Pharm Cumulative Review Flashcards
Stretch Reflex: Drugs modifying the reflex arc modulate excitatory or inhibitory synapses:
Decrease activity of 1a fibers
Enhance activity of inhibitory internuncial neurons
Baclofen
MOA: agonist at presynaptic GABAB receptors
Causes hyperpolarization and antagonizes the release of excitatory neurotransmitters
Therapeutic Use:
Reversible spasticity associated with multiple sclerosis or spinal cord lesions
Intrathecal administration (spinal cord injury, MS, and other spinal diseases)
ADRs: drowsiness, seizures, hypotension, confusion, dizziness, psychiatric disturbances
Tizanidine
MOA: alpha2-adrenergic agonist
Increases presynaptic inhibition of motor neurons
Therapeutic Use:
Muscle spasticity
Chronic migraine (?)
ADRs: drowsiness, hypotension, dizziness, dry mouth
Drugs Used to Treat Local Muscle Spasm
Carisoprodol
MOA: unclear
Therapeutic Use: short-term treatment of musculoskeletal pain
ADRs: drowsiness, dizziness
Cyclobenzaprine
MOA: unclear
Therapeutic Use: short-term treatment of muscle spasm; ineffective in spinal cord injury
ADRs: antimuscarinic effects, dizziness
Dantrolene
MOA: inhibits ryanodine receptor (RyR) calcium channel
Blocks release of calcium through sarcoplasmic reticulum, impairs muscle contraction
Therapeutic Use:
Spasticity associated with upper motor neuron disorders
Malignant hyperthermia
ADRs: generalized muscle weakness, sedation
A 43 y/o female becomes hypertensive and suffers a fatal acute coronary syndrome shortly after starting therapy on a drug. Autopsy reveals little in the way of coronary atherosclerosis, but ECG changes noted just before her death revealed significant myocardial ischemia in the myocardium served by the left anterior descending and circumflex coronary arteries. The cause of death is thought to involve coronary vasospasm. What drug most likely precipitated this event?
Bromocriptine for Parkinson’s disease
Ergotamine given to abort a migraine attack
Morphine for post-trauma analgesia
Phenytoin to manage generalized tonic-clonic seizures
Propofol for anesthesia induction
Answer: Ergotamine given to abort a migraine attack
- causes vasospasm
Bromocriptine is an ergot but is specific for dopamine
propofol, morphine, and phenytoin –> hypotension
Ergot Alkaloids
Agents: ergotamine, dihydroergotamine
MOA: cause constriction of peripheral and cranial blood vessels; may also effect presynaptic trigeminal nerve endings, inhibiting release of vasodilating peptides; agonist activity at 5-HT1D/1B receptors
ADRs: GI, prolonged vasospasm, abdominal pain, weakness, fatigue, paresthesias, drowsiness
CIs: obstructive vascular diseases, uncontrolled hypertension, hepatic or renal dysfunction, pregnancy
A 34 y/o female presents to her PCP with throbbing right-sided headaches. She experiences nausea, phonophobia, and photophobia with these headaches, but no aura. She usually has headaches 2 times/month. She is hypertensive and morbidly obese. Her only other medications include an oral contraceptive and hydrochlorothiazide. Which one of the following medications would you recommend for prophylaxis?
Amitriptyline Naproxen Propranolol Sumatriptan Valproic acid
Propranolol to help with hypertension
sumatriptan,
naproxen- acute migraine therapy
valproic acid- seizures
amitriptyline- depression
Migraine Prophylaxis
β-Adrenergic Antagonists
- metoprolol, propranolol
Calcium Channel Blockers
- verapamil
Antidepressants
- amitriptyline, venlafaxine, phenelzine
Anticonvulsants
- topiramate, valproate, divalproex sodium
A 24 y/o female presents with a history of frequent and severe migraine headaches. The decision is made to begin abortive therapy. Which of the following would be the most likely drug target? 5HT-1D/1B receptor B-adrenergic receptor D2 receptor GABA receptor Monoamine oxidase enzyme
5HT-1D/1B receptor
Serotonin (5-HT1D/1B) Agonists
Prototype: sumatriptan
MOA: activates 5-HT1D/1B receptors on presynaptic trigeminal nerve endings inhibiting release of vasodilating peptides [i.e., calcitonin gene-related peptide (CGRP)]; stimulates vasoconstriction, preventing vasodilation/stretching of pain endings
ADRs: altered sensations (tingling, warmth), dizziness, muscle weakness, fatigue, flushing, drowsiness, nausea, sweating, and neck pain; chest discomfort (1-5%)
CIs: coronary artery disease, angina, ischemic heart disease, uncontrolled hypertension
Two inhaled general anesthetics, A and B, have the following MAC values:
A – MAC 2%
B – MAC 100%
Based only on this information (note we have not named the drugs), which statement is true?
A. Drug A has a longer duration of action than Drug B
B. Drug A is more soluble in the blood than Drug B
C. Drug B causes greater analgesia and skeletal muscle relaxation than Drug A
D. Drug B requires a higher concentration of drug in inspired air for adequate anesthesia compared to Drug A
E. Drug B requires a significantly longer time (50X) to onset of adequate general anesthesia compared to Drug A
D. Drug B requires a higher concentration of drug in inspired air for adequate anesthesia compared to Drug A
Minimum alveolar concentration
Describes anesthetic potency
1.0 MAC = partial pressure of inhaled anesthetic, 50% of population remain immobile at skin incision
Value expressed as volume %
Successful anesthesia = 0.5 – 2 MAC
MAC is additive: 0.5 MAC of x + 0.5 MAC of y = 1 MAC
A 45 y/o male is admitted to the hospital to undergo a laparoscopic abdominal surgery. In the pre-operative waiting area, he is administered an agent which binds the GABA receptor (in the presence of GABA) to increase the frequency of channel opening. Which of the following was most likely administered? Benzocaine Dexmedetomidine Ketamine Midazolam Oxycodone
D. Midazolam
Benzocaine targets Na channel
Dexmedotomidine targets alpha 2
Ketamine–> NMDA
Oxycodone–> mu
A 45 y/o male is admitted to the hospital to undergo a laparoscopic abdominal surgery. Review of his medication record shows that an intravenous general anesthetic, which targets the GABA receptor and is formulated as a lipid emulsion, is administered for induction. What is/are the most likely adverse response(s) associated with the administration of this widely used drug?
Adrenocortical suppression
Emergence reactions and dissociative anesthesia
Malignant hyperthermia
Respiratory depression and hypotension
Seizures
Answer: Propofol–> respiratory depression and hypotension
Adrenocortical suppression is related to etomidate (used with CV patients)
emergence reactions and dissociative anesthesia– from ketamine
succinylcholine and volatile anesthetics –> malignant hyperthermia
A 40 y/o male presents with an upper respiratory viral infection. He is complaining of a severe sore throat, fever, cough, and runny nose. He would like a drug therapy recommendation to help alleviate his throat pain. You suggest an oral lozenge which decreases sodium ion permeability, inhibiting depolarization of the neuronal membrane. Which agent was most likely recommended? Benzocaine Bromocriptine Dexmedetomidine Ethosuximide Etomidate
Benzocaine
Local Anesthetics
Administration – drug is delivered directly to target organ
Loss of sensation in limited region of the body
Disrupts afferent neural traffic
May also cause muscle paralysis and suppression of somatic or visceral reflexes
A patient with Parkinson’s disease has signs and symptoms that can be considered “moderate” now, but they are worsening and not responding well to current drug therapy. The physician decides to empirically assess an antiparkinson drug that is a selective inhibitor of monoamine oxidase type B (MAO-B). What drug would that be? Benztropine Bromocriptine Carbidopa Rasagiline Ropinirole
Rasagiline
Benztropine is anti-muscarinic
bromocriptine is dopamine agonist
carbidopa is dopa decarboxylase inhibitor
A 70 y/o male presents with complaints of an increasingly stooped posture, tremors, and unsteadiness when he walks. Examination reveals a rest tremor of his right arm and leg, mild rigidity, and impaired rapid alternating movements in the right limbs. The physician decides combination drug therapy is appropriate at this time. Two agents are prescribed, what is the mechanism of action of the drug which works in the periphery rather than within the CNS? Dopa decarboxylase inhibitor Dopamine receptor agonist GABA receptor agonist Monoamine oxidase inhibitor Muscarinic antagonist
dopa decarboxylase inhibitor (allows more levodopa to the CNS, and smaller dose, and decreases side effects)
A 10 y/o male, who has been treated for epilepsy for a year, is referred to a periodontist for evaluation and probable treatment of massive overgrowth of his gingival tissues. Some teeth are almost completely covered with hyperplastic tissue. What is the mechanism of action for the drug most likely responsible for the oral pathology?
Answer: phenytoin stabilizes the inactivated form of the Na channel.
GABA pentin target calcium channel
benzos and barbituates target gaba receptors
A 22 y/o female was diagnosed with epilepsy after developing repeated episodes of generalized tonic-clonic seizures following a skiing accident. After initiating appropriate injectable drug therapy to address her seizures acutely, the decision is made to prescribe an agent which binds the synaptic vesicular protein SV2A. Once stabilized, what might be a unique adverse drug reaction that may arise during therapy? Gingival hyperplasia Hyponatremia Paresthesias Serious mood and behavioral changes Stevens-Johnson syndrome
levoterazepam –> Serious mood and behavioral changes
carbamazapine –> hyponatremia
carbamazapine and lamotragene -> Stevens Johnson (rash)
A 24 y/o female has just received a new diagnosis of focal seizures. She is otherwise healthy and her medication list contains only an oral contraceptive. If prescribed concurrently, which of the following drugs would be least likely to result in contraceptive failure? Carbamazepine Oxcarbazepine Phenobarbital Phenytoin Valproic acid
Answer; Valproic acid is an enzyme inhibitor
Phenobarbitol and phenytoin, carbamazepine and oxcarbazepine are inducers
Antiepileptic Drug (AED) Mechanisms of Action
Limit sustained, repetitive neuronal firing, mediated by promoting inactivated state of voltage-gated Na+ channels
Enhanced γ-aminobutyric acid (GABA) mediated synaptic inhibition, mediated by presynaptic/postsynaptic actions
Inhibition of voltage-gated Ca2+ channels
Enhanced Na+ Channel Inactivation (drugs)
carbamazepine phenytoin topiramate lamotrigine valproate zonisamide
Enhanced GABA Synaptic Transmission drugs
vigabatrin
valproate
tiagabine
GABA binding site: benzodiazepines and barbiturates
Reduced Ca2+ Channel Current drugs
valproate and ethosuximide
