Ouhsc Pharmacology Test 1

Front 1

acts on all α- and β-adrenoceptors in the body. If you
understand the actions of this prototype agent, the effects of all of the other
compounds will be clear. It is the primary catecholamine liberated from
the adrenal medulla and is not effective when given orally. Even when injected it
has a short duration of action. As a drug, it is given parenterally or by
inhalation.

Back 1

Epinephrine

Front 2

As this drug stimulates all adrenoceptors, its actions on the cardiovascular
system are complex. The overall effect will be the algebraic summation of two
opposing effects (α-adrenoceptor induced vasoconstriciton vs. β-adrenoceptor induced vasodialation).

Back 2

Epinephrine

Front 3

this drug has potent action on the heart where it stimulates the cardiac
β1- Adrenoceptors to increase heart rate and contractility. As with other drugs, changes in cardiac output are not sufficient to overcome direct effects on the blood vessels when they are opposing (i.e. the depressor effects of it are still observed when the α-adrenoceptors are blocked even though there is a pronounced increase in cardiac output). It acts on β2-adrenoceptors to relax bronchial smooth muscle in the treatment of asthma and for treating bronchospasm during anaphylactic shock.

Back 3

Epinephrine

Front 4

Among the most important actions of ________ are those concerning metabolism (i.e., providing energy substrates for fight or flight response).It acts via β- adrenoceptor mechanisms to increase adenylate cyclase
activity to form the second messenger cAMP that has the following metabolic effects:
1) Increases plasma glucose by breakdown of liver glycogen.
2) Inhibits synthesis of glycogen
3) Stimulates gluconeogenesis
4) Breaks down fats (triglycerides) to fatty acids.

Back 4

epinephrine

Front 5

this is the neurotransmitter released from sympathetic nerve endings acting on all α-adrenoceptors as well as β1-adrenoceptors. It is not clinicallyuseful as it is not orally effective and even parenterally is very short acting. A bolus
injection of it will increase blood pressure due to both vasoconstriction and increased cardiac output.

Back 5

Norepinephrine (NE)

Front 6

______in the peripheral nervous system is a metabolic precursor in the
formation of NE and EPI. In the CNS, it is an important neurotransmitter,
especially in the extrapyramidal motor system.

Back 6

Dopamine (DA)

Front 7

A CNS defect in _________is responsible for producing Parkinson’s disease. Agents that block ______ in the CNS also produce a syndrome similar to Parkinson’s disease.
Renal blood vessels appear to possess non-innervated dopamine receptors that produce vasodilation in the kidney. Consequently, infusion of this has been used to treat certain conditions where renal blood flow is compromised (e.g. certain shock states). At higher doses, it can also stimulate α- and β- adrenoceptors causing increased blood pressure and cardiac output.

Back 7

dopaminergic mechanisms

dopamine

Front 8

______ and ______are indirect acting sympathomimetics that are orally effective and readily enter the CNS. These are dangerous drugs with very limited therapeutic justification. They do produce a temporary elevation of mood and appetite suppression (anorexia) but tolerance to these effects develops rapidly. A rebound depression frequently develops and they quickly lose their anorectic action.

Back 8

Amphetamine and Methamphetamine

Front 9

________are highly toxic and can be lethal. Due to tolerance the ED50
increases but the LD50 remains unchanged. Chronic toxicity can mimic paranoid
schizophrenia. Fortunately, this is reversible upon drug withdrawal. The major
finding at autopsy is cerebral hemorrhage that may be secondary to intense
vasoconstriction of CNS blood vessels.

Back 9

Amphetamines

Front 10

what are theonly two valid medical uses for amphetamines.

Back 10

The first is in the
treatment of hyperkinetic children who sometimes respond to amphetamines bybecoming more sedate and thus increase their attention span. The other use is to treat patients suffering from narcolepsy.

Front 11

_________ is a mild CNS stimulant that is structurally related to
amphetamine. In large doses, like amphetamine, it will produce
generalized CNS excitation and may cause convulsions. Like amphetamines, this
drug has potential for abuse. The primary use for it is in
treatment of some children with attention deficit hyperactivity disorder.
It has a good oral bioavailability

Back 11

Methylphenidate

Front 12

__________ is one of the oldest drugs known to man, being used in Chinese
medicine for at least 3000 years. About half of its action is due to direct receptor
stimulation where like EPI it acts as an agonist on all α- and β-receptors in the body.
About half of its action is also indirect in that it releases NE from neuronal stores.

Back 12

Ephedrine

Front 13

This can be used as an oral treatment for bronchial asthma (β effect) and is
found in some over-the-counter medications for ear and nasal decongestion. It has also been used for it’s α effects as a pressor agent and in
ophthalmology to produce short lasting mydriasis without cycloplegia.

Back 13

Ephedrine

Front 14

_______may be better known to you by one of its common trade names –
‘Neo-Synephrine’. It is a direct acting sympathomimetic with primarily α-adrenergic
stimulating effects. It is orally effective only when given in extremely large doses
(200-300 times the i.v. dose) so its inclusion in some over-the-counter cold
medications is questionable. It is used as a pressor agent and in ophthalmology to
produce mydriasis. As a nasal spray, α-adrenergic stimulants caused local
vasoconstriction in the nasal airways along with less leakage of fluid. Unfortunately,
these sprays frequently cause a rebound congestion that is worse than the initial
congestion.

Back 14

Phenylephrine

Front 15

_______is an agonist (stimulant) of the α2 subtype of adrenergic receptors.
Although it produces a variety of short lasting autonomic effects outside of the brain,
its main action is long term stimulation of CNS α2 adrenoceptors. This paradoxically
reduces sympathetic tonic activity from the brain and consequently, it is used
to treat high blood pressure and other conditions where high sympathetic nerve
activity may produce untoward side effects. It also decreases activity of
neurons in the brain involved with pain pathways so it is also used as an analgesic
(pain reliever).

Back 15

Clonidine

Front 16

________is a modification of metaproterenol with the same clinical indications. It
is longer acting than metaproterenol but also has a higher incidence of cardiac side
effects. It is also used to prevent premature child birth.

Back 16

Terbutaline

Front 17

is a drug for treatment of asthma with indications essentially similar to
terbutaline. It is long acting with fewer cardiac effects than terbutaline.

Back 17

Albuterol

Front 18

__________is a long acting β2-adrenoceptor agonist that is commonly used to treat
bronchial asthma.

Back 18

Salmeterol

Front 19

______is a β2-adrenoceptor agonist that is approved for use to relax smooth
muscle of the uterus and to delay premature labor. As with the other “selective” β2
agonists, it must be given with caution because of possible cardiac side
effects. It is sometimes administered first i.v. to see if it is effective, and then
by the I.M. and oral routes. Although it is only about 30% absorbed orally, this is the
preferred route of administration.

Back 19

Ritodrine

Front 20

________is a synthetic catecholamine analog of dopamine that is a highly selective β1-adrenoceptor stimulant (does not stimulate dopamine receptors!). It increases cardiac output without the vasoconstriction associated with NE that would result in increased cardiac work. It is used for short-term treatment of cardiac insufficiency (e.g. organic heart disease or cardiac surgery).

Back 20

Dobutamine

Front 21

__________ is classified as a local anesthetic agent that also is a potent inhibitor of NE reuptake I. Its major implication in medicine is in the area of drug abuse and will be discussed in that section.

Back 21

cocaine

Front 22

_____________________are also potent inhibitors of catecholamine reuptake into
adrenergic nerve terminals. These drugs are used for their CNS effects in treating
pathological depression.

Back 22

Tricyclic antidepressants

Front 23

Drugs that block adrenergic receptors will produce effects that depend on the normal
neural control of the organs affected. α-Adrenoceptor blockade will be manifest as a reduction of _________

Back 23

systemic blood pressure.

Front 24

Troublesome side effects of ADRENERGIC RECEPTOR ANTAGONISTS would include postural hypotension, reflex tachycardia, nasal congestion, and failure of ejaculation. Side effects limit the therapeutic usefulness of general α-adrenoceptor blockade. β1-adrenergic blockade will mainly affect innervation to the ________ and _______

Back 24

heart and sympathetic control of renin release from the JG apparatus of the kidney.

Front 25

Drugs that occupy and consequently prevent the action of _________ are known as α-adrenoceptor blockers. Agents with preference for specific subtypes of α- adrenoceptors also are available, but virtually all of those considered for use in clinical medicine are either nonspecific or have a higher affinity for _______

Back 25

NE on α-adrenoceptors

α1-adrenoceptors.

Front 26

________ is a selective α1-adrenoceptor antagonist that does not produce the large reflex tachycardia seen with other α-adrenoceptor antagonists. For this reason,
it is useful for treating some hypertensive patients. The other untoward actions
of α adrenergic blockade persist. In addition, some patients respond with an extreme
hypotensive effect and loss of consciousness when it is first administered. To
avoid this “first dose” effect, initially less drug should be slowly administered.

Back 26

Prazosin

Front 27

______ and _______are prazosin-like drugs with a longer half-life which permits
once-per-day dosing. These drugs are commonly used to treat the symptoms of benign
prostatic hypertrophy.

Back 27

Terazosin and Doxazosin

Front 28

_________ blocks both β1-and β2-adrenoceptors, thus we classify it as being nonselective. It was initially used to treat cardiac arrhythmias, being effective not only due to its β blocking properties, but also because it is a potent local anesthetic (almost as potent as lidocaine). It was through clinical observations that it was noted to also be an effective antihypertensive drug. The mechanism by which β-adrenoceptor antagonists lower blood pressure remains unknown.

Back 28

Propranolol

Front 29

_________is primarily a β1-adrenoceptor antagonist with a higher affinity for β1- vs β2-
adrenoceptors, thus is referred to as “cardioselective”. It reduces plasma renin (β1) but
has less metabolic and bronchial effects.

Back 29

Metoprolol

Front 30

_________, like metoprolol, it is a cardioselective β1-adrenoceptor antagonist. However, it has a longer half-life and can be administered less frequently. It also produces less CNS side effects than seen with metoprolol. It is excreted primarily by the kidney so should not be administered to patients with severe renal disease.

Back 30

Atenolol

Front 31

________also is cardio-selective (β1-adrenoceptors blockade) with a very short half-life
when given intravenously (10-15 min). The ultrashort half-life is due to rapid hydrolysis
by cytosolic red blood cell esterases. It is used for acute emergency control of
ventricular heart rate in patients with atrial fibrillation or atrial flutter (particularly those
arrhythmias resulting from intraoperative anesthesia). Due to the short half-life, it
may be safer to use and more readily controlled in critically ill patients.

Back 31

Esmolol

Front 32

_______ was introduced for clinical use as a compound having both α and β blocking
properties. It is a nonselective β antagonist and an α1 selective blocker. It
appears to be an effective antihypertensive agent that decreases total peripheral
resistance with little reflex effect on heart rate or cardiac output.

Back 32

Labetalol

Front 33

___________ has actions similar to labetalol and, in addition is a “free radical scavenger” and consequently may protect the heart cells from damage. Because of this combined action, this drug is approved for use in treating certain patients with congestive heart failure.

Back 33

Carvedilol

Front 34

All neurons in the peripheral or central nervous system that releases acetylcholine (ACh) are referred to as _________

Back 34

cholinergic.

Front 35

Many organs (particularly smooth muscle of blood vessels) also have non-innervated
receptors for ACh on them. Non-innervated ACh receptors are generally of the
___________ type

Back 35

Muscarinic

Front 36

Thus, muscarinic stimulants will ___(do what to the body) when injected even though parasympathetic nerve stimulation cannot do this.

Back 36

lower blood pressure

Front 37

Drugs that increase cholinergic function can do this by what 2 methods

Back 37

either directly by stimulating cholinergic receptors (e.g., nicotinic or muscarinic stimulants)
indirectly by increasing the effectiveness of endogenous ACh (e.g., anticholinesterase drugs).

Front 38

________blocks the transport of choline and consequently will
eventually cause an inhibition of cholinergic function.

Back 38

Hemicholinium (HC-3)

Front 39

______prevents the release of ACh from the nerve terminal. Black widow
spider venom (latrotoxin) causes excessive fusing of the granules with the nerve
membrane that leads to excessive release and eventual depletion of the transmitter.

Back 39

Botulinum toxin

Front 40

M2
receptors are found in the _____ .

Back 40

heart

Front 41

M1 receptors are found in the

Back 41

GI tract and autonomic ganglia

Front 42

M2 - M5 receptors are found in the ______

Back 42

CNS

Front 43

Heart rate is slowed by stimulation of muscarinic receptors on atrial pacemaker cells. This is due to an increase in _____ permeability that causes a prolongation of phase 4 depolarization. _______ receptors produce little direct effect on force of ventricular contraction.

Back 43

K+
Muscarinic

Front 44

Although most blood vessels are not innervated by
cholingergicnerves, systemic administration of ACh and other muscarinic stimulants
produces a profound ________ and _____________. It is believed that ACh acts of non-innervated muscarinic receptors on endothelial cells of blood vessels
that, in turn, release an____________ to cause relaxation of the blood vessel smooth muscle.

Back 44

vasodilation and decrease of blood pressure
endothelium derived relaxing factor (EDRF)
(side note :EDRF is nitric oxide (NO).

Front 45

The eye is innervated by ____________nerves to the sphincter muscle of the
iris and to the ciliary body controlling shape of the lens. __________ agonists thus
produce pupillary constriction (miosis) and spasm of accommodation (cyclotonia).

Back 45

parasympathetic
Muscarinic

Front 46

__________ agonists increase tone and motility of the GI tract
from the lower esophagus to the rectum; only the smooth muscles of some sphincters
appear to relax (the lower esophageal sphincter is stimulated). Bladder motility is
similarly activated by __________receptors (especially the detrusor muscle) although the bladder sphincters relax.

Back 46

Muscarinic
Muscarinic

Front 47

Bronchiolar smooth muscle: Only a modest constriction is produced by ________ agonists in man. In asthmatic patients and in some experimental animals this effect is much greater.

Back 47

Muscarinic

Front 48

Secretory glands: Sweat glands are innervated by ______nerves that
paradoxically release _______(sympathetic-cholinergic system). Thus, _______receptor stimulation causes sweating. Lacrimal, salivary, bronchial and intestinal glands all possess __________receptors that augment secretion.

Back 48

sympathetic
ACh
muscarinic
muscarinic

Front 49

NMJ: All somatic nerves release _____, which activates ________-receptors at
the neuromuscular junction on the motor endplate of skeletal muscle.

Back 49

ACh
Nicotinic

Front 50

Autonomic ganglia: sympathetic and parasympathetic post-ganglionic neurons are stimulated by _______acting on________ receptors.

Back 50

ACh
Nicotinic

Front 51

Adrenal medulla: The synapse between the preganglionic sympathetic splanchnic nerve and chromaffin cells of adrenal gland is analogous to the ganglionic synapse. ACh produces release of __________ and ___________ by excitation of nicotinic receptors.

Back 51

epinephrine and norepinephrine

Front 52

CNS: Some cholinergic synapses in the brain and many in the spinal cord are ______

Back 52

nicotinic.

Front 53

This drug must be injected to have an effect. Intravenous administration will
produce a short-term stimulation of all cholinergic receptors in the body (even by this
route it will not enter the brain as it is highly charged). Because of its short duration of
action (broken down by cholinesterase) and lack of receptor specificity, it is
not used as a therapeutic agent.

Back 53

Acetylcholine

Front 54

________is the only one of the choline esters that has a well established clinical
utility. It has both the CH3 and NH2 substitutions as seen in both methacholine and
carbachol. This agent is refractory to AChase inactivation and has mostly muscarinic
stimulating effects. It is useful in treating post-operative urinary retention and atony of
the GI tract.

Back 54

Bethanechol

Front 55

In its pure form, it is an odorless, colorless liquid (turning brown when oxidized). The responses tothis drugs injection would include activation of all autonomic ganglia (including the adrenal medulla) and stimulation of the skeletal muscle endplate nicotinic receptors. If you know the predominant tone to the individual autonomic organs, you can then predict what the response to this drug would be in both the stimulating and blocking modes.

Back 55

Nicotine

Front 56

is derived from a certain type of mushroom and is responsible for one type (rapid onset type) of mushroom poisoning. ______ is a specific antidote and, if used, the prognosis is good. Alkaloids from different mushrooms produce poisoning (delayed onset type) by other mechanisms with a much poorer prognosis. This will stimulate all muscarinic receptors whether innervated or noninnervated

Back 56

Muscarine

Atropine

Front 57

Does muscarine stimulate innervated or non-innervated receptors

Back 57

both

Front 58

_______was originally isolated from a South American shrub and, like methacholine
and muscarine, it selectively activates muscarinic receptors. It is
not so highly charged (being a tertiary amine) and thus more
readily crosses membrane barriers. It is used to treat
glaucoma. Outflow of aqueous humor from the eye is enhanced
due to constriction of the iris sphincter muscle and the ciliary
body behind the iris. These events mechanically widen the
angle between the cornea and iris where aqueous outflow takes
place.

Back 58

Pilocarpine

Front 59

_______was originally isolated from the Calabar bean. Like ACh, it binds to
both the anionic and esteratic sites on the enzyme. It is not
highly charged (e.g. tertiary amine) and thus can readily enter
the CNS. It has little activity other than its action to
inhibit AChase.
Its main clinical use is topical for the treatment of glaucoma (like pilocarpine it produces
miosis and contraction of the ciliary muscle) due to increasing ACh concentrations at
synapses in the eye. Due to accessibility to both peripheral and central neurons,
it is the most rational agent of this type for the treatment of atropine
poisoning.

Back 59

Physostigmine

Front 60

______is one of several additional drugs available to treat myasthenia gravis.They are potent reversible anti-ACHASE compound. As treatment of this disease is along-term process, some patients develop tolerance or allergies to specific drugs. Other agents may be better tolerated.

Back 60

Pyridostigmine

Front 61

_________has a short duration of action as it binds tightly to only one of the enzyme sites (anionic site). Administration inhibits ACHASE only for minutes and thus it is valuable for the diagnosis of myasthenia gravis . During treatment with anticholinesterase drugs, patient may also exhibit skeletal muscle weakness that could be due to either too much ACHASE inhibition (cholinergic crisis) or insufficient ACHASE inhibition (myasthenic crisis). Due to its short action, it is beneficial in titration of the effective dose levels of longer acting anticholinesterase agents

Back 61

Edrophonium

Front 62

________is a CNS acting anticholinesterase drugs used to treat cognitive dysfunction
seen in patients with Alzheimer’s disease.

Back 62

Donepezil

Front 63

is a common insecticide used in agriculture. The drug itself is not an anti AChase compound but is converted by liver to the active agent paraoxon

Back 63

Parathion

Front 64

Muscarinic blocking drugs: ________and related compounds are very effective
competitive antagonists at all muscarinic cholinergic receptors. Agents of this class
have an important therapeutic role in ________, ________, and _________.

Back 64

Atropine

anesthesia, ophthalmology, and cardiology.

Front 65

Toxicological considerations of muscarinic blocking drugs are also important. ___________drugs with CNS selectivity are used in treating Parkinson’s disease. Muscarinic receptor antagonism will cause lack of motility and secretions of all __________innervated organs.

Back 65

Antimuscarinic
Parasympathetic

Front 66

__________is readily absorbed following oral administration. It is an alkaloid originally
derived from such plants as the deadly nightshade and has an
interesting history as a poison. It differs from scopolamine
in that it produces CNS excitation whereas scopolamine is a CNS
depressant

Back 66

Atropine

Front 67

______is very toxic to children who do not appear to be able to tolerate even very
small doses. _____ poisoning is characterized by hot dry skin; dilated pupils and
maniacal behavior (red as a beet…hot as a pistol…dry as a bone… and mad as a
hatter). Hat makers in early days were exposed to toxic levels of mercury used to press
felt! One pharmacological treatment for this drugs poisoning is to give an
anticholinesterase compound.

Back 67

Atropine
Atropine

Front 68

_________is an atropine like alkaloid that has a shorter duration of action and is
readily absorbed through the skin. It is mainly used to prevent motion sickness.

Back 68

Scopolamine

Front 69

________is one example of a less potent and much shorter acting muscarinic antagonist. Drugs of this type are more useful for general ophthalmological exams as atropine and scopolamine have a very prolonged effect

Back 69

Tropicamide

Front 70

___________is a synthetic muscarinic antagonist that is a quaternary amine and thus has fewer systemic (especially CNS) side effects. The drug is typically applied topically
to the airway by means of a metered inhaler. Its primary use is in patients with chronic obstructive pulmonary disease (COPD) by producing bronchodilation without reduction of volume or increase of viscosity of bronchial secretions (as is seen with atropine). It is a second line drug for treatment of bronchial asthma but appears to be
beneficial when combined with other bronchodilators.

Back 70

Ipratropium

Front 71

_____________is a CNS acting antimuscarinic drug that is used to relieve symptoms of Parkinson’s disease

Back 71

Benztropine

Front 72

_____________is an atropine-like agent that is often used to treat spasms of the bladder seen after urologic surgery and in some neurological disorders producing bladder hyperactivity. It can be administered either orally or topically (via catheter) to decrease tone of bladder smooth muscle and thus improve continence.

Back 72

Oxybutynin

Front 73

___________is the prototype ganglionic blocking drug. Presently, its only use is as an experimental tool. C6 blocks all autonomic ganglia but, does not compete with ACh at the nicotinic receptors found on the endplate region of skeletal muscle.

Back 73

Hexamethonium (C6)

Front 74

These are clinical indications for what drugs?

Paralytic ileus
Atony of bladder
Glaucoma
Nicotine addiction
Myasthenia gravis
Toxicological considerations
Dementia

Back 74

CHOLINOMIMETICS

Front 75

These are clinical indications for what drugs?


Ophthalmologic exam
Bladder hyperactivity
Cardiac effects
Bronchodilator
Motion sickness
Parkinsonism
Toxicological considerations

Back 75

CHOLINERGIC ANTAGONISTS

Front 76

These are clinical indications for what drugs?

Hemostasis
Nasal decongestion
Use with local anesthetics
Hyper- and hypotension
Cardiac stimulation
Bronchodilation
Allergic reaction
Appetite control
Narcolepsy
Behavioral disorders
Uterine motility
Opioid withdrawal

Back 76

SYMPATHOMIMETICS

Front 77

These are clinical indications for what drugs?

Hypertension
Glaucoma
Angina
Post-infarction prophylaxis
Congestive heart failure
Migraine
Stage fright
Cardiac arrhythmias
Essential tremor
Pheochromocytoma
Benign prostatic hypertrophy
Hyperthyroidism

Back 77

ADRENERGIC BLOCKERS

Front 78

there is more calcium inside or outside the cell

Back 78

outside

Front 79

there is more chloride inside or outside the cell

Back 79

outside

Front 80

potasium leaks out of the cell(faster or slower) than sodium leaks in

Back 80

faster

Front 81

there is more potasium inside or outside the cell

Back 81

inside

Front 82

there is more sodium inside or outside the cell

Back 82

outside

Front 83

transmitter receptor interaction number 1 involves

Back 83

drug goes thru the membrane to the transmitter

Front 84

transmitter receptor interaction number 2 involves

Back 84

drug interacts with the transmitter on the cell membrane

Front 85

transmitter receptor interaction number 3 involves

Back 85

drug interacts with the membrane bound receptor that opens up a pore

Front 86

transmitter receptor interaction number 4 involves

Back 86

drug interacts with a memnbrane bound receptor that activates GDT in GPT and amplifies the signal

Front 87

2 types of cholinergic drugs

Back 87

nicotinic and muscarninc

Front 88

two types of adrenergic drugs

Back 88

alpha receptor and beta receptor