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Medicine 1 > Week 11 - Pharmacology > Flashcards

Week 11 - Pharmacology Flashcards

1
Q

What are agonists?

What are antagonists?

A

Activate receptors

Block receptors

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2
Q

What are the types of drug actions?

A
  • Interact with ion channels
  • Activate / inhibit enzymes (statins, penicillin)
  • Inhibition of transporters / pumps
  • Interact with DNA (anticancer)
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3
Q

What are the sries of events for the action of salbutamol?

A

Binds to receptors

Receptor is activated

Receptor couples to G-protein

Association of alpha subunit

GDP-GTP

Activation of adenylyl cyclase

AMP-cAMP

Relaxation

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4
Q

What happens during modality?

A
  • Receptors respond to specific energy / modality
  • Specific sensation from type of receptor activated
  • Concentrate on simple somatosensory system
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5
Q

What is the role of the pacinian corpuscle?

A

Vibration and rapid movements

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6
Q

What are the properties of transduction?

A

Stimulation - touch / vibration –> sensory AP

Occurs at naked nerve terminal

Involves changes in ion channel activity

Non-propagated potential

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7
Q

What happens during encoding?

What is an adaptation of encoding?

A

Sensitivity = ability to encode and detect stimuli of wide range of strengths –> increase sensitivity = use neurons with different AP thresholds and population encoding (use large no. of neurons for small stimuli detection, + chance of detection)

Temporal change in output in response to a stimulus –> + sensitivity and + cellular efficiency

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8
Q

What is involved in pain?

What are the 2 types of pain?

A

Nerve response to noxious stimuli –> above normal range, can cause damage, withdrawal behaviour

Specialised nerve fibres –> myelinated = fast, sharp pricking acute pain (Aδ), mechanical mainly, unmyelinated = slow, dull ache (C fibres), polymodal (mechanical + thermal for example)

TRPV1s = burning, heat

Meissner’s Corpuscles = tingling, numbness

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9
Q

What are the properties of the autonomic nervous system?

A

Smooth + cardiac muscle –> sympathetic (positive heart inotropy and chronotropy, gut vasoconstriction, skeletal muscle vasodilation, + sensory awareness, sweat secretion) or parasympathetic

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10
Q

What happens during sympathetic flight or flight response?

A

Heart inotropy and chronotropy

Vasoconstriction in gut

Vasodilation in skeletal muscle

Sensory awareness – eg vision

Sweat secretion

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11
Q

What are the prevertebral ganglia?

A

Celiac ganglion

Superior cervical ganglion

Superior mesenteric ganglia

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12
Q

What is the sympathetic outflow from spinal cord III (cervical region)?

A

Follow blood vessel and enter skull

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13
Q

What is the sympathetic outflow from spinal cord IV?

A

Midline plecuses

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14
Q

What is included in the parasympathetic nervouse system?

A

Cranio-sacral outflow

Long-pre and short-post ganglionic fibres

Cranial nerves III (occulomotor), VII (facial), IX (glossopharyngeal), X (vagus)

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15
Q

Where do the parasympathetic cranial and sacral nerves lead to?

A
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16
Q

What tissues only have parasympathetic innervation?

A

Ciliary muscle

Constrictor pupillae

(eyes)

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17
Q

Which nerves are radial and circular eye ,muscles supplied by?

A

Radial = sympathetic

Circular = parasympathetic

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18
Q

What are the effects of parasympathomimetic drugs?

A

Agonists of parasympathetic systems (Miosis (pupil constriction), decrease in near point, decrease in intraocular pressure)

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19
Q

What are the effects of parasympatholytic drugs?

A

Blockers of parasympathetic systems (mydriasis (dilation of pupil), cycloplegia, increased intraocular pressure)

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20
Q

What are the effects of sympathomimetic drugs?

A

Agonists of sympathetic systems (mydriasis, increased IOP)

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21
Q

What are the effects of sympatholytic drugs?

A

Blockers of sympathetic systems (miosis)

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22
Q

What are the 4 adrenoceptor subtypes and their functions / properties?

A
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23
Q

What type of agonist is adrenaline and how does it work?

A

Directly acting sympathomimetics adrenoceptor agonist:

Used for cardiac arrest, sepsis and septic shock

Delivered intravenously

Stimulation of b1 starts / increases heart rate

Used for anaphylactic shock

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24
Q

What type of agonist is salbutamol and how does it work?

A

Directly acting sympathomimetics adrenoceptor agonist:

Beta-2 adrenoceptor agonist

Bronchodilation

Bronchial asthma

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25
Q

What type of drug are NA reuptake inhibtors and how do they work?

A

Indirectly acting sympathomimetic drugs:

TCAs for depression treatment –> enhances NA function and 5-HT, block reuptake by varicosity

Other effects enhanced

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26
Q

What type of drug are cocaine and amphetamine and how do they work?

A

Indirectly acting sympathomimetic drugs:

CNS stimulant and NA reuptake inhibitor

+ sympathetic excitation

Amphetamine = causes exocytotic NA from neuronal uptake

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27
Q

What are propranolol and prazosin and how do they work?

A

Adrenoceptor antagonists:

Prazosin = selectively blocks alpha receptor

Propranolol = selectively blocks beta receptor (B2 agonist so stop salbutamol effects) - is used for:

Ischaemic heart disease

Reduce cardiac load during heartbeat

Beta blockers

Is administered orally

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28
Q

How are muscarinic receptors characterised?

A

Activated by muscarine

Act via metabotropic events

Neural, cardiac and glandular are family members

Utilise different 2nd messengers

Act on different target proteins

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29
Q

When are muscarinic receptor agonists used theraputically?

What are some side effects?

A

Oxybutynin:

Used for incontinence

–Non-selective parasympatholytic or anti-muscarinic

–Prevents unwanted bladder contractions

–Side-effects same as atropine which include: blurred vision,

tachycardia, dry mouth

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30
Q

What are ophthalmic uses of muscarinic agonists?

How do they work?

A

Pilocarpine:

Glaucoma

  1. Constriction of circular muscle
  2. Opens up drainage channel
  3. ­ + aqueous humour drainage
    • intraocular pressure.
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31
Q

When is the muscarinic antagonist tropicamide used ophthalmically?

A

For ocular examination:

Mydriasis

  • Relaxation of circular muscle of iris
  • Relaxation of ciliary muscle
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32
Q

What are the actions of anticholinesterases?

Examples of drugs used?

A
  • Reversible
  • Competitive inhibitors

Physostigmine (used for glaucome, bladder stimulation and treatment for atropine poisoning)

Neostigmine (treatment for myasthenia graves)

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33
Q

What are the proeprties of irreversible anticholinesterases?

A
  • Non-competitive inhibitors
  • Insecticides
  • Covalently modify AChE organophosphorous compounds
34
Q

What are the symptoms of organophospho anticholinesterase poisoning?

A

Muscarinic effects =

  • Miosis
  • Salivation
  • Sweating
  • Bradycardia

Nicotinic effects =

  • Twitching
  • Paralysis

CNS effects =

  • Anxiety
  • Restlessness
  • Dizziness
35
Q

How do you treat anticholinesterase poisoning?

A

Anti-muscarinic:

  • Alleviate muscarinic symptoms by decreaseing mAChR availability
  • Use atropine to block mAChR

Dephosphorylate acetylcholinesterase

36
Q

What is the health belief model?

A
37
Q

What is the health belief model used for?

A
  • Help to predict, understand and address non-adherence to treatment
  • Better at predicting initiation of health protective behaviours (screening) than reducing health risk behaviour (smoking)
  • Useful framework for health promotion, for example increasing vaccination coverage
38
Q

What is the theory of planned behaviour?

A
39
Q

What is the concept of the theory of planned behaviour?

A
  • The idea of perceived behaviour control
  • Suggests what might be stopping someone from doing a behaviour
  • Judgments are based on if you have resources or opportunities to do behaviour
40
Q

What is the transtheoretical model (stages of change)?

A
41
Q

What is motivational interviewing and its properties?

A

Counselling which is patient centred and explores and resolves ambivalence about behaviour change

Useful = for peoplke unmotivated and unprepared for change

Not useful = for people motivated for change

It increases motivation and makes commitment to the change

42
Q

What are the function and properties of receptors?

A

Respond to messengers by initiating a signal

  • Selective binding site for endogenous hormone / transmitter
  • Act as molecular switches
43
Q

What are the 4 main receptor superfamilies?

A
  • Ligand gated ion channels
  • G protein coupled receptors
  • Catalytic receptors
  • Nuclear receptors
44
Q

What is drug affinity?

What is drug efficacy?

A

Ability of drug to bind to receptor

Ability of drug to activate receptor by conformational change, when bound

45
Q

What is an agonist?

What is an antagonist?

A

Has affinity and efficacy as it binds and activates receptor

Has only affinity as it binds but doesn’t activate receptor, instead blocks it

46
Q

What is KON?

What is KOFF?

What is KD and how do you work it out?

A

Forward rate of reaction

Reverse rate of reaction

Concentration of drug required to occupy 50% of receptors

KON / KOFF

47
Q

What does a low KD indicate?

A

High affinity

48
Q

What is EC50?

What is Rmax?

A

Effective concentration of agonist for 50% of its maximal response (Rmax)

Maximum response of a drug

49
Q

What does the presence of an antagonist do the agonist potency and maximum response?

A

Reduces EC50

Rmax is unchanged

50
Q

What are the properties of competitive antagonists?

What are the properties of uncompetitive antagonists?

A
  • Bind at same 3D site on target receptor as agonist
  • Have structural similarities
  • Bind to different binding site on target receptor
  • Have non-surmountable effects
51
Q

What is a xenobiotic?

What is intoxication?

What is toxic syndrome?

A

Foreign substance to our body

When compound reaches above safe maximum dose value

Toxic effects comprising a set of clinical fingerprints for a group of toxic chemicals

52
Q

How are xenobiotics classified?

A

Target organ classification

Use in the public domain (i.e. food colourings)

According to source

According to effects

According the physical state

According to biochemical properties

53
Q

What are the routes of eposure of xenobiotics?

A
  • Oral
  • Intranasal
  • Inhalation
  • Parenteral (non-GI tract)
54
Q

What are the duration and frequency of xenobiotics?

A

Acute = < 24 hours

  • One exposure or low dose continual exposure until 72 hours
  • Subacute = repeated exposure > 72 hours < 1 month

Chronic = > 3 months

  • Continuous or intermittent exposure
  • Subchronic = 1 - 3 months
55
Q

What are the 4 chemical interactions of toxic agents?

A

Agonistic

Antagonistic

Potentiation / Synergistic

Additive

56
Q

What are the harmful effects of toxins?

A
  • Asphyxiant (simple / chemical)
  • Irritant
  • Corrosive
  • Narcotic
  • Sensitiser
  • Toxic
  • Carcinogenic
  • Mutagen
  • Teratogen
57
Q

What is graded dose response?

A

Relationship of individual test subject or system to increasing / continuous dose of a chemical

58
Q

What is quantal dose response?

A

All-or-nothing response

Determined by distribution of responses to increasing doses in a population of test subjects

59
Q

What is theraputic dose ED50?

What is toxic dose TD50?

What is lethal does LD50?

A

Median effective dose - dose that produces effective dose in 50% of population taking it

Median toxic dose - dose which toxicity occurs in 50% of population taking it

Dose that causes death in 50% of animals tested

60
Q

What is IC50?

A

Inhibitory concentration:

Concentration necessary to inhibit 50% of a measured response in an in-vitro system

61
Q

What is the threshold dose?

What is NOAEL?

A

Point where toxicity first appears

No observed adverse effect level

62
Q

What is toxicokinetics?

What is toxicodynamics?

A

Considers rate chemical enters the body, the storage and metabolism and sebsequent excretion

Concerns dynamic interaction of a toxicant with a biological target and its biological effects

63
Q

What is pharmacokinetics?

What is ADME?

A

Time course of a drug from absorption to elimination, determining dose and how often

Absorption

Distribution

Metabolism

Excretion

64
Q

What are the 5 different drug frequency acronyms?

A

o. d. = once daily
b. d. = twice daily
t. d.s. = thrice daily
q. d.s. = four times daily
p. r.n. = as required

65
Q

What are the 5 different drug routes and their acronyms?

A

po = oral

im = intramuscular

iv = intravenous

sc = subcutaneous

neb = nebuliser

66
Q

What are the benefits of IV?

A

Rapid effects

Absorption circumvented

Good for emergency use

Permits dosage titration

Suitable for large volumes and irritating substances when diluted

67
Q

What are the disadvantages of IV?

A

+ risk of adverse effects

Risk from embolism

Not for oily or insoluble substances

Requires IV access

68
Q

What are the properties of the subcutaneous drug route?

A

Prompt from aqueous solutions

Slow and sustained

Suitable for insoluble suspensions and pellet implantations

Not suitable for large volumes

Possible pain or necrosis from irritating substances

69
Q

What are the properties of the intramuscular drug route?

A

Prompt from aqueous solution

Slow and sustained

Suitable for moderate volumes, oily vehicles and irritating substances

Painful

Danger from incorrect site of injection

70
Q

What are the 2 drug systemics?

When are IV used?

When are subcutaneous routes used?

A

Enteral (via GI tract) and parenteral (avoids GI tract)

Antibiotics, general anaesthetic

Insulin, heparin of low molecular weight

71
Q

What are the properties of oral drugs?

A

Solutions, suspensions, tablets, capsules

Interpatient variation

Variable bioavailability

Most convenient

Requires patient cooperation

72
Q

What are other drug routes?

A

Topical (eye drops)

Transdermal (patches)

Inhalation

Rectal

Sublingual

73
Q

What is the magnitude of drugg effect proportional to and other properties?

A

Concentration at site of action (plasma concentrations)

Needs to be within theraputic window so is effective but not toxic

74
Q

What are the properties of drug absorption?

A
75
Q

What is zero order and first order in pharmacokinetics?

A

Zero-order = rate independent of concentration –> occur when system is saturated

First-order = rate dependent on concentration

76
Q

What are the properties of IV injection?

What is salt factor?

A

?

Proportion of a dose of a drug that is actually the drug

77
Q

What is bioavailability?

How do you work out amount of drug?

A

Amount of administered drug that reaches systemic circulation / volume absorbed

Amount needed / F (bioavailability)

78
Q

What is volume of distribution?

A

Apparent volume in which drug is absorbed into the body

Vd = amount in body / concentration

In L or L/Kg

79
Q

What are the properties of drug elimination?

A

Metabolism and excretion

80
Q

What is clearance in pharmacokinetics?

A

Volume of plasma cleared of a drug per unit time

L/h

81
Q

What is k in pharmacokinetics?

What is t1/2 in pharmacokinetics?

A

Fraction eliminated per unit time

k = clearance / Vd

Time for concentration to decrease by 50%

Medicine 1 (28 decks)

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