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Pharmacology > 02 Noradrenergic pharmacology > Flashcards

02 Noradrenergic pharmacology Flashcards

1
Q

2.01 β2-RECEPTOR AGONIST

Short-acting: salbutamol (albuterol), terbutaline - actions

A

bronchodilation
(minimal action on heart: ↑rate and force)
relaxes uterine smooth muscle

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2
Q

2.01 β2-RECEPTOR AGONIST

Short-acting: salbutamol (albuterol), terbutaline - MOA

A

↓calcium-mediated contraction in bronchioles
↑cAMP which activates protein kinase A (PKA)
PKA inhibits myosin light chain kinase (MLCK) - the mediator of contraction

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3
Q

2.01 β2-RECEPTOR AGONIST

Short-acting: salbutamol (albuterol), terbutaline - abs/distrib/elim

A

given as required by inhalation for asthma
salbutamol, terbutaline: fast onset, short-acting (3-5h)
can also be given IV for severe airway disease or premature labour

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4
Q

2.01 β2-RECEPTOR AGONIST

Short-acting: salbutamol (albuterol), terbutaline - clinical use

A

asthma and obstructive airway disease (main use)
salbutamol and terbutaline for rapid relief of the acute attack
treatment of pre­mature labour, and hyperkalaemia

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5
Q

2.01 β2-RECEPTOR AGONIST

Short-acting: salbutamol (albuterol), terbutaline - adverse effects

A

tremors, tachycardia (sometimes dysrhythmias), nervousness, some peripheral dilatation
high-dose nebulised salbutamol drives potassium into cells and causes hypokalaemia - this is used for emergency management of hyperkalaemia

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6
Q

2.02 β1-RECEPTOR ANTAGONIST

Selective: atenolol, bisoprolol, etc.; non-selective: propranolol; mixed α/β: labetalol, etc. - actions

A

reduces BP in hypertensive patients by:
↓cardiac output
↓renin release
↓CNS-mediated sympathetic activity
in angina, slows heart rate and reduces metabolic demand

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7
Q

2.02 β1-RECEPTOR ANTAGONIST

Selective: atenolol, bisoprolol, etc.; non-selective: propranolol; mixed α/β: labetalol, etc. - MOA

A

blocks the action of endogenous and exogenous agonists on β1 receptors

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8
Q

2.02 β1-RECEPTOR ANTAGONIST

Selective: atenolol, bisoprolol, etc.; non-selective: propranolol; mixed α/β: labetalol, etc. - abs/distrib/elim

A

absorbed orally, with rapid onset of action
mainly metabolised in liver

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9
Q

2.02 β1-RECEPTOR ANTAGONIST

Selective: atenolol, bisoprolol, etc.; non-selective: propranolol; mixed α/β: labetalol, etc. - clinical use

A

ischaemic heart disease
congestive cardiac failure
cardiac arrhythmias
hypertension
migraine prophylaxis (propranolol)

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10
Q

2.02 β1-RECEPTOR ANTAGONIST

Selective: atenolol, bisoprolol, etc.; non-selective: propranolol; mixed α/β: labetalol, etc. - adverse effects

A

dangerous: bronchconstriction in asthma
potential heart block or worsening heart failure in patients with unstable cardiac conditions
decreased sympathetic warning to hypoglycaemia in diabetes
inconvenient: cold extremities, fatigue

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11
Q

2.03 α- AND β-RECEPTOR AGONISTS

Epinephrine (adrenaline) - actions

A

α1: vasoconstriction (thus ↑BP); contraction of uterus, GIT sphincters, bladder sphincter, radial iris muscle
α2: inhibits lipolysis, inhibits NA release
β1: increased heart rate
β2: bronchodilation, vasodilation (decrease in diastolic BP)

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12
Q

2.03 α- AND β-RECEPTOR AGONISTS

Epinephrine (adrenaline) - MOA

A

α1: activation of phospholipase C with generation of IP3 (which increases intracellular calcium and thus force of contraction)
β2: ↑cAMP activates protein kinase A (PKA); in smooth muscle, PKA reduces the contractile action; in cardiac muscle, PKA increases intracellular calcium and thus force of contraction

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13
Q

2.03 α- AND β-RECEPTOR AGONISTS

Epinephrine (adrenaline) - abs/distrib/elim

A

given IM or SC
plasma half-life 2min
metabolised by MOA and COMT

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14
Q

2.03 α- AND β-RECEPTOR AGONISTS

Epinephrine (adrenaline) - clinical use

A

anaphylactic shock
also added to local anaesthetic solutions to prolong activity of the anaesthetic

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15
Q

2.03 α- AND β-RECEPTOR AGONISTS

Epinephrine (adrenaline) - adverse effects

A

tachycardia, raised BP, anxiety

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16
Q

2.03 α- AND β-RECEPTOR AGONISTS

Epinephrine (adrenaline) - special points

A

phenylephrine and oxymetazoline are similar drugs except that they are α1-selective

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17
Q

2.04 α1-RECEPTOR ANTAGONIST

Selective: prazosin, doxazosin, tamsulosin; non-selective: phenoxybenzamine - actions

A

vasodilation (thus ↓BP)
↑heart rate (a reflex β-receptor response to the ↓BP)
↓bladder sphincter tone
inhibits hypertrophy of smooth muscle of bladder neck and prostate capsule

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18
Q

2.04 α1-RECEPTOR ANTAGONIST

Selective: prazosin, doxazosin, tamsulosin; non-selective: phenoxybenzamine - MOA

A

blocks the action of endogenous and exogenous agonists on α1 receptors
tamsulosin is an α1A-receptor antagonist that is “uro-selective”
phenoxybenzamine is a non-selective, irreversible inhibitor

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19
Q

2.04 α1-RECEPTOR ANTAGONIST

Selective: prazosin, doxazosin, tamsulosin; non-selective: phenoxybenzamine - abs/distrib/elim

A

selective agents are absorbed orally and metabolised by liver
prazosin has a shorter half-life of 3-4h (others are longer acting)

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20
Q

2.04 α1-RECEPTOR ANTAGONIST

Selective: prazosin, doxazosin, tamsulosin; non-selective: phenoxybenzamine - clinical use

A

for severe hypertension: prazosin, doxazosin (in combination with other agents)
for benign prostatic hypertrophy: doxazosin, tamsulosin
for phaechromocytoma: phenoxybenzamine

21
Q

2.04 α1-RECEPTOR ANTAGONIST

Selective: prazosin, doxazosin, tamsulosin; non-selective: phenoxybenzamine - adverse effects

A

orthostatic hypotension, dizziness
hypersensitivity reactions
insomnia
sometimes priapism
tamsulosin can cause abnormal ejaculation and back pain

22
Q

2.05 β1-RECEPTOR AGONIST

Dobutamine - actions

A

cardiac stimulant: increases contractility and thus cardiac output
it has less effect on heart rate and there is little vasoconstriction

23
Q

2.05 β1-RECEPTOR AGONIST

Dobutamine - MOA

A

acts mainly on β1 receptors causing G protein-mediated increase of cAMP, which increases calcium influx in the cardiac myocytes
minimal effect on β2 receptors

24
Q

2.05 β1-RECEPTOR AGONIST

Dobutamine - abs/distrib/elim

A

given IV
plasma half-life 2min
inactivated by MAO and COMT

25
Q

2.05 β1-RECEPTOR AGONIST

Dobutamine - clinical use

A

cardiogenic shock
low cardiac output hypoperfusion
(dopamine is a related drug used in these situations)

26
Q

2.05 β1-RECEPTOR AGONIST

Dobutamine - adverse effects

A

dysrhythmias

27
Q

2.06 α1-RECEPTOR AGONIST

Phenylephrine, xylometazoline, etc. - actions

A

vasoconstriction
nasal decongestion
pupil dilation without effect on accommodation

28
Q

2.06 α1-RECEPTOR AGONIST

Phenylephrine, xylometazoline, etc. - MOA

A

causes release of calcium from the sarcoplasmic reticulum
the increased calcium activates the contractile mechanism

29
Q

2.06 α1-RECEPTOR AGONIST

Phenylephrine, xylometazoline, etc. - abs/distrib/elim

A

given intranasally or topically in the eye
plasma half-life 3h (longer in the elderly)

30
Q

2.06 α1-RECEPTOR AGONIST

Phenylephrine, xylometazoline, etc. - clinical use

A

as nasal decongestant
for opthalmoscopy

31
Q

2.06 α1-RECEPTOR AGONIST

Phenylephrine, xylometazoline, etc. - adverse effects

A

hypertension, reflex bradycardia

32
Q

2.07 DRUGS THAT RELEASE NORADRENALINE

Amfetamine, methylphenidate, atomoxetine - actions

A

indirectly acting sympathomimetics
release NA from the varicosity, therefore has similar actions to NA and epinephrine, but weaker:
α1: vasoconstriction (thus ↑BP)
β1: increased heart rate
β2: bronchodilation
also a potent CNS stimulant

33
Q

2.07 DRUGS THAT RELEASE NORADRENALINE

Amfetamine, methylphenidate, atomoxetine - MOA

A

taken up by Uptake 1 into the varicosity, then into the vesicle by exchange with NA
the NA, now loose in the cytoplasm, is then released by exchange with amfetamine at Uptake 1

34
Q

2.07 DRUGS THAT RELEASE NORADRENALINE

Amfetamine, methylphenidate, atomoxetine - abs/distrib/elim

A

absorbed orally
plasma half-life ~12h
excreted unchanged in urine

35
Q

2.07 DRUGS THAT RELEASE NORADRENALINE

Amfetamine, methylphenidate, atomoxetine - clinical use

A

stimulant effects in narcolepsy
treatment of ADHD

36
Q

2.07 DRUGS THAT RELEASE NORADRENALINE

Amfetamine, methylphenidate, atomoxetine - adverse effects

A

increased BP, tachycardia
insomnia
psychosis with excessive doses

37
Q

2.08 SELECTIVE β3-ADRENOCEPTOR AGONIST

Mirabegron - actions and MOA

A

stimulates relaxation of bladder smooth muscle through increased cAMP concentrations

38
Q

2.08 SELECTIVE β3-ADRENOCEPTOR AGONIST

Mirabegron - abs/distrib/elim

A

given orally with peak plasma concentrations at 3-4h
metabolised and eliminated through multiple pathways, including renal and hepatic

39
Q

2.08 SELECTIVE β3-ADRENOCEPTOR AGONIST

Mirabegron - clinical use

A

urgency, frequency and/or incontinence in overactive bladder syndrome

40
Q

2.08 SELECTIVE β3-ADRENOCEPTOR AGONIST

Mirabegron - adverse effects

A

tachycardia
urinary tract infections

41
Q

2.09 α2-AGONIST PRODRUG

Methyldopa - actions

A

reduces release of NA
lowers blood pressure

42
Q

2.09 α2-AGONIST PRODRUG

Methyldopa - MOA

A

acts mainly in the CNS
is taken up into adrenergic neurons and converted into false transmitter methylnoradrenaline (methylnorepinephrine)
this is released and acts on the α2 adrenoceptors, decreasing the release of NA

43
Q

2.09 α2-AGONIST PRODRUG

Methyldopa - abs/distrib/elim

A

given orally
actively transported into CNS neurons
plasma half-life ~2h
duration of action ~24h

44
Q

2.09 α2-AGONIST PRODRUG

Methyldopa - clinical use

A

hypertension

45
Q

2.09 α2-AGONIST PRODRUG

Methyldopa - adverse effects

A

hypotension
transient sedation
dry mouth
diarrhoea
hypersensitivity reactions

46
Q

2.10 DOPA DECARBOXYLASE INHIBITOR

Carbidopa, benserazide - actions and MOA

A

levodopa is used to treat parkinsonism, but in the GIT and periphery it is metabolised by DOPA decarboxylase
this reduces the amount available to the CNS
the resulting GI and peripheral dopamine causes nausea and hypotension
carbidopa inhibits DOPA decarboxylase, thus increasing the availability of levodopa to the CNS and reducing the dopamine-mediated side effects

47
Q

2.10 DOPA DECARBOXYLASE INHIBITOR

Carbidopa, benserazide - abs/distrib/elim

A

usually given in combination with levodopa to treat parkinsonism
carbidopa cannot cross the blood-brain barrier so it affects only the peripheral metabolism of levodopa

48
Q

2.10 DOPA DECARBOXYLASE INHIBITOR

Carbidopa, benserazide - clinical use

A

an adjunct in treatment of parkinsonism

49
Q

2.10 DOPA DECARBOXYLASE INHIBITOR

Carbidopa, benserazide - adverse effects

A

hypotension
transient sedation
dry mouth
diarrhoea
hypersensitivity reactions

Pharmacology (34 decks)

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