Pharm Flashcards by Anya McDermott

Vincristine

Chemotherapeutic drug that causes peripheral neuropathy due to microtubule damage

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Bethanechol

Muscarinic antagonist for post operative ileus

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Pilocarpine

Musacrinic agonist used to increase secretions in ppl with Sjögren’s syndrome

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Tropicamide

Musacrinic antagonist producing mydriasis needed in eye exam

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Ipratropium

Muscarinic antagonist for COPD

Bronchodilates and inhibits bronchial glands

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Tolterodine

Muscarinic antagonist for urge incontinence

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Side effects of muscarinic antagonists

Constipation

Dry eyes

Dry mouth

Urinary retention

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Treatment for cholinergic excess

Atropine (muscarinic antagonist) and pralidoxime (chemical antagonist)

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Cholinesterase Inhibitor Poisoning

D-diarrhea
U-urination
M-miosis
B-bronchospasm
B-bradycardia
E-excitation (of skeletal muscles)
L-lacrimation
S-sweating
S-salivation

Respiratory failure and death

With cholinergic excess, muscarinic symptoms before nicotinic

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Mechanism of Action: Local Anesthetic

Reversible blocks voltage-gated Na+ channels to inhibit impulse conduction along nerve axons

Does not change resting potential

Neutral form required to enter membrane, but charged form required for binding to channel site

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Modulated Receptor Hypothesis

Local anesthetic binding is a function of the conformational state of the channel

LAs have higher affinity for receptors in activated and inactivated states than receptors in resting state

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Frequency Dependent Block

Repeated depolarizations produce more effective anesthetic binding

Fibers that fire at a faster rate are more susceptible to effects of LAs

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Vasoconstrictors and local anesthetics

Vasoconstrictors decrease absorption

Used with short and medium acting drugs to increase duration of local anesthesia by constricting blood vessels (concentrates drug where it is needed)

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Elimination of Esters

Plasma pseudocholinesterase yields PABA and derivatives

PABA can cause allergic reaction

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Elimination of Amides

Liver and cytochome P450

If impaired flow to liver, have increased amide serum concentration

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Adverse effects-local anesthetics

Systemic toxicity: first manifests as CNS toxicity, then cardiotoxicity
Local neural toxicity: can cause membrane damage leading to death of neuron; motor and sensory loss are seen; transient neurologic symptoms
Methemoglobinemia: prilocaine and metabolites act as oxidizing agent to convert hemoglobin2+ to 3+, which causes decrease oxygen delivery
Allergies: PABA metabolite of esters can cause IgE mediated allergy

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Cocaine

Stimulant, vasoconstrictor

Benzocaine

MetHb potential

Mepivacaine

Lowest pKa of injectable LAs

Vasoconstrictor–>longer duration

Prilocaine

MetHb potential

Bupivacaine

Risk of cardiotoxicty

Opioid receptor target

G-protein coupled receptors

Mu
Kappa
Delta

Opioid Mechanism of Action

Inhibitory process

Opioid binds to receptor on presynaptic neuron which inhibits the formation of cAMP

Decreased cAMP causes Ca2+ channels to close, preventing transmission of AP and release of NT

Opioid also binds to receptor on post-synaptic neuron, causing K+ channels to open and hyperpolarization of the cell, thus decreasing the firing of the neuron and decreasing excitability/pain

Acute effects of Opioids

Analgesia 
Respiratory depression
Euphoria
Cough Suppression
Miosis
Constipation 
Increased intracranial pressure

Euphoric effects of opioids

Decrease GABA in neuron | Increase dopamine release from neighboring neuron

Opioid effect on CNS

Sedation Toxicity: contraindicated for head injury because can cause increase intracranial pressure Respiratory depression: decreased response to carbon dioxide causes CO2 to rise, leading to cerebral vasodilation and increased intracranial pressure Give naloxone, not oxygen Major cause of death from overdose Cough suppression ``` Pupillary constriction (except meperidine) Miosis is visible sign of overdose ``` Nausea and vomiting Muscle rigidity

Meperidine

Opioid that causes mydriasis (contrary to the miosis caused by other opioids)

Opioid effect on cardiovascular system

Minimal effects, but may cause bradycardia, vasodilation, and orthostatic hypertension

Opioid effect on histamine release

Causes non-immunologic (non-allergic) release of histamine, including vasodilation and hypotension Skin redness, urticaria, pruritus

Opioid effect on smooth muscle

GI: decreases peristalsis, which can lead to constipation Biliary: induce spasmodic effects which may lead to biliary colic Urinary tract: anti-diuretic, so can cause urinary retention

Methynaltrexone

Medication used to treat opioid-induced constipation

Loperamide

Opioid used to treat diarrhea

Diphenoxylate

Opioid used to treat diarrhea

Opioid effect on pregnancy/neonate

Used to relieve pain in labor Fetus may become opioid dependent in utero because it courses the placenta May cause respiratory depression in baby

Opioid Overdose

Classic triad: 1. Miosis 2. Respiratory depression 3. Apnea, coma

Mechanism of Action: Nalaxone

Rapidly reverses opioid overdose by competing for opioid receptors (mu, kappa, and delta) Short half life

Methadone

Full mu agonist: Competes with opioids for mu receptor binding Long acting

Mechanism of Action: Cholinergic Drugs

1. Presynaptic transporter CHAT brings in choline and Na+ 2. ChAT assembles choline and acetyl CoA into acetylcholine 3. ACh is packed into vesicle using VAT (vesicle associated transporter) 4. Ca2+ channels open, allowing for an influx and exocytosis of vesicle 5. ACh binds to receptor on post synaptic neuron 6. ACh on autoreceptor is important negative feedback loop 7. Excess ACh is degraded by AChE

Nicotinic receptors

Ionotropic 5 subunits Nm=muscle type (on skeletal muscle endplate) Nn=neuronal type (on another neuron)

Muscarinic Receptor

Metabotropic 7 transmembrane domains M1, M3, and M5 rely on second messengers M2 and M4 open K+ channels