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FCA pharmacology > MTF PHARMA > Flashcards

MTF PHARMA Flashcards

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
Q

examples of low therapeutic index drugs

q7

A

Warfarin, vancomycin and digoxin are examples of drugs with a low therapeutic index.

21
Q

what do antagonists require to extert their effect

A

Antagonists require the presence of an agonist or partial agonist to
exert their effect

22
Q

Buprenorphine

7

A

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
Q

The efficacy of a partial agonist

q7

A

greater than zero but less than the full agonist, despite full
receptor occupancy

24
Q

tachyphylaxis ephedrine

q9

A

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
Q

MOA Edrophonium

A

reversibly binds to the
anionic and esteratic sites of acetylcholinesterase, rendering the enzyme incapable of
catalyzing the breakdown of acetylcholine

26
Q

Edrophonium clinical importance

A

short duration of action. It therefore has a diagnostic rather than a treatment role in
the management of myasthenia gravis

27
Q

what are carbamates

A

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
Q

MOA Neostigmine

A

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
Q

cyanide poisoning treatment

A

Dicobalt edetate

30
Q

lidocaine vs phases

A

prolongation of phase 0
refractory period is reduced owing to faster
repolarization (phase 3)

31
Q

Flecainide vs Lidocaine

A

Flecainide no effect on the refractory period but lidocaine reduces

32
Q

Example of pentameric family of receptors

q12

A

GABA A receptor and nicotinic Ach receptor

33
Q

q12

four different types of receptors

A

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
Q

Adverse drug reaction types with examples

q13

A

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
Q

Cytochrome P450 Inhibitors

q14

A

erythromycin, metronidazole, omeprazole, amiodarone, grapefruit juice and cyclosporin.

36
Q

Cytochrome P450 inducers
in common use include phenytoin, carbamazepine, rifampicin, chronic alcohol, barbiturates and cigarette smoking.

q14

A

phenytoin, carbamazepine, rifampicin, chronic alcohol, barbiturates and cigarette smoking.

37
Q

MOA Moclobemide

q15

A

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.

taken in conjunction with tyramine-containing foods (the ‘cheese reaction’) HYPERTENSIVE CRISIS

38
Q

physicochemical drug interection

q16

A

Physicochemical
interactions result from chemical or physical incompatibility, e.g. the activity of the acidic
heparin is terminated by the strongly basic protamine.

39
Q

Pharmacokinetic drug interections

q16

A

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
Q

pharmacodynamic drug interection

q16

A

Pharmacodynamic interactions occur as a
result of competition for the binding site of an enzyme or receptor

e.g. flumazenil and
benzodiazepines

41
Q

synergism

q16

A

Synergism occurs where the net effect of two or more drugs is more than the sum of the
individual actions.

42
Q

Example of Synergism

q16

A

remifentanil and propofol

43
Q

first-order kinetics

q17

A

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
Q

First order kinetic vs Enzyme

q17

A

enzyme activity is not rate-limiting. The more the substrate the more the Enzyme activity

45
Q

Zero order Kinetic

q17

A

zero-order
kinetics, the rate of change of plasma drug concentration is constant rather than being
dependent on the concentration of drug present

46
Q

Zero kinetic and enzyme activity

q17

A

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
Q

Why metabolism of ethanol is Zero kinetic

q17

A

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
Q

What molecules crosses The blood–brain barrier (BBB) and How

q18

A

active transport and
facilitated diffusion. Only lipid-soluble, low molecular weight drugs can cross by simple
diffusion, whilst large, polar molecules cannot

49
Q

Atropine vs glycopyrronium BBB

q18

A

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
Q

pharmacokinetic differences are seen in the elderly population

A

Older people
have a relative reduction in muscle mass with a resulting increase in the proportion of
adipose tissue; this increases VD.

please have a look

51
Q

The rapid onset of action of thiopentone when administered intravenously is as a result of

q20

A

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
Q

Thiapentone Pka

q20

A

pKa of 7.6

53
Q

factors affecting drug transfer across mother and fetus cells membrane

tq21

A

Low molecular weight, lipophilic, uncharged drugs are transferred with greater ease than larger, charged molecules

54
Q

Cisatracurium/atracurium vs propofol metabolism

q21

A

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
Q

Mivacurium/suxamethonium

q21

A

metabolized by butyrylcholinesterase (also known as
plasma cholinesterase and pseudocholinesterase, to differentiate it from acetylcholinesterase)

56
Q

Esmolol has a very short duration of action. WHY

q21

A

This is due to
rapid metabolism via ester hydrolysis by cholinesterase enzymes found in red blood cells.

57
Q

Low molecular weight heparins (LMWH),
e.g. enoxaparin toxicity what should we measure

q25

A

anti-Xa levels

FCA pharmacology (2 decks)

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