Opioids Opioids are derivatives of opium. Morphine is the pure alkaloid form. Katzung et. al relate the name of this pharmaceutical to Mor- pheus, the Greek god of dreams (2018, p. 553). Opioids may be administered via oral, intramuscular and subcutaneous pathways. First-pass elimination is dependent upon method of administra- tion. This class of narcotics induces analgesic effects by binding to protein receptors in the brain, spinal cord and possibly periph- eral nerve endings, associated with pain modulation. Opioids are administered in a wide variety of clinical presentations that involve pain perception in terms of sensory and affective (emo - tional) components. Typical effects also include subjective eupho- ria; sedation; depression of cough, respiratory, renal and uterine function; truncal rigidity; nausea/vomiting; decreased percentage of stage 3 and 4 sleep states; and constipation. General duration of effects vary from one to eight hours. Maximum efficacy is rela- tive to drug design and dosage. Common opioids also include hydromorphone, oxymorphone, methadone, fentanyl, codeine, hydrocodone and oxycodone. In the acute inpatient setting, opi- oids are commonly used to manage variable acute and chronic complaints. Opioids are commonly associated with tolerance and dependence, the nature of which is currently hypothetical. In ad - dition, opioids may also induce hyperalgesia, most often in the context of chronic pain. Physical therapy media and culture has developed a strong cam- paign against habitual prescription use and abuse of opioids. In- cidents of opioid-induced respiratory failure and death are signifi- cant. Opioid addiction is considered to be a crisis in the United States. It is estimated that the United States consumes approxi- mately 80 percent of the world’s opioids (Katzung, 2018, p. 569). Anticoagulants Anticoagulant drugs limit blood coagulation, and are commonly applied in clinical presence of thromboembolic disease, chronic atrial fibrillation, deep vein thrombi, pulmonary emobili, and ce- rebral vascular accidents (strokes). Heparin is a common antico- agulant administered via intravenous or subcutaneous injection to enhance the physiologic function of endogenous antithrombin, which effectively inhibits clot formation. While Heparin is more commonly applied to induce rapid anticoagulation, it presents poor bioavailability in parenteral form. In contrast, warfarin (aka Coumadin) is chemically structured to present with 100 percent bioavailability and a 36-hour half-life when administered orally, making it one of the most commonly prescribed drugs (Katzung, 2018, p. 614). Fibrinolytic drugs form the serine protease known as plasmin , which effectively lyses thrombi in rapid fashion, and may be invoked by endogenous activation of tissue plasminogen activators (t-PAs). Fibrinolytic pharmaceuticals, such as alteplase, reteplase and tenecteplase, are administered within clinically de - fined therapeutic windows in the presence of cerebral vascular accidents, in order to lyse cerebral thrombi and potentially reduce local brain tissue ischemia. In addition, anti-platelet agents, such as aspirin, prohibit cyclooxygenase-thromboxane interactions, and are a commonly prescribed anti-coagulant following myocar- dial infarction and/or stroke. Anti-coagulants inherently present increased risk of bleeding, whether spontaneous or due to trauma, relative to pharmaceu - tical dosage and duration of use. Primary concerns of physical therapist who may treat patients taking anti-coagulants in both inpatient and outpatient settings include negating fall risk, recog- nizing potential signs of acute hemorrhage, and enacting emer- gency response systems. Corticosteroids Synthetic corticosteroids are applied in general presentation of a wide variety of inflammatory and immunologic disorders. Syn- thetic corticosteroids enact anti-inflammatory and immunosup- pressive activity by inhibiting function of physiologic immunity mediators such as lymphocytes, macrophages, neutrophils, eosin- ophils and basophils (Katzung, 2018, p. 708). Local effects, such as those induced by dexamethasone, include vasoconstriction when applied at the dermal level. While dexamethasone has been commonly employed by physical therapists in outpatient clinical
local anesthetic precision to reduce required recovery periods following surgical intervention. Amendments in position during administration along with pharmaceutical choice may affect dura- tion of somatosensory versus motor effects. Risks associated with receiving local epidural anesthesia include neural injury as well as chronic persistent transient neurologic symptoms. While etiology of the adverse effects is not well understood, current evidence does not report connection between clinical effect and toxicity. This is an additional area of concern for physical therapists, as patients may present to outpatient clinics following orthopedic surgical intervention with complaints of transient neurologic pain, which inherently requires more of a pain science-based therapeu- tic approach. Muscle relaxants Muscle relaxants are most commonly applied either to induce controlled muscle paralysis during surgery and/or intensive/criti- cal care, or to diminish painful states of relative muscle spasticity. Muscle relaxants act by interrupting function of myelinated so- matic nerves, unmyelinated motor nerve terminals, nicotinic ace - tylcholine receptors, the motor end plate, muscle membrane and intracellular muscle contractile system (Katzung, 2018, p. 475). Neuromuscular blocking pharmaceuticals, such as succinylcho- line, vecuronium, cisatracurium and rocuronium, bind to acetyl- choline receptors at the neuromuscular junction. These drugs may be applied alongside general anesthesia during surgical interven- tion to enhance muscular relaxation and reduce tetanic twitches, reduce pharyngeal and laryngeal muscle spasms during endotra- cheal tube placement, and improve ventilatory compliance dur- ing mechanical ventilation (Katzung, 2018, p. 485). Antispasmodic and spasmolytic drugs are applied in the presence of peripheral musculoskeletal pathologies as well as upper motor neuron le- sions. These pharmaceuticals include benzodiazepines such as diazepam, botulinum toxin (Botox), baclofen, tizanidine and dan- trolene. Physical therapists may encounter patients receiving mus- cle relaxants in cases of cerebral palsy, cerebral vascular accident, spinal cord injury and multiple sclerosis. Parkinsonism and movement disorder pharmacology Pathologic movements such as rigidity, bradykinesia, tremors, chorea, tics, athetosis and dystonia characterize general move- ment disorders. Though not well understood, the majority of movement disorders are relatively associated with dysfunction at or near the basal ganglia. Specifically, the etiology of Parkinson- ism is associated with reduced dopaminergic production and ac- tivity in the basal ganglia. In turn, pharmacologic management of Parkinsonism revolves around supplying dopamine, most com- monly in the form of Levodopa, a metabolic precursor with chemi- cal characteristics suitable to cross the blood-brain-barrier, along with carbidopa, which decreases peripheral conversion of levodo- pa to dopamine. This pharmaceutical combination is known as sinemet . Common concerns associated with prolonged levodopa administration include adverse behavioral effects, “dopa”-dyski- nesias of the face and distal extremities, and fluctuations in clinical response (Katzung, 2018, p. 497). Additional dopamine receptor agonists, monoamine oxidase and catechol-o-methyltransferase inhibitors, may enhance the effects and prolong dopaminergic presence and activity. Physical therapists commonly treat patients with Parkinsonism across the rehab spectrum, including acute hospital inpatient admissions, acute neurologic inpatient facility rehab, skilled nursing facility rehab, home health, and/or outpa- tient settings. Therefore, knowledge pertaining to the interaction between the aforementioned pharmaceuticals and pathological progression may allot the best plan of care with regards to im- proving functional movement. Additional movement disorders, such as Huntington’s disease, may present pathologic movements associated with overactiv- ity in dopaminergic pathways. Huntington’s disease in particular may be pharmaceutically managed with combinations of beta- blockers, such as propranolol, benzodiazepines and antiepileptic drugs to reduce involuntary choreatic movements and associated dementia.
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