pharmacology 3 Flashcards

please remember to check on how metabolism is affected by certain drugs

1
Q

what is meant by systems framework

A

this is a framework that is used to give a system structure , the processes and the outcomes

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2
Q

factors that are involved in the work system

A

technology and tools
organisation
tasks
environment

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3
Q

what is meant by a systems approach to ADME

A

this means that there is a system that helps with the process of ADME and there are some likely consequences.

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4
Q

what does system comprise of

A

people
tools
tasks
organisation
environment

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5
Q

how does systems affect the absorption of a drug

A

1.people-that is factors that affect the individual person that is cognitive state of mind , other physiological factors ,inflammation , the fear that is within a person.
2.tools-that is the tools that are required to facilitate the absorption of the drugs that means presence of storage material etc.
3.tasks- refers to the tasks to be done before the administration of the drug that is shaking.
4.organisation - the money to buy the fridge , availability of support etc.
5. environment - temperature , design of material etc.

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6
Q

how does system affect the distribution of a drug

A

the systems that is people may have an adverse effect towards the insulin that is produced synthetically and they may not have a reaction towards natural animal insulin however the medical profession people refused their right to an informed choice of insulin treatment.

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7
Q

what is hypoglycaemia unawareness

A

this refers to the state of being unaware of the symptoms of a certain disease

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8
Q

how does the system affect distribution in the case of insulin

A

polymorphism ;this will affect the receptors of the drug , the drug solubility sometimes insulin may be more lipophilic in other people than in others , there could also be increased protein binding.

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9
Q

how does system affect metabolism of drugs

A

1.genetic variation of the CYP2C9 enzyme may lead to poor metabolism of the drug warfarin, example is people with 2 and 3 polymorphism will be poor metabolisers of the drug.
2.warfarin build up is a narrow therapeutic index.

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10
Q

how is excretion influenced by systems

A

Metformin: ‘biguanide’ – first-line drug treatment in T2DM
* Monotherapy or with other drugs (including thiazolidinediones)
* Effects are complex: reduces hepatic glucose production (inhibits
gluconeogenesis)
* Increases FAO in muscle; enhances insulin sensitivity
* Inhibits mitochondrial respiration in liver – lactic acidosis
* Not metabolised
* Excreted unchanged in urine (renal clearance much higher than GFR)

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11
Q

systems approach to renal excretion

A

1.Transporters involved in secretion that is OCT -2 ,MATE-1
2.polymorphic variants of the transporters .
3.Drugs like sulphonylureas and TZDs inhibit OCT activity.
4.H2RA cimetidine
5.kidney function dehydration.

6.other factors such as drinking factors for people with incontinence such as old people, often stress that tends to affect women more ,
7.persons with restricted mobility such as self catheterisation , restriction of fluids in the plane where there are no toilets .

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12
Q

how is methotrexate (MTX) affected by system.

A

1.15mg methotrexate (MTX), once weekly
(to be dispensed as 2.5mg tablets) example is folic acid.
2.Risks arise from systems issues like tablet strength confusion (2.5mg vs. 10mg).
Patient safety depends on understanding perspectives and workflows.

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13
Q

a systems approach to insulin

A

1.Absorption: Factors such as inflammation, injection technique, and temperature impact effectiveness.
2.Distribution: Variation in human vs. animal insulin; challenges like hypoglycemia unawareness.
3.Complexity in patient behavior (e.g., fear, depression) and tools (e.g., vials, monitoring).

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14
Q

a systems approach to warfarin

A

1.Metabolism affected by CYP2C9 polymorphisms and ethnic variations (e.g., *2, *3 alleles).
2.Narrow therapeutic index increases risks, demanding precise dosing and monitoring.

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15
Q

a systems approach to metformin

A

1.Excreted unchanged in the kidneys via OCT-2 and MATE-1 transporters.
2.Renal function, fluid intake, and physical barriers (e.g., accessing toilets) affect clearance.

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16
Q

what is drug to drug interactions

A

this is the modification of a drug`s effect by prior or concomitant administration of another drug ,herb ,foodstuff and drink

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17
Q

object drug

A

a drug whose activity is altered

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18
Q

precipitant drug

A

the agent that precipitates an interaction between a drug

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19
Q

reasons for drug to drug interactions

A

1.increasing action of drug for example co amoxiclav which is amoxicillin plus clavulanic acid.
2.antibiotic resistance -beta lactamase
3.efflux pumps - they prevent drugs from accumulating in the cells.
4.multidrug resistance

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20
Q

what are the factors that may cause drug interactions in patients

A

1.multiple prescribers
2.self prescriptioning that is the use of over the counter medication and the use of food supplements etc .
3.length of the hospital stay .
4.age
5.polymorphisms that is the different genetics contribute to the interactions between the drugs.
6.change in the blood levels for potent drugs will have a harmful effect.

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21
Q

drug interactions how do they affect absorption of the drug

A

they affect the rate at which the drug is absorbed.

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22
Q

what problem is formed when there is a complex formation that causes inhibition of absorption

A

there is a short half life that means a large amount of the drug is needed to achieve therapeutic levels rapidly .

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23
Q

chelation

A

process where drugs bind to the metals in the blood to form complexes that cannot be absorbed by the cells.

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24
Q

example of a drug that undergoes chelation

A

tetracycline and calcium

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25
Q

example of insoluble complexes that are formed by drugs

A

cholestyramine and warfarin

26
Q

examples of how drug interactions affect absorption of the drug

A

1.chelation.
2.formation of insoluble complexes
3.ionisation
4.gut flora
5.GI motility
6.delay

27
Q

gut flora , oral contraceptives and drug interactions

A

some gut flora produce enzymes that cause the re-uptake of the and conjugation of the drugs.
broad spectrum antibiotics cause the increase

28
Q

: Why might rate of absorption be clinically significant?

A

Issues arise when drugs have a short half-life or when therapeutic levels need to be achieved rapidly.

29
Q

How do tetracycline antibiotics interact with calcium?

A

Tetracyclines form chelates (complexes) with calcium, reducing their absorption.

30
Q

What happens when cholestyramine interacts with warfarin?

A

Cholestyramine binds to warfarin, forming insoluble complexes that reduce warfarin absorption.

31
Q

How do H2RAs, PPIs, and antacids affect drug absorption?

A

They reduce H⁺ and increase gastric pH, which can affect the ionization and absorption of acidic drugs like aspirin.

32
Q

Why does increased gastric pH reduce aspirin absorption?

A

Aspirin is a weak acid, and at higher pH, it becomes ionized, reducing its ability to cross membranes for absorption.

33
Q

How can broad-spectrum antibiotics interact with oral contraceptives?

A

Broad-spectrum antibiotics can disrupt gut flora, which reduces the enterohepatic recycling of oral contraceptives, leading to reduced effectiveness.( the plasma proteins for conjugation are no longer available )

34
Q

Where are most drugs absorbed in the GI tract?

A

Most drugs are absorbed in the small intestine due to its large surface area.

35
Q

How do anticholinergics and opiates affect GI motility?

A

They delay gastric emptying, slowing drug absorption

36
Q

What is the relationship between free and bound drugs in plasma?

A

Only the free drug (unbound) is active and available for therapeutic action.

37
Q

Which plasma proteins are primarily involved in drug binding?

A

Albumin: Binds acidic drugs.
α1-glycoprotein: Binds basic and neutral drugs.

38
Q

List examples of drugs that are >95% protein-bound.

A

Warfarin
Ibuprofen
Furosemide
Nifedipine
Clofibrate

39
Q

drug interactions and distribution of drugs

A

there is displacement of drugs when in the presence of other drugs which makes the drugs more active.

40
Q

Why is displacement of highly protein-bound drugs clinically significant?

A

Displacement increases the concentration of free drug, which can enhance its effect or toxicity.

41
Q

What determines the clinical effect of drug displacement?

A

Metabolic capacity (liver function).
Excretion capacity (kidney function).
Overall state of the liver and kidneys.

42
Q

how would drug interactions affect the distribution of a drug

A

The concentration of free (active) drug increases.
This can enhance therapeutic effects but may also cause toxicity.

43
Q

drug interactions and metabolism

A

this is caused when drugs inhibit or induce cytochrome CYP450

44
Q

lomitapide drug

A
45
Q

drug to drug interaction and metabolism

A

Drugs such as clarithromycin,
erythromycin, cimetidine, ketoconazole,
omeprazole, CCBs (diltiazem) inhibit
cytochrome P450 enzymes and so reduce
or stop the metabolism of many drugs

46
Q

drugs that induce cytochrome p450

A

Inducers: barbiturates, carbamazepine,
phenytoin, rifampacin and tobacco smoke
are potent inducers of cytochrome P450s

47
Q

how long does drug to drug inhibition tak e

A

hours

48
Q

how long does drug to drug induction take

A

weeks

49
Q

drug to drug interactions and excretion

A

-Loop diuretics and lithium
-Verapamil/diltiazem inhibit
digoxin excretion

50
Q

types of pharmacodynamics interactions

A

Pharmacodynamic actions of a drug are changed due to another drug
acting directly (same receptor) or indirectly (different receptors)

51
Q

example of direct drug interactions

A

antagonistic , synergistic and or agonistic

52
Q

example of direct antagonism

A

beta blockers they block causing no effect while beta agonists causing a reduction effect sam e effect physiologically though.

53
Q

what is meant by a synergistic effect

A

Both drugs produce the same pharmacological effect but may act through different receptors.
the effects could be additive or more than additive that is potentation.

54
Q

direct antagonism

A

Direct Antagonism: Opposing effects at the same receptor (e.g., β-blockers vs β-agonists).

55
Q

synergism

A

Same overall effect, through different mechanisms (e.g., atenolol + verapamil).

56
Q

adverse synergistic events

A

Drug combinations leading to undesired outcomes (e.g., warfarin + NSAIDs → bleeding).

57
Q

indirect antagonism

A

Drugs act at different sites but counteract each other’s effects (e.g., NSAIDs + anti-hypertensives).

58
Q

how does warfarin function

A

it is an anticoagulant and most of the warfarin is bound to plasma protein only a small percentage is active and free in the blood.

59
Q

reasons why warfarin intake might be dangerous

A

Absorption issues
* Distribution: plasma protein-binding (very
significant)
* Reliance on CYP2C9 (and also 3A4) for clearance
* Polymorphic variation: build up
* Food and drug interactions (NSAIDs)
* Inhibited by: broccoli, sprouts, spinach (Vit K rich)-increase vit K concentration inhibiting warfarin.
* Cranberry (anthocyanins metabolised by 2C9/3A4)-acts on CYP29 and causes reduced warfarin metabolism increasing the amnt of warfarin in circulation.
* -3 fatty acids from fish is an antiplatelet effect they synergise with warfarin to form an anti coagulant effect .

60
Q
A