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47 Cards in this Set
- Front
- Back
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What CNS disorders are Muscarinic Receptor Antagonists used to treat?
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Motion sickness
Parkinsonism and Psychoses Hay fever/colds |
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What GI/GU disorders are Muscarinic Receptor Antagonists used to treat?
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↑ in: GI tract activity and
secretions Bladder activity Glandular Secretions |
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What CV/lung disorders are Muscarinic Receptor Antagonists used to treat?
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↑HR and Conduction in AV node
Asthma and COPD Hay fever/Colds |
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What are the other use for Muscarinic Receptor Antagonists?
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Treatment of AChE toxicity
To induce mydriasis during eye examinations |
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What type of inhibiotn is present with Muscarinic Receptor Antagonists?
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Competitive and reversible (prevent agonist binding but have NO agonist activity)
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What determines Muscarinic Receptor Antagonist's effect magnitude?
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Existing parasympathetic and sympathetic tone
Agonist levels |
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What are the tissues that are most sensitive to Muscarinic Receptor Antagonists?
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Salivary, bronchial and sweat glands
Followed by eye and heart (vagal-mediated effects) |
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What are the tissues that are least sensitive to Muscarinic Receptor Antagonists?
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Urinary bladder and GI tract
Gastric secretions are the least effected of all |
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What causes the differences in tissue sensitivities to Muscarinic Receptor Antagonists?
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Parasympathetic tone
Involvement of reflexes Effects of interneuronal neurons |
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Are tissue sensitivities to Muscarinic Receptor Antagonists determined by receptor subtype? How do we know?
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No
The difference is still seen with atropine |
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What are the three classes of Muscarinic Receptor Antagonists?
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1. Naturally occurring
2. Synthetic Quaternary Ammonium Compounds 3.Synthetic Tertiary Ammonium Compounds |
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What are the properties of naturally occuring Muscarinic Receptor Antagonists?
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Organic esters = organic acid + base
Uncharged tertiary amines that enter the CNS |
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What is the effect of muscarinic blockers on the SA/AV node? What's the clinical use of this?
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vagolytic = ↑conduction
Tx of 2nd degree AV block or ↓ vagomimetic effects of glycosides (digitalis), which slow AV conduction |
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Why are muscarinic antagonists helpful in the early stages of an MI?
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Vagal tone can ↑ during early stages of an MI = ↓ nodal conduction & ↓HR
Muscarinic block can = ↑HR and ↓AV block |
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What effect can muscarinic antagonists have on blood vessels?
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They can block the vasodilation caused by muscarinic agonists.
Some patients experience flushing due to dilation of superficial vessels |
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What's the effect of muscarinic antagonists on the lung?
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bronchodilation
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What are muscarinic antagonists used in surgical prep?
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They decrease respiratory tract secretions.
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What drugs are used in the treatment of hayfever/cold
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OTC/anti-histamines that have large muscarinic antagonism components.
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When are muscarinic antagonists used to treat salivary issues? Side effects?
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Excessive salivation due to: heavy metal poisoning, Parkinsonism, or esophageal obstructions.
Side effects = dry mouth, difficulty swallowing |
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When are muscarinic antagonists used in GI issues?
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useful for treating conditions involving increased GI activity (they decrease tone and motility)
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When are muscarinic antagonists used with urinary tract issues?
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*Renal colic (stones) = relaxes ureter
*Enuresis in kids to ↑bladder capacity and ↓bladder contractions *Spastic paraplegia to ↓frequency of urination |
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What's the effect of muscarinic antagonists on sweat glands?
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Decreases secretion
Can = increased body temp and flushing (especially in kids/infants) |
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When are muscarinic antagonists needed to treat excessive AChE inhibition?
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Reversal of NM block after surgery
TX myasthenia gravis Insecticide poisoning Mushroom poisoning (muscarine) |
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What can cause muscarinic antagonist poisoning?
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Atropine, scopolamine etc.
H1 histamine receptor antagonists Phenothiazines Tricyclic antidepressants |
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What's the memory tool for muscarinic antagonist poisoning?
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Blind as a bat, mad as a hatter, red as a beet, hot as hell, dry as a bone, the bowel and bladder lose their tone, and the heart runs alone.
Can't see, spit, pee, or shit. |
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What's central anticholinergic syndrome?
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toxic changes seen with intermediate to high doses of atropine
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What are the symptoms of central anticholinergic syndrome?
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↓ concentration & memory drowsiness, sedation, coma excitation, hallucinations
ataxia, asynergia, disorientation EEG: ↓alpha waves and ↑ low-voltage slow waves |
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How can you confirm a diagnosis of Muscarinic Antagonist poisoning?
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Lack of typical responses to AChE inhibition (injection of physostigmine 1 mg, IM)
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How long can Muscarinic Antagonist poisoning last? What else can it look like?
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more than 48 hours
schizophrenic episode or alcoholic delirium |
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How do you treat Muscarinic Antagonist poisoning?
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AChE inhibition (1+ slow IV injections physostigmine) plus sedative for convulsions/excitation, artificial respiration if failure, and ice/alcohol sponges for fever.
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What makes ganglionic transmission complex & variable?
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*Modulating interneurons
*Large number of Nn subtypes *Both nicotinic and muscarinic receptors on postganglionics *Complex membrane potential changes in ganglionic neurons |
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What determines the effects of ganglionic blocking agents?
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Parasympathetic and sympathetic tone existing at innervated organs
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What are the effects of ganglionic blocking agents at the organs under predominantly parasympathetic tone?
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tachycardia
mydriasis and cycloplegia ↓in GI tone & motility, constipation Urinary retention Dry mouth |
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What are the effects of ganglionic blocking agents at the organs under predominantly sympathetic tone?
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↓ ventricle contractility
Vasodilation, ↑ peripheral blood flow, ↓BP, ↓ venous return, ↓ CO ↓ sweat gland secretion |
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What kind of surgery requires controlled hypotension?
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plastic, neurological & ophthalmologic
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What can happen in untreated autonomic hyperreflexia?
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Increased BP can = MI, stroke or retinal hemorrhage
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What have ganglionic blockers been replaced with? Why?
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nitroprusside and alpha blockers
Effects are more controllable and predictable |
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What are muscle relaxants used for?
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1. Treat malignant hyperthermia
2. Facilitate surgery and make anesthesia safer 3. Prevent muscle convulsions, spasms and spasticity |
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What is malignant hyperthermia?
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In patients with mutations in the ryanodine receptor Ca2+ release channel, inhalation anesthetics causes release of lots of Ca2+
= intense muscle contractions which elevates temp to unsafe levels |
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What are the 3 classes of muscle relaxants?
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1. Compounds that work directly on skeletal muscle
2. Centrally acting compounds 3. Neuromuscular blockers |
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How do neuromuscular blockers make surgeries safer and more efficient?
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↓ level of anesthetic required
Facilitate tracheal intubation ↓ fasiculations at the incision site Facilitate maintenance of ventilation |
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How are neuromuscular blockers in neurologic conditions?
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↓ spasticity due to tetanus in neurological diseases and multiple sclerosis
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How else are neuromuscular blockers used in hospital patients?
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Prevent bone fractures during electroshock therapy
Facilitate maintenance of respiration in the ICU |
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What are the three classes of neuromuscular blockers?
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1. Competitive (nondepolarizing) N-M blockers
2. Depolarizing blockers 3. ACh release blockers |
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What percentage Nm receptors must be inhibited for a complete block? What does the dose to reach this level depend on?
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90-95%
The drug, muscle location, and patient |
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Can muscles be activated after administration of competitive (nondepolarizing) N-M blockers? How?
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Yes
By stimuli that act downstream of the NM receptor (i.e. by electrical stimulation or ↑ external K+) |
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What's the duration of NM blockade influenced by?
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Route of metabolism
Nature of surgery and anesthetic Age, condition of patient (trauma, burns, lytes, organ function) ↓ levels or activity of BuChE |
