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Medicine 1 > Week 11 - Pharmacology > Flashcards

Week 11 - Pharmacology Flashcards

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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
What type of drug are NA reuptake inhibtors and how do they work?
Indirectly acting sympathomimetic drugs: TCAs for depression treatment --\> enhances NA function and 5-HT, block reuptake by varicosity Other effects enhanced
26
What type of drug are cocaine and amphetamine and how do they work?
_Indirectly acting sympathomimetic drugs:_ CNS stimulant and NA reuptake inhibitor + sympathetic excitation Amphetamine = causes exocytotic NA from neuronal uptake
27
What are propranolol and prazosin and how do they work?
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
28
How are muscarinic receptors characterised?
Activated by muscarine Act via metabotropic events Neural, cardiac and glandular are family members Utilise different 2nd messengers Act on different target proteins
29
When are muscarinic receptor agonists used theraputically? What are some side effects?
_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
30
What are ophthalmic uses of muscarinic agonists? How do they work?
_Pilocarpine:_ Glaucoma 1. Constriction of circular muscle 2. Opens up drainage channel 3. ­ + aqueous humour drainage 4. - intraocular pressure.
31
When is the muscarinic antagonist tropicamide used ophthalmically?
_For ocular examination:_ Mydriasis - Relaxation of circular muscle of iris - Relaxation of ciliary muscle
32
What are the actions of anticholinesterases? Examples of drugs used?
- Reversible - Competitive inhibitors Physostigmine (used for glaucome, bladder stimulation and treatment for atropine poisoning) Neostigmine (treatment for myasthenia graves)
33
What are the proeprties of irreversible anticholinesterases?
- Non-competitive inhibitors - Insecticides - Covalently modify AChE organophosphorous compounds
34
What are the symptoms of organophospho anticholinesterase poisoning?
Muscarinic effects = - Miosis - Salivation - Sweating - Bradycardia Nicotinic effects = - Twitching - Paralysis CNS effects = - Anxiety - Restlessness - Dizziness
35
How do you treat anticholinesterase poisoning?
_Anti-muscarinic:_ - Alleviate muscarinic symptoms by decreaseing mAChR availability - Use atropine to block mAChR _Dephosphorylate acetylcholinesterase_
36
What is the health belief model?
37
What is the health belief model used for?
* 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
What is the theory of planned behaviour?
39
What is the concept of the theory of planned behaviour?
- 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
What is the transtheoretical model (stages of change)?
41
What is motivational interviewing and its properties?
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
What are the function and properties of receptors?
Respond to messengers by initiating a signal - Selective binding site for endogenous hormone / transmitter - Act as molecular switches
43
What are the 4 main receptor superfamilies?
- Ligand gated ion channels - G protein coupled receptors - Catalytic receptors - Nuclear receptors
44
What is drug affinity? What is drug efficacy?
Ability of drug to bind to receptor Ability of drug to activate receptor by conformational change, when bound
45
What is an agonist? What is an antagonist?
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
What is KON? What is KOFF? What is KD and how do you work it out?
Forward rate of reaction Reverse rate of reaction Concentration of drug required to occupy 50% of receptors KON / KOFF
47
What does a low KD indicate?
High affinity
48
What is EC50? What is Rmax?
Effective concentration of agonist for 50% of its maximal response (Rmax) Maximum response of a drug
49
What does the presence of an antagonist do the agonist potency and maximum response?
Reduces EC50 Rmax is unchanged
50
What are the properties of competitive antagonists? What are the properties of uncompetitive antagonists?
- 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
What is a xenobiotic? What is intoxication? What is toxic syndrome?
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
How are xenobiotics classified?
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
What are the routes of eposure of xenobiotics?
- Oral - Intranasal - Inhalation - Parenteral (non-GI tract)
54
What are the duration and frequency of xenobiotics?
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
What are the 4 chemical interactions of toxic agents?
Agonistic Antagonistic Potentiation / Synergistic Additive
56
What are the harmful effects of toxins?
- Asphyxiant (simple / chemical) - Irritant - Corrosive - Narcotic - Sensitiser - Toxic - Carcinogenic - Mutagen - Teratogen
57
What is graded dose response?
Relationship of individual test subject or system to increasing / continuous dose of a chemical
58
What is quantal dose response?
All-or-nothing response Determined by distribution of responses to increasing doses in a population of test subjects
59
What is theraputic dose ED50? What is toxic dose TD50? What is lethal does LD50?
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
What is IC50?
_Inhibitory concentration:_ Concentration necessary to inhibit 50% of a measured response in an in-vitro system
61
What is the threshold dose? What is NOAEL?
Point where toxicity first appears No observed adverse effect level
62
What is toxicokinetics? What is toxicodynamics?
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
What is pharmacokinetics? What is ADME?
Time course of a drug from absorption to elimination, determining dose and how often Absorption Distribution Metabolism Excretion
64
What are the 5 different drug frequency acronyms?
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
What are the 5 different drug routes and their acronyms?
po = oral im = intramuscular iv = intravenous sc = subcutaneous neb = nebuliser
66
What are the benefits of IV?
Rapid effects Absorption circumvented Good for emergency use Permits dosage titration Suitable for large volumes and irritating substances when diluted
67
What are the disadvantages of IV?
+ risk of adverse effects Risk from embolism Not for oily or insoluble substances Requires IV access
68
What are the properties of the subcutaneous drug route?
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
What are the properties of the intramuscular drug route?
Prompt from aqueous solution Slow and sustained Suitable for moderate volumes, oily vehicles and irritating substances Painful Danger from incorrect site of injection
70
What are the 2 drug systemics? When are IV used? When are subcutaneous routes used?
Enteral (via GI tract) and parenteral (avoids GI tract) Antibiotics, general anaesthetic Insulin, heparin of low molecular weight
71
What are the properties of oral drugs?
Solutions, suspensions, tablets, capsules Interpatient variation Variable bioavailability Most convenient Requires patient cooperation
72
What are other drug routes?
Topical (eye drops) Transdermal (patches) Inhalation Rectal Sublingual
73
What is the magnitude of drugg effect proportional to and other properties?
Concentration at site of action (plasma concentrations) Needs to be within theraputic window so is effective but not toxic
74
What are the properties of drug absorption?
75
What is zero order and first order in pharmacokinetics?
Zero-order = rate independent of concentration --\> occur when system is saturated First-order = rate dependent on concentration
76
What are the properties of IV injection? What is salt factor?
? Proportion of a dose of a drug that is actually the drug
77
What is bioavailability? How do you work out amount of drug?
Amount of administered drug that reaches systemic circulation / volume absorbed Amount needed / F (bioavailability)
78
What is volume of distribution?
Apparent volume in which drug is absorbed into the body Vd = amount in body / concentration In L or L/Kg
79
What are the properties of drug elimination?
Metabolism and excretion
80
What is clearance in pharmacokinetics?
Volume of plasma cleared of a drug per unit time L/h
81
What is k in pharmacokinetics? What is t1/2 in pharmacokinetics?
Fraction eliminated per unit time k = clearance / Vd Time for concentration to decrease by 50%

Medicine 1 (28 decks)

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