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Y2 Pharmacology > Intro to pharmacology > Flashcards

Intro to pharmacology Flashcards

1
Q

what is pharmacology

A

study of drug action ( how drug interacts with living organisms and influences physiological function. More drug focused

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2
Q

What 2 concepts are pharmacology split into

A

pharmacodynamics ( effect of drug on body) + pharmacokinetics ( how body breaks down drug)

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3
Q

What is pharmacodynamics

A

effect of drug on body

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4
Q

What is pharmacokinetics

A

how body breaks down drug

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5
Q

what is the study of therapeutics

A

Drug prescription and treatment of disease. More ppl focused

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6
Q

What questions must you ask in pharmacodynamics

A

Where is the effect produced ?
Remember drugs can have different effects good and bad
Must be specific about location
What is the target for the drug ?
Remember in order for a drug to have an effect it must bind to a target
What response produced after interaction with the target ?

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7
Q

Where does cocaine act

A

Dopaminergic neurons in the nucleus accumbent to produce high

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8
Q

How does cocaine produce a high

A

Cocaine blocks dopamine reuptake protein on pre synaptic terminal hence dopamine not removed for synapse → more dopamine can bind to D1 receptor ( Dopamine 1) and cause euphoria

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9
Q

What are the 4 types of drug targets and name an example of a drug that woks on each

A

Receptors - nicotine
Enzymes - aspirin
Ion channels - local anaesthetic
Transport proteins - prozac (antidepressant)

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10
Q

What is drug selectivity

A

Effective drugs must bind with high selectivity for a target but may be hard in real life as a lot of things are structurally similar
Remember lock and key effect → if a drug is selective the drug ( the key) will only bind to one target ( the lock)

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11
Q

Why does dopamine antagonists produce side effects

A

Ie . Dopamine , Noradrenaline and serotonin and similar shapes so dopamine antagonists may also produce side effects due to reactions with noradrenaline + serotonin receptors

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12
Q

What is dose and how do you find out the correct dose for a drug

A

Dose helps with selectivity → first find the dose at which the drug is only selective for the intended receptor then you can find out what
dose the drug will have to be to get side effects ( acting on side receptors)

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13
Q

What are the 4 interaction drugs have with their receptors

A

Electrostatic interactions → most common . H bonds + van der waals
Hydrophobic interactions → important for lipid soluble drugs
Covalent bonds → least common as interactions tend to be irreversible
Stereospecific interaction → drugs exist as stereoisomers and interact with specific receptors

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14
Q

when a drug binds to a receptor what is formed

what happens if you increase conc of a drug

A

Drug receptor complex

Remember this is like an equilibrium reaction if increase conc of drug then equilibrium shift to right as more drug avialable to bind to receptors so more drug receptor complexes formed

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15
Q

What can drug interactions be divide

A

ntagonists + Agonists. Both can bind to receptors but only agonists can activate them. ( Lock and key mechanism : agonist ( key) that can open the receptor ( lock) but antagonists can fit but would jam the lock

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16
Q

What is affinity

A

: Strength of binding of drug to receptor. Linked to receptor occupancy aka the higher the affinity the more the drug binds with receptor

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17
Q

What is efficacy

A

ability of an individual drug molecule to produce and effect once bond to a receptor . Drugs can produce: complete , no or partial responses

Remember a drug can have no efficacy but high affinity

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18
Q

What are the 2 classes of agonists

A

Partial + full

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19
Q

What is potency

A

Conc / dose of a drug to produce a 50% tissue response ( EC50 / half maximal effective conc or ED 50 / half maximal effective dose)

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20
Q

What is the difference betweeen ED50 and EC50

A

look at example on docs

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21
Q

Which is more important potency or efficacy

A

efficacy is more important as you want to know if a drug can give max response. If 2 drugs have equal efficacy potency doesn’t matter as you can still prod max response in the less potent drug but administering it at a higher conc

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22
Q

What are the 4 factors to consider in pharmacokinetics

A

Absorption
Distribution
Metabolism
Excretion

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23
Q

What are the 4 most important carrier systems in pharmacokinetics

A

Renal tube ( allow excretion of drugs from body)
Biliary tract
Blood brain barrier ( allow drug access to certain tissues)
GI tract ( allow drug access to bloodstream due to absorption here + allow extrection)

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24
Q

What is absorption

A

Passage of drug from administration site into plasma aka process for drug transfer into blood. Linked to Bioavailability

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25
Q

what is bioavailability

A

fraction of initial dose that gains access to systemic circulation aka outcome/ how much drug transferred into blood

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26
Q

What are 5 ways to administer a drug

A 
Intravenous → bioavailability is 100% as all drug passes into circulation ( bulk transfer) 
Oral 
Inhalational 
Dermal ( percutaneous 
Intranasal
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27
Q

what are the 2 ways that drugs can move around the body

A 
Bulk flow transfer ( ie in bloodstream) 
Diffusional transfer ( movement across shot distances)
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28
Q

What are the 4 types of diffusional transfer

A

Pinocytosis ( vesicle transfer of drug ( drug surrounded by broken cell membrane ) ( RARE)
ie insulin access to brain
Diffusion across aqueous pores ( gapes in epi/endothelial cells) ( Uncommon as drugs unlikely to be smaller than 0.5nm in diameter)
Simple diffusion ( drug must be lipid soluable)
Carrier mediated transport ( sometimes need ATP)

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29
Q

why is bioavailality <100% for non IV drugs

A

Due to diffusion of drug through lipid membranes before it can get to bloodstream

30
Q

What are the 2 formes a drug is able to exist in

A

weak acid or base meaning that they will be Ionised / unionised

31
Q

Why are most drugs water soluble

A

Most soluble in water not lipid as most are orally administered and need to be dissolved in the GI tract

32
Q

What form are drugs more lipid soluble

A

Unionised form

33
Q

What 2 factors does ionisation of a drug depend on

A 
Dissociation constant ( pKa) of drug 
Most Weak acids have pka of 3 -5 
Most Weak bases pka of 8-10 
PH of body 
Remember if Pka of drug = pka of tissue then durg will be equally dissociated aka 50% ionised/ 50% unionised
34
Q

what happens to solubility of weak acids as PH

a) increases
b) decreases

A

For weak acids as PH decreases = unionised form dominated, PH increases = more ionised form

35
Q

what happens to solubility of weak bases as PH

a) increases
b) decreases

A

For weak bases PH increases - unionsed from more , PH decrease = ionized form more

36
Q

Where are weak acids more unioinsed

A

areas of low Ph like stoma

37
Q

Where are weak bases more unioinsed

A

Areas of higher Ph like blood and urine

38
Q

what is the pka of aspirin and morphine

A 
Aspirin = weak acid.  In ionised state donates H+ . has a Pka of 3.5 aka at PH 3.5 equally dissociated. 
Morphine = weak base. The ionised state accepts H+ . Has Pka of 8
39
Q

Will weak bases be trapped in stomach and weak acids trapped in blood?

A

No→ weak base may be poorly absorbed in stomach but when it enters the SI it will have access to transport proteins . Weak acids can be absorbed in stomach and move into blood but won’t remain trapped there due to tissues having transport proteins moving the drug from the blood into the tissue

40
Q

what are factors effecting distribution of drugs

A

1) Regional blood flow
2) Plasma protein binding
3) capillary permeability
4) tissue localisation

41
Q

What factors do amount of drug bound depend on

A

Free drug conc
Affinity for protein binding sites
Plasma protein conc

42
Q

Why is binding capacity important

A

Why is binding capacity important?
Albumin has 2 binding sites and a conc in the blood of 0.6mmol/ bringing the binding capacity to 1.2mmol/L
Plasma conc required for all drugs is less than 1.2mmol/l ⇒ therefore plasma proteins are NEVER saturated with drugs so they don’t get harmed. Differences are due to different affinity of drugs to receptors

Note → only free drugs can diffuse out of blood into tissue. Drugs bound to plasma proteins can’t leave until it dissociated from the protein

43
Q

how does regional blood flow effect distribution of drugs

A

Different tissues receive diff cardiac output. Higher cardiac output = higher blood flow = more drug distributed to those tissues
Remember distribution can increase / decrease depending on circumstance ie exercise will increase blood to muscles and decrease to stomach

44
Q

how does plasma protein binding effect distribution of drugs

A 
Drugs can bind to plasma proteins in circulation ( albumin is V good at binding to acidic drugs so acidic drugs tend to be more heavily plasma protein bound)
Amount of drug bound depends on : 
Free drug conc 
Affinity for protein binding sites 
Plasma protein conc
45
Q

What are the 4 capillary types and how does they effect distribution of drugs?

A

Continuous structure ( most cap have this) this means that lipid soluble drugs can diffuse through. If drugs aren’t lipid soluble then they will either be v small ( pass through gap junctions) or be transposed into tissues via carrier proteins

Blood brain barrier has tight junctions which makes it hard for drugs to access the brain as they can’t move through

Fenestrated →Circular winders in endothelial cells that allow for passage of small mr substances ie bloods example : kidney glomerulus ( important for excretion of drugs → small drugs can pass through in kidney tubules increase excretion )

Discontinuous → allows big gaps between capillary endothelial cells so drugs can easily diffue out of blood . example : Liver ( important as liver is key for metabolising drugs)

46
Q

how does tissue localisation effect distribution of drugs

A

Make up of the tissue determines diffusion gradient for lipid and water soluble substances
Ie Lipid soluble delta9 - TCH active component of cannabis diffuses into brain → equilibrium established → brain has higher fat content → diffusion grad weights towards higher retention in the brain → more localisation in brain
Water soluble drug diffuses into brain → equilibrium established → brain has lower water content → different grad means more of drug stays in plasma

47
Q

What is drug metabolism

A

Breaking down of the drug. Ideally want drugs to be lipid insoluble so they can stay in bloodstream and get excreted but this means they will have to effect. Metabolism involves conversion drugs → metabolites that are water soluble so easier to excrete

48
Q

What organ is the site for major drug metabolism

A

liver

49
Q

What enzyme n the liver is responsible for drug metabolism

A

Cytochrome P450

50
Q

What are the 2 stages of drug metabolism

A

Phase 1 and 2

51
Q

What happens in phase 1 of drug metabolism

A 
Phase 1 ( want to introduced a reactive group to drug)
Introduce reactive polar groups . Can occur by reduction , oxidation , hydrolysis
Most common is oxidation → note all oxidation reactions start with a hydroxylation step by CP450 system. Aim is to incorporate O into non activated hydrocarbons
52
Q

What enzyme carries out phase 1 drug metabolism

A

c P450

53
Q

What are prodrugs and when are they made

A

phase 1 can make pharmacologically active drug metabolites ( aka drug that only become active one metabolised. These are known as PRODRUGS . Active metabolites my also damage things ie ( liver damage in paracetamol overdose is due to metabolite not paracetamol)

54
Q

What happens in phase 2 of drug metabolism

A

Phase 2 ( add a conjugate to reactive grp)
Attachment of conjugate to make resulting metabolite inactive ( mostly) and less lipid soluble for excretion in urine . bile
Done using transferases enzymes ! rather then cp540 enzymes like in phase1

55
Q

qhat is first pass hepatic metabolism and why is this a problem

A

First pass hepatic ( presystemic ) metabolism :
Problem with oral drugs
Oral drugs administered → absorbed mostly from SI → enter hepatic portal blood supply → pass through liver → systemic circulation
This causes drug to be heavily metabolised so little active drug may reach systemic circulation ( note presystemic metabolism is needed for Prodrug activity)

56
Q

What is the solution to presytemic metabolism and why is this solution not perfect

A

Solution : increase dose
Prolem : extent of metabolism varies in ppl so amount of drug reaching systemic circulation also varies→ causes hard to predict drug + side effects

57
Q

What enzyme carries out phase 2 of drug metabolism

A

Transferases not cp540 like in phase 1

58
Q

What are 4 routes for excretion of drugs

A 
Routes for excretion: 
Excreted via lungs ( ie alcohol → think alcohol breath test) 
Breast milk 
Urine ( *) 
Bile  (*) 
*most excreted this way
59
Q

what are the 3 mayor ways for drugs to exit the kidney ( most effective secretion method)

A

Glomerular filtration
active tubular secretion ( reabsorption_ ,
passive diffusion across tubular epithelium

60
Q

What happens in glomerular filtration

A

Allows drug molecules of molecular weight <20,000 to diffuse into glomerular filtrate. → therefore smaller drugs are excreted quicker

61
Q

What happens in active tubular secretion

A

Most important method as 80% of renal plasma passes onto blood supply to PCT and isn’t filtered out by glomerulus so more drugs are delivered to PCT
PTCT capillary endothelial cells have 2 active transport systems to transport drugs against conc grad : 1 for acidic drugs and the other for basic

62
Q

what happens in passive diffusion across tubular epithelium

A

Generally leads to reabsorption from kidney tubule. 99% of water filtered is reabsorbed and lipid soluble drugs go back into the blood
Factors influencing reabsorption:
Drug metabolism → phase 2 metabolites more water soluble than parent drug → less well reabsorbed
Urine PH → can vary from 4.5 - 8. Acidic drugs better absorbed at lower PH and basic drugs at higher PH

63
Q

What causes variation of excretion of drugs

A

Drugs used these 3 processes of excretion by the kidney differently which causes variation of excretion of drugs ( this is also impacted on by metabolism. Phase 1 + 2 produce more water soluble metabolites that are easier to excrete)

64
Q

How do drugs get excreted in biliary excretion

A

Liver cells transport drugs from plasma to bile ( use transported similar to kidney)
Is really good at removing Phase 2 glucuronide metabolites
Drugs go into bile → intestine → excreted in faeces

65
Q

What is enterohepatic recycling and what does it do

A

Prolongs drug effect

Glucuronide metabolite transported to bile
Metabolite excreted into SI where it is hydrolysed by hut bac releasing glucuronide conjugate
Loss of glucuronide conjugate increase lipid solubility of molecules
Increased lipid solubility increase reabsorption from SI back into hepatic portal blood system for return to the liver
Molecule reuters to liver where a probation will be metabolised by a proportion ma escape back into system circulation to continue having effects

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Y2 Pharmacology (1 decks)

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