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s3 - MSK, Derm, Cardio, Neuro, Pharm > Pharmacology > Flashcards

Pharmacology Flashcards

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Dermatology Board Prep flashcards
1
Q

Bioavailability/f is

A

the proportion of administered drug that reaches systemic circulation

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2
Q

Give 4 of the Lipinski rules

A
  • molecular weight <500
  • Less than 5 H-bond donors
  • Less than 10 H-bond acceptors
  • log p<5
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3
Q

How do drugs that obey 1st order kinetics behave?

A
  • a constant FRACTION of drug is removed
  • the time to remove the drug is independent of dose
  • has a constant half life
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4
Q

How do drugs that obey 0 order kinetics behave?

A
  • a constant AMOUNT of drug is removed
  • the bigger the dose, the longer time taken to remove it
  • as dose decreases, and mechanism is no longer saturated, process returns to 1st order
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5
Q

Volume of Distribution (Vd) =

A

Total amount of drug ÷ plasma drug concentration

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6
Q

Plasma Clearance (CL) =

A

Rate of elimination ÷ plasma drug concentration

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7
Q

Dosing Rate x F =

A

CL x Target Conc

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8
Q

Multiple dosing leads to steady state to balance rate of absorption with elimination, the time taken to reach steady state is

A

4-5 times the drugs half life

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9
Q

Name a drug that may be given to treat postural hypotension?

A

fludrocortisone - acts on mineralocorticoid receptors to increase Na+ receptors

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10
Q

Local anaesthetics are more non-ionised/permeable in what pH?
Why?

A

LAs are weak bases. They are more permeable in alkaline conditions.

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11
Q

What happens if LAs enter the CNS?

A

-initially stimulation, then depression

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12
Q

What happens if LAs enter the CVS?

A
  • blocked Na+ channels so less Ca2+ influx and decreased force of contraction
  • vasodilation due to symp. inhibition so BP drop
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13
Q

Give 4 routes of LA administration?

A
  • surface
  • nerve block
  • spinal
  • epidural
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14
Q

Give 3 reasons LA may be administered with Adrenaline.

A
  • keeps it localised
  • inhibits absorption from ECF->blood (less toxicity)
  • prevents bleeding
  • prolongs its action
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15
Q

Give a disAdv of administering LAs with Adrenaline.

A
  • can get local hypoxia esp. in extremities

- absorption of adrenaline can cause arrhythmias

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16
Q

Where does drug metabolism mainly occur, what is its purpose?

A
  • in liver, makes drug more water soluble

- less drug reabsorbed

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17
Q

What happens in the following drug metabolism:

  • Phase I
  • Phase II
A

I-adds chemically reactive groups by oxidation making them more polar and reactive
II-increases water solubility by conjugation

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18
Q 
Renal Clearance (ml/min) = 
-units?
A

-urine drug conc/plasma drug conc

drug/min drug/ml

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19
Q

What 4 things influence ADME?

A
  • Age (neonates, elderly)
  • Genetics
  • Drug metabolising enzymes (g.f. juice, alcohol)
  • Disease (liver/kidney)
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20
Q

Give 3 Advs of monitoring drug conc.

A
  • confirm patient adherance/individualise doseage
  • determine toxicity/presence of other drugs
  • useful in postmarket surveillance
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21
Q

What characterises a type A ADR?

A

-predictable, dose dependent, not lethal

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22
Q

How can a hypersensitivity reaction occur to a large molecular weight drug (often as bound to plasma proteins)?

A

They are a ‘hapten’ (identified by immune system), upon encountering again you have primed mast cells -> histamine release, anaphalaxis

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23
Q

3 forms of pharmacoviligince:

A
  • Yellow Card (no denumerator)
  • Black Triangle (new drug-take caution)
  • Green Form (anyone on new drug, everything recorded, numerator&denumerator)
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24
Q

Where is there sympathetic activity induced via Ach acting on Musc receptors?

A
  • sudomotor nerves to eccrine sweat glands

- pilloerrector muscles

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25
Q

Where do opiods act? By which mechanism? To do what?

A
  • act at Gai receptors, mainly mu
  • at periphery, in dorsal horn & periaq. grey
  • to decreases pain by decreasing synapic transmission
26
Q

Opiods mechanism of action:
Presynaptically…
Postsynaptically…

A

Pre…opiod binds to mu, decreased VGCC so less NT release. Also stimulates K+ channels->hyperpolarisation
Post…opens K+ channels –> hyperpolarisation

27
Q

How do opiods decrease pain in the periaq. grey?

A

They switch on neuronal areas involved in analgesia by disinhibiting the inhibitory interneurone (more stimulation)

28
Q

How do opiods lead to feelings of euphoria?

A
  • opiods disinhibit GABAergic interneurones in reward areas

- more DA release and DAergic transmission

29
Q

Why are opiods often given with metoclopramide?

A

Opiods cause vomiting by activating the CTZ, this prevents it.

30
Q

If orally, where would opiods be mainly absorbed and why? Why are opiods given IV?

A
  • they are weak bases, pka-8, would be in intestines

- have a high 1st pass metabolism/low f

31
Q

What opiod partial agonist with long half life is given for heroin withdrawal?

A

Buprenorphine

32
Q

At which receptors do the following act?

  • alcohol
  • phencyclidine hallucinogens
A
  • alcohol at GABAa receptors

- phencyclidine hallucinogens- NMDA antagonist

33
Q

How do amphetamines like methylphenidate act?

Effect?

A
  • Displace DA from bouton

- increased alertness, euphoria, confidence, BP, less appetite

34
Q

How do psychotomimetics like ecstacy act? Effect?

A
  • inhibit M.Amine Transporters, more 5HT&DA release

- more DA causes euphoria but depletion -> irritable mood after

35
Q

How do central stimulants like cocaine act? Effect?

A
  • block catecholamine uptake so more DA, NA and 5HT
  • activates HPA axis so increases cortisol
  • euphoria, locomotor stimulation
36
Q

How does alcohol lead to good/reward feelings?

What is alcholism treated with?

A
  • the potentiated GABA-mediated inhibition disinhibits the mesolimbic DAergic neurones and releases endogenous opiod peptides
  • Disulfiram (acetaldehyde accumulates so alcohol is iyk)
37
Q

How and where does Nicotine act? Effect? Treatment?

A
  • on nic Ach a4B2 receptors (lots in VTA&hippocampus) so more NT, opiod peptides, alertness, addictive
  • treat via nicotine patches/buprion/varenicline
38
Q

To maintain homeostasis upon excessive drug use, how does your body desensitise the continually activated receptors?

A
  • arrestin binds and de-activates the receptors effect

- hyperpolarises it via K+ efflux

39
Q

What is Lofexidine’s mechanism of action? (given to supress withdrawal effects of opiod abuse, or clondine for alcohol abuse)

A

central a2 agonist, inhibits excessive NT release

40
Q

What pharmacological agents are used for treating motion sickness? How are they given? -remember more = more side effects

A

-Musc. Ach R Antagonists e.g. scopolamine
-Histamine 1 Antagonists e.g. dyphynhydramine
(separately if mild, mixed if bad, both +DA antagonists)

41
Q

What are the most common GABAa subunits?
Where does GABA bind to the receptor?
What does activation of GABAa receptors cause?

A

2a, 2B, gamma
GABA binds between a and B subunits
Hyperpolarisation by opening Cl- Channels

42
Q

Where on the GABAa receptor do the anxiolytic drugs: barbituates bind? What about benzodiazepines?

A

Barbituates bind at allosteric sites on a/B subunits

Bezodiazepines bind between a and gamma subunits at a regulatory site, stabilising GABAa R as open

43
Q

Barbituates are GABAa agonists, why are they no longer used for anxiety? Now used for?

A
  • “dirty”/many SEs, also glycine agonist, blocks ca2+ NT release… v powerful at increasing inhibition
  • epilepsy, general anaesthetic, capital punishment
44
Q

Flumenazil is a competitive GABAa antagonist used for overdose of which anxiolytic drug class?

A

Benzodiazepines

45
Q

What are 3 S.E.s of the anxioltytic drug class, Benzodiazepines?

A
  • drowsy
  • confusion
  • forgetfullness
  • resp depression
46
Q

Midazolam, zolpidem and lorazepam are types of which drug? What are they used for? How do you choose which to give?

A

Benzodiazepines used for: anxiolytic, anticonvulsant, muscle relaxant, sedative, amnesic
Choice based on duration of action

47
Q

What are Z drugs? What are they used for?

A

GABAa modulators, bind between a and gamma subunits (like benzodiazepines)
-Hypnotics

48
Q

What is the mechanism of action of 5HT-1 R agonists like buspirone which treats general anxiety disorder?

A
  • activate pre 5HT1 autoreceptors, these inhibit 5HT release so less activity of NAergic neurones/less arousal
  • overtime due to less 5HT you have neuroadaptation to increase it (uptake inhibited, less pre-autoreceptors)
  • Seratonin levels overall increase. Takes time.
49
Q

What is fluoxetine (Prozac) used to treat?

What is the mechanism of action?

A
  • for social phobias, panic, nausea, sexual dysfunction

- its s 5HT re-uptake inhibtior

50
Q

How are B-blockers used in the treatment of anxiety?

A

They reduce peripheral manifestations

51
Q

What are 2 uses of Histamine 1 R Antagonists?

A
  • treat allergenic/inflammatory disease
  • have hypnotic/sedative effects
  • act centrally to treat insomnia (maybe result of anxiety)
52
Q

MAO inhibitors rapidly increase monoamines. Early non-selective irreversible drugs caused a big NA rise after eating cheese/wine, why? Effect?

A

Indirect sympathomimetic amines such as amphetamine and TYRAMINE increase release of monoamines.
Effect=headache, severe HT, intracranial haemorrhage..

53
Q

Moclobemide is a reversible inhibitor of MAOa (RIMA), so in case of excess NA, RIMA is displaced and excess is broken down. They still have some SEs, name 3

A
  • postural hypo
  • increased appetite, weight gain
  • Antimusc effects (blurred vision, constipation..)
  • excessive central stimulation (tremors, insomnia…)
54
Q

How do TCAs act? e.g. amitriptyline, imipramine, lofepramine…

A
  • inhibit NA/5HT reuptake so increased conc in cleft

- chronically, down regulates B1, a1, 5HT2, 5HT1a/1d

55
Q

2 side effects of TCA?

A
  • anticholinergic/antimuscarinic (dry mouth, blurred vision)
  • antihistaminergic (weight gain, sedation)
  • a-antagonistic (low BP, postural hypo, tachycardia)
56
Q

Give 3 reasons TCAs have a narrow therapeutic index/are undesirable?

A
  • antipsychotic drugs, steroids..inhibit TCA metabolism
  • TCAs potentiate effects of alcohol & anaesthetics
  • Overdose is toxic (heart attack, convulsions..)
  • TCA cant be used in elderly/dementia (confusion) or heart disease (block K+ channels->dysrhythmia)
57
Q

How do SSRIs (e.g. fluoxetine; sertraline; paroxetine, cetalopram) act?
Block reuptake and increase 5HT in cleft …

A
  • cause downregulation of the 5HT1A autoreceptors which disinhibits 5HT neurone so more 5HT is released
  • the increased 5HT ‘normalises’ the post synaptic receptors (thought to be upregulated in depressed as low 5HT activity)
58
Q

3 Advs of SSRIs

A
  • safer, better tolerated
  • no anticholinergic/antimuscarinic SE so better compliance
  • shorter t 1/2, less severe withdrawal effects
  • 5HT2A R -> antidepressant, anti OCD effect
59
Q

3 disAdv of SSRIs

A
  • take longer to act
  • 5HT2A R -> insomnia, sexual dysfunction
  • 5HT3 R -> nausea, GI disturbances, headaches
60
Q

What is buproprion mechanism of action? Its used to treat….

A
  • inhibits NA/DA uptake (not 5HT)

- treats nicotine dependence

s3 - MSK, Derm, Cardio, Neuro, Pharm (9 decks)

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