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166 Cards in this Set

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What are the targets for drug action?
Enzymes, receptors, carriers, ion channels.
What is receptor occupancy related to?
The concentration of the drug
The higher the affinity of the drug for the receptor...
The lower the concentration that it produces occupancy
What are the two main characteristics of reversible competitive antagonism?
Concentration-effect curve is shifted to the right with no change in steepness. Dose ratio increases linearly with antagonist concentration, which is used to measure the affinity of the antagonist for the receptor
What is dose ratio?
Dose ratio is the ratio by which agonist concentration has to be increased in the presence of the antagonist in order to restore a given level of response
What does an inverse agonist do?
Reduces the level of constitutive activation-Possible for receptors to have natural levels of activation with no ligand bound.
What do a) Agonists
b) Antagonists
c) Inverse agonists
Show according to the two state model?
a) Bind to activated state (equilibrium to right)
b) Equal affinity for both states
c) Greater affinity for resting state, (equilibrium to left)
What is a partial agonist?
Can occupy all the receptors but does not produce the full response
What is the concept of spare receptors?
That full agonists can produce a maximal response without occupying all the receptors
What is a) Chemical antagonism
b) Pharmokinetic antagonism
c) Competitive antagonism
d) Irreversible antagonism
e) Physiological antagonism
a) Interaction in solution e.g. DIMERCAPROL.
b) Affecting absorption, metabolism or excretion.
c) Interrupts receptor-effector linkage.
d) Both drugs binding to same receptor
e) Two agents producing opposite effects
What is tachyphylaxis?
loss of a drug's effect when given continuously e.g. change in receptors, enhanced metabolism.
Fractional occupancy is equal to...
Concentration of the Agonist X Concentration of the receptor divided by the total number of receptors.
Law of mass action
What does the position of the agonist dose-response curve depend on?
Kd (dissociation constant,) Efficacy, tissue, response
What does absorption depend on?
Lipid solubility
Blood flow at site of administration
Route of administration
What does drug absorption depend on in the GIT?
Splanchic blood flow
Particle size
GIT motility
Physicochemical factors
What are the two routes for enteral administration?
Oral, rectal
What are the four routes of parenteral administration?
Intrathecally-If need to cross BBB
Intramuscular-Absorption depends on blood flow and diffusion rate.
Subcutaneous-Skilled admin
Intravenous-Slow infusion, stabilises plasma conc.
What are the five subcutaneous routes?
Nasal-For peptides
Topical-Poor absorption
Inhalation-Rapid adjustments of plasma conc.
Sublingual-Rapid, avoids 1st pass
Eye drops-No damage to kidney
Where do drugs often accumulate?
In fat and tissues with a high melanin content and sometimes bone and teeth e.g. Tetracyclines.
What does distribution depend on?
Blood flow
Lipid solubility
Diffusion barriers
Tissue binding
Plasma protein binding
What are the two stages in drug breakdown in the liver?
P450 enzymes
1-Catabolic-Hydrolysis, oxidation and reduction.
2-Anabolic-Conjugated using sulfate etc to less active compound usually
How does the liver excrete drugs?
In bile (can be reactivated by hydrolysing, releasing free drug in intestine)-Enterohepatic circulation
How does the kidney excrete drugs?
Glomerular filtration
Active tubular secretion
Passive diffusion
Highly polar drugs not reabsorbed and excreted in urine-Basic drugs better in acidic urine as it is ionised.
What does dose interval depend on?
Plasma half life, follows exponential time course.
What happens in saturation kinetics?
In normal states, linear line where steady state is directly proportional to dose, in saturation kinetics when the therapeutic dose is exceeded, steady state cannot be reached.
How does conjugation work?
Adds a polar group to make the drug more soluble.
What factors may affect drug elimination?
Age, thyroid, liver function, blood pressure, kidney function.
What is phase 1 of clinical studies when making a new drug?
Healthy volunteer testing with ethics commitee approval
What is phase 2 in drug production?
Certificate from CSM, small scale trials, not dose controlled
What happens in phase 3 in drug development?
Large scale, double blind and placebo trials
What is phase 4 of drug production?
Product licensed and drug marketed
How does a virus penetrate a cell?
By pinocytosis.
What drugs can block viral nucleic acid synthesis?
What inhibits translation?
Acyclovir, Foscarnet
What drug can inhibit the penetration of a virus and what is this used on?
What is its mechanism of action?
AMANTIDINE, use on Influenza A as prophylaxis.
Blocks ion channel associated with entry of virus via endosome.
What is the mechanism of action of ZANAMIVR? What is it used for?
Influenza A and B
Neuraminidase inhibitor blocking budding and cleaves glycosides.
When would a DNA polymerase inhibitor be used?
Herpes simplex 1 and 2, zoster, cytomegalovirus
What is the mechanism of ACYCLOVIR?
Phosphorylated via viral thymidine kinase
acyclo GMP
Inhibits viral DNA polymerase
Terminated viral DNA chain extension.
What is GANCICLOVIR a derivative of? Why should it be used with caution?
Guanosine derivative, toxic to host replicating cells.
What drug is a synthetic nucleoside that alters viral nucleotide synthesis?
What are examples of reverse transcriptase inhibitors?
ZIDOVUDINE, analogue of thymidine modified sugar.
Phosphorylated to triphosphate, inhibiting Reverse transcriptase.
DIDANOSINE-Adenosine analogue
non-nucleoside RT inhibitor
Used in AIDS
What does SAQUNAVIR inhibit?
What are the problems with this?
Aspartate protease
Dcresases structural proteins and enzymes.
Inhibits P450 enzymes, lipodystrophy.
What is the regime for AIDS?
HAART-2RT inhibitors and a protease inhibitor
What are the four types of allergic reactions?
Type 1-Food, asthma-Anaphylactic hypersensitivity.
Type 2-Antibody dependent cytotoxic hypersensitivity.
Type 3-Complex mediated hypersensitivity-Joints
Type 4-Cell mediated hypersensitivity-Tcells/lymphocytes-Insect bites
What is the beneficial effect of chemotherapy due to?
Quantitative differences in cell numbers
What does gram negative bacteria have that gram positive doesn't?
Lipopolysaccharide and protein coat.
What parasites have little exoerythrocytic stage and which ones have this stage?
Plasmodium falciparum + P. Malariae

P.vivcux, P.ovale
How does chloroquine work?
Concentrates in parasite lysosome, inhibits Hb metabolism by inhibiting haem polymerase, increased haem is toxic to the virus.
Used at acute and chemoprophylaxis stage.
Why can chloroquine not be used for p. falciparum and what is used instead?
Has aquired resistance, maybe ejecting the drug from itself.
Use quinine, mefloquine instead.
What does Pyrimethamine do?
Inhibits dihydrofolate reductase which decrease the amount of co-factor needed in DNA synthesis
What inhibits the conversion of pABA to folate at acute and chemoprophylaxis stages?
What is MEBENDAZOLE used for and how does it work?
Used for threadworms
Binds to beta tubulin preventing the formation of microtubules.
What would you use for GI roundworms?
PIPERAZINE-Inhibits nerve transmission at worm NMJ-GABA agonist
Which drug causes a selective calcium increase in muscle and consequential paralysis?
How do AMPHOTERICANS work? Which drug is similar?
Bind to ergosterol in fungal membranes forming an ion channel pore, cells lose potassium.
Used for GIT infection or systemic infection.
What inhibits the synthesis of ergosterol?
What are the consequences?
Decreases membrane fluidity and replication, inhibits the formation of hyphae in yeast.
What is FLUCONAZOLE used for and what are its side effects?

What would be used for superficial infections?
Systemic infections, rarely liver toxicity.

TERBINAFINE-Inhibits squalene epoxidase (squalene to ergosterol)
Squalene accumulates which is toxic
What are the common side effects of anti-cancer drugs?
Bone marrow suppression
Impaired wound healing
GI tract damage
Nausea and vomiting
Hair loss
Impaired growth in children
What type of drug is CYCLOPHOSPHAMIDE and what are its side effects?
Pro drug activated by P450 binds to DNA, highly reactive used as an anticancer drug
May cause haemorrhagic cystitis-ACROLEIN MESNA given to try and protect.
How does CISPLATIN cause DNA denaturation?
What are side effects?
Intrastrand cross-linking, given by IV infusion.
Serious nephrotoxicity-Need hydration.
Severe nausea
How does DOXORUBICIN work and what type of drug is this?
Side effects?
Binds to DNA inhibiting DNA and RNA ayntheis. Also stablilised DNA/topoisomerase 2 complex.
Cardiotoxic, hair loss local necrosis at IV site.
Which drug breaks up DNA chains and where is it most effective?
Side effects?
BLEOMYCIN, at G2 stage.
Hyperpyrexia, allergies, pulmonary fibrosis
What drugs in chemotherapy affect spindle formation and how do these work?
Inhibit cell divison at metaphase, and tubulin polymerisation.
Must be administered by IV.
neurotoxic Reduced W.B.C's
Side effects?
Stabilises microtubules in polymerised state, administered by IV.
Breast cancer
Bone marrow, allergies, neurotoxicity
Side effects?
Folate agonist, inhibiting dihydrofolate reductase.
Bone marrow supression, pneumonitits, nephrotoxicity.
What else can be used to treat Cancer?
Hormones e.g. glucocorticoids
Hormone antagonists-Tamoxifen/Flutamide
Biological response modifiers-Interferons
Radioisotopes-e.g. Thyroid
How are side effects of chemotherapy drugs controlled?
Drug combinations intermitently
Anti-emetics for nausea e.g. 5HT antagonists.
Harvest bone marrow
Correct management of infection
What are newer approaches to chemotherapy?
More selective drugs
Angiogenesis-Stop blood supply
Mutant adenovirus lyses tumour cells when P53 is not present (as in cancer)
Selective antagonist for neuronal sub-type nicotinic receptor.
Not competitive
Blocks all effects of autonomic stimulation
What type of receptors are present:
a)Pre-ganglion automomic
b)Post-ganglion parasympathetic?
a)Nicotinic Ach
b)Muscarinic Ach
How many muscarinic receptor sub-types are there and what do these do?
M2=Heart, smooth muscle
What are the effects of muscarinic agonists such as MUSCARINE, PILOCARPINE?
Increased secretions,gut motility.
Bradycardia, bronchoconstriction, urinary frequency, constriction of pupil, vasodilation via activation of receptors which are not innervated.
What are the result of muscarinic antagonists such as ATROPINE?
Decreased secretions and gut motility, tachycardia, bronchodilation, urinary retention (stopping miticuration reflex) dilation of pupil.
What is used to treat
a) Depression?
b) Parkinsons?
c) Cardia arrythmias?
d) schizophrenia?
e) Motion sickness?

What are all of these?
a) Imipramine
b) Benzhexol
c) quinidine
d) chlorpromazine
e) promathazine

What may drugs such as pilocarpine be used for?
What may drugs such as ATROPINE be used for?
Heart failure (which is sometimes due to excessive parasympathetic stimulation,) premeds, asthma, chronic bronchitis(Ipratropium,) eye examinations.
What is Noradrenaline synthesised from?
made into DOPA by tyrosine hydroxylase
to Dopamine by dopa decarboxylase
Made to Noradrenaline by dopamine beta hydroxylase
To adrenaline by PNMT
How many types of adrenoreceptor are there and what do they do?
alpha 1-Smooth muscle contraction
alpha 2-Vasoconstriction, also pre-synaptic.
Beta 1-Increase heart rate and contractility
Beta 2-Relax smooth muscle
In what instances is adrenaline used in combination with other drugs?
As a vasoconstrictor with local anaesthetics (alpha)
In cardiac failure (beta 1)
Anaphylactic shock (alpha/beta)
What agonist is used as:
a) Nasal decongestant?
b)For hypertension?
b) CLONIDINE on alpha 2
What are alpha antagonists used for?
benign prostatic hyperplasia (Prazosin)
Impotence (phentolamine)
What are beta antagonists used for and what are two examples?
Propanolol, metoprolol (beta 1 only)
Angina, cardiac arrhythmias
Anxiety states
In anaesthetics, which type of linkage metabolises first?
Ester linkage first, amide linkage second, only suitable for short procedures.
How do local anaesthetics work?
At what pH is there more of the charged ion?
Block voltage gated ions channels from inside the neurone.
Acidic pH
What are examples of short, medium and long acting anaesthetics?
How may local anaesthetics be administered?
Infiltration-Straight into the tissue
Nerve block-Into nerve trunk
Spinal-Subarachnoid space
Epidural-Childbirth-Fewer neuralgic effects
What are the unwanted effects of local anaesthetics?
Tremor, agitation, convulsions, respiratory failure
decreased contractility of cardiac muscle
dilation of b.v-Bradycardia
What do Inotropic drugs do?
Affect contractility of the heart, clinically used to increase cardiac output in heart failure (when CO is insufficient for the metabolic needs of the body)
What could be the causes of heart failure?
Ischaemic heart disease
What do positive inotropic drugs do?
Increase contractility by increasing intracellular calcium
What type of drug is DIGOXIN and what is its mode of action?
Cardiac glycoside
Inhibits sodium/potassium atpase
Intracellular Na+ increases
Efficiency of Na+/Ca2+ exchange decreases
Ca increases intracellularly
Contractility increases
What are the side effects of DIGOXIN?
Increase resting membrane potential of cardiac myocytes-Arrhythmias
Neurological disturbance
What are sympathomimetic inotropes?
How do they produce this effect and on what receptor?
Mimic the affect of sympathetic activity i.e. Adrenaline and Noradrenaline on B1.
Bind, cyclic AMP makes Ca channels stay open longer increasing intracellular Ca.
Which beta 1 agonist is highly specific in the heart?
What about beta 1 and 2?
DOBUTAMINE-Short half-life, by IV for emergencies
How do they work?
Phosphodiesterase inhibitors type 3 selective.
Inhibits PDE, level of cAMP increases.
More calcium channels, more contractility
What other drugs may be useful for cardiac failure?
Diuretics-Decrease blood volume
Vasodilators-Inc. systemic volume
What part of the nervous system are blood vessels controlled by?
Some e.g. erectile tissue are controlled by MAchR but most are controlled by sympathetic NS.
What does 5-HT do with respect to tyrosine synthesis?
What is this useful in?
Inhibits alpha methyl tyrosine blocking the conversion of tyrosine to DOPA-Hypertension
What does Carbidopa treat?
What does Disulfiram treat?
Parkinsons by blocking dopa decarboxylase.
Alcoholics, severe reaction with alcohol causing aldehyde to accumulate in the blood
What does RESERPINE do?
Inhibits NA transport into the vesicles, depleting stores-Hypertension.
What does GUANETHIDINE prevent?
Exocytosis of NA containing vesicles.
Therefore sympathetic stimulation blocked and decreased BP
Where is uptake one and what is it blocked by?
From synapse to neuron, blocked by IMIPRAMINE (anti-depressant)
What is monamine oxidase blocked by?

What is Catecholo-methyltransferase blocked by?

What do beta2 receptors in skeletal muscle do?
In respiratory system?
At which type of adrenoreceptor is ISOPRENALINE more potent?
At Beta receptors, evidence for different types of receptor.
Name and agonist and an antagonist at:-
a) Alpha 1
b) Alpha 2
c) Beta 1
d) Beta 2
a) Phenylephrine, prazosin
b) Clonidine, Tohimbine
c) Dobutamine, metoprolol
d) Salbutamol, butoxamine
Which agonists/antagonists on adrenoreceptors have no clinical use?
Tohimbine and Butoxamine.
Which receptors does ADRENALINE work preferentially on?
What does it do?
Beta receptors
Increases CO and vasodilation
When is the only time that you would use vasoconstrictors such as PHENYLEPHRINE for shock?
To treat acute hypotension after surgery
How does CLONIDINE produce a decrease in blood pressure?
Although it acts on alpha 2 receptors, those in the brain are activated causing a centrally mediated decrease in blood pressure.
What are the following used for?
a) Dobutamine
b) Prazosin
c) Phentolamine
d) Propranolol
a) Cardiac failure, longer acting than adrenaline.
b) Raynauds disease
c) Impotence, vasodilatation blocking ejaculation.
d) Angina, cardia arrythmias, hypertension.
How do beta blockers work?
What effect do they have in the kidney?
Decrease CO
May lead to resetting of baroreceptors
Blocks b1 receptors in kidney that initiate renin release--Angiotensin--Vasoconstriction.
How is vasodilation produced?
How does calcium enter the cell?
With a decrease in intracellular calcium levels.
By voltage gated channels and metabotropic action working at adrenergic receptors
What effect does HYDRALAZINE have on the blood vessels?
What are the side effects?
Increase in cyclic GMP, increase protein kinase activity, dec Ca2+
Increase in prostaglandin release

Headache, reflex tachycardia, sweating
How dose MINOXIDIL work?

What are the side effects?
K+ is free to move, causes hyperpolarisation, therefore the threshold is harder to reach

Tachycardia, oedema, hypertrichosis.
What side effect is unique to DIAZOXIDE?
Which drug has arterial and venous effects with regards to vasodilation?
How does it work?
What are the side effects?
Sodium Nitroprusside
NO release caused guanylyl cyclase activation and rapid increase in cGMP.

Cyanide groups can cause metabolic failure-Dose limited-EMERGENCIES.
How do calcium channel blockers work and what are some examples?
Verapamil, dihydropyridines
No calcium induced calcium released-No actin and myosin binding.
What are drugs for Angina aimed at doing?
What are some examples?
Improving coronary flow
Decreasing cardiac work
Use:-Beta blockers
Glyceryl trinitrate-Sublingual-Fast but short duration
Works by increasing guanyl cyclase
Calcium channel blockers
What would be used to try and prevent damage to the brain after a stroke?
Calcium channel blockers
What are the three categories of Eicsanoids?
Where are Ecosanoids stored and produced?
What is the source?
Semen only
Various parts of the body
Arachidonic acid, esterified in membrane
What is production of Eicsanoids regulated by?
Chemicals e.g. hormones and other autacoids
Mechanical stress on endothelial cells
Calcium influx activates PLA2
What is production of Eicsanoids regulated by?
Chemicals e.g. hormones and other autacoids
Mechanical stress on endothelial cells
Calcium influx activates PLA2
What is production of Eicsanoids regulated by?
Chemicals e.g. hormones and other autacoids
Mechanical stress on endothelial cells
Calcium influx activates PLA2
What is the cyclo-oxygenase pathway?
Prostaglandins and thromboxanes in this process
COX-1 in most cells
COX-2 in inflammatory cells
Endothelium-PGI2 and Platelets-TXA2
What do non-selective NSAIDS inhibit?
Selective NSAIDS?
COX-1 and COX-2

Inhibit the expression of COX-2
Induce the expression of lipocortin which inhibits PLA2
What causes vasodilation and vasoconstriction with regards to Eicosanoids?
PGE2 and PGI2, Leukotrienes


Leukotrienes also increase Pcap and inflammation.
What do eicosanoids do in the respiratory system?
Prostanoids can cause brochoconstriction or bronchodilation.
Leukotrienes cause bronchoconstriciton.
What type of voltage gated calcium channels are found in cardiac and smooth muscle?
What are calcium entry blocking drugs used for?
Hypertension, angina-Dihydropyridines, diltiazem
Antiarrhythmics-Verapamil, diltazem
Cerebral ischaemia-Nimodipine
What are the side effects of Calcium entry blocking drugs?
Cardiac failure when in combination with beta blockers
Headache, postural hypotension, flushing nausea, constipation (Verapamil) and bradycardia (diltiazem)
What other type of voltage operated channels (apart from L-type) are there?
N-type-Low-ish threshold-Neuronal
P-type-Purkinje cell, high threshold, transient
What are clinically relevant targets of calcium channel blockers?
Dec force of heart contraction
Impaired conduction at AV node
Vasodilation of SM and coronary vessels.
How do class 4 antidysrhythmic drugs work and what is the risk?
Slow nodal conduction by blocking slow inward ca2+ current prolonging phase 2 and refractory period.

Risk of heart failure
What does Verapamil do in Angina?
Slow conduction at nodes
Decrease contractility, inc o2 demand

Coronary vasodilation, better perfusion
Peripheral vasodilation, decrease o2 demand need slow release to avoid reflex tachycardia.
What does ETHOSUXIMIDE do?
Prevents phasil mode of firing in thalamocortical neurones, blocks low threshold inward Ca2+ current.
What are natural bronchodilators?
VIP and NO
Which sensory nerves control bronchiole diameter?
C fibres and irritant receptors

Releases substance P and neurokinin A.
What anti-asthma drug is given by a subcutaneous mini pump?

What is the newer version of SALBUTAMOL?
TERBUTALINE-Brittle asthma

SALMETEROL-Lipid soluble side chain, longer lasting
What are the side effects of bronchodilators?
Tremor, headaches, tachycardia (b1 on heart) anxiety, may worsen the disease process.
What would be used in COPD/intractable asthma?
IPRATROPIUM, OXITROPIUM with a nebuliser, awkward in glaucoma altered drainage of aqueous humour.
What drug may be given orally for prophylaxis as a bronchodilator?

Side effects

What is the mechanism?
Low therapeutic index

Nausea, headache, insomnia, diuresis, arrythmias, convulsions

Inhibition of PDE increasing cGMP
Give an example of a leukotriene antagonist.

How does SODIUM CROMOGLYCATE work in Asthma?
MONTELUKAST given orally in exercised induced asthma.

Stabilises mast cells and inhibits axon reflexes and Tachykinin antagonist.
What are the side effects of GLUCOCORTICOIDS?
Raises blood glucose
Suppresses pituitary adrenal axis-Cannot produce steroids
What is becoming a first line treatment for Asthma?
Inhaled BECLMETHASONE as there are few side effects such as sore throat, thrush, husky voice
May reverse beta 2 receptor desensitisation
What are histamine receptors like?
Three types, all G-protein coupled, metabotropic, different 2nd messenger targets.
What are the 2nd messenger targets and antagonists in:
a) Phospholipase C activation-CHLOROPHENYRAMINE
What does histamine do on H1?
Increase permeability of capillaries
Vasodilation of capillaries
GIT contraction
What is the triple response with regards to histamine?
Redding due to small vessel dilatation
Wheal (oedema) caused by an increase in Pcap.
Histamine induces AP's. Receptive ending releases neuropeptides, Distant vessels vasodilate.
Where are H2 receptors found?
Gastric mucosa, cardiac muscle and the brain (neural inhibiton)
Where are H3 receptors found?
Associated with neurones mediating neurotransmission.
IN ENS inc motor activity of SM
Small amount in skin
Give an example of an old antihistamine drug and its side effects.
Crosses the BBB
Anti-muscarinic effects

PROMETHAZINE causes alpha 1 receptor antagonism
5-HT antagonist
Dry mouth, GIT disturbance, blurred vision
Give an example of a new H1 antagonist.
More selective, less sedative.
What are other uses of H1 antagonists?
Motion sickness-CINNANZINE
Asthma-Perhaps in the initial stages
Give an example of a use of H2 antagonists, and a drug name.
For excess acid

GIT disturbance, dizziness, confusion.

What are the side effects?
Respiratory stimulant, affects CO2 and O2 chemoreceptors enhancing electrical activity.

Bad side effects including arrhythmias, tremor, convulsions, dizziness.
Give an example of a general anaesthetic acting as a respiratory depressant.
HALOTHANE, ISOFLURANE decrease response of central CO2 chemoreceptors, inc CO2 in plasma and affects acid base balance.
Give an example of an injected general anaesthetic.

How do these work?

Increases inhibitory neurotransmission via GABAa, inc Cl- channel opening, hyperpolarisation further from threshold.
What are BENZODIAZEPINES used for?
What is an example?
Pre-anaesthetic, anxiolytics

Decreased hypoxic drive-Peripheral action.
How does alcohol work as a respiratory depressant?
Inhibits the carbon dioxide response
Inc GABAa transmission
Dec NMDA transmission

Threshold for fatal RD is v.high
How do OPIOIDS act at the respiratory centres?

What types of receptors are there?
M2=In resp centre

Decreases CO2 receptor sensitivity
What is the mechanism of action of FENTANYL?
G-protein coupled receptors
K+ channels open, cell becomes hyperpolarised and therefore cannot detect changes in plasma CO2.
What is an example of an opioid receptor antagonist?
What is the effect of benzodiazepines and alcohol?
Benzodiazepines and general anaesthetics?
Additive effect, potentially fatal.
Increases depressant effect