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Pharmacology > Cholinoreceptor Blocking Agents > Flashcards

Cholinoreceptor Blocking Agents Flashcards

0
Q

PNS Blocking agents: Pharmacokinetics

A 
Absorption and Distribution
   - Rapidly absorbed
   - Crosses BBB
   - Given topically or injected
Metabolism and excretion
   - Eliminated via hepatic metabolism and urinary excretion 
   - 2-3 hour half life
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1
Q

Parasympathetic Blocking agents: Belladonna poisoning

A

Mad as a hatter (delirium)
Red as a beet (vasodilation)
Blind as a bat (can’t accommodate for near vision), mydriasis (maximal pupillary dilation)
Hot as hell (block sweating)

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2
Q

Atropine: mechanism

A

Competitive antagonist of Ach at muscarinic sites

Doesn’t distinguish between different subgroups of muscarinic receptors

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3
Q

Atropine: Action

A

GIT
Glandular secretions decreased
Bronchial smooth muscle and secretory glands
Heart
- Varies with dose and with vagal tone of individual
- Small doses
- May produce an initial temporary bradycardia
Peripheral action causes progressively increasing tachycardia by blocking muscarinic receptors on the SA node pacemaker
Blood vessels
- Most don’t have PNS innervation
- Cholinergic sympathetic vasodilator fibers to blood vessels are blocked
- Blocks generalized vasodilation caused by direct-acting muscarinic agonists
Eye
- Mydriasis (dilation)
- Relaxation of ciliary muscle
- Can precipitate acute glaucoma in patients with narrow anterior chamber angle
- Decreased lacrimal secretions

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4
Q

Atropine: Flush

A

Dilation of cutaneous vessels

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5
Q

Atropine: Adverse effects

A 
Xerostomia (dry mouth)
Blurred vision
Increase IOP
Urinary retention
Constipation
Anhidrosis
Tachycardia
Asthma ( bronchoconstriction)
CNS
"Can't pee, can't see, Can't spit, can't shit"
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6
Q

Atropine: Treatment of overdose

A

Gastric lavage (if oral)
Supportive measures for maintenance of circulation and respiration
Lowering body temperature
Physostigmine
- Once was used (increases Ach)
Diazepam, lorazepam, barbiturates to control CNS excitation

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7
Q

Atropine: Therapeutic Uses

A 
Inhibition of secretions
Preanesthetic med
Bradycardia
Intestinal hypertonicity
Muscarinic agonist poisoning
Peptic ulcer disease
asthma and respiratory disorders
Renal and biliary colic
CNS
   - Parkinsons
   - Motion sickness
Overactive bladder
   - Tolterodine [ Detrol]
       - Offers no advantage over long acting anticholinergics
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8
Q

Scopolamine (cholinergic blocker) (TransdermScop, Inopto-Hyoscine)

A 
Topical 
Motion sickness
Opthomology 
Midwives
   - Produced amnesia
Crosses BBB
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9
Q

Homatropine: USe

A

Opthamology

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10
Q

Ipratropium: USe

A

Respiratory diseases

Inhalers

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11
Q

Ganglionic stimulants and blockers

A

Nicotine

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12
Q

Nicotine (ganglionic stimulant): Mechanism

A

Stimulates ganglion cells by depolarizing the postsynaptic membrane, resulting in stimulation like Ach
Larger doses of nicotine stimulation followed by block of the ganglia
- Nicotine stays on receptors preventing stimulation by Ach
Addictive

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13
Q

Nicotine: Actions

A

NMJ
- Stimulation followed by depression (depolarizing block)
CNS
- Stimulation of CV, Respiratory, and vomiting centers in medulla
- Tremors
- After quitting can have a hard time concentrating sometimes

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14
Q

Nicotine: agents

A

Nicorette
Transdermals
Chantix

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15
Q

Nicotine: Toxicity

A

Depends on age
Fatal dose
- 1 drop of liquid (amount in 2 cigarettes)
- Ingest of nicotine by kids especially vomiting usually, limiting exposure

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16
Q

Ganglionic Blocking agents: Mechanism

A

Competitive inhibition of Ach of autonomic ganglionic sites

17
Q

Ganglionic Blocking Agents: Pharmacokinetic action

A

Can be predicted with knowledge of the autonomic innervation of effector organs

18
Q

Ganglionic Blocking Agents: Adverse Effects

A

orthostatic hypertension, dilation of pupils and blurred vision, dry mouth, urinary
Hesitancy constipation, impotence in males, numerous other side effects

19
Q

Ganglionic Blocking Agents: Agents

A

Trimethaphan
Mecamylamine
Hexamethonium
- First two used in treatment of hypertensive emergencies

20
Q

Agents that Inhibit Cholinergic Transmission: Main drug

A

Botulinum Toxin Type A (Botox)

21
Q

Botulinum Toxin: Mechanism

A

Inhibits release of Ach at the neuromuscular junction and in cholinergic neurons in the ANS

22
Q

Botulinum Toxin: Uses

A

Ophthalmological disorders
Movement disorders
Cosmetic uses
Can cause a decrease in sweating

23
Q

Botox in strabismus

A

Can help straighten out the eyes

24
Q

Neuromuscular blocking agents: Effects

A

Control of muscle contraction

Interfere with transmission at the neuromuscular end plate causing paralysis

25
Q

Classification of neuromuscular blockers

A

Nondepolarizing neuromuscular blockers I (tubocurarine)
Nondepolarizing neuromuscular blockers II: (other)
Depolarizing neuromuscular blockers (succinylcholine)

26
Q

Neuromuscular pharmacological categories

A

Competitive antagonists of Ach at the NMJ
- Tubocurarine
Depolarizing agonists
- Produce a depolarizing block at the NMJ (succinylcholine)

27
Q

Competitive Antagonist Agents

A

Curare, d-tubocurarine

28
Q

Curare alkaloids, d-tubocurarine: Mechanism

A

At NMJ curare like agents compete with Ach for cholinergic receptors at the motor end-plate of skeletal muscle
Curare has little intrinsic activity but competitively blocks the action of Ach
Is reversible
- Increase Ach to reverse effect of curare by using CHE inhibitors

29
Q

Curare: Absorption, Distribution and fate of Tubocurarine

A

Not absorbed orally
Can’t cross BBB or placenta
Rapid initial distribution followed by slower elimination phase
- Onset within 4-6 minutes after IV administered
- Lasts 1 hour after single dose
- Second dose as late as 24 hours after first dose
- Less drug is needed to produce same degree of paralysis
Excreted in urine

30
Q

Curare, d-tubocurarine: Pharmacological Actions

A

Fairly selective at NMJ
- Produce paralysis
Order of symptoms
- Skeletal muscles become weak/ flaccid
- small rapid moving muscles, then limbs, neck, and trunk
- intercostals and lastly diaphragm paralyzed
Histamine release
- Flushing
- Hypotension
- Excessive bronchial and salivary secretions and bronchospasms
- Mass cells
- Pouring out of mass cells
- Degranulation of mass cells

31
Q

Curare: Adverse effects

A

Hypotension
Bronchospasms and excessive secretions
Respiratory failure
Patients with myasthenia gravis extremely sensitive

32
Q

Curare: Drug interactions

A

General anesthetics
Quinidine, lidocaine and other local anesthetics and antiarrhythmics
Aminoglycoside antibiotics
CCB

33
Q

Curare: Clinical uses

A

Adjunct to surgical anasthesia to induce skeletal muscle relaxation and facilitate manipulations during surgery
Orthopedic procedures
Facilitate intubation with an endotracheal tube
Decrease intensity in electroshock therapy
Diagnostic for myasthenia gravis

34
Q

Depolarizing blocking agents

A

succinylcholine

35
Q

Succinylcholine: Mechanism

A

Produces a depolarization of the motor end-plate like Ach which produces a transient muscle activation
Persistent depolarization and blocks NMJ
Can’t be antagonized by cholinesterase inhibitors

36
Q

Succinylcholine: Action

A

Before paralysis, depolarizing agents evoke transient muscular fasciculations
Has intrinsic activity
Ultra-short duration and rapid onset
Brief duration due to rapid hydrolysis by cholinesterase enzymes of liver and plasma
If prolonged depolarization, muscle cells may loose significant quantities of K
- Accompanies skeletal muscle contraction
- If you have a leaky membrane (trauma membrane) showing hyperkalemia
- Could stop the heart

37
Q

Succinylcholine: CV Effects

A

Stimulate all cholinoreceptors including nicotinic receptors in both SNS and PNS and the adrenal medulla, and muscarinic receptors in the heart
Low doses can produce bradycardia
Larger doses can produce hypertension and tachycardia

38
Q

Cholinesterase inhibitors: Action

A

Accentuate the neuromuscular blockade

39
Q

Succinylcholine:Myasthenia gravis

A

Resistant, going to need a higher dose

40
Q

Succinylcholine: Adverse effects

A

Cardiovascular effects from stimulation of parasympathetic of sympathetic ganglia
Respiratory failure
Malignant hyperthermia

Pharmacology (13 decks)

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