Week 10 - Pharmacology Flashcards
1
Q
what is a drug?
A
any individual chemical that has an effect on the body, good or bad.
2
Q
what is a medicine?
A
mixtures of chemicals, including a drug or drugs, packaged up for patient consumption to treat a pathology or symptom
3
Q
what is a prescription?
A
a “written order, which includes detailed instructions of what medicine should be given to whom, in what formulation and dose, by what route, when, how frequently and for how long”
4
Q
what is the difference between pharmacodynamics and pharmacokinetics?
A
pharmacodynamics is what the drug does to the body (both begin with D) and pharmacokinetics is what the body does to the drug
5
Q
what is an agonist?
A
An agonist is a ligand that binds to a receptor and produces a conformational change, signalling for the initiation of some kind of biological response
6
Q
what is an antagonist?
A
An antagonist is a ligand that binds to a receptor without producing a conformational change and initiating an intracellular signal.
7
Q
what is a partial agonist?
A
A partial agonist is a ligand that activates a signalling pathway to an extent less than the maximum potential of the receptors available
8
Q
what is an inverse agonist?
A
a ligand that produces the opposite effect to the full agonist when it binds to a receptor
9
Q
what is a competitive antagonist?
A
A competitive antagonist occupies a receptor that would otherwise be occupied by an endogenous molecule and prevents that endogenous ligand from binding.
will not reduce Emax, just the dose needed to reach it
10
Q
what is a non-competitive antagonist?
A
interferes with the receptor response in other ways. It binds to a site called an allosteric site, which just means a site other than the agonist binding site, and generally brings about some conformational change that prevents the receptor from working. will reduce the Emax
11
Q
what is an irreversible antagonist?
A
a particular form of non-competitive antagonist characterised by antagonism that persists, even after the antagonist has been removed. The antagonism can only disappear when new proteins or enzymes are synthesized. Aspirin, for example, is an irreversible antagonist.
12
Q
what is receptor affinity?
A
a measurement of how strong the attachment between the drug and receptor is, and how long it will take to dissociate
13
Q
what is efficacy?
A
the extent to which a drug can produce a response when it is bound to all available receptors.
14
Q
what is ED50?
A
The ED50 is the dose that produces a response that is half of the Emax.
15
Q
what is potency?
A
the amount of drug required for a given response. This is related to how well the drug binds to a receptor, so tends to correlate with affinity, but is also related to the amount of response that the drug will produce, so is also related to efficacy.
Higher potency drugs will require lower concentrations of doses, so the potency is what determines the recommended drug dosage. this is important in drugs with adverse effects, as we tend to want to give the most potent drug
16
Q
how much do prescriptions cost the NHS?
A
Prescriptions cost NHS around £15 billion/year or 10% of all healthcare costs
17
Q
what can drugs do?
A
• Treating life threatening diseases • Treating risk factors • “lifestyle drugs” o Feel better/improving the perceived quality of life/ sense of well-being • Hedonistic enjoyment
18
Q
why are medicines a problem?
A
- 7% of hospital admissions
- 15% of hospital patients have drug-related complication
- Prescribed drugs are now a leading cause of mortality
19
Q
what are most receptors?
A
glycoproteins
drug-receptor complex formation is reversible with the biological response being proportional to the fraction of receptors bound
20
Q
types of receptors for drugs
A
Channel-linked receptors
G-protein -coupled receptos
kinase-linked receptors
DNA-linked receptors
other kinds of ‘receptor’ – more targets rather than true receptors
• enzyme targets
• voltage-sensitive ion channels
• transporter proteins
21
Q
what is therapeutic efficacy?
A
the concept of efficacy is not restricted to comparing the effects of drugs that act at the same receptor
the term therapeutic efficacy is used to describe the comparison of drugs that produce the same therapeutic effects on the biological system but do so via different pharmacological mechanisms
22
Q
what is the therapeutic index?
A
the ratio between the ED50 of therapeutic affect and adverse effects
mostly the dose to do half the possible harm will be 100X greater than that to do half the possible good
23
Q
how does interpersonal variation arise?
A
Arises because of various factors (e.g. differences in receptor number and structure, receptor-coupling mechanisms and physiological changes resulting from differences in genetics, age, health etc)
24
Q
what is desensitisation?
A
Biological response to a drug diminishes when it is given continuously or repeatedly
Tachyphylaxis – desensitization that occurs very rapidly
Tolerance- more gradual loss of response to a drug – over days or weeks
25
causes of desensitisation
downregulation of receptor numbers
changes in receptor function or structure
exhaustion of mediators such as depletion of signalling molecules
physiological adaptation
increased drug metabolism - repeated exposure to a drug increases the liver's capacity to metabolise it
26
what are the four stages of pharmacokinetics?
* Absorption
* Distribution
* Metabolism
* Excretion
27
what are the methods of absorbtion?
```
• Enteral
o Oral (PO)
o Buccal (under the tongue)
o Sublingual (SL)
o Rectal (PR)
• Parenteral
o Intravenous (IV)
o Intramuscular (IM)
o Subcutaneous (SC)
o Inhaled (INH)
• Topical application (directly onto site)
```
28
what must an oral medication be to be successful?
* Be swallowed
* Survive gastric acid
* Avoid unacceptable food binding
* Be absorbed across the gastro-intestinal mucosa
* Survive hepatic first-pass metabolism and the enterohepatic circulation
29
benefits of oral
* Convenient
* Simple
* Can be easily self-administered
30
benefits of intravenous
* No concerns about absorption
* Rapidly achieved high drug concentrations
* No “first pass” effect
31
benefits of intramuscular
* Simple to administer
* Unpredictable rate of absorption
* Painful
32
benefits of subcutaneous
* Can be administered parenterally
* Absorbed well from subcutaneous fat
* Can be injected by patients
33
which methods of administration have the first pass effect?
oral and gastric
34
how are nitrates given?
under the tongue as they do not survive the gastric route
35
what does the speed drug distribution depend on?
the level of protein binding in plasma (mostly to albumin, which causes slower distribution) and water/lipid solubility
high water solubility and protein binding will mean the drug stays in the blood for longer.
more lipid soluble will distribute faster
size of the molecule is also a factor
36
what are the four phases of pharmacokinetics?
absorbtion, distribution, metabolism, excretion,
37
what is the volume of fluid of the different body compartments?
plasma - 4L
interstitial fluid - 12L
intracellular fluid - 32L
38
how to work out the volume of distribution?
C0 = D/Vd
C0 is the initial plasma concentration
D is the amount of drug administered
Vd is the amount of drug that has distributed
39
what is the livers effect on drugs?
reduces biological activity, increases water-solubility (for excretion)
Phase I metabolism – oxidation in microsomal mixed function oxidase system (usually inactive after)
Clinically, phase I is really important because this is the site of a lot of drug interactions as some drugs can induce/inhibit metabolism of other drugs.
Phase II metabolism – conjugation by either acetylation or glucuronidation
Drug can be excreted straight away, undergo both phases, just phase I, just phase II
40
how can drugs affect metabolism?
• Induce metabolism
o Produce more metabolising enzymes
Anti-epileptic drugs such as phenytoin
Chronic alcohol
• Inhibit metabolism
o Produce less metabolising enzymes
Erythromycin
important when administering drugs which require stable plasma concentrations such as warfarin
41
describe first-pass metabolism
* After oral does
* Must pass the gut wall and liver
* Can be metabolised before reaching the systemic circulation
* Pro-drugs can be activated this way
42
what are the ways a drug can be excreted?
* Kidney main organ of excretion (renal) (low weight water soluble drugs)
* Biliary excretion (common for drugs that undergo conjugation with glucuronide and drugs with a larger molecular weight)
* Faeces
* Breast milk
* Sweat
43
what happens to highly lipid soluble drugs?
cannot be excreted as they are reabsorbed in the kidney
44
what is entero hepatic circulation?
After liver metabolism, drugs or drug metabolites enter the bile and are carried into the intestinal lumen. There some drugs will be excreted in faeces (faecal excretion). Drugs that are sufficiently lipid soluble may be reabsorbed and re-enter the portal vein. This recycling between the liver, bile, gut and portal vein is known as entero-hepatic circulation.
It prolongs the residence time of drugs in the body, and therefore their effects.
The recycling of glucuronide conjugates requires the presence of bacterial flora. These bacteria have enzymes capable of hydrolysing conjugates, reverting the conjugate to a phase I metabolite that can be reabsorbed. Broad-spectrum antibiotics and other drugs that can inactivate or kill the bacterial flora can therefore reduce reabsorption and drug availability.
45
what is drug clearance?
Drug clearance can be defined as the volume of plasma which is completely cleared of drug per unit of time; it is usually defined as volume divide by time (ml/min or L/hr). It is predominantly caused by liver metabolism and renal excretion. Clearance is related to half-life in a way that drug with a high rate of clearance have a short half-life.
46
what is bioavailability?
Bioavailability is the fraction of the administered dose of unchanged drug that reaches systemic circulation. For drugs that are given intravenously their bioavailability is 100%, as all of an intravenous dose will enter the systemic circulation. However, this is not the case for drugs given via other routes (such as oral route). Therefore the definition of oral bioavailability is the AUCoral/AUCintravenous for the plasma concentration-time graph, expressed as a percentage.
47
what does bioavailability depend on?
* Gastric acid destruction
* Formulation (enteric coated, slow release)
* First-pass metabolism
* Solubility, ionization, food, diarrhea
48
how is steady state reached?
by repeating doses before the first dose of the drug has been eliminated
this causes the drug to accumulate in the body and reaches steady state after 5 HALF LIVES (not doses)
steady state is when drug absorbtion and elimination are equal
49
what is important about steady state?
there will be peaks and troughs in drug concentrations but should be within therapeutic range
these peaks and troughs do not occur in IV - drip
50
what is the problem with adherence and keeping drug exposure constant?
with low frequency dosing, the difference between troughs and peaks will be greater (may be subtherapeutic range or cause adverse effects) but many patients will be unwilling to adhere to multiple doses a day
modified release formulations can solve this
51
when would we use loading doses?
with drugs with a long half life such as digoxin
otherwise it would take a long time to reach steady state (5 half lives)
subtherapeutic before it reaches steady state so larger initial dose is given to reach steady state faster
52
what is zero-order (saturation) kinetics?
- constant amount of drug cleared in unit time
- saturated the mechanism for clearing it
- elimination rate reaches a maximum
- if the drug is administrated at a faster rate than its clearance, it will progressively accumulate
53
what is first order (exponential) kinetics?
- Rate of metabolism or elimination of the drug depends on its concentration
- Exponential decrease in concentration over time
- Constant fraction of drug is cleared in unit time
- predictable
half life of a drug only applies to first order kinetics
54
describe long half life drugs
- slow to reach steady-state
- loading dose may be needed
- slow to be eliminated
- less regular dosing
55
describe short half life drugs
- rapid steady-state
- fine control
- not suitable orally
- more regular dosing required
56
what is an adverse effect?
A response from a medicinal product which is noxious and unintended.
57
what is a side effect?
any effect caused by a drug other than the intended therapeutic effect, whether beneficial, neutral or harmful
58
types of adverse effect
Type A (augmented) – predictable from the known pharmacology of the drug and dose-related, common, usually mild
Type B (bizarre) – unrelated to the known pharmacology of the drug and idiosyncratic, rare, often severe, unpredictable
59
why should prescribing be done with caution in pregnancy
Teratogenic drugs – affect cell division/DNA synthesis -thalidomide, alcohol, cytotoxins, steroid
altered growth - tetracycline, smoking
interference with uterine muscles during labour - beta blockers
postpartum effects - opioids
60
what is drug toxicity?
adverse effects which occur because the plasma concentration has risen above the therapeutic dose
61
why are adverse effects a problem?
Reduce adherence, lose quality of life, litigation problems
62
describe the yellow card scheme
```
detects unrecognised ADCs
• Indication of predisposing factors
• 3-4% of all ADRs are reported
• 10% of all serious ADTs are reported
• Reporting rate was high after release but has fallen
```
changes may include: restriction of use, reduction in dose, product withdrawn, warnings
63
risk factors for ADRs
age (due to polypharmacy, poor clearance, reduced physiological reserve*),
female sex (a lot of medications are not tested very well on females before being released on the drug market)
taking a large number of medicines (increases the risk of drug interactions),
neonates,
genetic factors
allergy,
disease (hepatic or renal as it will affect drug metabolism and excretion)
and adherence problems.
polypharmacy and taking alternative medication
64
what symbol do new drugs have?
black triangle
65
what is the autonomic NS split into?
sympathetic and parasympathetic
66
where are the adrenal glands and what do they do?
superior aspect of each kidney
linked to the sympathetic NS
store catecholamines (synthesised from phenylalanine) to be released in times of physical or psychological stress (most noradrenaline is converted to adrenaline)
67
what does the sympathetic NS do?
- increases heart rate
- increases contractility (force of contraction) of ventricular myocardial muscle
- increases stroke volume (volume of blood pumped by the heart with each beat)
- vasoconstriction
in most arterial circulations which increases resistance to flow thereby reducing local blood flow
o increases peripheral vascular resistance and blood pressure
- vasodilation
o smooth muscle relaxation in large arteries and arterioles supplying skeletal muscles
- venoconstriction increases venous return to the
- Constricts renal arterioles - reduces urine production
- Renin secretion - catalyses the production of angiotensin I which is coverted to angiotensin II which causes vasoconstriction and stimulates the release of aldosterone which leads to sodium retention - both lead to more urine retention
- Bronchodilatiation - more oxygen
- Stimulates more viscous saliva
- Decrease peristalsis
- Constricts sphincters
- Stimulates glycogenolysis - converting glycogen into glucose
- Stimulates lipolysis
relaxes smooth muscle in the bladder and contricts sphincters to preventing urination
- Contraction and relaxation of myometrium to help labour
- Pupil dilation
- Muscle tremor
- Platelet aggregation
- Sweating
68
what are the four targets of catecholamines?
Actions of neurotransmitter on alpha1-adrenoreceptor cause vasoconstriction of blood vessels.
Actions of neurotransmitter on alpha2-adrenoreceptor (located in presynaptic membranes) are slightly different than on other adrenoreceptors. Noradrenaline released from the presynaptic terminals inhibits its own release via feedback inhibition.
Actions on neurotransmitter on beta1-adrenoreceptors (mainly found in the heart) increases force and rate of contraction.
Actions on neurotransmitter on beta2-adrenoreceptors (mainly found in the lung and blood vessels). In the lung it causes relaxation of smooth muscle in the bronchi, and in if the blood vessels it causes vasodilatation.
69
describe alpha agonists
alpha 1 - noradranaline, adrenaline, phenylephrine
alpha 2 - clonidine
rarely used other than topical for the nose
Adverse effects – hypertension, tachycardia, angina
70
describe beta agonists
Non-selective (act at both beta1 and beta2) are adrenaline, isoprenaline (will cause an increase in rate and force of heart contraction, dilatation of bronchi and vasodilation), Adrenaline is used in emergency situations such as cardiac arrest and anaphylaxis.
Dobutamine is beta1 selective so it will cause an increase in rate and force of heart contraction, and is used in severe heart failure.
Salbutamol is beta2 selective and will lead to dilation of bronchi. Inhaled salbutamol is used to treat asthma and intravenous salbutamol to prevent premature labour (inhibition of smooth muscle).
- Adverse effects
o Tachycardia, palpitations (beta 1)
o Tremor, hypokalaemia (beta 2)
71
describe alpha antagonists
(‘alpha-blockers’) tend to end in -zosin: prazosin, doxazosin are alpha1 antagonists where they stop/reduce vasoconstriction. They are indicated for the treatment of hypertension and benign prostatic hypertrophy (prazosin will cause the relaxation of smooth muscle in bladder neck and prostate to relax, making urination easier and therefore reducing the symptoms of BPH).
Adverse effects are hypotension, dizziness and nasal congestion (as they will cause the blood vessels in your nose to dilate).
72
describe beta antagonists
(‘beta-blockers’) tend to end in -olol. Similar to beta agonists, they differ in their selectivity for beta1 and beta2 receptors. Propranolol which is not selective, so has an effect on both beta1 and beta 2 receptors where it will lead to decreased force and rate of heart contraction, as well as stopping the dilatation of the bronchi and blood vessels.
Atenolol is more selective as its actions are primarily on the beta 1 receptors where it will reduce the rate and force of heart contraction.
Beta 1 blockers are indicated for hypertension, angina pectoris and heart failure (indicated for heart failure as they cause inhibition of chronic beta-1 stimulation-induced myocardial apoptosis/necrosis/inflammation).
Beta 2 blockers are indicated for the treatment of tremor (prevent stimulation of beta2 receptors in skeletal muscle).
Adverse effects of beta1-blockers are bradycardia and heart failure
ADRs of beta2-blockers are bronchospasm, cold peripheries and lethargy.
73
what is important to remember about atenolol?
Importantly, no drugs are totally selective, and they will have effects on other receptor subtypes at high enough concentrations. This means that although atenolol primarily has effects at beta 1 receptors, it can also have effects on beta 2 receptors, meaning that atenolol should not be given to people with asthma as it could lead to excessive airway narrowing.
74
what are non-depolarising blockers of the neuromuscular junction?
o Antagonize the nicotinic cholinergic receptor
o Based on curare alkaloids
o Atracurium, rocuronium, vecuronium, pancuronium
can be used as mucle relaxants during surgery
75
what are depolarising blockers of the neuromuscular junction?
o Initial agonism of the receptor (with depolarization) followed by continued binding and shutting of the ion channel
o Suxamethonium (two linked Ach molecules)
Broken down by acetylcholinesterase but more slowly than Ach
Mimics ACh at the neuromuscular junction
Its action cannot be reversed
Genetic variant atypical plasma cholinesterase can cause prolonged paralysis and may require ventilation assistance
76
what are anticholinesterases?
• Anticholinesterases reduce the rate of breakdown of Ach
o Reversal of neuromuscular blockade – induced as a part of anaesthesia
o Increasing cholinergic activity in the brain – for alzheimers
Myasthenia gravis
Diagnosed with short-acting anti-cholinesterases (e.g. edrophonium)
Treatment with long-acting anti-cholinesterases (neostigmine)
Pyridostigmine, physostigmine, rivastigmine, donepezil, galantamine are all inhibitors of acetylcholinesterase.
77
what is dangerous about anticholinesterases?
Some anti-cholinesterases are nearly irreversible because they contain a phosphate ester bond and resist hydrolysis so act for many hours
Dangerous because neuromuscular junction rendered unresponsive and causing widespread muscle paralysis and respiratory failure and a cholinergic crisis in the autonomic nervous system
These are extremely poisonous and include the nerve agent sarin and various insecticides
Powerful hydrolyzing agent, pralidoxime (PAM) can be administered rapidly before the cholinesterase binding is acetylated and becomes completely irreversible
78
what is Dantrolene?
Dantrolene is a peripherally acting muscle relaxant. It acts on skeletal muscle by inhibiting calcium release from the sarcoplasmic reticulum (calcium necessary for the interaction between actin and myosin). Dantrolene therefore prevents muscle contraction and is indicated in severe spasticity of voluntary muscle and malignant hyperthermia (can occur in some people after they are exposed to volatile anaesthetics
79
how can drugs now be designed?
based on their targets on a computer
80
what is the cost of developing a drug?
can take 12-15 years and cost up to £1 billion including failed attempts
81
what is the preclinical phase of clinical trials for?
to test the safety of a drug in humans - tested on model organisms or in vitro (cells and tissues)
determine doses associated with toxicity, revisibility, carcinogenicity etc
82
what are the three Rs in animal testing?
Reduce, replace, refine
83
what are the stages of clinical trials?
Phase I - fewest number - 20-80 - healthy people - to establish basic pharmacokinetic (ADME) and pharmacodynamic (beneficial and adverse effects) properties over a dose range
Phase II - 100-200 - to test effectiveness and dosage
Phase III - 100-1000 - critical phase as it determines if the drug is safe and effective enough to be licenced
Phase IV - 100s - 1000s - after the drug has received licensing regulatory approval - confirm effectiveness and safety and screen rarer side effects
84
what are treatment trials ?
asses the effects of treatments for a particular disease process or symptoms (e.g. is a certain drug effective in reducing blood pressure).
85
what are prevention trials?
asses the ability of a certain practice/treatment to prevent the occurrence of significant healthcare events in the future (such as reducing the incidence of stroke).
86
Typical inclusion criteria are
appropriate diagnosis, age, stage of disease.
87
Typical exclusion criteria are
medical conditions (renal or hepatic failure), women of child-bearing potential, specific drugs that the patients are on.
88
what is parallel group design?
where one group received treatment A, and one group received treatment B, and their outcomes are assessed at the end of the trial.
89
what are factorial design studies?
Factorial design studies can be quite complicated but the simplest version is known as a 2x2 factorial design. In a 2x2 factorial design participants are randomly allocated to one of four combinations of two interventions: A and B. These combinations are A alone, B alone, both A and B; neither A nor B (control). This study design allows us to compare the experimental interventions with the control, compare the experimental interventions with each other, and investigate possible interactions between them. What we mean by this is that we can compare the sum of the effects of A and B given separately and their the effects when they are combined. At the end of the trial the outcomes of all groups are assessed.
90
what are diagnostic trials/screening trials?
assess methods of detecting disease (such as blood tests).
91
what are quality of life studies?
assess the impact of treatments on quality of life for patients rather than strict medical outcomes.
92
what is cross-over design?
a repeated measurements design such that each patient receives different treatments during the different time periods, i.e., the patients cross over from one treatment to another during the course of the trial. Their outcomes are assessed before crossing over. This is different to a parallel design in which patients remain on that treatment throughout the duration of the trial.
The reason the crossover design is used is that fewer patients might be required in the crossover design in order to attain the same level of statistical power or precision as a parallel design because each patient serves as his/her own matched control. Every patient receives both treatment A and B.
93
randomisation groups
Stratified – by characteristic (size may vary e.g. more young men than young women)
Blocked – by time (randomising small consecutive groups) disadvantage of small block sizes is that it is possible to guess some allocations, thus reducing blinding in the trial.
Clustered – by geographical location
94
blinding
Single blind – the patient doesn’t know which treatment he/she is getting
Double blind – neither doctor nor patient knows
Triple blind – observer doesn’t know either
95
what are observational studies?
observing the progression of patients exposed to different drugs and compare outcomes
96
what should outcome measurement be?
clinically relevant - should be directly relevant to patients
objectively measured - should not be open to interpretation which can introduce bias especially if the observer is not blind to the treatment allocation
97
what are the ethical issues of clinical trials
```
equipoise (balance of interests)
informed consent must be given
the scientific quality of the study
statistical manipulation
interpretation of data
publication of data - such as failing to publish it
```
98
what is RAMMbo?
Recruitment - were the subjects representative of the target population
Allocation - was the trial randomised (were the groups comparable)
Maintenance - Were the groups treated equally during the trial
Measurements
- blinded - Were the patients and clinicians blinded to treatment
- observations - were the measurements objective and standardised
99
what is complementary medicine?
Complementary medicine is a therapeutic approach that is used together with conventional medicine
100
what is alternative medicine?
alternative medicine is a therapeutic approach used instead of conventional medicine.
101
how many cancer patients use CAM?
3-25%
102
how many adults use CAM?
20-60%
103
what happens in the parasympathetic nervous system?
ACETYLCHOLINE is released from
postganglionic nerve endings
The two subtypes of receptor are nicotinic (ligand-gated ion channels) and muscarinic (GPCRs), named for their specific ligands - on effector tissues - called cholinergic receptors
The ganglia (relay centres/synapses, described above) are located close to the effector organ, in contrast the sympathetic NS.
104
what are the types of muscarinic receptor?
Muscarinic receptors M1, M3 and M5 ACTIVATE the phospholipase C pathway
M2 and M4 INHIBIT the adenylate cyclase pathway
105
actions of the parasympathetic NS
```
Bronchoconstriction
• Bradycardia
• Hypotension
• Salivation
• Sweating
• Pupil contraction
• Peristalsis
```
106
Cholinomimetic drugs
Direct acting agonists: acetylcholine, bethanechol, pilocarpine and muscarine (latter three muscarinic)
107
what are anti-muscarinic drugs?
often competitive antagonists of M receptors, and as such will have sympathetic effects:
Ipratropium: used in asthma and COPD to promote bronchodilation
Atropine: used in myocardial infarction (to stimulate heart), pre-anaesthetic (to prevent respiratory secretions), ophthalmological tests (to dilate pupil) and to counteract cholinomimetic poisoning •
Benztropine: used in Parkinson’s to restore cholinergic/dopaminergic balance
108
what is a cholinergic crisis?
fluid from every orifice
109
Tetracycline action
Tetracycline inhibits the binding of tRNA in translation.
110
Erythromycin action
Erythromycin inhibits translocation of ribosomal subunits during translation.
111
Streptomycin action
Streptomycin inhibits the formation of the initiation complex.
112
Chloramphenicol action
Chloramphenicol inhibits peptidyl transferase
113
whats special about dobutamine
short half life - 2 mins
114
what drugs are affected by gastric acid?
insulin and benzylpenicillin
115
what drugs are effected by first pass metabolism?
morphine
116
why is paracetamol widely available?
high therapeutic index
| unlike warfarin, digoxin, theophylline, insulin
