AMiddle-Aged Caucasian Man with Anxiety
AMiddle-Aged Caucasian Man with Anxiety
Thecase study is about a 46-year old white male who works as a welder.His primary care physician refers the man to psychiatry after a tripto the emergency room where he showed symptoms of a heart attack. Thepatient indicated instances of chest tightness, shortness of breath,and a feeling of impending doom. He has light hypertension butmanages it with low sodium diet he is also a little overweight. Thepossibility of myocardial infarction was ruled out in the emergencyroom, and the electrocardiogram did not reveal significant results.The client admits that he occasionally consumes 3-4 beers to counterwork-related stress. The patient takes care of his aging parents andencounters stress at the workplace. The mental health exam revealsthat the client is alert and oriented however, he does not have anysuicidal or homicidal thoughts. The psychiatric-mental healthpractitioner (PMHNP) administered the Hamilton Anxiety Rating Scale(HAM-A) and revealed a score of 26. The PMHNP diagnosed the clientwith generalized anxiety disorder. The PMHNP made three treatmentdecisions for the patient the first was to apply Zoloft 50 mg podaily, start Imipramine 25 mg po BID, and useBuspirone.
Thefirst treatment option was Zoloft that was taken orally at 50milligrams daily. Zoloft is used to treat depression, panic attacks,obsessive-compulsive disorders, post-traumatic stress disorder, andanxiety. The medication was chosen because of its ability to lessenanxiety attacks within the shortest time possible. Pharmacodynamicsis the impact that medication has on the body while pharmacokineticsis the way the body reacts to the drug. Pharmacokinetics involves theprocesses of absorption, distribution, metabolism, and excretion ofmedications (Jann et al., 2016). Their mechanism of action typicallydescribes them as selective serotonin reuptake inhibitors (SSRIs)with the binding ability towards the serotonin transporter. Thetreatment works by restoring the balance of serotonin, which is anatural substance in the brain. The treatment undergoes an extensivefirst-pass metabolism, its principal initial pathway of metabolismbeing N-demethylation. It has a plasma termination half-life of62-104 hours (Devane et al. 2016, p. 250). The 50 mg dosage waschosen because of the weight of the client. His weight would make itpossible to absorb the medication. The expected result for the drugwas the reduction in panic attacks the outcomes were achieved aftertaking the medication for the first few months. The medicationincreased the client’s appetite, thus resulting in significantweight gain, and he experienced constant change in moods while on thedrug. The PMHNP informed the client that whenever he felt that he washaving an anxiety attack, he was free to call at any time. He wasalso advised that if his calls were not picked he could be calledback immediately. The client was notified of the benefits and sideeffects of the medication as required by the code of ethics.
Thesecond treatment option was to begin Imipramine at 25 mg, which istaken orally twice in a day. Imipramine belongs to the tricyclicgroup of antidepressants and it is known to be useful in thetreatment of anxiety attacks (Almatura et al., 2013). The expectedresults of the medication are reduced panic or anxiety attacks andelevated moods. However, the results differed with the desiredresults since the client experienced insomnia. Notably, insomniaensured that the patient did not get enough sleep therefore, he wasalways fatigued, thus increasing the risk of panic attacks triggeredby stress. As noted earlier, the client’s management at work isharsh therefore, if his productivity was lowered, it would stresshim out hence, leading to more anxiety attacks. Apart from insomnia,the patient also experienced constipation, weight gain, frequentsleepiness, and increased sweating. Imipramine works by preventingthe neuronal reuptake of neurotransmitters, norepinephrine, andserotonin (Devane 2016, p. 258). It binds the serotonin, which is asodium-dependent transporter and norepinephrine carrier,thuspreventing the reuptake of norepinephrine and serotonin by thenerve cells. Apart from inhibiting neurotransmitters re-uptake, thedrug causes down-regulation of cerebral cortical beta-adrenergicreceptors and reigniting of postsynaptic serotonergic receptors withchronic use, thus leading to an enhanced serotonergic transmission(Lader 2015, p. 425). It takes approximately two to four weeks forthe effects of the drug to be effective. Imipramine is rapidlyabsorbed after it is taken orally. Bioavailability is about 43percent, and the peak plasma concentration is attained at 1-2 hoursafter intake (Lader 2015, p. 428). Food does not influence the drugabsorption. Forty percent of the orally administered drug is secretedin urine within one day and seventy percent in three days. Slightamounts are eliminated in feces through biliary elimination.Imipramine has a half-life of 8-20 hours. Imipramine toxic signsprogress from depression, irregular breathing, convulsions, anddeath. As mentioned earlier, the client consumes alcohol, and it isvital to avoid such consumption when on Imipramine. The patientwasinformed of the risks and benefits of the drug before commencing thetreatment plan. The client was also told that he could call the PMHNPif he had any question regarding the use of the drug or if he feltlike he was relapsing.
Thethird treatment option was to begin Buspirone. Buspirone (BuSpar) isan anti-anxiety medication used to treat symptoms such as anxiety,fear, tension, irritability, pounding heartbeat, and dizziness.Buspirone attaches to serotonin receptors on neurons in the dorsalraphe and finally to the neurons located in the hippocampus.Therefore, it prevents the discharge rate or the receptors containingneurons in the dorsal raphe (Jann et al., 2016). Buspirone alsoattaches at dopamine receptors, which prevents the dopamine receptorsfrom working. Buspirone increases firing in the locus ceruleus, anarea of the brain where norepinephrine cell bodies are present inhigh concentration (Almatura et al., 2013). The mechanism ofbusiprone results in prevention of serotonergic activity andreactivity of noradrenergic and doperminergic cells. Buspirone isused in the treatment of generalized anxiety. The reason the PMHNPchose the medication is its benefit since it does not causedrowsiness and does not cause physical dependence. Buspirone isdifferent from typical anxiolytics since it does not causeanticonvulsant or muscle relaxant effects. It is also evident thatbuspirone highly binds to serotonin receptors. Besides, it has aminimal binding ability for brain D2-dopamine receptors. However,recent studies suggest that buspirone may have unintended effects onother neurotransmitter systems (Wu et al. 2014, p. 498). The drug iseasily assimilated in humans its bioavailability is low and changeseasily because of the large first pass metabolism. The drug binds toproteins at a rate of 95% that is about 70% bound to albumin, and30% bound to alpha 1 –acid glycoprotein. 29% to 63% of the drug issecreted primarily as metabolites through urine within one day (Wu etal. 2014, p. 500). 18% to 38% of the secretion is accounted for infecal matter (Jann et al., 2016). Buspirone has a half-life of 2-3hours however, the action of a single dose takes a long time thanthe listed half-life suggests. Some of the symptoms of toxicityinclude nausea, dizziness, stomach upsets, dizziness, and smallpupils. The client was warned to avoid alcohol, grapefruit, andgrapefruit juice while under medication. The medication significantlyreduced anxiety symptoms and was the best choice among the medicinessince it had minimal side effects the drug achieved the expectedresults.
Insummation, the case study is a 46-year old white male who works as awelder. His primary care physician refers the man to psychiatry aftera trip to the emergency room where he indicated symptoms of a heartattack. The patient showed cases of chest tightness, shortness ofbreath, and a feeling of impending doom. The psychiatric-mentalhealth practitioner (PMHNP) administered the Hamilton Anxiety RatingScale (HAM-A) and revealed a score of 26. The PMHNP diagnosed theclient with generalized anxiety disorder. The PMHNP made threetreatment decisions for the patient the first was to begin Zoloft 50mg po daily, start Imipramine 25 mg po BID, and applyBuspirone. Thereason Zoloft was chosen was its ability to lessen anxiety at theshortest time possible. Their mechanism of action typically describesthem as selective serotonin reuptake inhibitors (SSRIs) with thebinding ability towards the serotonin transporter. The treatmentworks by restoring the balance of serotonin, which is a naturalsubstance in the brain. The treatment undergoes an extensivefirst-pass metabolism, its principal initial pathway of metabolismbeing N-demethylation. It has a plasma termination half-life of62-104 hours. Imipramine belongs to the tricyclic group ofantidepressants and is known to be effective in the treatment ofanxiety attacks. The expected results of the medication are reducedpanic or anxiety attacks and elevated moods. However, the resultsdiffered with the desired outcomes since the client experiencedinsomnia. Notably, insomnia ensured that the patient did not getenough sleep therefore, he was always fatigued, thus increasing therisk of panic attacks triggered by stress. Buspirone (BuSpar) is ananti-anxiety medication used to treat symptoms such as anxiety, fear,tension, irritability, pounding heartbeat, and dizziness. The reasonthe PMHNP chose the drug is its benefits since it does not causedrowsiness and physical dependence. The medication significantlyreduced anxiety symptoms and was the best choice among themedications since it had minimal side effects the drug achieved theexpected results.
Altamura,A. C., Moliterno, D., Paletta, S., Maffini, M., Mauri, M. C.,&Bareggi, S. (2013). Understanding the pharmacokinetics ofanxiolytic drugs.Expertopinion on drug metabolism & toxicology,9(4),423-440.
DeVane,C. L. (2016). Clinical Pharmacokinetics and Pharmacodynamics ofAnxiolytics and Sedative/Hypnotics.InAppliedClinical Pharmacokinetics and Pharmacodynamics ofPsychopharmacological Agents(pp. 247-266). Springer International Publishing.
Jann,M. W., Penzak, S. R., & Cohen, L. J. (Eds.).(2016). AppliedClinical Pharmacokinetics and Pharmacodynamics ofPsychopharmacological Agents.Springer.
Lader,M. (2015).Generalized anxiety disorder.In Encyclopedia ofPsychopharmacology (pp. 699-702).Springer Berlin Heidelberg.
Wu,C. K., Huang, Y. T., Lee, J. K., Juang, J. M. J., Tsai, C. T., Lai,L. P., … & Lin, L. Y. (2014). Anti-anxiety drugs use andcardiovascular outcomes in patients with myocardial infarction: anational wide assessment. Atherosclerosis,235(2),496-502.