Instructions for Discussion Replies to 6 DQS

DO NOT JUST REPEAT SAME INFORMATION, DO NOT JUST SAY I AGREE OR THINGS LIKE THAT. YOU NEED TO ADD NEW INFORMATION TO DISCUSSION.

1- Each reply should be at least 200 words.

2- Minimum One Peer reviewed/scholarly reference ( NO MAYO CLINIC/ AHA)

3- APA 7th edition style needs to be followed.

4- Each response should have reference at the end of each reply

5- Reference should be within last 4 years

Q-1

TRIGEMINAL NEURALGIA (TN)

Presentation

Facial pain without associated neurologic deficit is essential in the diagnosis of trigeminal neuralgia. There is a restriction to the trigeminal nerve in the common distributions noting for the pattern, quality, duration and consistency of pain. In patients with symptomatic trigeminal neuralgia, bilateral involvement is more frequent. Distributions of the trigeminal nerve are: V1 ophthalmic, V2 maxillary and V3 mandibular. (Obermann, 2019).

Etiology

In the majority of patients, the etiology is associated with trigeminal nerve compression. Compression occurs to 80% to 90% of patients demonstrated focal compression of the trigeminal root at the root entry zone. Posterior fossa tumors can also produce symptoms imitating trigeminal neuralgia (TN). TN is twenty times more common in multiple sclerosis patients compared with the general population. MS patients with TN usually demonstrate demyelinating plaques in the pons that encompass the root entry zone of the trigeminal nerve (Obermann, 2019).

Common Differential Diagnosis

Dental caries, dental fracture, mandibular osteomyelitis, temporomandibular joint syndrome, migraine, glossopharyngeal neuralgia, post-herpetic neuralgia, temporal arteritis, or atypical facial pain (Bourenne et al., 2017).

Diagnostic Work-Up

Diagnosis is clinical with a history of outburst of sharp, superficial, stabbing, burning or intense pain lasting for up to 2 minutes. Triggers such as tooth brushing, eating, cold, and touch are common. Although most patients do not complain of neurologic deficit and are asymptomatic between episodes, patients are fearful of repeat attacks because of its intensity. Other important history to rule out TN are facial trauma, herpetic outbreak, rash or facial droop (Obermann, 2019).

Treatment Plan

Carbamazepine is the only anti-convulsant medication with efficacy proven in ramdomized controlled trials in TN and is typically first-line therapy. Seventy percent to seventy five percent of patients show at least partial improvement on Carbamazepine. Long-term use may be associated with decreased efficacy (Bourenne et al., 2017). Oxcarbazepine, a derivative of Carbamazepine with fewer drug-drug interactions, appear equally efficacious and may even be useful in patients with Carbamazepine resistant TN. There is some evidence for the effectiveness of Topiramate (Bourenne et al., 2017).

Referrals/Consultation

Patients started on medical therapy should be evaluated regularly for adverse reactions, documentation of efficacy of treatment, and/or dose adjustment until adequate pain control is achieved. Following uncomplicated surgical treatment, patients should be reevaluated about 1-week post-procedure to document resolution of symptoms and evaluate for the presence of complications. Subsequent evaluations are performed at longer time periods based on level of symptomatic relief, pain recurrence, and patient desire to wean medications (Bourenne et al., 2017).

Preventive Measures

No preventive strategies have been identified. However, patients may learn to avoid activities that trigger pain. Eat soft food, at room temperature warm or cool. Avoid food that trigger attacks such as caffeine and citrus fruits or other triggers that have caused pain in the past. If wind triggers pain, wear a scarf wrapped gently around the face in windy weather (Bourenne et al., 2017).

Reference:

Bourenne, J., Hraiech, S., Roch, A., Gainnier, M., Papazian, L., & Forel, J. (2017). Sedation and neuromuscular blocking agents in acute respiratory distress syndrome.

Annals of Translational Medicine, 5(14), 291-291. doi:10.21037/atm.2017.07.19

Obermann, M. (2019, April 17). Recent advances in understanding/managing trigeminal neuralgia. Retrieved March 30, 2021, from https://f1000research.com/articles/8-505

Q-2

Peritonsillar abscesses generally occur after tonsillitis and a localized collection of pus occurs between the tonsillar capsule and constrictor muscle (Gupta, 2020). The patient generally presents with a sore throat, possible referred ear pain, painful swallowing, halitosis, drooling if unable to swallow, muffled speech, neck pain, inability to open mouth, and possible fever/chills, body aches, etc. If it extends further the patient could be in respiratory distress. Differentials include tonsillitis, mononucleosis, pharyngitis, dental abscess, epiglottitis, AIDS, and malignancies.

The workup would include CBC, throat cultures, rapid strep, Antibody test (r/o infectious mono), ultrasound of neck to help with aspiration guidance, CT soft tissue of the neck, aspiration of pus, physical exam, and history, CRP if worried about systemic sepsis. The gold standard of diagnosis is to aspirate the pus, do an incision and drainage, or tonsillectomy. If the provider is not comfortable with doing the aspiration then a consult would need to go out to an otolaryngology, ENT, or general surgeon depending on the setting/hospital services that you have (Galioto, 2017). The most common bacteria involved are Group A streptococcus and Streptococcus milleri and initial antibiotics should be broad spectrum to cover these such as penicillin VK 500mg and metronidazole 500mg Q6H, Augmentin 875 BID, clindamycin 300-450mg Q8H, or third generation cephalosporins (Galioto, 2017). Corticosteroids and analgesics are the other therapies that can be added. The patient could need close supervision during the first few days to monitor for complications.  Complications include aspiration of pus, airway obstruction, thrombophlebitis, deep neck infection, or puncture/hemorrhage from carotid artery. The reasons for admission are dehydration, airway concern, persistent dysphagia, and failure of outpatient management. In the geriatric population is less heard of but when it is a differential diagnosis could be lymphoma in this setting. Follow up could include tonsillectomy since there is typically a high rate of reoccurance.

Gupta G, McDowell RH. Peritonsillar Abscess. [Updated 2020 Jul 21]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2021 Jan-. Available from: 

https://www.ncbi.nlm.nih.gov/books/NBK519520/

Galioto NJ. Peritonsillar Abscess. Am Fam Physician. 2017 Apr 15;95(8):501-506. PMID: 28409615.

Q-3

Deep neck infections frequently arise from the tonsils, parotid glands, cervical lymph nodes, dental and periodontal structures. Clinical presentation is variable and based on whether the infection is local or systematic. In addition to fever and neck pain, associated symptoms might include dental pain, dysphagia, stridor, dysphonia, trismus, and respiratory distress. Inspection of the neck may reveal asymmetry, redness, swelling,  and regional lymphadenitis (Maharaj, Ahmed, & Pillay, 2019).

Malignancy would be on my differential list, as well as an infectious process such as an abscess. Infection can easily spread from dental abscesses, sublingual or submaxillary salivary glands, or oral infections following trauma. Medial displacement of the uvula along with tonsillar asymmetry would suggest a peritonsillar abscess. Ludwig’s angina can lead to life-threatening airway obstruction if untreated and should be part of the differential. It should be suspected when there is cellulitis on the floor of the mouth, along with drooling and inability to swallow. Cervical adenitis would also be suspected when patients present with sore throat, cough, fever, chills, or have other upper respiratory manifestations (Motahari et al., 2015).

 Diagnosing deep neck infection includes computed tomography with contrast and magnetic resonance imagining. Although not adequate for deep infections, ultrasound is useful to differentiate an abscess from phlegmon, which is unbounded and can keep spreading out along tissue. A chest x-ray would show active infection including tuberculosis, a foreign body, mediastinitis, pneumomediastinum, or empyema. I would order a CBC to look for leukocytosis, and blood cultures which may reveal frequently encountered microorganisms such as Streptococcus, Staphylococcus aureus, Klebsiella, gram-negative rods, and fungi. Furthermore, the type of causative organism would be influenced by the presence of risk factors such as immunocompromised state, diabetes, and intravenous drug use (Motahari et al., 2015).

Intravenous nafcillin or vancomycin plus gentamycin, ampicillin/sulbactam, or clindamycin are generally accepted initial choices. For MRSA infections, vancomycin or linezolid plus cefepime can be used. Consultation with infectious disease and ENT specialists, surgery, and oncology would be appropriate. Surgical drainage becomes necessary with persistent draining wounds or for infections not responding to standard medical management (Caccamese & Coletti, 2018).

Caccamese, J. F., Jr, & Coletti, D. P. (2018). Deep neck infections: clinical considerations in aggressive disease. Oral and maxillofacial surgery clinics of North America, 20(3), 367–380. https://doi.org/10.1016/j.coms.2008.03.001

Maharaj, S., Ahmed, S., & Pillay, P. (2019). Deep Neck Space Infections: A Case Series and Review of the Literature. Clinical medicine insights. Ear, nose and throat, 12, 1179550619871274. 

https://doi.org/10.1177/1179550619871274

Motahari, S. J., Poormoosa, R., Nikkhah, M., Bahari, M., Shirazy, S. M., & Khavarinejad, F. (2015). Treatment and prognosis of deep neck infections. Indian journal of otolaryngology and head and neck surgery : official publication of the Association of Otolaryngologists of India, 67(Suppl 1), 134–137. https://doi.org/10.1007/s12070-014-0802-7

Q-1

Adrenal Insufficiency (Addison’s Disease)

Etiology

The most common cause of Addison’s disease (80 to 90%) in developed countries is by dysfunction of autoimmune system with antibodies directed against the adrenal cortex or 21-hydroxylase, a steroid involved in biosynthesis of aldosterone and cortisol, present in patients with autoimmune dysfunction (Huecker, 2021). Tuberculosis is another cause in endemic countries. Less common origins are infectious disease that results in destruction of the adrenal glands, systemic fungal infection, opportunistic infections secondary to HIV, metastatic malignancies, medications, and some conditions that interfere with cortisol synthesis (Huecker, 2021).

Clinical Manifestations

Substantial weakness associated with mucocutaneous hyperpigmentation, hypotension and/or postural hypotension and salt craving (Huecker, 2021).

Common Presentation

Fatigue is commonly reported by patients maybe described as weakness or tiredness, anorexia, weight loss, hyperpigmentation evident in mucosa and sun-exposed areas notable in palmar crease, scars and areas of friction. Hyponatremia is a result of decreased aldosterone production. Salt craving is specific to Addison’s disease but is only demonstrated by 16% of patients (Huecker, 2021).

Consultant orders for diagnostic test

The first diagnostic test I will order is the morning plasma cortisol level between 8 am and 9 am when the cortisol levels peak. If the patient’s cortisol level is 3 to 18 mcg/dL, I will order further testing with ACTH stimulation test also known as Cosyntropin test. It is ordered when morning serum cortisol does not confirm or exclude adrenal insufficiency (Mongioì et al., 2019). This test can be performed at any time of the day. Cosyntropin is a synthetic derivative of adrenocorticotropic hormone (ACTH) that is used in the evaluation and diagnosis of patients with adrenocortical insufficiency. The pharmacologic profile of Cosyntropin is similar to that of purified natural ACTH. If cortisol levels below 18 micrograms/dL are found at either 30 or 60-minutes after ACTH stimulation, the diagnosis of adrenal insufficiency is highly likely (Mongioì et al., 2019).

Treatment

Oral glucocorticoid and mineralocorticoid replacement therapy is given in physiologic doses for life. I will prescribe a short-acting glucocorticoid such as Hydrocortisone 15-30 mg/day PO in 2 divided doses 8am and 4pm. I will provide education so they know when to increase replacement doses appropriately when febrile, vomiting or in preparation for elective surgical procedures, stress, trauma, infection and pregnancy (Huecker, 2021). Persistent fatigue is evident of insufficient dosage. Excessive weight gain or facial plethora is present of over-replacement (Huecker, 2021).

Preventive Care

Patient education is important in the prevention of adrenal crisis. A regular review by an endocrinologist, in the months following diagnosis and then six to 12 months thereafter, is recommended after a pertinent acute presentation with an adrenal crisis. Patients need to be encouraged to make relevant adjustments to their own medication, in the absence of their treating physician, and to adapt their dose according to individual needs (Dineen et al., 2019).

Reference:

Dineen, R., Thompson, C. J., & Sherlock, M. (2019). Adrenal crisis: Prevention and management in adult patients. Therapeutic Advances in Endocrinology and Metabolism, 10, 204201881984821. doi:10.1177/2042018819848218

Huecker, M. (2021, February 07). Adrenal insufficiency. Retrieved April 06, 2021, from https://www.ncbi.nlm.nih.gov/books/NBK441832/

Mongioì, L. M., Condorelli, R. A., Barbagallo, F., Cannarella, R., La Vignera, S., & Calogero, A. E. (2019). Accuracy of the low-dose acth stimulation test for adrenal insufficiency diagnosis: A re-assessment of the cut-off value. Journal of Clinical Medicine, 8(6), 806. doi:10.3390/jcm8060806

Q-2

Hyperprolactinemia is a condition resulting from elevated serum prolactin that occurs from prolactinomas and from a pituitary adenoma. Transient mildly elevation from transient factors such as food, exercise, stress, and chest wall stimulation and moderate elevation can be caused by pregnancy, primary hypothyroidism, renal failure, cirrhosis, and medications such as metoclopramide, calcium-channel blockers, phenothiazines, SSRIs, and risperidone (Jain, & Katznelson, 2019). Any sellar tumors may compress the pituitary stalk, reduce the dopamine delivery to the gland leading to elevation of prolactin levels up to 150 ng/ml.

The majority of patients are asymptomatic due to concomitance of other diseases and some may develop hypogonadism symptoms such as galactorrhea, menstrual disorders, fertility problems, gynecomastia in men, and neuroradiological abnormalities (Vilar, Vilar, Lyra, & da Conceicao Freitas, 2019). Diagnosis by history to rule out other causes of pregnancy, drug-induced or secondary diseases such as hypothyroidism, and renal failure. Lab test for elevated prolactin levels, imaging study CT or MRI and differentiate from other pituitary tumors by gel filtration or polyethylene glycol precipitation (Kasum, Orešković, Čehić, Šunj, Lila, & Ejubović, 2017). Macroprolactinomas are a tumor size more than >10 mm in greatest diameter and produce prolactin levels of > 150 ng/ml (Jain, & Katznelson, 2019).

Consult to an endocrinologist is appropriate for the management of prolactinoma and for neurosurgery for surgical treatment and oncologist for radiotherapy for failed medical and surgical therapy and OB/GYN consultation if the condition coexists with pregnancy and lactation.

Treatment is by dopamine agonist such as bromocriptine started at 1.25 mg at bedtime and slowly titrated up to 2.5 mg twice a day and cabergoline is expensive than bromocriptine and better tolerated at a dose of 0.25 mg once weekly and titrated up to 1 mg twice a week (Jain, & Katznelson, 2019). Lab monitoring of prolactin levels and intermittent MRI is needed to monitor the effectiveness of therapy. Transsphenoidal surgery is indicated when the medical treatment fails or due to cystic tumors which do not respond to dopamine agonist. A radiotherapy is also an option who fails medical and surgical therapy. Management of postoperative complications such as anterior pituitary insufficiency and diabetes insipidus, sinusitis and perforation of nasal septum and CSF leakage, meningitis, intracranial hemorrhage, epistaxis, and visual deficits. Follow-up visits with endocrinology and neurosurgery. Education and counseling regarding monitoring of those complications and to report on time and have extra glucocorticoid tablets and medical identification alert for them.

Reference.

Jain, S.H., & Katznelson, L. (2019). Pituitary disorders. In S.C. McKean, J.J. Ros, D.D. Dressler & D.B. Scheurer. (2nd ed.), Principles and practice of hospital medicine, 2e. Vol.1 (PP.1248-1251). Retrieved from https://lccn.loc.gov/2016022668

Vilar, L., Vilar, C. F., Lyra, R., & da Conceicao Freitas, M. (2019). Pitfalls in the diagnostic evaluation of hyperprolactinemia. Neuroendocrinology, 109(1), 7-19. Retrieved from https://www.karger.com/Article/Abstract/499694

Kasum, M., Orešković, S., Čehić, E., Šunj, M., Lila, A., & Ejubović, E. (2017). Laboratory and clinical significance of macroprolactinemia in women with hyperprolactinemia. Taiwanese journal of obstetrics and gynecology, 56(6), 719-724. Retrieved from https://www.sciencedirect.com/science/article/pii/S1028455917302413

Q-3

Adrenal crisis is a life-threatening condition that is caused by low levels of cortisol that is produced by the adrenal gland (Elshimy, et al.,2020). Cortisol is essential to maintain glucose, suppress immune response in relation to the body response to stress. Generally, there is something that stresses the body to go into a crisis such as infection, dehydration, stress, etc. It generally occurs in patients with known adrenal insufficiency from primary or secondary causes. In stressful situations the patients cannot replace the used cortisol sending them into a crisis. Most are caused by undiagnosed Addison’s disease, followed by infiltrative diseases, iatrogenic causes, pituitary causes, and medications. Symptoms of Adrenal crisis are headache, weakness, fatigue, nausea vomiting, low blood pressure, confusion, electrolyte abnormalities, abdominal pain, and fever.

Patients present usually very sick and appear in shock and will need to get collateral information such as adrenal insufficiency issues. Initial symptoms are nausea/vomiting, fever, abdominal pain, hypotension, altered mental status. They may have hyperpigmentation of the skin, have Cushingoid symptoms from chronic steroid use, fevers, and could slip into a coma if cortisol levels are depleted (Rathbun, et al.,2020). Obtaining labs such as CMP, CBC, cortisol levels, ACTH, aldosterone, renin, and thyroid function. The electrolytes may show dehydration with hyponatremia, hyperkalemia, hypoglycemia, and acute renal injury. Treatment includes fluid replacement (2-3L of NS or 5% dextrose) glucocorticoid replacement (hydrocortisone 100mg bolus first followed by 100-300mg per day for another 2-3 days (Puar, et al., 2016). The rapid correction of hyponatremia should be avoided, and treatment of fluids should be titrated to urine output. Long term treatment includes hydrocortisone, prednisone, or methylprednisolone, or fludrocortisone acetate (if aldosterone is low), and making sure the patient gets enough salt in the diet.

Elshimy G, Alghoula F, Jeong JM. Adrenal Crisis. [Updated 2020 Nov 20]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2021 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK499968/

Rathbun KM, Nguyen M, Singhal M. Addisonian Crisis. [Updated 2020 Dec 8]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2021 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK441933/

Puar, T. H., Stikkelbroeck, N. M., Smans, L. C., Zelissen, P. M., & Hermus, A. R. (2016). Adrenal crisis: Still a deadly event in the 21st century. The American Journal of Medicine, 129(3). doi:10.1016/j.amjmed.2015.08.021