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year 1 flash cards > TOPIC 10 - pharmacology > Flashcards

TOPIC 10 - pharmacology Flashcards

1
Q

what are the two branches of pharmacology?

A
  • pharmacodynamics

- pharmacokinetics

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2
Q

what is pharmacodynamics?

A

specific to drug or drug class/way drugs act in body at specific points:

  • interation with cellular component
  • concentration effect relationship
  • modification of disease progression
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3
Q

what is pharmacokinetics?

A

non specific general processes/ quantitive study of drugs movement in the body:

  • absorption from site of administration
  • time to onset of effect
  • elimination from the body
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4
Q

what is a generic name?

A

approved or official name

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5
Q

what is the chemical name?

A

based on its chemical structure

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6
Q

what is the use name?

A

categorised according to use.

eg. anti-inflamatories, pain killer, contraceptives

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7
Q

what is the effect name?

A

some drugs categorised due to biological response in the body. eg. pain killer

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8
Q

what are + to oral route of transmission?

A
  • convenient
  • safe
  • economical
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9
Q

what are - to oral route of transmission?

A
  • cannot be used for drugs inactivated by 1st pass metabolism or that irritate the gut
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10
Q

what is first pass metabolism?

A

metabolism occurs prior to and during absorption

when the drug travels to the liver and gets broken down so 100% of the drug is not absorbed

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11
Q

what are + to intramuscular route of transmission?

A

(muscles are water based, so drugs have to be water based)

  • suitable for suspensions and oily vehicle
  • rapid absorption fro solutions
  • slow and sustained absorption from suspensions
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12
Q

what are - to intramuscular route of transmission

A
  • may be painful

- may cause bleeding at site of injection

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13
Q

what are + to subcutaneous route of transmission

A

(fat layer so drugs tend to be more fat loving)

- sutiable for suspensions and pellets

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14
Q

what are - to subcutaneous route of transmission

A
  • cannot be used to deliver large volumes of fluid as layer quite small
  • cannot be used for drugs that irritate cutaneous tissue
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15
Q

what are + to intravenous route of transmission

A

(straight into vein and circulation, bypass 1st pass metabolism)

  • bypasses absorption yielding immediate effect
  • 100% immediate bioavailibiltiy
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16
Q

what are - to intravenous route of transmission

A

poses more risk for toxicity: cant remove it once given if person has reaction

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17
Q

what are + to buccal route of transmission

A

(placement of tablet under cheek)

  • rapidly absorbed
  • avoids 1st pass metabolism
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18
Q

what are - to buccal route of transmission

A
  • effective only for low doses as space under cheek small

- drugs must be water and lipid soluble

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19
Q

what are + to transdermal route of transmission

A

(on skin, eg. nicotine patches)

- avoids 1st pass metabolism

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20
Q

what are - to transdermal route (eg.nicotine patches) of transmission

A

effective only for low doses of drug that are highly lipids soluble as has to cross the skin layer

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21
Q

what are + to inhalation route of transmission

A

-produce localised effect

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22
Q

what are - to inhalation route of transmission

A
  • drug particles must be correct size

- dependent on patient technique

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23
Q

what are + to intrathecal route of transmission

A

(administration into spinal chord into brain)

- local and rapid effects

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24
Q

what are - to intrathecal route of transmission

A
  • requires expert administration

- may introduce infection/ toxicity

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25
Q

what are + to epidural route of transmission

A

(administered into epidural sac close to spinal chord)

provides a targeted effect

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26
Q

what are - to epidural route of transmission

A
  • risk of fialure

- risk of infection

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27
Q

what are + to topical route of transmission

A

( application to skin)

- non-invasive and easy to administer

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28
Q

what are - to topical route of transmission

A
  • poorly lipid soluble not absorbed via skin or mucous membranes- drug must be very lipophilic
  • very slow absorption
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29
Q

what is modified dose forms

A

less frequent administration of a drug as drugs released over a long period of time

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30
Q

benefits of using modified dose forms

A
  • improved patient adherence
  • reduction in incidence and severity of GIT effects
  • improved control over therapeutic plasma conc.
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31
Q

dis advantages of using modified dose forms

A

cost more per unit than conventional forms

  • possibilty of unsafe dosage if used incorrectly or in failure of MR tablet
  • rate of transmit through GIT. limits the max period for which a therapeutic response can be maintained
  • variability in physiological factors, eg. GIT,pH,enzymes, food ect. influence drug bioavailbity
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32
Q

how can we get incorrect route of transmission

A
  • oral medications given intravenously
  • intramuscular preparations administered intravenously
  • epidural and intravenous lines mix- up
  • using intravenous medications orally
  • intrathecal administration instead of intravenous admistration

incidents can result it adverse outcomes, inc death

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33
Q

what is ADME

A
  • administration
  • distribution
  • metabolsim
  • elimination/excreation
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34
Q

what happens when the drug is administered orally

A
  • its absorbed and goes through the first pass metabolism
  • metabolised by liver
  • distribution to systemic circulation, tissue spaces and cells via the hepatic portal vien from liver
  • pharmacological action in target tissue
  • metabolised by the liver
  • excretion via kidneys, lungs, faces

same process when drug administered via injection but no first pass metabolism in liver - straight to systemic circulation

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35
Q

what is absorption

A

Transfer of the drug from the site of administration into the general or systemic circulation

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36
Q

in first pass metabolism is all of the drug absorbed from the gut?

A

no only proportion of drug absorbed

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37
Q

what factors affect oral absorption

A
  • Particle size and formulation
  • GIT enzymes/AIDS
  • GIT motility
  • Physicochemical factors
  • Food
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38
Q

why is particle size and formulation important in oral absorption?

A

– time taken for drug to disintegrate to small enough size for distribution
– compound must be small enough and lipid soluble to cross gut wall

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39
Q

why is GIT enzymes/acid important in oral absorption?

A

GI tract acidic but less acidic than stomach so breakdown from stomach can continue to smaller particles in GIT

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40
Q

why is GIT motility important in oral absorption?

A
  • GIT constantly moving
    – rate which gastroempties occurs determines rates drug delivery to gut and absorbed to blood stream to go to right area to be absorbed
    -Hyper-motility- gut moving too fast= diarrhoea = lack of absorption = not staying in small intestines long enough to be absorbed
    Hypo-motility= constipation – gut not able to move and open our bowels
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41
Q

why is physiochemical factors important in oral absorption?

A
  • drug size

- point at which drug disintegrates

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42
Q

why is food important in oral absorption?

A

eg. Take with food, on empty stomach – compounds in food may contain electrolytes which effect how drug absorbed

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43
Q

are drugs acids or bases?

A

both
properties of whether acidic or basic determine how drug will work and where it will be absorbed
NB- For drugs to pass membrane have to be uncharged

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44
Q

are acidic drugs ionised or unionised in stomach?

A

Acids are compounds that can dissociate to donate one or more protons= become ionised in stomach

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45
Q

are basic drugs ionised or unionised in stomach?

A

Bases are proton acceptors= Start off being charged and then become unionised

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46
Q

what is the degree of ionisation dependent on?

A

pH of their environment- whether they are in stomach or small intestine

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47
Q

what is distribution

A
  • movement of drug in body
    -The process by which the drug is transferred reversibly
    •from the general circulation into the tissues as concentrations in blood increase
    •from the tissues into blood as blood concentrations decrease
  • needs to have free movement in different areas
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48
Q

what is the distribution of a drug dependent on?

A

lipid solubility, ionisation and physiological ph of envriroment

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49
Q

how does distribution normally happen

A

Mainly occurs by passive diffusion of un-ionised form across the cell membrane

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50
Q

what is the volume of distribution

A

Volume of plasma that accounts for total amount of drug

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51
Q

what is volume of distribution used for

A

•Used to determine the loading dose necessary for a desired blood concentration of a drug, half life and how long take to be cleared
•Also used for estimating a blood concentration in the treatment of overdose
- proteins have large role in this

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52
Q

what factors effect drug distribution

A
  • plasma protein binding
  • specific drug receptor sites in tissues
  • regional blood flow
  • lipid solubility
  • disease
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53
Q

why is plasma protein binding important in distribution of drugs

A
  • helping transfer drugs to site of action
  • protein binding can enhance or detract from drugs performance
  • Agents that are minimally protein bound penetrate tissues better than those highly protein bound as less difficult to leave protein and carry out job
  • Drug only effective when unbound
  • eg. low albumin can effect how well protein binds to protein and how much free drug we have
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54
Q

what barrier do dopamine agonists cross

A

blood brain barrier

results are CNS based and effect CNS

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55
Q

why is regional blood flow important in distribution of drugs

A

more blood flow= better distribution

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56
Q

why is lipid solubilty important in distribution of drugs

A

like drugs more lipophilic – can cross into different tissues as all made of lipids

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57
Q

why is the drug protein complex important

A
  • allows for distribution of drug

- if highly protein bound= difficult to break

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58
Q

what proteins do drugs become bound to in a drug protein complex

A
  • Binding of drugs with albumin and glycoproteins

* Reversible structure

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59
Q

what happens if you administer a highly protein binding drug to a patient who is already taking a drug that is highly protein bound

A

•Results in displacement of drug already bound to protein
•Produces increased unbound concentration of drug and biological activity
-If drug is widely distributed in tissues, the increase in unbound drug is rapidly redistributed to body tissues and unbound plasma concentration rapidly returns to negligible amount

60
Q

are changes in plasma protein binding significant?

A

only for drugs which are greater than 90% bound to plasma proteins

61
Q

what drugs are bound to albumin

A
  • furosemide
  • ibuprofen
  • phenytoin
  • thiazides
  • warfarin
62
Q

what drugs are bound to glycoproteins

A
  • chorpromazine
  • propranolol
  • tricyclic antidepressents
  • lidocaine
63
Q

what must a drug be to be able to cross membranes

A
  • not bound to protein

- Drugs needs to be lopophilic to move around

64
Q

how are drugs transported across the membrane

A
  • Passive diffusion
  • Transporters
  • Membrane pores
  • Vesicle mediated transport (Pinocytosis)- molecules engulfed by cell membrane and vesicle formed which then releases molecule in cell
65
Q

why do we metabolise drugs?

A

to alter drugs to facilitate their removal from the body

66
Q

what are the 4 roles of drug metabolism

A
  • Activation of inactive drug:
    Drug should only have affect on certain part of body
    Liver breaks down drugs to active form
    -Production of active drug with increased activity from active drug
    When drug broken down again produces more active compound so can manage symptoms even more
  • Inactivation of active drugs
    Once drug has had effect- eliminate from system
  • Change in the nature of the activity: Sometimes drug metabolism changes structure of drug so much no longer has effect
67
Q

what are the 4 major metabolic barriers a drug must overcome in first pass metabolism

A
  • intestinal lumen: digestive enzyme secreted by mucosal cells and pancreas- certain enzymes break down proteins and stop them being absorbed
  • intestinal wall: rich in enzymes- further metabolism
  • liver- major site of drug metabolism
  • lung: cells of lung= high affinity for many drugs and are site of metabolism for lots of hormones

this means slow breakdown of drug throughout our system

68
Q

what are the phases of metabolism

A

phase 1: reaction (oxidation,reduction and hydrolysis)- lipophilic drug made into more reactive drug
-phase 2: reaction/cojugation: drug made more hydrophilic and so water soluble to be excreted from kidneys

69
Q

what factors effect drug metabolism

A
  • first pass effect
  • hepatic blood flow: good blood supply= better breakdown
  • liver disease: could mean some enzymes are not present
  • genetic factors
  • other drugs
  • age
70
Q

what is CYTOCHROME P450 (CYP450) system

A

• A large family of enzymes and individual one is called an isoenzyme.

71
Q

how do isoenzymes break down drugs?

A

•Substrate: drug metabolised by isoenzyme

  • Then introduce a drug which is enzyme inducer/inhibitor for same isoenzyme
  • result depends on whether inducer or inhibitor
72
Q

what do enzyme inducers do

A

•Enhance production of liver enzymes which breakdown drugs
•Faster rate of drug breakdown
End up with smaller levels of substrate = less drug in system

73
Q

what do enzyme inhibitors do

A

•Inhibit production of enzymes which breakdown drugs
•Reduced rate of drug breakdown
So more drug in system as its not being broken down efficiently enough

74
Q

How is paracetamol metabolised normally

A

undergos conjugation turning into inactive metabolites paracetamol glucuronide and paracetamol sulphate

75
Q

what kind of additional metabolism takes place if we have an overdose of paracetamol

A

conjugation pathway oversaturated so oxidation pathway used
1- oxidation
2- produces N-acetly-p-benzoquinoneimine (NAPQI)= toxic metabolite- effets liver
3- cysteine derivatives

We use acetylcysteine to push it back down conjugation pathway – to get inactive not toxic metabolites

76
Q

what is bioavailibility

A

Proportion of a dose that reaches systemic circulation

77
Q

what effects bioavailibitly

A

taking drug orally - not 100% drug in systemic ciruclation

- Intravenous route- 100% in systemic circulation

78
Q

what is bioequivalence

A

Two or more chemically or pharmaceutically equivalent products – similar dosage forms but from diff companies

79
Q

why is bioequivalnce useful

A

may be appropriate to replace one product with another without causing clinical problems

80
Q

where does get eliminated

A

liver or kidney

81
Q

what does elimination via the liver depend on?

A
  • blood flow to the liver

* activity of the enzymes in the liver

82
Q

what do liver enzymes do

A

chemically alter the drug to form ‘metabolites’ which are:
•inactive
- water soluble so kidneys can get rid of it
•equally or more active than the parent drug

83
Q

how elimination via the kidney get rid of drug

A

Any ionised lipid soluble drugs eliminated by urine

84
Q

what is clearence

A

Volume of blood/plasma cleared of drug per unit time

  • This includes metabolic as well as renal and biliary clearance
  • Clearance does not indicate the amount being removed
85
Q

whats half life

A

time taken for the conc to reduce by 50%

When drug undergoes 5 half lives = drug cleared from system

86
Q

what is creatinine

A
  • Creatinine is a substance produced in skeletal muscle when skeletal muscles broken down which is excreted through the kidneys
  • It is neither passively reabsorbed nor actively secreted
  • Estimation of creatinine clearance, gives idea of how well kidney function is estimates clearance of drugs filtered at glomerulus
87
Q

why might patients have a raised creatinine level

A

renal failure OR
have more muscle mass
test doesn’t take that into consideration

88
Q

why might patients have a decreased creatinine level

A

renal failure OR

old age, not as much muscle mass

89
Q

what is the COCKCROFT GAULT EQUATION

A

Gives real idea of renal function

= {(140-Age) x Weight x Constant} /Serum Creatinine

Age in years
Weight in kilograms
Serum creatinine in micromol/litre
Constant 1.23 for men 1.04 for women

90
Q

does age affect absorption?

A
  • in elderly generally unchanged

- in children unrelaible in neonates

91
Q

does age affect distribution?

A

in children and elderly fat components of body mass tends to be proportionally greater- act as resevior

92
Q

does age affect metabolism?

A

in infants = reduced capacity = immature liver = drug effects prolonged

in elderly = reduction = impaired liver function = effects more pronounced, last longer

93
Q

does age effect excretion

A

in children reduce capacity die to immature kidneys

in elderly reduction due to impaired glomerular filtration rate

94
Q

what are the three properties of drugs?

A

affinity, efficacy and potency

95
Q

what is drug affinity?

A

the chemical forces that cause the drug to bind to the receptor site
(drugs with low affinity= need high conc to have effect)

96
Q

what is drug efficacy?

A

the extent of functional change in response to a drug binding to a receptor
-relative ability of drug receptor complex to produce a response
(high efficacy drugs = only need few receptors bound to drug for output)

97
Q

what is drug potency?

A

dose of drug needed to produce a biological effect (higher efficacy/affinity = lower dosage)
(highly potent= larger response at low conc)

98
Q

what is an agonist?

A

drug that binds to receptors and initiates a cellular response - normally mimic naturally occurring hormones
- have high affinity and efficacy= strongly bound to receptor

99
Q

what is a partial agonist?

A

act on same receptor but do not produce a maximal response no matter how much receptors activated (eg debutamine mimic noradrenaline)

100
Q

what is an inverse agonist?

A

acts on same receptor but produces an opposite affect (eg naloxone reverses opioid toxicity)

101
Q

what is an antagonist?

A

drug that binds to receptors but does not initiate a cellular response
- has affinity but no efficacy

102
Q

what is a competitive antagonist?

A

reversibly bind to same site as the agonist but does not activate it

103
Q

what is a non-competitive antagonist?

A

irreversibly binds to an allosteric site(not the active site) to prevent activation of the receptor
- changes structure of molecule completely = no resposne

104
Q

what kind of dose response curve is used to compare drugs and what shape does it produce?

A
  • log scale

- sigmoidal

105
Q

what is drug threshold?

A

dose that produces a just-noticeable effect/ lowest dose we can give

106
Q

what is ED50?

A

dose that produces 50% of maximum response

107
Q

what is ceiling?

A

lowest dose that produces maximal effect

- max dose of drug we can give

108
Q

what is relative potency?

A

ED50(lower potency drug)/ ED50(higher potency drug)

- potency good way to see which agonist has higher affinity for given receptor

109
Q

will an agonist + competitive antagonist reach a maximum response?

A

yes - sigmoidal curve still produced, just shifted right as takes longer to reach maximum
- because of reversible binding, agonist can still bind to sites

110
Q

will an agonist + non-competitive antagonist reach a maximum response?

A

no - cannot be reached as antagonist binds irreversibly and changes the structure of the molecule
- some response can still be reached as agonist can occupy receptor site before antagonist (curve shifted right )

111
Q

what are the 4 general mechanisms of drug action?

A
  • action on receptors
  • action on synapses
  • enzyme action
  • inhibit cell transport
112
Q

how do histamine H2 receptor antagonists (ranitidine, cimetidine) work?

A 
block H2 receptor 
- inhibiting action of histamine
- reduces cAMP formation 
- reduced gastric induced acid secretion
all happens in the gut
113
Q

what is gastric acid secretion stimulated by?

A

histamine, acetylcholine and gastrin

114
Q

what is the function of acetylcholine (Ach)?

A

enables muscle action, learning and memory

115
Q

what does low levels of acetyl choline cause?

A

Alzheimer’s disease

116
Q

what is the function of noradrenaline?

A

helps control alertness and mood, increases heart rate

117
Q

what does low noradrenaline cause?

A

depression

118
Q

what does high noradrenaline cause?

A

insominia

119
Q

what is the function of dopamine?

A

influences movement, attention and emotion

120
Q

what does low levels of dopamine cause?

A

parkinson’s disease

121
Q

what does high levels of dopamine cause?

A

schizophrenia

122
Q

what is the function of Gamma Amino Butyric Acid (GABA)?

A

major inhibitory neurotransmitter

123
Q

what does low levels of GABA cause?

A

anxiety

124
Q

what is the function of serotonin (5-HT)?

A

affects sleep, mood, hunger and arousal

125
Q

what does low levels of serotonin cause?

A

depression

126
Q

what do SSRI’s do?

A

selective serotonin reuptake inhibitors - block reuptake of serotonin so more in synaptic cleft, so more stimulation of receptors

127
Q

what do TCA’s do?

A

tricyclic antidepressants - block reuptake of serotonin and noradrenaline but can cause cognitive impairment (so don’t use in old people)

128
Q

what is released following tissue injury that triggers COX?

A

arachidonic acid

129
Q

what does COX 1 do?

A

cytoprotective prostaglandins

  • protect gastric mucosa
  • protect renal perfusion

thromboxanes
- aid platelet aggregation

130
Q

what does COX 2 do?

A

inflammatory prostaglandins

  • recruit inflammatory cells (inflammation, vasodilation)
  • sensitise skin pain receptors
131
Q

what do NSAIDs do?

A

non-steroidal anti-inflammatory drugs

  • eg iburpfen and aspirin
  • inhibit cycloxeganses
132
Q

what do ACE inhibitors do?

A

inhibit angiotensin converting enzymes

  • prevent angiotensin 1 –> 2
  • reduce blood pressure
133
Q

what do ARB’s do

A

angiotensin II receptor antagonist
- block action of angiotensin II receptors
= no vasoconstriction or aldosterone release

134
Q

what do calcium channel blockers do?

A

bind to calcium channels on smooth muscle, block influx of calcium —> smooth muscle relaxation and decreased heart rate

135
Q

what are the three classes of calcium channel blockers?

A
  • dihydropyridines - most smooth muscle selective (most commonly used- work mostly on vascular points)
  • phenylakylamine - selective to myocardium, less effective vasodilator (work mostly on calcium channels near the heart)
  • benzothiazepine - cardiac depressant and vasodilator

Last 2 more work more on calcium channels near heart – more cardioselctive = make sure don’t work too well

136
Q

what do local anaesthetics (LAs) do?

A
  • produce a transient and reversible loss of sensation in restricted area of the body without loss of consciousness
  • cause depression of excitation in nerve endings or inhibition of conduction process
  • Used for analgesia too – for pain management not just during procedure but also post operatively
137
Q

what is the general structure of LAs?

A
  • lipid-soluble hydrophobic aromatic group
  • charged hydrophilic amine group
  • can be joined by and an amide or ester bond (bond determines class of drug)
  • are weak bases-proton acceptors = become unionised
138
Q

what are the properties of ester LAs?

A
  • rapidly hydrolysed
  • breakdown product = PABA
  • PABA associated with allergic and hypersensitive reactions
  • eg cocaine and amethocaine
139
Q

what are the properties of amide LAs

A
  • relatively stable and safer than esters
  • hypersensitivity reactions rare
  • eg lignocaine, bupivacaine and prilocaine
140
Q

which LA is more commonly used and why?

A

amides - more stable and so can be stored for longer as ester linkage is more commonly broken down

141
Q

what is the LA mode of action?

A

intracellular blockage of Na+ channels

  • therefore nerve signal not transmitted as no action potential = if pain is being experienced nit registered by the brain
  • blocking sodium channels we work on nerves= decrease ability for conduction= vasodilation by causing smooth muscles relax – working on CNS and heart rate also
142
Q

what are potential adverse affects of LAs?

A
  • can cause myocardial depression and vasodilation as block Na+ channels in conduction system of heart
  • restlessness or convulsions- effects on CNS
  • adrenaline causes constriction of vessels, less distribution , prolonging action and producing nearly bloodless field
143
Q

how are ester LAs metabolised?

A

(except cocaine)

broken down by plasma esterases to inactive compounds and have a short half life

144
Q

how are amide LAs metabolised?

A

hepatically by amidases, half life is longer and can accumulate if given by repeated doses or infusion

145
Q

where are LAs administered

A

usually to site

146
Q

why would you never use ACE inhibitors and ARBs together?

A

no additional benefit as work at different points of cycle

147
Q

what are the side effects of NSAIDs such as ibuprofen?

A
  • GI irritation- no longer COX1 to protect gastric mucosa

- fluid retention- no longer protect renal perfusion and so kidneys

year 1 flash cards (23 decks)

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