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Phase 2a Gold Standard > ICS - Pharmacology > Flashcards

ICS - Pharmacology Flashcards

1
Q

Specificity vs sensitivity

A

Specificity - Number of true negatives
Sensitivity - Number of true positives

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2
Q

Alcohol units equation

A

(alcohol % by volume * volume of liquid in ml)/1000

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3
Q

Sympathetic vs parasympathetic nervous system

A

Sympathetic (Nad) - fight or flight
Pupil dilates
Increased heart rate
Bronchodilation
Decreased GI motility and secretion
Detrusor relaxes
Ejaculation

Parasympathetic (Ach) - rest and digest
Pupil constricts
Decreased HR
Bronchoconstriction
Increased GI motility and secretion
Detrusor muscle in bladder contraction
Penis points (erection)

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4
Q

Define Pharmacokinetics

A

How the body affects the drug:
Absorption, Distribution, Metabolism, Excretion (ADME)

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5
Q

Explain drug absorption, distribution, metabolism, excretion (Pharmacokinetics)

A

Absorption - Route and entry into body
Distribution - Drug distributed in plasma according to properties and size, may be taken up by organs
Metabolism - Drugs metabolised in kidney (small/water soluble) or liver (hydrophobic)
Excretion in urine or faeces

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6
Q

First pass vs second pass metabolism

A

First - Metabolism before drug reaches systemic circulation (gut/liver wall metabolism, bioavailability reduced)

Second - Actual metabolism (Phase 1 - CYP450, Phase 2 - conjugation)

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7
Q

Define Pharmacodynamics

A

How the drug affects the body

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8
Q

Name 4 drug targets

A

Usually proteins
1. Receptors
2. Enzymes (COX-1 and ACE)
3. Transporters (e.g. PPI, Diuretics)
4. Ion channels (CCB, local anaesthesia)

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9
Q

Define summation, synergism, antagonism, and potentiation (physicochemical)

A

Summation - Drugs used together and effect is as you would expect (1+1=2)
Synergism - Drugs used together and effect greater than expected (1+1>2)
Anatagonism - effect less than expected (1+1=0)
Potentiation - Drug A given with Drug B, increases effect of Drug B without effecting Drug A (1+1=1+2)

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10
Q

Routes of administration

A

Oral
IM
IV
Sublingual
Inhaled
Topical
Rectal
Intrathecal (into CSF)

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11
Q

Define bioavailability

A

Amount of drug taken up as proportion of amount administered

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12
Q

Bioavailability of IV drugs

A

1, or 100%

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13
Q

Factors affecting drug absorption

A

Motility - Certain drugs e.g. codeine affect gut motility. Impaired transit=reduced absorption
Acidity - certain drugs (antacids,PPI) can affect pH so absorption of drugs
Solubility - Eating high fat food with a fat soluble drug can cause the drug to dissolve: no absorption

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14
Q

Factors affecting drug distribution

A

Protein binding causes reduced concentration of drug in plasma. This can be overcome by using another protein binding drug to make the first one more bioavailable.

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15
Q

Effect of amiodarone in patient taking warfarin

A

Amiodarone is a protein binding drug. Will mean less warfarin binds to protein so plasma concentration will be higher

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16
Q

Importance of metabolism in pharmacokinetics

A

Enzyme induction or enzyme inhibition can cause increased or decreased effect of drug.

E.g. morphine metabolised to morphine-6-glucuronide by CYP450. Drug A inhibits CYP450 leaving more morphine in blood, increasing effect.

Drug B induces CYP450, increasing metabolism of morphine, less effect.

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17
Q

Examples of excretion in pharmacokinetics

A

Furosemide causes increased but dilute urine. As a result, drug clearance, particularly of gentimicin, is decreased.

pH of urine can be altered to purposefully remove drugs from blood.

E.g. weak bases are cleared quicker if urine acidic, and weak acids are cleared faster if urine is alkali. Therefore urine pH can be changed to alter excretion.

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18
Q

Give the 4 types of receptors

A
  1. Ligand-gated ion channels
  2. G protein coupled receptors (most common - opioids act here)
  3. Kinase linked receptors
  4. Cytosoloic/nuclear receptors
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19
Q

Explain action of ligand-gated ion channel

A

Pore forming membrane proteins that allow ions to pass through shifting electrical charge distribution

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20
Q

Explain G protein coupled receptors

A

GPCRs consist of large polypeptide chains that go intracellular and extracellular.

On activation, G proteins catalyse exchange of GDP (guanosine diphosphate) to GTP (guanosine triphosphate), causing signal cascade

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21
Q

Explain kinase linked receptors

A

kinases catalyse phosphorylation.

Binding of ligand on extracellular side causes phosphorylation of tyrosines on intracelullar side, allowing it to recruit intracellular signal mediating components.

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22
Q

Explain Cytosolic/ nuclear receptors

A

Intracellular molecules that modify gene transcription upon steroid hormone ligand binding.

N domain on outside, C on inside, zinc fingers bind to DNA.

23
Q

Give examples of how chemical/receptor imbalance can lead to pathology

A

Chemical increase: Allergy (increased histamine)
Chemical decrease: Parkinson’s (decreased dopamine)

Receptor increase: Mastocytosis (increased c-kit receptors)
Receptor decrease: Myasthenia gravis (loss of ACh receptors)

24
Q

Define agonist/antagonist

A

Ligands that bind to a receptor and activates it

25
Q

Define Potency and EC50

A

Potency - measure of how well a drug works, as measure of amount of drug given to produce an effect of a given intensity.

(highly potent drug produces more effect than a less potent one at the same concentration)

EC50 - concentration that gives half the maximal response

26
Q

Define full/partial agonist

A

An agonist that can elicit a maximal response, no matter how great a concentration is required.

Partial agonists have a maximum efficacy lower than 100% response.

27
Q

Define efficacy

A

the ability of an intervention to produce a desired or intended result (or for a ligand to activate a receptor)

28
Q

Define intrinsic activity, and provide equation for it

A

ability of drug-receptor complex to produce maximum functional response

IA = E(max) of partial agonist ÷ E(max) of full agonist

E(max) = max efficacy

29
Q

Example question.

Drug A starts providing response at lower concentration than Drug B. However, Drug B can provide a greater overall response. Which is more efficacious, and which is more potent?

A

Drug A more potent. Drug B more efficacious.

As drug A more effective at lower doses, but drug B can achieve greater % response

30
Q

Define antagonist

A

A compound that reduces the effect of an agonist

31
Q

Define competitive antagonism and explain how it affects dose-response curve

A

Competitive antagonists bind to receptor, preventing agonist from having an effect. This shifts curve to right - more agonist required to achieve same effect

32
Q

Define non-competitive antagonism and explain how it affects dose-response curve

A

Non-competitive antagonist binds to allosteric (non-agonist) site, preventing its activation. Shifts curve right and down - agonist can bind but cannot activate the receptor, so Emax cannot be reached.

33
Q

Define affinity

A

The ability of a ligand to bind to a receptor

34
Q

Why can antagonists have high affinity but always 0 efficacy

A

Antagonists can bind well to receptors but never activate them

35
Q

What will happen to drug action when irreversible antagonists are added to a receptor?

A

Less receptors will be available so response will be slower. Drug-response curve will shift right. Max effect will still be possible but will need higher concentrations.

(spare receptors exist for full agonists, however there are no spare receptors for partial agonists)

36
Q

Why can activation of receptors cause different responses in different tissues

A

Signal amplification in different tissues cause comparatively increased/decreased responses.

37
Q

Define inverse agonism

A

A drug that binds to the same receptor as an agonist but induces a response opposite to that of the agonist

(Efficacy of full agonist = 100%, efficacy of antagonist = 0%, efficacy of inverse agonist < 0%)

38
Q

Drug tolerance vs desensitisation

A

tolerance is a slow reduction in agonist effect over time

desensitisation is rapid, due to receptor degrading, uncoupling, internalising etc.

39
Q

Statins MoA

A

HMG-CoA reductase inhibitors.

Block rate limiting step in cholesterol pathway

40
Q

3 effects of NSAIDs

A

Analgesic
Anti-pyretic
Anti-inflammatory

41
Q

NSAID MoA

A

COX inhibitors

42
Q

Aspirin MoA

A

Non selective COX inhibitor (COX1+COX2)

43
Q

3 types of protein ports

A
  1. Uniporters: Energy from ATP pulls molecules in
  2. Symporters: Co transport, movement of one molecule pulls another with it
  3. Antiporters: One substance moves against gradient, using energy from second substance moving down gradient
44
Q

What pathology are Epithelial Sodium channels implicated in?

A

Heart failure

45
Q

Define afferent signals

A

Signals towards brain/spinal cord

46
Q

Define efferent signals

A

Signals away from brain/spinal cord

47
Q

Define adrenergic

A

Relating to noradrenaline

48
Q

Define cholinergic and muscarinic/nicotinic

A

Relating to ACh and its receptors.
Musc/nico are types of Ach receptor

49
Q

Sympathetic nerve system anatomy properties

A
  • 2 nerve system
  • Preganglionic nerve in lateral horn of spinal cord (T1-L2)
  • Sympathetic ganglia in chain beside vertebrae
  • Preganglionic fibre synapses with post ganglionic in chain
50
Q

Treatment of C diff infection

A

Vancomycin or metronidazole 4x10 days

51
Q

Explain adverse drug reactions

A

Rawlins classification
Augmented - Common (dose related)
Bizarre - Odd (allergy/non dose related)
Chronic - Taking for long time (dose and time e.g. HPA suppression of steroids)
Delayed - Months/years after (time e.g. teratogenesis, cancer - has drug in PMH caused?)
End of use - Withdrawal

52
Q

Treatment of opioid overdose

A

Methadone
Naloxone

53
Q

Side effects of steroids

A

CUSHINGOID MAP
Cataracts
Ulcers
Striae
Hypotension
Infection
Necrosis of bone
Growth restriction
Osteoporosis
Increased ICP
Diabetes type 2
Myopathy
Adipose hypertrophy
Pancreatitis

Phase 2a Gold Standard (29 decks)

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