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House Pharmacology > Muscarinic And Nicotinic Blockers > Flashcards

Muscarinic And Nicotinic Blockers Flashcards

1
Q

The efferent (motor) division of the PNS is sub-divided into ______ Nervous System and the ______ Nervous System.

A

Somatic

Autonomic

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2
Q

The somatic nervous system innervates the ______ muscles.
The ANS supplies motor impulses to ____ muscle, _____ muscles and to the glandular epithelium.

A

skeletal

cardiac; smooth

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3
Q

The ANS is divided into ______ and ______ systems.

A

sympathetic and the parasympathetic

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4
Q

Autonomic efferent pathway uses ___ neurons arranged in ___ to integrate CNS to the peripheral organs.
Somatic efferent pathway, however, uses _____ neuron for the integration of CNS to the skeletal muscles

A

two; series

a single

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5
Q

Cholinergic Transmission: Site Differences

Skeletal Muscle

Neurotransmitter:_______
Receptor type: _______

A

Acetylcholine

Nicotinic

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6
Q

Cholinergic Transmission: Site Differences

Autonomic Effectors
š š š
Neurotransmitter: _______
Receptor type:_________

effector coupled to receptor by _______

A

Acetylcholine

Muscarinic

a G protein

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7
Q

Cholinergic Transmission: Site Differences

Autonomic Ganglia

Neurotransmitter: ______
Receptor type: _____

A

Acetylcholine

Nicotinic

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8
Q

Nicotinic Receptor Agonists

These are drugs that mimic the action of acetylcholine at __________ receptor sites.

Examples include: ???

A

nicotinic acetylcholine

nicotine, acetylcholine, choline, epibatidine, lobeline, varenicline and cytisine

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9
Q

Ganglion stimulants

These are drugs which stimulate the ___ receptors in ___________ ganglia.

A

nicotinic

both sympathetic and parasympathetic

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10
Q

Ganglion stimulants

The dominant receptors are the _________.

In addition, there are subsidiary ___________________________________ receptors

A

nicotinic NN

M1, M2, adrenergic, dopaminergic, aminergic and peptidergic

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11
Q

autonomic ganglion is a one transmitter – one cell junction system

T/F

A

F

autonomic ganglion is not merely a one transmitter – one cell junction, but a complex system

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12
Q

therapeutic application of ganglion stimulants??

A

There is no therapeutic application of ganglion stimulants , as no useful purpose could be served by stimulating both sympathetic and parasympathetic ganglia concurrently.

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13
Q

Ganglion stimulants

Nicotine is available as ________ for treating nicotine dependence and as an aid to smoking cessation.
It ameliorates the symptoms of _________ but does not completely ______

A

transdermal patches

nicotine withdrawal

suppress craving.

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14
Q

Varenicline:

As a ___________, it reduces both the __________ and ________ of cigarettes and other tobacco products. Through these mechanisms it can assist some patients to quit smoking.

A

partial agonist

craving for and the pleasurable effects

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15
Q

ANTICHOLINERGIC DRUGS

Also known as Cholinergic Antagonists, ___________

A

Parasympatholytics

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16
Q

ANTICHOLINERGIC DRUGS

If via the nicotinic receptors, they are referred to as “______,” and “________.”

A

Ganglion blockers

Neuromuscular blockers

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17
Q

Muscarinic Receptor Subtypes:

M1
Location: ____ neurones , _____

Functions: Improves learning, memory, motor functions
Gastric glands:____ release, ___ secretion
Salivary: ____eased secretion

Clinical Effects: _____ Secretion
Clinically Selective Anticholinergic Drugs:

____,_____,____,______

A

CNS; Stomach

histamine; acid ; incr

Hydrogen Ion

Pirenzepine, Telenzepine, Dicyclomine, trihexyphenidyl

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18
Q

M1 is It is primarily a _____ receptor

A

neuronal

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19
Q

M2:

Location: ____,_____
- Functions: SA node: ____polarization, (enhanced or reduced?) rate of impulse generation
- AV node: (enhanced or reduced?) conduction velocity
- Atrium: (shortening or lengthening ?) of APD, (enhanced or reduced?) contractility
- Ventricle: (enhance or reduced?) contractility
- Presynaptic terminals/Cholinergic nerve endings of peripheral and central neurones : reduced ACh release
- CNS: tremor, analgesia

A

Heart, CNS

hyper ; Reduced; reduced

Shortening; Reduced

Reduced

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20
Q

M2 receptor exert (excitatory or inhibitory?) effects, mainly by increasing ___ conductance and by (stimulating or inhibiting?) _____ channels. Thus, its activation is responsible for the vagal ____ of the heart, as well as presynaptic ______ in the CNS and periphery.

A

inhibitory

K+; inhibiting; calcium

inhibition

inhibition

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21
Q

M2:

Clinical Effects: ______
Clinically Selective Anticholinergic Drugs: _______,_________

A

Bradycardia

Tripitamine, Methoctramine

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22
Q

M3:
Effects mainly (excitatory or inhibitory?) , except on the ______ muscle, where its activity is mediated through the release of ___, to produce vaso______.

A

excitatory; vascular smooth; NO

dilatation

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23
Q

M3:

  • Location : ______,_____,_______,_____

Clinical Effects
CNS - Visceral smooth muscle (contraction or relaxation?)
- Iris (pupillary (constriction or dilatation?)

A

Smooth muscles, endocrine glands, lungs, pancreas

Contraction

Constriction

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24
Q

M3

Clinical effects

-Ciliary muscle (contraction or relaxation)
- Exocrine glands (______)
- Vascular endothelium (release of ___ to produce vaso____)

Clinically Selective Anticholinergic Drugs:

Mention 4

A

Contraction

Secretion

NO; dilatation

Darifenacin, Solifenacin, oxybutynin, tolterodine.

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25
Q

M4:
They function as (inhibitory or excitatiry?) autoreceptors for ACh.
When activated M4 receptors (inhibit or stimulate ?) ACh release in the striatum. Antagonist:_______

A

inhibitory

Inhibit

Himbacine

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26
Q

Atropine

Is sufficiently lipid (soluble or insoluble?)

A

Soluble

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27
Q

Atropine -from _______(_____)

Hyoscine- from ________-(_____).

Both are ______\ compds

A

Atropa belladonna

deadly nightshade

Datura stramonium

thorn apple

tertiary ammonium

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28
Q

Atropine

readily penetrate the BBB.

T/F

A

T

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29
Q

Semi-synthetic derivatives: Homatropine, Atropine methonitrate, Tiotropium, Ipratropium (quaternary amine) and Hyoscine butyl bromide
Synthetic: Cyclopentolate, Propantheline, Oxyphenonium, Glycopyrolate, Dicyclomine, Valethamate, Pirenzepine and Tropicamide (quaternary amine

A

Lmao

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30
Q

Atropine (prototype)

Effect on heart rate: causes ______, but in low doses it causes a _______, which results from a central action, increasing vagal activity.

Eye: Pupillary dilatation (mydriasis), which makes the eye _______. Relaxation of ______ causes paralysis of accommodation (cyclopegia), as a result, ___ vision is impaired.

A

tachycardia; paradoxical bradycardia

unresponsive to light

ciliary muscle

near

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31
Q

Effects of atropine

GIT: (enhanced or Reduced ?) motility

Other smooth muscles: ______,____, and _______ tract are all relaxed by atropine

A

Reduced

Bronchial, biliary and urinary

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32
Q

Effects of atropine

CNS: Atropine produces mainly (inhibitory or excitatory?) effects.

Low doses cause _______, higher doses cause ________

These central effects could be opposed by _________ drugs

A

Excitatory

mild restlessness

agitation and disorientation.

anticholinesterase

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33
Q

__________ is an effective antidote to atropine poisoning

A

Physostigmine

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34
Q

Hyoscine (low dose) causes marked ____ but is similar to ______ in high dosage.

A

sedation

atropine

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35
Q

Hyoscine also useful as an _____ and used in _____ sickness.

A

antiemetic

motion

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36
Q

Atropine-like drugs affect ________ system, reducing _______ movement and ______ in Parkinson’s disease.

Body temperature: (Increase or decrease)

Local anaesthestic: Atropine produces a mild anaesthetic action on the ___

A

extrapyramidal

involuntary

rigidity

Increase

cornea

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37
Q

Pharmacokinetics of atropine

Absorption: is (slow or rapid?) after ____ and local admn of the tertiary amines.

Systemic absorption of inhaled quaternary dugs is _____

Elimination: Atropine (__% is metabolised in the liver and the remaining ————-

Half-life: approx. __

A

Rapid; oral

Minimal

50

excreted unchanged in the urine.

4h

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38
Q

Between hyoscine and atropine , which penetrates the BBB better and which is more completely metabolized?

A

Hyoscine is more completely metabolized and penetrates the BBB better.

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39
Q

Summary of AntiCholinergic Effects

In the CNS- list 5

In the eye- list 3

In the heart- at low and high dose

In the bronchioles- list 2

A

Sedation, hallucination, drowsiness, antiparkinsonism, amnesia

Mydriasis, cyclopegia, lacrimal glands become dry and sandy

Initial bradycardia at low doses then tachycardia

Bronchodilation, decrease in bronchial secretions

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40
Q

Summary of AntiCholinergic Effects

In the GIT- tone, motility, emptying time

Urinary tract- tone, emptying

A

Relaxation, decrease motility, antidiarrheal, prolongs gastric emptying time

Relaxation of the bladder wall, urinary retention

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41
Q

Summary of AntiCholinergic Effects

Glands

Skeletal muscles

A

Decrease secretion, salivation, lacrimation, sweating

None

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42
Q

Anticholinergic Toxicity

Symptoms Mnemonic

-____ as a hare ( ______ )
-____ as a bone (___)

  • ____ as a beet (____)
  • ____ as a bat (____)
  • ____ as a hatter (______)
A

Hot; Hyperthemia
Dry; dry skin
Red; flushed
Blind; mydriasis
Mad; delirium

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43
Q

Management of anticholinergic Toxicity

1) Control hyperthemia using _______

  1. Agitation may require
    -____________
    -________(Benzodiazepines)
  2. If ingested, ____
  3. Antidote: ________ (1-3 mg s.c or i.v arrests both central and peripheral effects)
A

cold sponging or ice bags

physical restraints
- chemical restraints

gastric lavage

Physostigmine

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44
Q

Why physostigmine as antidote and not Neostigmine

A

Neostigmine is ineffective for central effects

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45
Q

Clinical uses of Anticholinergic drugs

As Antispasmodic:

Useful for intestinal and renal colic, ____

For _______ diarrhoea, but not _____ diarrhoea

Spastic constipation, _______ syndrome

Urinary frequency and urgency, ______ in children

_________

A

abdominal cramps

nervous and drug-induced ; infective

irritable bowel

enuresis

Dysmenorrhoea

46
Q

Clinical uses of Anticholinergic drugs

Bronchial asthma, Chronic Obstructive Pulmonary Disease (COPD):
- They produce broncho_____ and dry up _______ in the respiratory tract

A

dilatation

excessive secretions

47
Q

Clinical uses of Anticholinergic drugs

As Antisecretory:
- as _______ medication, especially when irritant general anaethetics (ether) are used to check increase salivary and bronchial secretions.
- in ________, they decrease gastric secretion. Histamine H2 receptor antagonists are however preferred.
- to check excessive sweating and salivation in _______
- in ________, they reduce reflex secretions

A

pre-anaesthetic
Peptic ulcer

Parkinsonism

pulmonary embolism

48
Q

Clinical uses of Anticholinergic drugs

Mydriatic and Cyclopegic:

  • For _____: since in testing error of refraction, both mydriasis and cyclopegia are needed

For Therapy: used for ____,______,____,_____

A

Diagnosis

Iritis, choroiditis, keratitis and corneal ulcer

49
Q

Clinical uses of Anticholinergic drugs

As cardiac Vagolytic: it counteracts _______ and ________ where increased vagal tone is responsible

A

bradycardia and partial heart block

50
Q

Clinical uses of Anticholinergic drugs

For Central Action:

Motion Sickness: _____ is most effective. Drug should be administered ______.

A

Hyoscine

prophylactically

51
Q

In Parkinsonism: which is more useful, Anticholinergic drugs or L-DOPA

A

L-DOPA

Anticholinergic drugs are Less effective than L-Dopa, only useful in mild cases

52
Q

Hyoscine is used to produce _____ and ______ during labour and in maniacal states.

A

sedation and amnesia

53
Q

Clinical uses of Anticholinergic drugs

To antagonize muscarinic effects of drugs and poisons: _______ is the specific antidote for Anti ChE and early mushroom poisoning.

A

Atropine

54
Q

_______ interfere with absorption of anticholinergics

A

Antacids

55
Q

Antinicotinic Drugs

Antinicotinic drugs sub-divided as:
-________ e.g. Hexamethonium, Trimethaphan, Mecamylamine
-___________ e.g. Suxamethonium, Decamethonium, Tubocurarine, Atracurium,

A

Ganglion blockers

Neuromuscular blockers

56
Q

Ganglion blockers

All ganglion-blocking drugs of interest are (synthetic or semi synthetic ?) amines.

A

Synthetic

57
Q

__________, the first to be recognized as being a ganglion blocker, has a very (short or long ? duration of action.

A

Tetraethylammonium (TEA)

Short

58
Q

Effect of ganglion blockers on veins

-Vaso_____
-_____ of blood
- ____eased venous return

A

Dilation

Pooling

Decr

59
Q

Effect of ganglion blockers on Arterioles

-Vaso_____
-_____eased peripheral blood flow
-____tension

A

Vasodilation

Incr

Hypo

60
Q

Why are ganglion blockers not frequently used??

A

Ganglion blockers are not too frequently used because more selective autonomic blocking agents are available.

61
Q

Clinical Applications:

__________ blocks central nicotinic receptors and has been advocated as a possible adjunct with the transdermal nicotine patch to reduce nicotine craving in patients attempting to quit smoking.

A

Mecamylamine

62
Q

_______ is occasionally used in the treatment of hypertensive emergencies.

And is a ____ blocker

A

Trimethaphan

Ganglionic

63
Q

Neuromuscular Blockers

They block neuromuscular transmission at the ______, causing ____ of the affected skeletal muscles.

A

neuromuscular junction

paralysis

64
Q

Neuromuscular Blockers

This action is accomplished either by acting presynaptically via ____________(e.g. _______ and _____); or by acting postsynaptically at the _____________(NMJ blocking agents).

A

inhibition of ACh synthesis or release

botulinum toxin and tetanus toxin

Ach receptors of the motor end-plate

65
Q

Two different kinds of functional blockade may occur at the neuromuscular end plate, therefore clinically used drugs fall into two categories:

________ Blocking Agents

________ blocking agents .

A

Non-Depolarizing

Depolarizing

66
Q

Non-Depolarizing Blocking Agents: Act by (competitively or non-competitively?) blocking ACh at NM receptor

Blockade could be reversed through administration of ________

A

competitively

cholinesterase inhibitor.

67
Q

Depolarizing ( _________ Blockers): agonists at NM receptors.

They act by _________ the receptors
-_________ (Suxamethonium)
- __________

A

Non-Competitive

over-stimulating

Succinylcholine; Decamethonium

68
Q

Depolarizing agonists at NM receptors.

Initial stimulation is accompanied by ______ of skeletal muscle (______)

With continued agonist effect, _______ cannot be maintained, and therefore, the continuous depolarization results in a ___________(____) .

Muscles are ____ and have _____ tone.

A

initial twitching; fasciculations

skeletal muscle tone

functional muscle paralysis (flaccid paralysis)

weak; little or no

69
Q

Depolarizing agonists at NM receptors.

Prototype is ______ (ultra-___ acting). Must be given by continuous i.v. infusion if prolonged paralysis is required.

A

succinylcholine

Short

70
Q

NEOSTIGMINE or any cholinergic agent can be used TO REVERSE DEPOLARIZING BLOCK

T/F

With reason

A

F

DO NOT USE NEOSTIGMINE (or any cholinergic agent) TO REVERSE DEPOLARIZING BLOCK. It will make it worse, one, since adding acetylcholine will only help contribute to depolarization, and two, because neostigmine also binds to and blocks the action of pseudocholinesterase, which is needed to break down SCh.

71
Q

____ is the only truly safe reversal agent for succinylcholine.

A

Time

72
Q

Actions of neuromuscular blockers
1. Skeletal muscle –

Intravenous injection of non-depolarizing blockers rapidly produces muscle _____ followed by ___ paralysis.

_________ muscles (fingers, extraocular) are affected first; paralysis spreads to hands, feet, arm, leg, neck, face, trunk, intercostal muscle then _____, and _____ stops.
Recovery occurs in the _____ sequence.

A

weakness; flaccid

Small fast response

diaphragm
Respiration

reverse

73
Q

Actions of neuromuscular blockers
1. Skeletal muscle

Depolarizing blockers produce initial _____ a few seconds before inducing ____.

____ occurs within 45-90 sec, but lasts only 2-5 min; recovery is (slow or rapid?) .

A

fasciculation

paralysis

Apnoea

rapid

74
Q

Actions of neuromuscular blockers

Autonomic ganglia – the cholinergic receptors in autonomic ganglia being nicotinic, ________ NMJ blockers (especially the [newer or older?] drugs, d-TC) produce some degree of ganglionic blockade.

A

competitive; older

75
Q

Actions of neuromuscular blockers

Histamine release –____ releases histamine from mast cells, which produces ___tension, broncho___, ___eased respiratory secretions and ____.

_____ may also be simultaneously released from mast cells.

A

dTC
Hypo; spasm; incr; flushing

Heparin

76
Q

Actions of neuromuscular blockers

CVS – dTC produces significant (rise or fall?) in BP, due to
i._______
ii. _____ release
iii. ( Enhanced or Reduced?) venous return, resulting from paralysis of limb and respiratory muscles. Heart rate may ___ease, due to vagal ganglionic blockade.

A

Fall

ganglionic blockade
Histamine

Reduced
Incr

77
Q

All newer non-depolarizing drugs have negligible effects on BP and HR.

T/F

A

T

78
Q

Actions of neuromuscular blockers

GIT – The ganglion blocking activity of competitive blockers may enhance ______ after abdominal operations.

CNS – All NMJ blockers are _______ compounds, and ( do or do not?) cross the BBB. However, dTC when injected in the cerebral ventricles or when applied to the brain cortex, produces ______- like effect.

A

paralytic ileus

quaternary

Do not

strychnine

79
Q

NM BLOCKERS

mode of administration
Ability to cross cell membrane
Volumes of distribution
BBB

A

IV or IM
can’t
Low
Can’t penetrate

80
Q

When given NM blockers, which gets affected first?

Muscles with high or low blood supply

A

High

81
Q

NM blockers’ effect on drugs metabolized by the liver and drugs excreted by the kidney

A

Increases the half life of those excreted by the kidney

Shortens the half life of those metabolized by the liver

82
Q

Succinylcholine is rapidly _____ by plasma _______ to ______ and then to __________

A

hydrolysed

pseudocholinesterase

succinyl monocholine

succinic acid and choline

83
Q

Pseudocholinesterase deficient patients suffer from _____ and ______ lasting for _____

A

muscle paralysis and apnoea

Hours

84
Q

The main difference between the two classes of NMJ blockers is in the ________

A

reversal of blockade.

85
Q

Non-depolarizing blockers are reversed by _______ drugs, since they are _______ antagonists of ACh.

A

acetylcholinesterase inhibitor

competitive

86
Q

_______ NM blockers cause the tetanic fade

A

non depolarizing

87
Q

Phase I Block

Perijunctional ____-Channel cannot reopen until the end plate ______ which cannot happen as long as the __________

A

Na

repolarizes

depolarizing muscle relaxant continues to bind to ACh receptors.

88
Q

Phase II Block:
After a period of time, prolonged end-plate depolarization can cause (well or poorly?) understood changes in the ________ that result in a Phase II block.

A

Poorly

ACh receptor

89
Q

Tetanic Fade refers to the diminishing ______ response under the effect of either a ________ agent, or a muscle that is under a _____________ agent.

A

muscle twitch

non- depolarizing neuromuscular blocking

phase II depolarizing neuromuscular blocking

90
Q

Neuromuscular Junction Disease:

Autoimmune disorders, in the case of neuromuscular diseases, tend to be ____ mediated, __ cell mediated, and result in an antibody improperly created against a motor neuron or muscle fiber protein that interferes with synaptic transmission or signalling.

A

humoral; B

91
Q

Myasthenia gravis

-comes from the Greek and Latin words meaning “_________________.”

The most common form of MG is a (acute or chronic?) autoimmune neuromuscular disorder that is characterized by _________ of the (voluntary or involuntary ?) muscle groups.

A

grave muscular weakness

Chronic; fluctuating weakness

Voluntary

92
Q

Myasthenia gravis occurs in all races

MG occurs in only females

MG occurs only at adulthood

MG is not thought to be directly inherited nor is it contagious.

MG does occasionally occur in more than one member of the same family.

T/F

A

T

F(both genders)

F(any age)

T
T

93
Q

In myasthenia gravis, the immune system produces ____ that block or destroy many of the individual’s muscles’ ______ for the neurotransmitter called _____.

A

antibodies; receptor sites

acetylcholine

94
Q

Myasthenia gravis

This waxing-and-waning weakness of muscles, worsening with use and improving with rest, is a hallmark of this particular disease. There typically are periods when you may notice more symptoms ( _________), interspersed with periods when symptoms decrease or disappear ( _______ ).

A

called an exacerbation

remission

95
Q

MG

The disease most commonly affects muscles that control ____ and _____ movement, so the first symptoms you notice may be ______ and/or ______ or ______.

The majority will go on to develop weakness in other muscle groups within _________

A

eye and eyelid

eyelid drooping

blurred or doubled vision

one or two years.

96
Q

_________ is also known as a plasma exchange. This process removes ______ from the blood, which may result in an improvement in muscle strength.

It is a (short or long?) -term treatment. The body continues to produce the harmful antibodies and weakness may recur. Plasma exchange is helpful before surgery or during times of extreme MG weakness.

A

Plasmapheresis

harmful antibodies

Short

97
Q

Complications of Myasthenia Gravis

One of the most dangerous potential complications of MG is _______. This consists of life- threatening muscle weakness that can include ______
Individuals with MG are at a higher risk of developing other autoimmune disorders such as _______ and _____

A

myasthenic crisis

breathing problems.

lupus and rheumatoid arthritis.

98
Q

There are two types of medications used to treat MG.
_________: temporarily relieves the symptoms of MG.
___________: attack the disease at its source.

A

Anticholinesterases

Immunosuppressants

99
Q

Anticholinestarases:
These agents include _______,_____,_______

A

pyridostigmine, neostigmine, and edrophonium.

100
Q

Anticholinestarases:

Pyridostigmine is used for ______

Neostigmine is generally used only when _________
Edrophonium is primarily used as a _____ to predict the response to _____-acting cholinesterase inhibitors.

A

maintenance therapy.

pyridostigmine is unavailable.

diagnostic tool

longer

101
Q

_____ significantly relieves MG symptoms for a large majority of myasthenics.

This drug is not as fast acting as ______, but it is faster than other _______, and it is relatively inexpensive. While prednisone can be very effective in treating myasthenia, it carries the risk of serious side effects

A

Prednisone

anticholinesterases

immunosuppressants

102
Q

Monoclonal antibodies.

One of the newer therapies used to treat myasthenia gravis that is resistant to traditional approaches is the ________
This treatment is given as ______ IV infusions repeated every ___ months. A similar __________, also is being investigated.

A

monoclonal antibody rituximab.

four weekly

six

monoclonal antibody, eculizumab

103
Q

Competitive NM blockers

Based on Duration of Action

Long-acting: d-______,______,_____,______

Intermediate-acting: _____,____,_____,______,________

Short-acting: ________

A

Tubocurarine, Pancuronium, Doxacurium, Pipecuronium

Vecuronium, Atracurium, Cisatracurium, Rocuronium, Rapacuronium

Mivacurium

104
Q

Competitive NM blockers

Based on chemical structure
- ____ Compounds: ( _____ properties)

-________ (BZIQ): (____________ )

A

Steroidal; vagolytic

Benzylisoquinoline

histamine realease

105
Q

Competitive NM blockers

Based on chemical structure
- Steroidal Compounds:
It includes ____,_____,———,_____,———-

  • Benzylisoquinoline (BZIQ):
    It includes d- ____,______,_____ ,______,____,______
  • Others: includes _____,_____
A

Pancuronium,Vecuronium, Pipecuronium, Rocuronium, Rapacuronium.

Tubocurarine, Metocurine, Doxacurium, Atracurium, Mivacurium, Cisatracurium

Gallamine, Alcuronium

106
Q

List the quaternary indirect choline agonists

List the tertiary indirect choline agonists

A

Pyrido, neo, edro

Physo, riva, galantamine, donepezil

107
Q

The steroidal NMJ drugs has _______ at the end

benzisoquinolins drugs has _____ at the end

A

curonium

curium

108
Q

________ and _______ were the most potent inducers of CYP2D6 followed by _________ and ______

A

Dexamethasone and corticosterone

prednisolone and cortisol

109
Q

Nicotine is gotten from ______

A

Nicotiana tobacum

110
Q

Hyoscamine is ???

A

Atropine

111
Q

Selective Nicotinic Agonists:
Natural
- ____________
-_____________

Synthetic
-______________
-_____________

A

Nicotine (small doses)
Lobeline

Dimethyl phenyl piperazinium (DMPP)
Tetramethyl ammonium (TMA)

House Pharmacology (50 decks)

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