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Pharm Block 1 > Cholinergics > Flashcards

Cholinergics Flashcards

1
Q

Where are M (muscarinic) receptors located?

A

Muscarinic receptors are located:

  • Effector tissues and innervated by parasympathetic fibers
  • Very select postganglionic sympathetic targets (sweat glands)
  • Endothelium (non-innervated tissue)
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2
Q

What are sites of cholinergic action?

A

Cholinergic transmission occurs at neural junctions where acetylcholine is the neurotransmitter:

  • All autonomig ganglia
  • Postganglionic termini of parasympathetic fibers (post-synaptic)
  • Postganglionic termini of sympathetic cholinergic fibers (sweat glands) (post synaptic)
  • Adrenal medulla (specialized sympathetic ganglion)
  • Termini of somatic motor nerves to skeletal muscle (neuromuscular junctions/motor end plates)
  • CNS
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3
Q

What are the actual effects of IV Ach?

A

1) Hierarchy of accessibility from blood:
- Endothelial cells
- Parasympathetic/sympathetic effector tissues
- NMJ
- Ganglia
- CNS
2) Ach is rapidly cleared from the blood
- Plasma => pseudocholinesterase
- Further limits access to less perfused sites

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4
Q

What is cholinergic syndrome/ extreme muscarinic over activation?

A

DUMBBELLSS:

  • Diarrhea (and Diaphoresis) and abdominal cramping
  • Urination
  • Miosis (pinpoint pupils)
  • Bradycardia (muscarinic) or Tachycardia (nicotinic)
  • Bronchorrea (increased secretions) or Bronchoconstriction (wheezing)
  • Emesis (Nausea and Vomiting)
  • Lacrimation
  • Lethargy
  • Salivation
  • Sweating

or

SLUDGE:

  • Salivation
  • Lacrimation
  • Urination (detrusor)
  • Defecation (anal sphincter)
  • GI
  • Emesis
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5
Q

What are the clinical signs of muscarinic activation?

A

DUMBBELLSS/ SLUDGE

AND:

1) Hypotension
2) Paradoxical bradycardia

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6
Q

What is the pathophysiology of hypotension in muscarinic over activation?

A
  • Activation of noninervated M3/M5 on endothelial cells
  • Rapid activation of endothelial NO (nitric oxide) synthase
       =\> NO diffuses into vascular smooth muscle cells

   =\> NO stimulates guanlylate cyclase (GTP -\> cGMP)

   =\> cGMP binds to myosin light chains to relax vascular smooth muscle cells --\> vasodilation --\> lowered BP
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7
Q

What are nonspecific receptor direct acting cholinomimetic drugs?

A

1) ACh
2) Carbachol

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8
Q

What are some important direct acting cholinomimetic muscarinic agonists?

A

1) Methacholine
- Methylated ACh, has quaternary ammonium so poorly absorbed
- Aerosol challenge to Dx bronchial hyperreactivity (asthma)
- Hyperreactive airways respond with bronchoconstriction to lower concentrations

2) Bethanechol
- Formerly used to relieve GI dysmotility syndromes such as postsurgical ileus
- Largely replaced by metoclopramide, stimulates presynaptic D2 receptors to trigger ACh release

3) Pilocarpine (plant alkaloid)
- Used topically in the eye to relieve glaucoma

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9
Q

What are some important direct acting cholinomimetic nicotinic agonists?

A

1) Nicotine
2) Varenicline (Chantix™)

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10
Q

What are some important indirect acting cholinomimetic cholinesterase inhibitors?

A

Short acting:
- Edrophonium

Intermediate acting

  • Neostigmine
  • Physostigmine

Long acting

  • Echothiophate
  • Parathion
  • Malathion
  • Sarin
  • Soman
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11
Q

What are some important indirect acting cholinomimetic presynaptic drugs?

A

Metoclopramide

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12
Q

What are the characteristics of Nicotinic receptor agonists?

A

1) Nn receptors in all autonomic ganglia,
- Post synaptic, on efferents to soma of postganglionic neurons
- Also in the CNS
2) Nm at NMJ on skeletal muscle
3) Ligand gated Na+/K+ channels
- When pore is open, Na+ goes into cell, K+ comes out
- More Na+ goes in than K+ comes out, net +ve charge in → membrane depolarizes
- Depolarization triggers action potential

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13
Q

Why are muscarine and Ach not therapeutically useful?

A

1) THey do not arrive at junctions in the organized fashion needed fro a synchronized physiological response
2) Too many side effects

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14
Q

Describe the nicotine addiction mechanism.

A

Nicotine⇒nicotinic receptors in the nucleus accumbens and prefrontal cortex => increase in mesolimbic reward system => dopamine

- when dopamine falls =\> cravings

* Nicotine patches are used to help with nicotine addiction but there is a risk of nicotine poisoning (especially in children)

  • Chantix works through different receptors and not through the reward system
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15
Q

What are the effects of nicotine receptor overactivation?

A

Initial activation –> subsequent deactivation:

  • Initial depolarizatin leads to muscle fasciculations
  • Prolonged receptor occupancy with Ach leads to receptor phosphorylation and inactivation (depolarization–desensitization blockade)

* Result is a paradosical flaccid paralysis which cannot be practically reversed until the agonist is cleared

  • Most critical concern is the effect on skeletal muscle/diaphragm
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16
Q

How is nicotine generally absorbed in poisoning?

A

Nicotine is rapidly absorbed orally/through the skin.

  • Poisoning leads to rapid stimulation of parasympathetic/sympathetic ganglia and adrenals
    - This causes depolarization–desensitization blockade
  • Flaccid paralysis demands respiratory support
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17
Q

What are the major clinical signs of nicotine poisoning?

A

* Sympathetic tends to predominate

1) Tachycardia
2) Hypertension
3) Nausea/vomitting/diarrhea/salivation
4) Urinary incontinence
5) Cold sweat
6) Syncopy,collapse,unconsciousness
7) Flaccid paralysis

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18
Q

What is Varenicline/Chantix?

A

Varenicline is used to treat nicotine addiction. It is an anicotinic receptor partial agonist—it stimulates nicotine receptors more weakly than nicotine itself does.

As a partial agonist, it both reduces cravings for and decreases the pleasurable effects of cigarettes and other tobacco products.

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19
Q

What drug class is Varenicline?

A

Pharmacologic class: Very selective and potent competative partial agonist of a2-b4 nicotinic receptors

Therapeutic class: smoking cessation

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20
Q

Describe the pharmacodynamics of varenicline.

A

Pharmacodynamics:

  • CNS mesolimbic dopamine
  • Partial a4-b2 stimulation prevents low dopamine and cravings
  • Prevents nicotine from creating dopamine surges
  • No chemical reward
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21
Q

Describe the pharmacykinetics of varenicline.

A

Pharmacokinetics:

  • Well absorbed
  • Peak 4 h, t1/2 = 24 h
  • Excreted primarily in urine as unchanged drug
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22
Q

What special considerations should be made for patients on varenicline?

A

Special considerations:

  • Reports of suicidal thoughts and aggressive and erratic behavior→ Patients and caregivers should be instructed about the importance of monitoring for neuropsychiatric symptoms and to communicate immediately with the prescriber the emergence of agitation, depression, unusual changes in behavior, or suicidality.

*Psychiatric patients – use extreme caution.

  • Contraindicated in pregnancy/lactation.
  • Causes drowsiness, caution operating machinery
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23
Q

What is the dose/route of varenicline?

A

Route/dose:

  • 1 mg PO BID for healthy adults
  • 0.5 mg PO BID for renal impairment CrCl < 50 ml/min
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24
Q

What should be monitored in patients on Varenicline?

A

Neuropsychiatric symptoms

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25
Q

What do cholinesterase inhibitors block?

A

Cholinesterase inhibitors block true AchE, plasma ChE, RBC AchE:

  • Plasma ChE is inhibited first
  • Plasma ChE neutralizes AChE inhibitors & protect neural AChE
  • Assays available for plasma ChE and AChE on RBCs membranes
  • Useful in diagnosis and prognosis of cholinesterase inhibitor poisonings
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26
Q

What are the side effects of AChE inhibitors?

A

1) Muscarinic side effects (DUMBBELSS)
- Reversible by muscarinic blocking drugs (next lecture)
2) Nicotinic effects

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27
Q

What is the mechanism for AChE?

A

1) Anionic site binds quaternary ammonium cation
2) Esteric site is catalytic, hydrolyzes ACh ester bond
- Ester Bonding to acetyl group → liberate choline
- Rapid hydrolysis releases acetate
3) Enzyme ready for next ACh

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28
Q

How do short acting AChE inhibitors work?

A

1) Short acting are competitive inhibitors => do NOT form ester bond to AChE

2) Edrophonium
- Highly charged, does not cross BBB
- Given I.V. (onset 1 min) or I.M. (onset 2 – 10 min)
- Extremely short lived effects (5-10 min IV; 5-30 min IM)
- Dx of myasthenia gravis (90-95% accuracy)

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29
Q

Describe the salient features of myasthenia gravis.

A

1) Autoimmune disease
2) Antibodies against a thymocyte epitope cross react with NMJ
3) Attack and destroy motor end plates, over months/years, causing impairment of neurotransmission
4) Patients complain of muscle weakness and rapid muscle fatigue
5) By transiently inhibiting ChE, edrophonium makes more ACh available in the synapse to restore transmission
- Patients note rapid increase in muscle strength

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30
Q

What is the mechanism of action of intermediate AChE inhibitors (Carbamates)?

A

Mechanism of action:

1) Bind anionic and esteric sites
2) AChE forms an ester bond to the carbamoyl group
3) This bond hydrolyzes slowly, over hours
4) Effects last much longer than those of edrophonium

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31
Q

What are the clinical uses of intermediate AChE inhibitors?

A

Used to treat:

1) Myasthenia gravis
2) Reverse the paralytic effects of nondepolarizing blockers of the NMJ (Nicotinic antagonists – NOT nicotinic agonists)

* also used as insecticide

32
Q

What is the mechanism of physostigimine (intermediate acting carbamate)?

A

1) Uncharged and lipid soluble so it crosses the BBB
- ChE inhibitors in the CNS have dangerous effects
- Not useful in myastenia gravis (strictly a peripheral disease)
2) Occasionally used to treat CNS signs of muscarinic blockers

33
Q

What are the uses of neostigmine (intermediate acting carbamate)?

A

1) Designed with quaternary ammonium group to keep it out of the CNS
2) Just peripheral effects so useful for myasthenia gravis
- Too little drug is inadequate to restore transmission → myasthenic crisis (respiratory paralysis, flacid paralysis)

  • Too much results in depolarization-desensitization blockade → cholinergic crisis (respiratory paralysis, flacid paralysis)
  • IV edrophonium can distinguish between the two states
34
Q

Describe the action of organophosphates (long acting AChE inhibitor).

A

1) Organophosphates:
- Over 50,000 organophoshpate AChE inhibitors
- Covalently bond the esteric site → phosphorylated enzyme
- Bond may require hundreds of hours to hydrolyze
- Some of the agents split off an alkyl group at which point the phosphorylation is irreversible (aging)

35
Q

Name various types of organophosphates.

A

1) Drugs (Echothiophate)
- Once used to treat narrow angle glaucoma (largely replaced)

2) Insecticides:
- A frequent source of poisoning
- Parathion, extremely toxic insecticide, poorly metabolized
- Malathion, “mammal friendly” insecticide

3) Nerve gas, weapons of mass destruction
- Sarin
- Soman

36
Q

How is organophosphate poisoning managed?

A

1) Supportive treatment

  • Manage DUMBBELSS/SLUDGE with muscurinic blockers (e.g. atropine)
  • Aggressive respiratory support

2) Antidote: Pralidoxime (2-PAM)
- Must be given in a timely manner
- Rescues muscular function
- Contraindicated in poisoning by carbamate ChE inhibitors

** * Makes worse due to competitive inhibition of AChE**

37
Q

Nonspecific anticholinergics only act in a __________fashion

A

Nonspecific anticholinergics only act in a **indirect **fashion

ie => botulinum toxin

38
Q

Specific anticholingergics only act in a _______ fashion.

A

Specific anticholingergics only act in a direct fashion.

1) Muscarinic antagonists

2) Nicotinic anticholinergics
- NN specific (NMJ blockers)
- Depolarizing NM cholinolytic agonists
- Nondepolarizing NM antagonists
- NN blocker (ganglionic blockers)

39
Q

Name the G coupled protein, second messenger, and effector for: alpha-1, M1, M3, M5 muscarinic receptors

A

G coupled protein: alpha q/11, PLC open membrane, Ca channels

Second messenger: Increase PLC

Effector: PKC

40
Q

Name the G coupled protein, second messenger, and effector for: alpha-2, M2, M4, D4

A

G coupled protein: alpha, inhibits adenylate cyclase,

Second messenger: decrease cAMP (increase PLC, PLD, PLA2)

Effector: PKA/PKC

41
Q

Name the G coupled protein, second messenger, and effector for: Beta 1-3, D1

A

G coupled protein: alpha s (activates), activates adnylate cyclase

Second messenger: icnrease cAMP

Effector: PKA

42
Q

What are the types of muscarinic receptors (USMLE)

A

a. G-protein coupled receptors (GPRCs)
b. 5 major types (M1 – M5)
* *c.M3 in most tissues**
d. M2 in heart
e. M1 in gastric parietal cells
f. M4 & M5 in CNS
g. M1, M3, M5 use Gq (odd ones are queer)
i. Gq (Queer) stimulates phospholipase C
ii. Leads to elevated Ca+2
h. M2, M4 (uses Gi)
i. Gi Inhibits adenylyl cyclase
ii. Activates K+ channels

43
Q

What are major types of Muscarinic Antagonists (M-specific anticholinergics)?

A

1) Atropine
2) Scopolamine

44
Q

What type of ligand gated receptors are Nicotinic receptors?

A

Nicotinic receptors are Na+/K+ channels ligand gated channels and are pentamers composed of several possible subunits.

 - alph 1-10
 - beta 1-4
 - delta 
 - gamma
45
Q

What are the two major types of Nicotinic receptors?

A

1) NM (muscle) in skeletal muscle (NMJ)
- Predominantly 2(alpha-1), 1-beta, 1-delta, 1-gamma

2) NN (neuronal) in autonomic ganglia & CNS
- 12 different combinations of a and b
- Ganglionic is alpha-3, alpha-5, 3(beta-2)
*Chantix™ is selective for 2(alpha-2), 3(beta-4) neuronal receptors

46
Q

What are the various types of N-specific anticholinergics?

A

1)NM-specific (NMJ blockers)

*Depolarizing NM cholinolytic agonists (ie Succinylcholine)

*Nondepolarizing NM antagonists (Prototype: d-Tubocurarine)

  - Benzylisoquinolines (d-Tubocurarin and Cisatracurium) 
  - Aminosteroid (Pancuronium, Vercuronium, Rocuronium)

2) NN-specific (ganglionic blockers)
*Trimethaphan

47
Q

What are the effects and mechanism of muscarinic blockers/antagonists?

A

Example: Atropine (plant alkaloid)

Effects: “Parasympatholytic”

  • Predominantly appear to block parasympathetic transmission at end organs
  • Can also effect sweat glands, CNS

Mechanism: Reversible blockade

  • Inverse agonists
    • M receptors have constitutive activity that is enhanced by ACh
    • Inverse agonists shift equilibrium M(active) → M(inactive)
    • In the absence of neurotransmission, inverse agonists produce an inhibitory effect
48
Q

What are the determinants of selectivity for a muscarinic blocker/antagonist?

A

1) Tertiary amine forms
2) Quaternary amine derivatives
3) M1, M2, M3 selectivity agents

49
Q

What are the characteristics of tertiary amine forms (muscarinic antagonists)?

A

1) Atropine and many derivatives
2) Uncharged, fat soluable
3) Both peripheral and CNS effects

50
Q

What are the characteristics of quarternary amine derivatives (muscarinic antagonists)?

A

1) Always charged
2) Predominantly peripheral effects

51
Q

What are the characteristics of M1-3 selectivity agents?

A

1) Only show selectivity in vitro
- Each M blocker shows unique tissue response hierarchy

  - Atropine sensitivity highest in salivary, bronchial, and sweat glands
  - Atropine potency highest in heart, bronchial and GI muscle

2) Clinically they are “non-selective”
3) Clinical actions not predicted by in vitro activity

52
Q

What are the effects of Atropine?

A

1) Common cause of pediatric poisonings
2) Effects: Anti-DUMBBELSS
- Unapposed sympathetic actions

53
Q

What are the signs of atropine toxicity?

A

* Toxicity causes:

1) Psychological effects
2) Visual deficits
3) Global dehydration
4) Elevated body temperature
5) Redness
6) Excessive urination
7) Bronchodilation
8) Constipation => blocks GI motility
9) Cardiovascular effects => HTN and Tachycardia

54
Q

What are the neurological symptoms of Atropine toxicity

A
  • Delirium, hallucinations (unclear CNS effects)
    • Can be confused with schizophrenia
    • Self destructive acts
    • Treatment: Phyzostigmine
55
Q

What are the visual deficits associated with atropine toxicity?

A
  • Mydriasis (pupil dilation)
    - Inhibition of miosis (constriction of the iris sphincter muscle)
    - Photophobia
    - Opthalmologists use short duration blockers, not atropine
  • Blurred vision (cycloplegia)
    • Inhibition of cilliary muscle constriction
    • Impaired near vision
  • Exacerbates closed angle glaucoma
56
Q

What signs are associated with dehydration in atropine toxicity?

A

1) Dry mouth
- Inhibition of salivation
- “I can’t spit”, intense thirst, difficulty swallowing
2) Dry skin (anhydrosis)
- Inhibition of thermoregulatory sweat glands
3) Dry eyes
- Inhibition of lacrymation
4) Bronchial secretions
- Anesthesia adjunct

57
Q

Describe the characteristics of elevated body temperature in atropine toxicity.

A
  • Elevated body temperature => secondary to anhydrosis
  • Unclear CNS effect
  • Most dangerous in pediactrics (can be fatal)
    • Not responsive to usual antipyretics
    • Requires physical cooling methods (ice bath/blankets)
58
Q

What is the mechanism behind excessive urination in atropine toxicity?

A

1) Block of detrusor muscle
2) Urinary retention
3) Bladder catheterization => also post surgery

59
Q

What are the uses for scopolamine ( muscarinic antagonist)?

A
  1. Motion sickness
    • Reduces vertigo, post surgical nausea
    • Transdermal patches
      • Impaired near vision
      • Prolonged use: delerium (Mad as a hatter)
  2. Anesthetic adjuvant
    • Induces amnesia
    • Reduces bronchial secretions (Dry as a bone)

*Side effects

  • Atropine- like effects
  • CNS depression/excitation
60
Q

What are the uses for Dicyclomine?

A

Irritable bowel and minor diarrhea

  • M3 selective competitive antagonist
  • Given by mouth or intramuscularly
  • Short half life but effects last up to 6 hrs
61
Q

What drugs inhibit acid secretion in peptic ulcers?

A

1) Methscopolamine
2) Pirenzepine
3) Propantheline

62
Q

What drugs are used in urinary urgency/bladder spasms?

A

1) Oxybutynin
2) Glycopyrrolate

63
Q

What are some uses of mydriatic eye drops?

A

1) Retinal examation
- Tropicamide: shortest duration of action (15 - 60 min)
- also scopolamine & atropine
2) Post surgical prevention of synechiae
- Adhesion of the iris to the cornea or lens
- Atropine: duration 5 – 6 days
- Homatropine: duration 12-24 h

64
Q

What muscarinic blockers are used for asthma and COPD?

A

1) Ipratropium or Tiotropium (TID – QID/3-4 times a day => aerosol delivery)
- Anticholinergics are first line therapy in persistent COPD
- Nonselective M antagonist
- Quaternary amine, low CNS penetration, low systemic absorption
- Inhibits bronchoconstriction
- packaged with albuterol (b2-agonist) for asthma

65
Q

What is given in the case of cholinergic poisoning?

A

IV Atropine is given in cholinergic poisoning

  • Given until signs of anti-cholinergic effects appear
  • Given with pralidoxime for organophosphate poisoning
66
Q

What are the 3 categories of nicotinic blockers/anticholinergics?

A

1) Depolarizing NM antagonists (NMJ blockers)
- Succinylcholine
2) Nondepolarizing NM antagonists (NMJ blockers)
- Prototype: d-Tubocurarine

  • Aminosteroids (Pancuronium, Vercuronium, Rocuronium)
  • Benzylisoquinolines (Cisatracurium, d-Tubocurarine)
    3) NN blocker (ganglionic blockers)
  • Trimethaphan
67
Q

What are the effects/uses of Nm blockers?

A

1) NM blocker side effects: Ganglionic blockade or CNS
- Nm blockers inhibit skeletal muscle activity during surgery

2) NN ganglionic blocker side effects: NMJ blockade or CNS
- Only 1 useful Gangionic (NN) blocker: Trimethaphan

68
Q

What are the effects of nicotinic receptor over-activation?

A

1) Initial activation → subsequent deactivation
2) Initial depolarization leads to muscle fasciculations
3) Prolonged receptor occupancy with ACh leads to receptor phosphorylation and inactivation (termed: depolarization-desensitization blockade)
4) Result is a paradoxical flaccid paralysis which cannot be practically reversed; have to wait until agonist is cleared
5) Over activation of the nicotinic receptor produces a net K+ efflux from muscle → hyperkalemia
* *Only 1 useful agent: succinylcholine**

69
Q

What are the general characteristics of succinylcholine (depolarizing Nm blocker)?

A

1) A dimer of ACh => functions like ACh
2) Used of short surgical procedures and intubations
3) Semi-selective for NMJ
4) Easy to control actions
- IV controlled drip: titrate to the desired degree of relaxation
- IV bolus: rapid onset & short duration (< 10 min)
5) Rapidly cleared by plasma cholinesterase
- Patients lacking plasma ChE are paralyzed for many hours
- Initially effects large muscles: chest and abdomen, then neck and legs

70
Q

What are the adverse side effects of succinylcholine?

A

1) Muscle fasciculations → post surgical pain
2) Hyperkalemia
3) Histamine release
- Warmth, vasodilatation
4) Malignant hyperthermia (very rare)
- Involves halogenated inhalation anesthetics
- Massive release of Ca++ from the sarcoplasmic reticulum => muscle rigidity
- Uncontrolled increase in skeletal muscle oxidative metabolism
- ↓ pO2, ­ pCO2 (acidosis), ­ temperature, muscle ridgidity

Treatment: O2, bicaRbonate, ice baths, hyperventilation,dantrolene (blocks the ryanodine receptor)

71
Q

What are the contraindications for succinylcholine use?

A

1) Family Hx of malignant hyperthermia
2) Hyperkalemia (if severe –> cardiac arrest)
3) Burns, trauma, tissue injury
4) Heart failure (arrhythmias)

72
Q

What are the effects of d-Tubocurarine (a nondepolarizing NM Blocker)?

A

Produces paralysis in fully conscious patients

  • Never give such a drug to an unanesthetized patient
  • Never let a patient emerge from anesthesia before reversing the paralysis

** * Can reverse with Neostygmine**

73
Q

How does botulinum toxin induce toxicity (botulinum toxin = indirect anticholinergic)?

A

Botulinim mechanism of action:
- Binds receptors and is endocytosed
- Light chain escapes from vesicles
- Light chain cleaves SNARES
so no docking => No Ach released

74
Q

What are the effects of botulinum toxin?

A

1) At the NMJ causes flaccid paralysis (ie no wrinkles)
2) At muscarinic junctions: Atropinic effects

75
Q

What are the applications for Botulinum toxin (BoTox)?

A

1) Cosmetic (wrinkles)
2) Prevent axillary hyperhydrosis (arm pit sweating)
3) Strabismus (unaligned eyes)
4) Blepharospasm (uncontrolled eyelid twitching)
5) Spasmodic torticollis => neurologic disorder causing erratic head movements
6) Anal achalasia to heal fissures

Pharm Block 1 (16 decks)

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