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MTF PHARMA Flashcards

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1
Q

What are Racemic mixtures?

q1

A

Racemic mixtures are mixtures of different enantiomers in equal proportions

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2
Q

Recemic mixtures and volatile agents

q1

A

All of the volatile agents, with the exception of sevoflurane, are racemic mixtures

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3
Q

Other examples of Recemic mixtures

q1

A

Other
examples include racemic bupivacaine, ketamine, atropine and racemic epinephrine.

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4
Q

Bupivacaine vs levobupivacaine

Q1

A

Levobupivacaine, by virtue of the fact that it is one of the optical isomers of bupivacaine

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5
Q

what is enantiomer

q1

A

Enantiomers are a pair of molecules that exist in two forms that are mirror images of one another

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6
Q

ketamine forms

q2

A

S(+)-ketamine
R(–)-ketamine

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7
Q

difference between S(+)-ketamine
R(–)-ketamine

q2

A

1.It produces less intense emergence phenomena.

  1. has greater affinity for the
    NMDA receptor than R(–)-ketamine, meaning that it is three times as potent an analgesic.

3.S(+)-ketamine is thought to produce less direct cardiac depression; therefore the risk of
cardiac ischaemia is lower.

4.Recovery is more rapid with S(+)-ketamine.

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8
Q

Advantage of levobupivacaine (the S-enantiomer) over bupivacaine and other local anaesthetics

q2

A

its potential for reduced toxicity

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9
Q

Ropivacaine vs Bupivicaine

q2

A

Ropivacaine is prepared as the pure S-enantiomer (the R-enantiomer is less potent and more
toxic).

The main differences between it and bupivacaine lie in its pure formula, improved side
effect profile and lower lipid solubility.

This lower lipid solubility may result in reduced
penetration of the large myelinated Aβ motor fibres, so that these are initially spared

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10
Q

what determines the duration of
drug action

q3

A

the higher the degree of protein binding, the greater the duration of
action

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11
Q

Alfentanyl vs Fentanyl

q3

A

Alfentanil is almost seven times less lipid-soluble
than fentanyl yet its onset is much more rapid

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11
Q

Alfentanil is almost seven times less lipid-soluble
than fentanyl yet its onset is much more rapid

why?

q3

A

This is due to various factors, including the
fact that it has
smaller volume of distribution and lower pKa than fentanyl (meaning that
at physiological pH a greater fraction of alfentanil is unionized).

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12
Q

why is addition of sodium
bicarbonate to lidocaine

q3

A

by raising the pH of the solution, this increases the proportion of
unionized local anaesthetic, enabling it to penetrate nerve membranes more readily Thus,
speed of onset is increased

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12
Q

dose–response curve X and Y

q4

A

Dose is plotted on the x-axis and the response on the y-axis

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12
Q

Bupivicaine vs Lidocaine in placenta

q3

A

Bupivacaine is more highly bound than lidocaine, so less crosses the placenta

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12
Q

The log10 dose–response curve determines what

q4

A

potency

the more potent a drug, the further
to the left it will lie on a dose–response curve and indeed the steeper the curve will be

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13
Q

what determines the speed of onset of the drug action

q3

A

Ionization of the drug

Although lipid solubility reflects the ability of a drug to cross the ce

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13
Q

what is ED50

A

This
is the dose of the drug that produces 50% of the maximal response.

The
ED50 can be determined from the log10 dose–response curve and used to define potency

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14
Q

The effect of an antagonist on the dose–response curve of an agonist

A

shift it to the
right

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15
Q

MOA: ondansetron

A

is highly selective as an antagonist at the 5HT3
receptor. It has actions centrally and peripherally

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16
Q

MOA ketamine

A

Ketamine is a non-competitive antagonist at the NMDA-type glutamate receptor. It
causes a dose-dependent depression of the CNS, resulting in a dissociative state characterized by analgesia and amnesia

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17
Q

MOA dexmedetomidine

A

Dexmedetomidine is a specific α2-adrenergic receptor agonist

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18
Q

what is therapeutic index

A

therapeutic index,
which is a ratio of LD50:ED50

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19
Q

what is the measurement units of therapeutic index

A

has no unit

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20
examples of low therapeutic index drugs | q7
Warfarin, vancomycin and digoxin are examples of drugs with a low therapeutic index.
21
what do antagonists require to extert their effect
Antagonists require the presence of an agonist or partial agonist to exert their effect
22
Buprenorphine | 7
Buprenorphine is a partial agonist at the μ-opioid receptor and as such is used in opioid addiction programmes. | This means that partial agonists can act as competitive antagonists
23
The efficacy of a partial agonist | q7
greater than zero but less than the full agonist, despite full receptor occupancy
24
tachyphylaxis ephedrine | q9
Ephedrine is an example of a drug that, with repeated doses, displays tachyphylaxis. The rapid loss of response to repeated doses of ephedrine is attributed to depletion of noradrenaline stores at sympathetic nerve terminals, which ephedrine indirectly stimulates
25
MOA Edrophonium
reversibly binds to the anionic and esteratic sites of acetylcholinesterase, rendering the enzyme incapable of catalyzing the breakdown of acetylcholine
26
Edrophonium clinical importance
short duration of action. It therefore has a diagnostic rather than a treatment role in the management of myasthenia gravis
27
what are carbamates
related to carbamic acid. The carbamylated complex has greater stability than the acetylcholinesterase–edrophonium complex. Therefore the duration of action of carbamates is longer | neostagmine and physostagmine
28
MOA Neostigmine
binds to the anionic site of acetylcholinesterase and results in the formation of a carbamylated enzyme complex | It is an analogue of the naturally occurring compound physostigmine
29
cyanide poisoning treatment
Dicobalt edetate
30
lidocaine vs phases
prolongation of phase 0 refractory period is reduced owing to faster repolarization (phase 3)
31
Flecainide vs Lidocaine
Flecainide no effect on the refractory period but lidocaine reduces
32
Example of pentameric family of receptors | q12
GABA A receptor and nicotinic Ach receptor
33
# q12 four different types of receptors
Type 1: Ligand gated ion channel. Examples: nicotinic acetylcholine receptor and GABAA. Type 2: G-protein coupled receptor. Examples: muscarinic acetylcholine receptor and opioid receptors. Type 3: Enzymes e.g. tyrosine kinase. Example: insulin receptor. Type 4: Intracellular receptors (which act via gene transcription). Examples: steroid and thyroid hormones
34
Adverse drug reaction types with examples | q13
Type A reactions are predictable and dose dependent, e.g. hypotension following propofol administration. Type B reactions are also known as idiosyncratic drug reactions. These are less common than Type A reactions. They are unpredictable, dose independent and unrelated to the known pharmacological properties of a drug reactions usually involve the immune system. Anaphylaxis (IgE medi | These
35
Cytochrome P450 Inhibitors | q14
erythromycin, metronidazole, omeprazole, amiodarone, grapefruit juice and cyclosporin.
36
Cytochrome P450 inducers in common use include phenytoin, carbamazepine, rifampicin, chronic alcohol, barbiturates and cigarette smoking. | q14
phenytoin, carbamazepine, rifampicin, chronic alcohol, barbiturates and cigarette smoking.
37
MOA Moclobemide | q15
is a reversible monoamine oxide (MAO) inhibitor used to treat depression. It selectively inhibits MAO-A, resulting in a reduced breakdown of serotonin, noradrenaline and dopamine. ## Footnote taken in conjunction with tyramine-containing foods (the ‘cheese reaction’) HYPERTENSIVE CRISIS
38
physicochemical drug interection | q16
Physicochemical interactions result from chemical or physical incompatibility, e.g. the activity of the acidic heparin is terminated by the strongly basic protamine.
39
Pharmacokinetic drug interections | q16
Pharmacokinetic interactions occur due to the effects of co-administered drugs on absorption, distribution, metabolism and elimination. For example, β-blockers reduce cardiac output, which may reduce the distribution of other drugs to their site of action. P
40
pharmacodynamic drug interection | q16
Pharmacodynamic interactions occur as a result of competition for the binding site of an enzyme or receptor | e.g. flumazenil and benzodiazepines
41
synergism | q16
Synergism occurs where the net effect of two or more drugs is more than the sum of the individual actions.
42
Example of Synergism | q16
remifentanil and propofol
43
first-order kinetics | q17
This means that plasma levels of the drug are proportional to the amount of drug present (i.e. an exponential function – the rate of change of drug A is proportional to the concentration of A)
44
First order kinetic vs Enzyme | q17
enzyme activity is not rate-limiting. The more the substrate the more the Enzyme activity
45
Zero order Kinetic | q17
zero-order kinetics, the rate of change of plasma drug concentration is constant rather than being dependent on the concentration of drug present
46
Zero kinetic and enzyme activity | q17
otherwise known as saturation kinetics, indicating that enzyme activity cannot be increased by increasing substrate concentration. A good example is the metabolism of ethano
47
Why metabolism of ethanol is Zero kinetic | q17
Humans metabolize ethanol at a constant rate, regardless of how much we have ingested. This is because the enzyme alcohol dehydrogenase requires a co-factor for its reaction, which is only present in small amounts
48
What molecules crosses The blood–brain barrier (BBB) and How | q18
active transport and facilitated diffusion. Only lipid-soluble, low molecular weight drugs can cross by simple diffusion, whilst large, polar molecules cannot
49
Atropine vs glycopyrronium BBB | q18
Whilst atropine readily crosses the BBB (it is an uncharged, tertiary amine), glycopyrronium does not, due to its quaternary, charged nitrogen. This means it is far less likely to produce the centrally mediated confusion or sedation seen with atropine use
50
pharmacokinetic differences are seen in the elderly population
Older people have a relative reduction in muscle mass with a resulting increase in the proportion of adipose tissue; this increases VD. ## Footnote please have a look
51
The rapid onset of action of thiopentone when administered intravenously is as a result of | q20
The rapid onset of thiopentone is due to high blood flow to the brain (hence increased drug delivery to the desired site of action), the high degree of lipophilicity low degree of ionization at physiological pH
52
Thiapentone Pka | q20
pKa of 7.6
53
factors affecting drug transfer across mother and fetus cells membrane ## Footnote tq21
Low molecular weight, lipophilic, uncharged drugs are transferred with greater ease than larger, charged molecules
54
Cisatracurium/atracurium vs propofol metabolism ## Footnote q21
like other IV induction agents, is predominantly metabolized via conjugation by the cytochrome P450 system in the liver Cisatracurium, like its parent compound atracurium, does undergo hepatic metabolism, however the majority of the drug undergoes Hofmann elimination, a pH- and temperaturedependent degradation of the drug
55
Mivacurium/suxamethonium ## Footnote q21
metabolized by butyrylcholinesterase (also known as plasma cholinesterase and pseudocholinesterase, to differentiate it from acetylcholinesterase)
56
Esmolol has a very short duration of action. WHY ## Footnote q21
This is due to rapid metabolism via ester hydrolysis by cholinesterase enzymes found in red blood cells.
57
Low molecular weight heparins (LMWH), e.g. enoxaparin toxicity what should we measure ## Footnote q25
anti-Xa levels

FCA pharmacology (2 decks)

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