Lecture 4 Flashcards
Why are muscarinic antagonists used in opthamology? Which drug is preferred
- dilate the eye for exam: Mydriasis
- administered directly into eye
- Produce cycloplegia
- Tropicamide preferred
when would you not use a muscarinic antagonists in an opthamology exam
- in a patient with glaucome
- it will increase intraocular pressure
Why is atropine used after an MI
- atropine used to decrease bradycardia due to excessive vagal stimulation and/or reverse heart block
Which muscarinic antagonist is used in surgery to prevent excessive vagal reflexes
Glycopyrrolate
Which muscarinic antagonist is used in the treatment of COPD and in acute asthma
- Ipatropium (Atrovent)
- Tiotropium (Spiriva)
Which muscarinic antagonist is used to treat overactive bladder
Tolterodine (Detrol)
- selective M3 receptor antagonist
Which muscarinic receptor is used to treat bladder spasms after prostate surgery
Oxybutynin (Ditropan)
- blocking muscarinic receptors decreases bladder tone and spasm
what is the main side effect of Oxybutynin
dry mouth
what are the main side effects of Tolterodine (Detrol)
- dry mouth
- blurred vision
which muscarinic antagonist is used to treat motion sickness
Scopolamine
Scopolamine has what CNS effects
- sedation
- short term memory loss
- euporia
- toxicity: hallucinations
List the side effects of muscarininc antagonists
- dry mouth
- decreased bronchial secretions
- tachycardia
- mydriasis, cycloplegia
- decreased GI motility
- urinary retention
- dry skin
- decreased sweating
atropine overdose: use mneumonic
- dry as a bone, blind as a bat, red as a beet, mad as a hatter”
- dry mouth, mydriasis, tachycardia, hot flushed skin, agitation and delirium.
treatment for atropine poisoning
- Treatment is supportive and symptomatic
- cholinesterase inhibitor, diazepam (Valium) to prevent seizures
- ice bags and ethanol to reduce body temperature
- assist respiration
Many classes of drugs have anticholinergic effects, and poisoning may occur with these drugs. Name these classes of drugs
- tricyclic antidepressants
- antihistamines
- phenothiazine antipsychotics.
Treatment of choinergic agonist or AChE inhibitor toxicity (e.g. pesticide, nerbe gas, or mushroom poisonint)
-
Atropine used to block muscarininc effects
- inject until pupils dilate and mouth is dry
Describe what happens at the neuromuscular junction when a nerve is depolarized
- The motor nerve terminal releases ACh when a stimulus travels down the axon
- ACh diffuses to the nicotinic receptor (NM) located on the skeletal muscle
- ACh binds and the Na+ channel opens and Na+ enters the cell
- This causes depolarization of the end plate membrane, resulting in a change in the end plate potential
- If the postjunctional end plate potential is sufficient, the adjacent muscle will depolarize, and the action potential will be propagated along the muscle fiber, and the muscle contracts
- ACh is rapidly broken down by acetylcholinesterase (AChE)
- If the action of ACh is prolonged sufficiently, the nicotinic receptors desensitize. At that point, the membrane can no longer be depolarized by ACh
Name the two types of neuromuscular junction blocking agents:
-
Nondepolarizing Block: The first are non-depolarizing, competitive antagonists, produce direct blockade.
- They bind to the receptor, and cause blockade, holding the channel in a closed position. Because they are competitive antagonists, their effect can be overcome by increasing ACh.
-
Depolarizing block.
- the depolarizing action is prolonged, so that subsequent release of ACh does not have any effect, since the endplate is already depolarized. With time the endplate desensitizes.
when are neuromuscular blockers used clinically
produce paralysis in surgery
- the patient treated only with a neuromuscular blocking will be paralyzed and awake.
What drug is the only depolarizing neuromuscular blocker
Succinylcholine
Describe a nondepolarizing block
- block receptor, prevent effect of ACh
- inhibit muscle contraction
- competitive, compete with ACh for nicotinic receptors
- reverisible with addition of ACh
how can nondepolarizing block be reversed
- since they bind competitively, the block can be reversed by increasing the amount of ACh in the synaptic cleft
- Cholinesterase inhibitors such as neostigmine are used to reverse the action of the non-depolarizing blockers
Do non-depolarizing drugs have a CNS effect?
- no CNS effect
- Highly ionized
non-depolarizing drugs affects which muscles first
- onset of action 1-6 minutes- causes motor weakness
- small muscles affected first (hand, eye, jaw, larynx)
- then larger muscles (trunk)
- respiratory muscles last
clinical presentation: which drug was given
- initial contraction before paralysis
- very brief action with rapid onset
- Succinylcholine: depolarizing blocker
- depolarized before blocking
which blockage is given for procedures where a very rapid and short-acting effect is needed, such as a tracheotomy or intubation
succinylcholine: depolarizing blockade
with succinycholine administration, list muscles that are effected first, second, and last
- arm, neck, legs
- facial and pharyngeal
- respiratory muscle
duration of succinylcholine effect
5-10 min
route of administration of non-depolarizing drugs
must be given via IV
succinylcholine is metabolized by
plasma pseudocholinesterase
what can effect the metabolization of succinylcholine
- There are genetic differences in ability to metabolize succinylcholine, which are expressed in terms of dibucaine number.
- Dibucaine is a local anesthetic that causes inhibition of AChE.
- A dibucaine inhibition of 80% is normal, but if it is only 20%, then the effects of succinylcholine can last for hours, instead of a few minutes.
- If a family member has had problems with succinylcholine, a dibucaine number may be obtained prior to using it.
explain the adverse effect of succinylcholine in relation to potassium
- During prolonged depolarization of the Na+ channel, K+ flows out of the muscle cell.
- In some patients, especially those with burns or who have nerve degeneration, succinylcholine administration may cause a pronounced release of potassium into the blood.
- If this rise is high enough, cardiac arrest may occur.
- This is a life-threatening situation, especially in patients with congestive heart failure
contraindications to administering succinycholine
- extensive soft tissue damage
- severe burns
- nontraumatic rhabdomylosis
- quadriplegia, paraplegia
- muscular dystrophy
- children under 8 yo, unless emergency
NMJ blockers effect is enhanced by what drugs
- some inhaled anesthetics
- aminoglycoside Abx: depress evoked ACh release
- tetracyclines: chelate Ca2+
describe ganglion receptor blockers
- block nicotine receptors at all autonomic ganglia
- non-depolarizing ganglia
effect of ganglion receptor blockers on autonomic nervous system
will decrease the total output of the ANS
- their effects will be similar to that of inhibiting both sympathetic and parasympathetic inputs. The effects will depend on the predominant tone to an organ
Name the ganglion blockers. which is used clinically
- Mecamylamine
- Hexamethonium
can ganglion blockers enter the CNS? What are the effects?
Mecamylamine can enter CNS
- causes sedation
- mental status affected
- movement affected
ganglion blockers effect on eyes
- cycloplegia
- the ciliary muscle is primarily affected, causing cycloplegia with loss of accommodation
- mild dilation of pupil
- The pupil receives both parasympathetic and sympathetic innervation, so effects on the pupil vary
ganglion blockers effect on blood vessels
- BV have mostly sympathetic innervation
- vasodilation, drop in BP (parasympathetic effects)
- Orthostatic hypotension
ganglion blockers effect on heart
- sympathetic and parasympathetic
- Contractility of the heart is reduced, and tachycardia occurs due to a decrease in vagal tone
ganglion blockers effect on GU system
- bladder tone reduced
- urinary retention with BPH
- erection/ejaculation reduced
ganglion blockers effect on sweating
No sweating
- but temperature control is maintained by vasodilation
