Seizure Disorders Pathophysiology and Pharmacological Intervention (Coursework Sample)

Seizure Disorders Pathophysiology and Pharmacological Intervention
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Introduction
Pharmacology involves the study of drug and their effect on living systems following administration. Nurses ought to possess a vast background in pharmacology to offer patients adequate information about medication regarding dosages, interactions with other drugs and the possible side effects. Lack of experience in this area may put the patients at risk and hence the improved efforts to incorporate pharmacology education in nursing curriculum (Barkhouse-MacKeen and Murphy, 2013). Half-life is described as the action period of a drug within an organism within which the concentration of the medicine can be reduced to half its concentration in the blood plasma.
Such background is vital to improving treatment outcomes and the quality of life for epileptic patients by ensuring patient-centered care. With the increasing need to access medicines faster and more efficiently, prescription drug duties are extended to the whole medical staff hence the need for a qualification in pharmacology (Barkhouse-MacKeen and Murphy, 2013). This paper seeks to provide insight on seizure disorders which continue to affect many worldwide, and the role nurses can play in understanding its pathophysiology and pharmacological interventions.
Disease process
Seizure disorders entail episodes of neurologic dysfunction where abnormal neuronal firing manifests as changes in sensory perception, behavior, motor control and autonomic function. In epilepsy, recurrent seizures arise spontaneously from aberrant electrical activity in the brain. These activities stem from the cellular biochemical processes that enhance neuronal hyperexcitability and hypersynchrony (Johannessen-Landmark and Patsalos, 2010)). In hyper synchronization, the generation of an impulse results in multiple neurons firing to bring about seizures. These disorders have a heterogeneous clinical expression, etiologies, and pathophysiology.
The pathogenesis of seizures is either idiopathic or reactive. For instance, in reactive seizures, the normal nonepileptic tissue is involved where hypoglycemia patients react to excessively low blood sugar. Brodie (2010) argues that meningitis and encephalitis lead to the inflammation of cerebral tissues hence causing seizure disorders. Other reasons include hypoxia, severe dehydration, and hyponatremia. Idiopathic seizures involve the chronically epileptic tissue. Drugs such as amphetamines, cocaine and withdrawal from opiates may lead to seizures development or exacerbation.
The hypersynchronous discharges in seizures begin in the cortex and spread to neighboring tissues. Seizure initiation has two distinctive concurrent events including the high-frequency firing of action potentials and the hype synchronization of neurons. Calcium ions gain entry into the neuronal membrane results in prolonged depolarization and action potential bursts followed by a rapid repolarization and a hyperpolarization (paroxysmal depolarizing shift).
GABA receptors, potassium ions efflux or chloride ions influx mediate the subsequent hyperpolarizing after-potential (Johannessen-Landmark and Patsalos, 2010). Seizure propagation occurs when activation can excite neighboring neurons spreads partial seizures within the brain. As a result, the surround inhibition is lost thus the seizure activity spreads via cortical connections and long association pathways. Usually, regions of surrounding inhibition formed by inhibitory neurons are meant to prevent the spread of the bursting activity together with hyperpolarization.
With adequate activation, neighboring cells are recruited resulting in three outcomes. To begin the repetitive discharges lead to an increase in the extracellular potassium ions hence depolarizing the adjacent neurons. Second, calcium ions accumulate in the presynaptic terminals hence causing a greater release of neurotransmitter. Lastly, there is the activation of NMDA excitatory amino acid receptors hence more calcium ion influx and activation of neurons (Brodie, 2010).
The persistent depolarization of the neurons in the cortical region causes gradual variations in the neuronal integrity and local homeostasis thus manifesting as ionic fluxes, altered gene expression, nerve arborization and synaptic reorganization. Ultimately, irreversible damage to the cells occurs causing cell loss. At the physiologic level, there is an increased metabolic demand in the brain followed by increased blood flow to the brain and increased anaerobic respiration. Later, the autoregulation of the brain disintegrates as the cerebral blood flow reduces due to organ dysfunction and systemic hypotension. Prolonged severe disorders are associated with cardiac dysfunction, hypoxia, and cerebral edema thus explaining the high mortality (Sreenath et al., 2010).
Medical Treatment
Benzodiazepines are administered as a conventional management of seizure disorders. These include lorazepam, an initial dose of 2-3 mg twice or thrice a day and a 1-2 mg for maintenance. Its therapeutic effect is longer, and the medication is associated with lower risks of respiratory suppression and venous thrombophlebitis. Benzodiazepine drugs mediate the condition through an antagonistic effect on the GABA receptors thus exerting an inhibitory effect on the neurons. At high concentrations, they limit the repetitive neuronal firing. Lorazepam is administered by parenteral and oral routes. The primary adverse effects include sedation and suppression of the respiratory system. Lorazepam has a greater duration of action (Sreenath et al., 2010).)
Phenytoin, also known as Dilantin (18 mg) is relatively cheap, has a greater duration of action and familiarity with medical professionals. Some of the adverse effects include drug rashes, hypotension, eosinophilia, unstable serum concentrations, and irritative thrombophlebitis. The medicine induces the P450 system hence increasing the metabolism of other medications that are prescribed concurrently. The concentration of the plasma has an influence on the half-life of phenytoin which is typically 24 hours. The drug is bound to albumin, and hence, the level of free and unbound Dilantin is dependent on the albumin levels (Johannessen-Landmark and Patsalos, 2010).
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