be excreted and parts that will go into systemic circulation
  • Used in phase I of metabolism
  • Adds oxygen on to drug
  • Oxygen charged, for most molecules will be enough to make it hydrophilic and then excreted
54
Q

Describe the metabolism of drugs in the liver

A
  • 2 phase reaction
  • Phase I (catabolism) may be sufficient to iinactivate then excrete
  • Phase II is synthetic conjugation
55
Q

Describe phase I of drug metabolism in the liver

A
  • Drug oxidised/reduced/hydrolysed
  • Add oxygen on to drug via CYP450
  • Oxygen charged, makes molecule hydrophilic
  • Can now be excreted
  • If not water soluble enough then processed by phase II
56
Q

Describe phase II of drug metabolism in the liver

A
  • If phase I not enough, transferases add on chemical groups
  • Increases water solubility
  • Once water soluble then can excrete drug in urine
57
Q

Where is CYP450 found within the cell and why?

A
  • Endoplasmic reticulum
  • Large membrane surface area, more likely for lipophilic drugs to end up on endoplasmic reticulum
  • Adjacent to/forms continuum with nucleus
58
Q

What is meant by “first pass/presystemic” with regard to drugs?

A
  • First pass metabolism is when a drug reaches the liver, liver acts on drug and metabolises it, excrete it in part before going on to systemic circulation
  • Reduces concentration of drug that will reach systemic circulation
  • From Gi initial concentration) to portal sstem to liver then broken down adn some excreted
  • Rest into blood
59
Q

What is the importance of the enterohepatic circulation in drug metabolism?

A
  • Blood from GI goes to liver via portal system
  • Contains drugs
  • Metabolised in liver, reducing concentration in systemic circulation
  • Protects body from drugs/xenobiotics
  • Drugs can return to GI in the bile
60
Q

Explain how variable drug responses are possible

A
  • Genetic variability, polymorphism
  • Intra-species differences in CYP enzyme activity
  • One patient may respond differently to another
  • Variable drug responses lead to drug toxicity
  • Extensive, poor and ultrarapid metabolisers
61
Q

Describe the drug activity where genes encode for an extensive metaboliser

A

Some drug activity

62
Q

Describe the drug activity where genes encode for a poor metaboliser

A

Increased drug activity

63
Q

Describe the drug activity where genes encode for an ultrarapid metaboliser

A

Drug activity decreased

64
Q

Describe how interaction between drugs is related to CYP enzyme function

A
  • Allosteric control of CYP
  • Products of metabolism of one drug affects the action CYP450 has on another drug
  • May be inhibition of CYP, so increased drug activity of drug 1 (where drug 2 metabolites inhibit CYP450)
  • May be stimulation of CYP so decreased drug activity of drug 1

GI (31 decks)

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