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Co-morbidity Exam > Interactions > Flashcards

Interactions Flashcards

1
Q

what are pharmacokinetic interactions

A

interactions which can affect the process by which drugs are absorbed, distributed, metabolised or excreted

(ADME INTERACTIONS)

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2
Q

what are pharmacodynamic itneractions

A

interactions that occur when the effect of drug A is altered by the presence of drug B without affecting its pharmacokinetics

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3
Q

what are CYP450 enzymes and how do they work?

A

haemoprotein metabolising enzymes

they are major enzymes involved in drug metabolism
they are primarily involved in phase 1 monooxygenase reactions
the source of oxygen is the oxygen joined to the heme co-factor

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4
Q

please draw the mechanism of CYP oxidation

A

aliphatic hydroxylation

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5
Q

what will happen if drug A is a CYP substrate and drug B is a CYP inhibititor?

A

drug a concentration will increase

risk of toxicity

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6
Q

what will happen if drug A is a CYP substrate and drug B is a CYP inducer?

A

drug A concentration will decrease
reduced substrate A efficacy
risk of therapeutic failure

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7
Q

what is the rate of onset of effect for CYP inducers? and why?

A

gradual onset and offset

this is because the process is slow and involves increased DNA transcription and synthesis of new CYP enzymes

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8
Q

what affects the length of effect of the CYP inducer?

A

half life of the inducer
time to make new CYP proteins
rate of degeneration of new CYP proteins

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9
Q

what is the rate of onset of effect for CYP inhibitors? and why?

A

rapid onset of action

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10
Q

how long does the effect of CYP inhibiting enzymes last

A

may be a long lasting effect (depends on the exact MOA)

may be long lasting depending on how long it takes to make new enzymes

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11
Q

what are the two methods of inhibiting CYP enzymes

o

A

oxidative metabolism

n-oxidation

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12
Q

how does oxidative metabolism act to inhibit CYP enzymes?

A

capable of alkylating either the protein or the prosthetic heme group

blocks the enzyme action
prevents its return to function until a new CYP enzyme is produced

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13
Q

how does n-oxidation act to inhibit CYP enzymes?

A

if the inhibitor contains an amine functional group
can lead to formation of an irreversible metabolic intermediate between a nitrogen group and the heme iron (prevents complete function)

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14
Q

Inhibitor or inducer?

rifampicin

A

inducer

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15
Q

Inhibitor or inducer?

carbemazapine

A

inducer

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16
Q

Inhibitor or inducer?

phenobarbital

A

inducer

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17
Q

Inhibitor or inducer?

phenytoin?

A

inducer

18
Q

Inhibitor or inducer?

nevirapine

A

inducer

19
Q

Inhibitor or inducer?

pioglitazone

A

inducer

20
Q

Inhibitor or inducer?

st. johns wort

A

inducer

21
Q

Inhibitor or inducer?

sulfamethazazole

A

inhibitor

22
Q

Inhibitor or inducer?

amioderone

A

inhibitor
(not the parent dug amioderone itself but its metabolites
it is the inhibitory metabolites of amioderone that are responsible for causing the drug drug interaction)

23
Q

Inhibitor or inducer?

cimetadine

A

inihibtor

24
Q

Inhibitor or inducer?

fluoxetine

A

inhibitor

25
Q

Inhibitor or inducer?

fluxonazole

A

inhibitor

26
Q

Inhibitor or inducer?

ritonavir

A

inhibitor

27
Q

what is the role of ritonavir in highly active antiviral therapy?

A

used in combination with other retrovirals

ritonavir is rarely used for its own retroviral activity but remains widely used as a “booster” for other protease inhibitors

it has these abilities because of its off-target inhibitory action agains CYP3A4

ritonavir is sacrificed to the CYP enzymes
it is a potent CYP enzyme inhibitor
it reduces the metabolic action of the enzymes
therefore it prevents other protease inhibitors being metabolised by the CYP enzymes and so BOOSTS their therapeutic action of the other antiretrovirals !!

28
Q

what is Pglycoprotein

A

it is a transmembrane molecular pump that acts to protect our cells from toxic molecules

it is the most characterised memeber of the ABC-transported subfamily of proteins

29
Q

what is special about the PgP structure that makes it really good

A

cone shaped intracellular cavity allows it to accept a wide range of structurally diverse substrates

30
Q

explain the process of PgP action

A

1) PgP sits in the cell membrane and searches for foreign hydrophobic molecules

2) when it finds a foreign hydrophobic molecule it grabs it deep within the protein and then it flips to a new conformation
(substrate binding initiates ATP recruitment)

3) the new conformation has an opening towards the outside of the cell and the molecule is ejected out of this opening

(the whole process if powered by ATP to ensure the process occurs in a timely manner)

31
Q

what happens in the interaction between anioderone and digoxin

A

amioderone increases the serum concentration of digoxin but inhibiting the Pgp that facilitates the elimination of digoxin from the body

amioderone may also influence the serum concentrations of digoxin bu changing the tissue distribution of digoxin (Vd)

32
Q

name 3 interactions that can occur between a drug molecule and PgP

A

hydrophobic interaction (weak electrostatic forces, Van Der Waals )

hydrogen bonding

aromatic cage formation (align electrons with the drug)

33
Q

what are antacids made of

A

they are chemically week bases formulated as salts

hydroxides, tricilates, carbonates

34
Q

how can antacids cause drug drug interactions

A

because of their effect on pH
they increase gastric pH (make it less acidic and more alkaline) therefore this impacts on pH dependent dissolution

as most drug molecules contain an ionisable functional group, changes in pH will have a knock on effect fo the dissolution profiles of any co-administered drugs

as dissolution is the rate limiting step of drug administration from a solid dosage form changes in drug dissolution due to changes in stomach pH can therefore lead to enhanced or reduced absorption

chelation
occurs between polyvalent metallic ions (magnesium or aluminium) and organic mocules
form an insoluble ring complex in solution that cannot be absorbed

35
Q

what is the problem with using antacids with ketoconazole

A

ketoconazole is a weak base pH approx 3
it is therefore nearly insoluble at pH 4 but is soluble at acidic pH

if the gastric ph is raised >4 for a period longer than gastric emptying (10-20 mins)
then the drug may reach the small intestine before dissolution has taken place therefore absorption will be decreased as the drug will not be in solution when it reaches the small intestine therefore it cannot be absorbed

36
Q

what is the problem with using mallow with tetracyclines

A

reduces the oral bioavailability of the tetracycline and its metabolites bu 80%
(the same effect doesnt occur when using omeprazole) this means that tetracycline chelates with the metal ions in the antacids and forms an insoluble complex
as the tetracycline has formed the insoluble complex it cannot be absorbed and therefore cannot exert its therapeutic effect.

37
Q

where can pharmacodynamic reactions occur

A

at the receptor (where it binds)

or the effector (the therapeutic effect that it has)

38
Q

please give an example of a negative interaction at the receptor

A

salbutamol (beta 2 agonist)

propranolol (non selective beta antagonist)

39
Q

please give an example of a positive interaction at the effector

A

using a combination of ACE inhibitor and calcium channel blockers to treat hypertension

both have different MOA but exert the same final effect of reducing blood pressure

40
Q

please give an example of a negative interaction at the effector

A

using carvedilol (beta blocker) and verapamil (CCB)

both have cardiac suppressant effects
can cause serious cardio depression e.g bradycardia, systole, sinus arrest :-(

Co-morbidity Exam (18 decks)

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