Pharmacology Mid-Term Exam

Front 1

how Gs alpha subunit (Gs protein) works

Back 1

activate adenylate cyclase - increased activity of CAMP dependent protein kinase

Front 2

how Gi alpha subunit (Gi protein) works

Back 2

inhibit adenylate cyclase (AC) - decreases production of cAMP from ATP - decreased activity of cAMP dependent protein kinase

Front 3

how Gq subunit works and its products work

Back 3

activates PLC - cleaves PIP2 to DAG and IP3
DAG binds to membrane
IP3 as soluble structure released into cytosol and binds to IP3 receptors (calcium channels) in endoplasmic reticulum (ER) increasing cytosolic concentration of calcium

Hint 3

PLC - phospholipiase C
PIP2 - phosphatidylinositol 4,5, bisphosphate
DAG - diacyl glycerol
IP3 - inositol 1,4,5, triphosphate

too much calcium in cell - malignant hyperthermia (Treated by inhibiting activity of Ca2+)

Front 4

role of transport proteins: ABC pumps

Back 4

small molecules across membranes

Hint 4

phospholipids, lipophilic drugs

Front 5

role of transport proteins: P type proteins

Back 5

ions against a gradient and usually get phosphorylated during transport

Hint 5

sodium potassium pump

Front 6

role of transport proteins: P type proteins

Back 6

ions against a gradient and usually get phosphorylated during transport

Hint 6

sodium potassium pump

Front 7

role of transport proteins: V type pumps

Back 7

ATPase - use energy released by ATP hydrolysis to move proteins against the concentration gradient (affect the pH)

Hint 7

influenza virus entry

Front 8

role of transport protein: F type pumps

Back 8

proton pump that produces ATP

Front 9

what do you find from dose-response curves?

Back 9

potency (EC50), Efficacy (Emax), type of drug (full agonist, partial agonist, inverse agonist), toxicity, steepness of curve (safety)

Front 10

pharmacokinetic parameters that determine t1/2

Back 10

clearance, volume of distribution

Front 11

half life determines

Back 11

duration of action, time taken to reach steady state, dosing frequency

Front 12

effects of repeat dosing depends on

Back 12

dosing interval, plasma half-life (t1/2)

Front 13

difference between first order clearance and zero order clearance

Back 13

first order clearance - rate of clearance is directly proportional to concentration of drugs. the more drug you have, the faster it is metabolised. half life is constant

zero order: half life increases as concentration increases. elimination rate is constant

Front 14

example of drug with big Vd

Back 14

lipid soluble drugs:
imipramine (antidepressant), chlorpromazine (antipsychotic)

Hint 14

get into CNS - cross blood brain barrier

Front 15

example of drug with small Vd

Back 15

lipid insoluble drugs:
warfarin (blood thinner)

Hint 15

cannot cross blood brain barrier

Front 16

what to look for from plasma-concentration-time profile

Back 16

1) clearance, 2) half life, 3) distribution

Hint 16

to compare generic drugs, need the same area under curve (AUC) and the same tmax

Front 17

uses for area under curve (AUC)

Back 17

1) compare clearance of a drug in different individuals after administration of the same dose (the larger the area, the smaller the clearance)
2) bioavailability of a drug
- compare the amount of drug that reaches the systemic circulation after different routes of administration (iv or orally)

Front 18

in phase I (functionalisation) of drug metabolism, what does CYP450 do?

Back 18

- responsible for the synthesis and catabolism of cellular molecules (bile salts, steroids, vitamin D, fatty acids)

Front 19

in phase I (functionalisation) of drug metabolism, what doesn't CYP450 do?

Back 19

- oxidation of amines (noradrenaline) and 5-HT (monoamine oxidase)
- oxidation of ethanol by alcohol dehydrogenase
- reduction reactions
- hydrolysis reactions (aspirin, lignocaine)

Front 20

type A adverse effect

Back 20

high morbidity
low mortality
dose dependent
usually mild
usually response to dose adjustment
high incidence (80% of ADR)
predictable

Front 21

type B adverse effect

Back 21

high morbidity
high mortality
dose independent
usually serious
unpredictable

Front 22

type C (continuous)adverse effect

Back 22

consequence of long term use
adaptive changes (development of drug tolerance and physical dependence)
rebound phenomenia

Front 23

type D (delayed) adverse effect

Back 23

appearance of delayed drug effects
may be acceptable if benefit of drug outweighs risk

Hint 23

carcinogenesis

Front 24

type E adverse effect

Back 24

related to drug withdrawal
uncommon

Hint 24

opiate with drawal syndrome, myocardial ischaemia after abrupt cesation of B blockers

Front 25

examples of narrow therapeutic index drugs (W,L,D,P,G,A,5)

Back 25

warfarin
lithium
digoxin
phenytoin
gentamycin
amphortericin B
5 fluoroucacil

Front 26

EU verbal descriptors of harm

Back 26

verbal - frequency - probability
very common - over 10% - more than 1 in 10
common - 1~10% - 1 in 100 to 1 in 10
unconmmon - 0.1~1% - 1 in 1000 to 1 in 100
rare - 0.01%~0.1 - 1 in 10,000 ~ 1 in 1000
very rare - less than 0.01% - less than 1 in 10,000

Front 27

sympathetic fibres
- neurotransmitter
- receptors
- exception

Back 27

- noradrenaline
- alpha or beta adrenoreceptors
- exception: sweat gland

Front 28

parasympathetic fibres
- neurotransmitter
- receptors

Back 28

- acetylcholine
- muscuranic or nicotinic (motor fibres) cholinergicreceptors

Front 29

other neurotransmitters

Back 29

NO, 5HT, ATP, GABA, dopamine, excitatory amino acids (glutamate and aspartate, neuropeptides)

Front 30

sympathetic adrenergic neurotransmission: alpha 1 receptor

Back 30

vasoconstriction, increased BP, mydriasis (pupil dilation), contraction of smooth muscle, exocrine gland secretion, neuronal excitation

Front 31

sympathetic adrenergic neurotransmission: alpha 2 receptor

Back 31

inhibition of NA release, decreased secretion of acqueous humor and insuline

Front 32

sympathetic adrenergic neurotransmission: beta 1 receptor

Back 32

cardiac stimulation, increased heart rate, heart contraction increased renin secretion, increased heart rate/contraction

Front 33

sympathetic adrenergic neurotransmission: beta 2 receptor

Back 33

vasodilation, bronchodilation, smooth muscle relaxation, glycogenolysis, uptake of K+ into the skeletal muscle

Front 34

sympathetic adrenergic neurotransmission: beta 3 receptor

Back 34

liplysis in adipose tissue

Front 35

what is the difference in adrenergic nerve ending and cholinergic nerve ending?

Back 35

adrenergic: tyrosin, dopamine, storage, NA release
cholinergic: choline, acetylcholine, storage, Ach release

Front 36

parasympathetic cholinergic neurotransmission: muscuranic 1 receptor (neural)

Back 36

modulation of neurotransmission

Front 37

parasympathetic cholinergic neurotransmission: muscuranic 2 receptor (cardiac)

Back 37

slowing of heart rate and conduction

Front 38

parasympathetic cholinergic neurotransmission: muscuranic 3 receptor (glandular)

Back 38

contraction of smooth muscles and stimulation of glandular secretions, vasodilation

Front 39

difference between direct, indirect and mixed acting adrenergic agonists

Back 39

direct - binds to receptor and stimulate
indirect - no action receptor, make more neurotransmitter (stimulate storage vesicles, prevent neurotransmitter and prevent reuptake)
mixed - both direct and indirect activity

Front 40

adrenoreceptors agonists - direct acting - pharmacological effect, clinical use, side effect - dobutamine

Back 40

- cardiac stimulation (beta 1) and vasodilation (beta 2)
- cardiogenic shock, acute heart failure, cardiac stimulation during heart surgery
- arrhythmias

Front 41

adrenoreceptors agonists - direct acting - pharmacological effect, clinical use, side effect - adrenaline/epinephrine

Back 41

- vasoconstriction, increased BP (alpha 1), cardiac stimulation (beta 1), bronchodilation (beta 2)
- anaphylactic shock, cardiac arrest, ventricular fibrilation, reduction in bleeding during surgery, prolongation of the action of local anaesthetics
- hypertension, vasoconstriction, arrhythmias

Front 42

adrenoreceptors agonists - direct acting - pharmacological effect, clinical use, side effect - salbutamol and salmeterol

Back 42

- smooth muscle relaxation, bronchodilation (beta 2)
- asthma, premature labour
- tachycardia, arrhythmias, tremors, peripheral vasodilation

Front 43

adrenoreceptors agonists - direct acting - pharmacological effect, clinical use, side effect - phenylpherine (extnsive metabolism by MAO in gut)

Back 43

- vasoconstriction, increased blood pressure, and mydriasis (pupil dilation) (alpha 1)
- nasal decongestion in viral and allergic rhinitis, ocular decongestion in allergic conjunctivitis, BP maintainance
- bradycardia, hypertension

Front 44

adrenoreceptors agonists - indirect acting - pharmacological effect, clinical use, side effect - amphetamine

Back 44

- increase in NA release
- CNS stimulant in narcolepsy appetite suppressant
- hypertension, tachycardia, dependence

Front 45

adrenoreceptors agonists - indirect acting - pharmacological effect, clinical use, side effect - cocaine

Back 45

- inhibition of noradrenaline uptake
- local anaesthesia, also used to stop nosebleeds due to vasoconstriction of alpha 1 receptor
- hypertension, cardiac damage, necrosis of nasal mucosa (abuse) - tachycardia

Front 46

adrenoreceptors agonists - mixed acting - pharmacological effect, clinical use, side effect - pseudoephedrine

Back 46

- vasoconstriction (alpha 1)
- nasal decongestion in viral and allergic rhinitis
- hypertension, tacycardia, insomnia, dependence

Front 47

adrenoreceptors agonists - mixed acting - pharmacological effect, clinical use, side effect - ephedrine

Back 47

- vasoconstriction (alpha 1)
- nasal decongestion in viral and allergic rhinitis
- hypertension, tacycardia, insomnia, dependence

Front 48

adrenergic agonists relevance to dentistry

Back 48

- indirect adrenergic agonists more wide spread effects - targets enzymes

Front 49

adrenergic antagonists - alpha blockers - MOA, phamacological effects, clinical use, side effects - prazosin

Back 49

- competitive alpha 1 blocker
- cause vasodilation, decrease vascular resistance and blood pressure, relax bladder, neck and prostate
- hypertension, urinary retention due to benign prostatic hyperplasia
- hypotension, tachycardia, nasal congestion, urinary urgency

Front 50

adrenergic antagonists - beta blockers (mainly to CVD by decreasing HR) - MOA, phamacological effects, clinical use, side effects - phentolamine

Back 50

- competitive alpha and alpha 2 blocker
- cause vasodilation, decrease vascular resistance and blood pressure
- hypertension due to pheochromocytoa, necrosis, ischemia after injection of alpha-adrenergic receptor agonists
- hypotension>tachycardia, nasal congestion

Front 51

adrenergic antagonists - beta blockers (mainly to CVD by decreasing HR) - MOA, phamacological effects, clinical use, side effects - atenolol

Back 51

- beta 1 blocker (selective)
- decreases cardiac rate, output, AV node conduction and O2 demand decreases blood pressure
- hypertension, angina pectoris acute emyocardial infarction, arrhythmia
- cardiac failure, hypoglycemia, possible bronchoconstriction

Front 52

adrenergic antagonists - alpha and beta blockers - MOA, phamacological effects, clinical use, side effects - propranolol

Back 52

- beta 1 and beta 2 blockers (non selective)
- decreases cardiac rate, output, AV node conduction and O2 demand decreases blood pressure
- hypertension, angina pectoris cardiac arrhythmias, migraine headache, acute thyroxicosis, acute myocardial infarction
- cardiac failure > bronchoconstriction, hypoglycemia - be concerned when sitting patient back up quickly (orthostatic hypotension)

Front 53

adrenergic antagonists - alpha and beta blockers - MOA, phamacological effects, clinical use, side effects - carvediol

Back 53

- beta 1 and beta 2 blockers, alpha 1 blockers, 5~10x more potent beta blocker than alpha
- causes vasodilation, decreases heart rate and blood pressure in patients with hypertension, increases cardiac output in patients with heart failure
- hypertension, heart failure
- as for beta blockers + renal failure

Front 54

adrenergic antagonists relevance to dentistry

Back 54

- syncope
- alpha 2 antagonists may cause xerostomia (poor OH, dental caries, candidiasis)
- beta blockers - will cause cardiac depression, propranolol may cause bronchodilation
- hypertensive after administration of anaesthetics containing adrenaline
- orthostatic hypotension

Front 55

differences between direct and indirect acting cholinergic agonists

Back 55

direct (muscuranic and nicotinic)
indirect (Ach inhibitors)

Front 56

cholinergic agonists - direct acting - choline esters -phamacological effect, clinical uses, side effects - acetylcholine

Back 56

- M and N
- miosis during opthalmic surgery
- for muscarinic agonists (bronchoconstriction, hypotension, DUMBELS, contraindications: asthma, hyperthyroidism, coronary insufficiency

Front 57

cholinergic agonists - direct acting - choline esters -phamacological effect, clinical uses, side effects - bethanecol

Back 57

- M and N
- post operative urinary retention, oral used for xerostomia
- for muscarinic agonists (bronchoconstriction, hypotension, DUMBELS, contraindications: asthma, hyperthyroidism, coronary insufficiency

Front 58

cholinergic agonists - direct acting - choline esters -phamacological effect, clinical uses, side effects - carbachol

Back 58

- M and N
- glaucoma, miosis
- - for muscarinic agonists (bronchoconstriction, hypotension, DUMBELS, contraindications: asthma, hyperthyroidism, coronary insufficiency

Front 59

cholinergic agonist - direct acting - plant alkaloids - phamacological effect, clinical uses, side effects - muscarine

Back 59

- M and N
- None
- - for muscarinic agonists (bronchoconstriction, hypotension, DUMBELS, contraindications: asthma, hyperthyroidism, coronary insufficiency

Front 60

cholinergic agonist - direct acting - plant alkaloids - phamacological effect, clinical uses, side effects - nicotoine

Back 60

- N
- smoking cessation

Front 61

cholinergic agonist - direct acting - plant alkaloids - phamacological effect, clinical uses, side effects - pilocarpine

Back 61

- M>N
- glaucoma (constricts cillary muscles to drain aqueous humour), xerostomia

Front 62

cholinergic agonist - indirect (cholinerase inhibitors) - short acting quarternary alcohols - phamacological effect, clinical uses, side effects - edrophonium

Back 62

- bind anionic site only preventing Ach access. Ionic bond readily reversible-brief action
- used in diagnosis of myasthenia gravis
- mainly due to muscarinic stimulation - DUMBLES. Nicotinic effects only at higher doses. inhibition causes same effect as Ach 'overdose'

Front 63

cholinergic agonist - indirect (cholinerase inhibitors) - medium acting - phamacological effect, clinical uses, side effects - neostigamine, physotigamine (longer acting)

Back 63

- carbarnyl transfer to ser 203 at anionic site, then slow hydrolysis
- reversal of neuromuscular block, myasthenia treatment, alzheimer's disease (doneprezil, tacrine)
- mainly due to muscarinic stimulation - DUMBLES. Nicotinic effects only at higher doses. inhibition causes same effect as Ach 'overdose'

Front 64

cholinergic agonist - indirect (cholinerase inhibitors) - irreversible block - phamacological effect, clinical uses, side effects - echothiopate, dyflos

Back 64

- with labile group. phosphorylate ser 203 at active site; bond stable and thus long lasting
- eye drops for glaucoma

Front 65

cholinergic antagonists - nicotinic neuromuscular and ganglionic blocking agents - non depolarising (tubocurarine analogues) - MOA, phamacokinetics, use - mivacurium, atracurium, vecuronium, pancuronium

Back 65

- competitive antagonist of Ach at NM receptors in skeletal muscle
- first paralyses small and rapidly moving muscles, finally intercoastal muscles and diaphragm - respiration cease (relaxation of abdominal muscles)
- muscle relaxatior

Front 66

cholinergic antagonists - nicotinic neuromuscular and ganglionic blocking agents - depolarising - MOA, phamacokinetics, use - suxamethonium

Back 66

- Ach analogue. sustained at neuromuscular junction- causes depolarisation block. rapid onset.
- metabolised by plasma cholinersterase (avoid anticholinesterases)
- brief endoscopy, orthopaedic manipulation, side effect: muscle fasciculation, contraindication: neuropathies, myopathies, burns/severe trauma

Front 67

cholinergic antagonists - muscarinic antagonists - MOA, phamacokinetics, use - pirenzepine

Back 67

- M1 selective
- inhibition of gastric acid secretion

Front 68

cholinergic antagonists - muscarinic antagonists - MOA, phamacokinetics, use - hyoscine (scopolamine)

Back 68

- reversible competitive blockage
- anti-emetic, antispasmodic for intestinal spasms

Front 69

cholinergic antagonists - muscarinic antagonists - MOA, phamacokinetics, use - impratropium

Back 69

- reversible competitive blockage
- bronchodilation

Front 70

cholinergic antagonists - muscarinic antagonists - MOA, phamacokinetics, use - atropine

Back 70

- reversible competitive blockage
- increase heart rate by blocking effects of vagus nerve; anticholinesterase and mushroom poisoning

Front 71

difference between depolarising and non-depolarising neuromuscular blockers

Back 71

nicotinic antagonists (neuromuscular blockers)
- non depolarizing (majority)
* blocks Ach receptors
* competitive antagonist at Ach at NM receptors in skeletal
* tubocurarine analogues - mivacurium, atracurium, vecuronium, pancuronium
- depolarizing
* agonists at Ach receptors
* zudamethonium
* depolarization block
* rapid onset

Front 72

cholinergic antagonists relevance to dentistry

Back 72

- few uses
- muscle relaxation
- insertion of tracheal tubes for general anaesthesia

Front 73

mode of actions of drugs used to treat arrhythmias

Back 73

- class I - sodium channel blockers - quinidine, lidocaine, flecainide
- class II - beta blockers - atenolol and propranolol
- class III - potassium channel blockers - amiodarone, sotalol
- class IV - calcium channel blockers - verapamil

Front 74

adverse effects of drugs used to treat arrhythmias

Back 74

- class I - sodium channel blockers - hypotension, arrhythmias, GIT distress, throbocytopenia
- class II - beta blockers - cardiac depression, bradycardia, bronchospasm (propranolol), insomnia, depression
- class III - potassium channel blockers - hypotension, arrhythmia, skin discolouration, thyroid dysfunction, pulmonary fibrosis, dry cough (amiodarone)
class IV - calcium channel blockers - hypotension, dizziness, GIT bleeding, gingival hyperplasia

Front 75

relevance of drugs used to treat arrhythmias to dentistry

Back 75

- orthostatic hypotension
- adrenaline - systemic increase - arrhythmia
- antimuscarinic affect of quinidine - cause xerostomia
- thrombocytopenia (quinidine) (oral haemorrhaging)
- verpamil causes gingival hyperplasia (calcium channel blockers)

Front 76

mode of actions of drugs used to treat heart failures

Back 76

- vasodilators - decreasing oxygen requirements - ACE inhibitors (captapril, enalaprill), angiotensin receptor antagonists (iosartan), Digoxin, phosphodiesterase inhibitors
- inotropic affects - increase heart contraction force - dobutamine (beta 1 agonists)

Front 77

adverse effects of drugs used to treat heart failures

Back 77

- ace inhibitors (captapril, enalapril) - renal failure, hypotension, angiodemia, hyperkalemia, dry cough
- angiotensin receptor antagoninst (iosartan) - hypotension and hyperkalemia
- digoxin - high toxicity, will cause GIT problems, arrhythmias and CNS effets (confusion, vertigo, visual disturbances)
- phosphodiesterase inhibitors (amrinone) - inhibits phosphodiesterase III and therefore, increase camp- cause arrhythmias
- dobutamine (beta 1 receptor agonists) - increases heart rate, may cause hypertension, arrhythmias and tachycardia

Front 78

relevance of drugs used to treat heart failures to dentistry

Back 78

- cause arrhythmia - adrenaline
- do not use adrenaline with digoxin - digoxin overdose is seen with increased salivation
- orthostatic hypotension - using anaesthetics and putting the chair up quickly

Front 79

principles behind the treatment of angina

Back 79

- vasodilators - nitrates, calcium blockers - nitrates (glyceryl trinitrates, isorbide initrate) will cause relaxation in vascular smooth muscle, calcium blockers - acting on phase 2 - verapamil and nifidapine, verapamil - calcium blockers, nifidipine - smooth muscle vascular relaxation
- cardiac depressant - calcium blockers - beta blockers (atenolol and propranolol)
- potassium channel activators - nausea, dizziness, hypotension, tachycardia, myalgia, headaches (diazoxide, nicorandil, minoxidil), and hyperglycemia (diazoxide)
- perhexiline

Front 80

mode of action of drugs used to treat angina

Back 80

- beta blockers
- calcium channel blockers
- potassium channel activators
- nitrates - releasing nitrous oxide

Front 81

adverse effects of drugs used to treat angina

Back 81

- nitrates - glycerol trinitrates and isorbide dinitrates - hypotension, tachycardia, headaches, dizziness
- calcium channel blockers - verapamil and nifidapine - gingival hyperplasia, GIT bleeding
- beta blockers - atenolol and propranolol - bradycardia, cardiac depression, bronchospasm (propranolol), insomnia and
- potassium channel activators - (diazoxide, nicorandil, minoxidil) - flushing, nausea, headaches, dizziness and myalgia and hyperglcemia (diazoxide)

Front 82

relevance to drugs used to treat angina to dentistry

Back 82

- hypotension from beta blockers and potassium channel activators and nitrates
- tachycardia - nitrates and nifidapine and potassium channel activaors - (beware of retraction cords, stress and adrenaline use)
- gingival hyperplasia for verapamil