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NR 603 APEA Predictor 2024/2025: Latest Exam Questions and Solutions, Exams of Nursing

A collection of multiple-choice questions and answers, along with detailed explanations, covering various topics related to the nr 603 apea predictor exam. The questions are designed to test knowledge and understanding of key concepts in the field of medicine, particularly in areas such as neurology, cardiology, and emergency medicine. Valuable for students preparing for the nr 603 apea predictor exam, as it offers a comprehensive overview of potential exam questions and provides insights into the correct answers and underlying rationales.

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2024/2025

Available from 11/01/2024

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NR 603 APEA PREDICTOR 2024/

LATEST EXAM WITH ALL POSSIBLE

QUESTIONS AND VERIFIED CORRECT

SOLUTIONS (RATIONALES

PROVIDED)/GRADED A+

Question In addition to life saving interventions, what prescription medication will most benefit this patient at this time? Answer Choices 1 Furosemide (loop diuretic) 2 Prednisone (glucocorticoid) 3 Tranexamic acid (antifibrinolytic agent) 4 Labetolol (beta blocker) 5 Nimodipine (calcium channel blocker) ANS: 5 Nimodipine (CCB) Nimodipine, a calcium channel blocker, has been shown to improve outcomes in patients following aneurysmal SAH. The mechanism of action is thought to be prevention of ischemia. Glucocorticoids (e.g., prednisone) are often utilized in patients with SAH because they offer symptomatic relief of headache and neck pain, but they have not been proved to decrease cerebral edema. Antifibrinolytic agents (e.g., Tranexamic acid) can be utilized in patients with a diagnosed aneurysm who cannot undergo directed treatment, but they are not routinely used following aneurysmal rupture. Labetalol (a beta blocker) may be utilized to treat elevated BP, but it must be used with caution because it can also decrease cerebral perfusion. Diuretics (e.g., furosemide) have no identified role in the treatment of aneurysmal SAH. A 75-year-old man is involved in a motor vehicle accident and strikes his forehead on the windshield. He complains of neck pain and severe burning in

his shoulders and arms. His physical examination reveals weakness of his upper extremities. What type of spinal cord injury does this patient have? A anterior cord syndrome B central cord syndrome C Brown-Séquard syndrome D complete cord transection E cauda equina syndrome ANS: B Central Cord Syndrome the central cord syndrome involves loss of motor function that is more severe in the upper extremities than in the lower extremities, and is more severe in the hands. There is typically hyperesthesia over the shoulders and arms. Anterior cord syndrome presents with paraplegia or quadriplegia, loss of lateral spinothalamic function with preservation of posterior column function. Brown-Séquard syndrome consists of weakness and loss of posterior column function on one side of the body distal to the lesion with contralateral loss of lateral spinothalamic function one to two levels below the lesion. Complete cord transection would affect motor and sensory function distal to the lesion. Cauda equina syndrome typically presents as low back pain with radiculopathy. A 37-year-old man fell from a ladder as he finished hanging the Christmas lights on his house. The right side of his head hit the alley cement, and he lost consciousness for about 1 minute; he woke up with a headache, but he had no other complaints. A few hours later, the patient is brought to the emergency room by his neighbor because of an intense headache, confusion, and left hand hemiparesis. On examination, the patient has a bruise located over the right temporal region, mydriasis, and right deviation of the right eye, papilledema, and left extensor plantar response. An emergency CT scan of the head without contrast reveals a lens-shaped hyper-density under the right temporal bone with mass effect and edema. What is the most likely diagnosis? Answer Choices 1 Epidural hematoma 2 Subdural hematoma

3 Subarachnoid hemorrhage 4 Intracerebral parenchymal hemorrhage 5 Acute meningitis ANS: 1 Epidural Hematoma Epidural hematoma most often results from a traumatic tear of the middle meningeal artery. Although a lucid interval ranging from minutes to hours followed by altered mental status and focal deficits is typical for epidural hematoma, this clinical picture is only encountered in up to 1/3 of the patients. The collection of blood between the skull and dura mater causes an evident mass effect with ophthalmic

4 nerve palsy and the contralateral hemiparesis. Surgical evacuation of the clot via burr holes is the treatment of choice. Subdural hematoma results from a traumatic rupture of the bridging veins that connect the cerebrum to the venous sinuses within the dura. This venous hemorrhage will result in a gradual increase of the hematoma, with a progressive clinical picture over days or weeks. The CT scan will show a concave, crescent-shaped hyper-density compared to the convex, lens-shaped hyper-density in epidural hematoma. Subarachnoid hemorrhage is the result of an aneurysm rupture; the most common is the congenital berry aneurysm. The clinical picture is of a sudden, severe headache with meningeal irritation. A CT scan will show blood in the subarachnoid space, and a lumbar puncture will reveal xanthochromia CSF. Intracerebral parenchymal hemorrhage is most likely caused by hypertension complicated with Charcot- Bouchard aneurysms. The blood accumulates into the brain substance and most commonly involves the basal ganglia. Acute meningitis is not associated with trauma. Fever and signs of meningeal irritation dominate the clinical picture. Lumbar puncture, indicated if there are no focal neurological signs on clinical examination, will be the diagnostic procedure. The CT scan of the patient presented in this case is characteristic for epidural hematoma, and there is no indication for a lumbar puncture. A 1-year-old boy presents with increasing lethargy. He is barely responsive, and his parents deny any trauma or injury. What is the most common cause of nontraumatic altered levels of consciousness? Answer Choices 1 Seizure disorder 2 Diabetic ketoacidosis 3 Inborn errors of metabolism 4 Toxic

5 ingestion 5 Infectio n ANS: infection Awareness of self and the surrounding environment or consciousness may be altered into different abnormal states of consciousness. Consciousness can shift from loss of clear thinking or confusion, usually accompanied by disorientation, to delirium, a succession of confused and unconnected ideas manifested in children as extreme mental and motor excitement, to lethargy, a profound type of slumber where movement or speech is limited, to stupor or deep sleep where arousal is achieved only by repeated vigorous stimuli, finally to coma, unresponsiveness to even painful stimuli. Non-traumatic coma is most common in infants and toddlers with another smaller peak of occurrence in adolescence. The most common cause of non-traumatic altered level of consciousness in children is infection of either the brain (encephalitis), meninges (meningitis), or both; infections account for more than 1/3 of cases. Prolonged seizures, anticonvulsive therapy, and postictal states can also lead to altered levels of consciousness. The most common metabolic cause of alteration of consciousness is diabetic ketoacidosis, which can occur at any age, but is most common in adolescence. Caused by severe insulin deficiency, hyperglycemia and ketogenesis lead initially to polyuria, polydipsia, hyperpnea, vomiting, and abdominal pain. As the process progresses, hyperosmolar dehydration and acid/base and electrolyte disturbances occur. Advanced stages alter level of consciousness and can lead to coma. Alterations of consciousness due to inborn errors of metabolism that present with electrolyte and glucose abnormalities typically present in infancy. The availability of gluconeogenic precursors or the functions of the enzymes required for production of hepatic glucose are affected. Metabolic defects causing hypoglycemia include glycogen storage disease, galactosemia, fatty acid oxidation defects,

6 carnitine deficiency, several of the amino acidemias, hereditary fructose intolerance, and defects of other gluconeogenic enzymes. Toxic ingestion and exposure are very common in toddlers and adolescents, with a toddler's ability to explore his environment filled with often brightly colored medications and intentional ingestion by adolescents typically involving over-the-counter medications or psychotropic drugs such as antidepressants. A 44-year-old man starts to notice that his eyelids are drooping. Some time afterwards, his jaw becomes weak. He has difficulty swallowing and also experiences weakness in his limbs. He is quite embarrassed when he eats because he must use his hand to help support his jaw. His weakness gets progressively worse. Finally, he seeks medical attention. His physical examination demonstrates the weakness in his limbs; however, no sensory defects are present. A Tensilon test is done and is positive. His doctor is concerned about an associated malignancy. What is the underlying pathology of this disease? Answer Choices 1 Inhibition of acetylcholine release 2 Blockage of the sodium channels 3 Demyelination 4 Subacute combined degeneration of the spinal cord 5 Antibodies to the acetylcholine receptor ANS: 5 5 Antibodies to the acetylcholine receptor Antibodies directed towards the acetylcholine receptor at the neuromuscular junction are seen with myasthenia gravis. This man has myasthenia gravis. Ocular muscle weakness, ptosis, dysphagia, and limb weakness can all be seen with myasthenia gravis. When the initial symptom is ocular weakness, Eaton Lambert Syndrome is extremely unlikely. Eaton Lambert Syndrome tends to not involve the extra-ocular muscles or the muscles involving chewing, swallowing, or speech.

7 The Tensilon test is used in the diagnosis of myasthenia gravis. The Tensilon test consists of the administration of edrophonium. Edrophonium is a quick acting anticholinesterase. Thymic tumors are associated with myasthenia gravis. Thymic tumors are also referred to as thymomas. Approximately 10 - 15% of patients with myasthenia gravis have an associated thymoma. The majority of patients with myasthenia gravis have hyperplasia of their thymus. Botulinum toxin inhibits acetylcholine release. The site of action is at the neuromuscular junction. Botulinum toxin is an enterotoxin produced by Clostridium botulinum. Botulism can result from incorrectly canned foods.

Tetrodotoxin is a toxin produced by puffer fish. The sodium channels are blocked by tetrodotoxin. The blockage of the sodium channels interferes with the inflow of sodium. As a result, the propagation of nerve and muscle action potentials is affected. Demyelination refers to the loss of myelin around the axon. Several disorders result in demyelination. An example of a demyelinating disease is multiple sclerosis. Subacute combined degeneration of the spinal cord is also called combined systems disease. Subacute combined degeneration of the spinal cord is a neuropathy secondary to B12 deficiency. It is seen in patients with pernicious anemia, especially pernicious anemia that has been present for quite some time. Symptoms include paresthesias and a loss of proprioception. A 74-year-old man presents after his wife witnessed him grab his head in pain and fall to the floor. He has not regained consciousness. His current blood pressure is 150/96 mm Hg, and his heart rate is 65 bpm. Emergent head CT shows a subarachnoid hemorrhage. A 31-year-old woman presents with a purpural rash covering her arms, legs, and abdomen. She also has fever, chills, nausea, abdominal tenderness, tachycardia, and generalized myalgias. Prior to the development of the rash, the patient noted that she had a headache, cough, and sore throat. Laboratory studies were positive for Gram-negative diplococci in the blood, along with thrombocytopenia and an elevation in PMNs. Urinalysis showed blood, protein, and casts. Vital signs are as follows: PB 92/66, P 96, RR 14, T 39. The patient denies any foreign travel and does not have any sick contacts. However, she does work part time as a nurse in a local hospital. Question The patient is diagnosed with Meningococcemia; she is admitted to the hospital and placed in respiratory isolation. What major course of therapy should this patient receive? Answer Choices 1

Steroids 2 Supportive care 3 Antibiotics 4 Transfusion 5 Bactericidal/permeability-increasing protein ANS:

Antibiotics Antibiotics are the treatment of choice for meningococcemia. The preferred drug for active infection is penicillin G. For those allergic to penicillin, chloramphenicol and cephalosporins (ie, cefotaxime, cefuroxime) may be used as alternatives. Patients will also receive supportive care, but antibiotic therapy must be initiated quickly if the patient is to survive. Intensive care placement may be necessary if organ failure is imminent. Ventilatory support, inotropic support, and IV fluids are necessary in some. If adrenal insufficiency occurs, corticosteroid replacement may be considered. A central venous line helps to provide large amounts of volume expanders and inotropic medications for adequate tissue perfusion. Steroids have not been shown to play a major role in the treatment of meningococcemia. However, they have been used in addition to antibiotic therapy. In the case of adrenal insufficiency, for example, steroid replacement has been shown to be beneficial. Transfusion does not generally play a major role in treatment. If the patient suffers from a devastating coagulopathy, blood or blood products may be replaced as necessary. Bactericidal/permeability-increasing protein is a protein stored in the granules of neutrophils. It binds to endotoxin in vitro and neutralizes it. This technique is experimental, and it is not used in everyday treatment of meningococcemia. In myasthenia gravis, weakness is a result of insufficient acetylcholine transmission at the neuromuscular junction; however, weakness can also occur with overdosing of the cholinergic medications used to treat myasthenia. What symptom helps differentiate a myasthenic crisis from a cholinergic crisis? Answer Choices 1 Respiratory failure 2 Bilateral ptosis 3 Muscle fasciculations

4 Diplopia 5 Normal muscle stretch reflexes ANS: 3 Muscle Fasiculations Signs of cholinergic overdosage include muscle fasciculation, rhinorrhea, lacrimation, salivation, increased bronchial secretions, nausea, or diarrhea. The presence of any of these suggests that the patient's weakness may be due to cholinergic crisis. The other signs are due to weakness and can occur in either condition.

A 54-year-old man presents after having a generalized seizure. The patient is HIV positive, but he has been unable to afford antiretroviral therapy since losing his job 2 years ago. Other than cachexia, the physical exam is unremarkable. Upon further inquiry, the patient also notes that he has become short- tempered and hypercritical; at times, he seems confused. An MRI of the brain is performed, and it reveals several cortical ring-enhancing lesions. Question What is the most likely diagnosis? Answer Choices 1 AIDS dementia complex 2 Cryptococcal meningitis 3 Cytomegalovirus encephalitis 4 Progressive multifocal leukoencephalopathy 5 Toxoplasma encephalitis ANS: Toxoplasma encephalitis The patient's symptoms and MRI findings are most consistent with the diagnosis of toxoplasma encephalitis. Toxoplasmosis is the most common cerebral mass lesion among HIV-positive patients. Infection with the Toxoplasma gondii parasite is relatively common and usually asymptomatic. Reactivation occurs in HIV positive patients due to failing cellular immunity, and it causes a multifocal necrotizing encephalitis. Seizures may be the initial manifestation of central nervous system (CNS) infection; other common clinical manifestations include focal neurologic deficits, such as impaired speech and hemiparesis. Personality change, lethargy, headache, and confusion are also observed. The MRI in patients with toxoplasma encephalitis characteristically reveals multiple, ring-enhancing lesions with surrounding edema; these lesions usually occur bilaterally in the frontal and parietal cortices. AIDS dementia complex describes a constellation of cognitive symptoms

seen among HIV positive patients. The condition occurs when HIV virus disseminates to the CNS. Within the CNS, the virus tends to concentrate in the basal ganglia and subcortical regions. Symptoms include a constellation of cognitive, behavioral, and motor disturbances that cause varying degrees of functional impairment. Characteristic MRI findings include non-enhancing white matter, cerebral atrophy, and ventricular enlargement. The diagnosis requires that other central nervous system infections, carcinoma, as well as general medical conditions and substance abuse have been excluded. Cryptococcal meningitis is caused by the encapsulated fungus Cryptococcus neoformans. Among HIV positive patients, the illness may be the result of new infection or reactivation of latent infection. Presenting signs are often nonspecific; they include headache, fever, change in mental status, and nausea or vomiting. Nuchal rigidity and photophobia may also be present, and elevated intracranial pressure is not uncommon. MRI findings vary, but they include lesions in the basal ganglia; meningeal enhancement, cerebral edema, and shrunken ventricles may also be seen. Cytomegalovirus (CMV) infection causing encephalitis is usually observed in patients with evidence of

CMV infection at other sites. MRI findings vary, but they often show areas of focal necrosis within the brain parenchyma, meninges, or periventricular regions. Symptoms typically reflect progressive dementia, with episodes of confusion, apathy, and focal neurologic deficits. Progressive multifocal leukoencephalopathy is often a fatal disorder; it is caused by reactivation of a latent JC viral infection. Focal neurologic deficits such as hemiparesis and gait disturbance are often the initial presenting symptoms; they are followed by progressive cognitive decline, coma, and death. The MRI commonly reveals multiple, non-contrast enhancing foci in cerebral white matter. A 37-year-old woman presents to her GP surgery with a history of right- sided facial weakness and peri- auricular discomfort since she awoke this morning. She is afebrile. Question What is the most likely diagnosis?

Answer Choices 1 Trigeminal neuralgia 2 Bell's Palsy 3 Multiple sclerosis 4 Myasthenia gravis 5 Primary lateral sclerosis ANS: 2 Bell's Palsy Explanation The correct answer is Bell's palsy, which is a condition typically with sudden onset that affects the facial nerve, causing unilateral facial weakness. Trigeminal neuralgia presents with sharp pain on one side of the mouth that radiates to the ipsilateral ear, eye, or nostril. Multiple sclerosis is a demyelinating disorder, causing a multitude of symptoms that typically include diplopia or blurred vision early on, then an insidious onset of progressive weakness, numbness, and/or tingling in the extremities. Myasthenia gravis commonly presents with ptosis and diplopia, as well as difficulty swallowing, fatigue, and muscle weakness. Primary lateral sclerosis is an upper motor neuron disease that causes limb weakness, stiffness, and fasciculations. A 62-year-old man presents with vision problems and difficulty swallowing. Over the last week, he has had a constellation of symptoms; they began with numbness and tingling in his feet and progressed to weakness that now affects both lower and upper extremities. Within the last day, he has started to notice difficulty swallowing and double vision. He also feels it is difficult for him to take a big breath. His past medical history is noncontributory, and he takes no medications. Exam reveals bilateral absence of patellar and ulnar reflexes. A lumbar puncture is performed to confirm the diagnosis. Question

What cerebrospinal fluid (CSF) finding is most likely? Answer Choices 1 Decreased CSF glucose content 2 Decreased CSF protein content 3 Elevated CSF polymorphonuclear cell count 4 Elevated CSF protein content 5 Elevated CSF lymphocyte count

Elevated CSF proteins Correct response is elevated CSF protein content. Symmetrical ascending paralysis as described in this patient is indicative of Guillain-Barré syndrome (GBS). The cause of GBS is unknown, but it is generally thought to be an inflammatory autoimmune process. More than half of patients with GBS report an antecedent illness. The antibodies produced in response to antigens present in the infectious agent are thought to cross-react with components of human neurons, prompting an acute postinfectious demyelinating process. Lumbar puncture characteristically reveals elevated CSF protein content. Other results are normal, although the white blood cell count may be somewhat elevated. Decreased CSF glucose and increased polymorphonuclear cell counts are seen in acute bacterial meningitis. Decreased CSF glucose and elevated CSF lymphocyte counts are commonly seen with meningitis caused by fungi. Viral meningitides usually presents with elevated lymphocyte counts, normal CSF glucose, and normal or slightly elevated CSF protein levels. A 70-year-old woman is brought to your attention by her family because of the slowly progressive gait disorder, the impairment of mental function, and urinary incontinence. About 1 year ago, she started having weakness and tiredness in her legs, followed by unsteadiness; her steps became shorter and shorter, and she also experienced unexplained backward falls. She is becoming emotionally indifferent, inattentive, and her actions and thinking have became "dull". Over the past month, she has started having urinary urgency and involuntary leaking of urine. Besides multivitamins and local application of the Timolol for glaucoma, she takes no other medications; there are no other symptoms. Question What is most likely the best method of treating the patient's urinary problems? Answer Choices 1 Antimuscarinic drug (Tolterodine) 2 Antibiotic (Sulfamethoxazole/trimethoprim ) 3 Acetylcholinesterase inhibitor

(Donepezil) 4 Ventriculoperitoneal shunt 5 Kegel exercises ANS: 4 Ventriculoperitoneal shunt Clinical triad of slowly progressive gait disorder, followed by impairment of mental function and then sphincteric incontinence strongly suggests the presence of normal-pressure hydrocephalus. Ventricular expansion is the cause of symptoms, and surgical CSF shunting is the main treatment modality. The potential benefit from surgery is usually evaluated by testing gait, cognition, and micturition before and after CSF drainage. Antimuscarinic Tolterodine is an antispasmodic that is used for symptomatic treatment of urinary incontinence in patients with an overactive bladder (urge incontinence). Antimuscarinic drugs are

contraindicated in patients with glaucoma. A urinary tract infection will probably manifest with a strong, persistent urge to urinate, burning sensation when urinating, passing frequent, small amounts of urine that has unusual smell and the appearance. Your patient has no such signs and symptoms; therefore, in this case, antibiotics are not indicated. Donepezil is used to treat dementia, but in the case of normal-pressure hydrocephalus, the problem is anatomic (the distortion of the periventricular limbic system and frontal lobes), and the best treatment is probably surgical. Kegel exercises can prevent or control urinary incontinence and other pelvic floor problems in cases of pelvic sphincter weakness. However, pelvic sphincter weakness will probably manifest as stress incontinence. A 5 - month-old male infant presents after a seizure involving all 4 limbs. His mother tells you that he was born full term without any complications, and he was well until 2 days ago when he developed a fever. He vomited multiple times yesterday and was irritable. He has not had diarrhea or a cough. He was given antipyretic medication for his fever. He has no known allergies. His immunizations are up-to-date. His developmental milestones have been in accordance with his age. On physical exam, his temperature is 102.7 F, and his pulse is 154/min; BP is 90/50 mmHg, and RR is 20/min. He is lethargic, pale, and focal neurological deficits are present. His anterior fontanel is bulging. You suspect that he has bacterial meningitis. Question After drawing blood samples for investigations, what is the most appropriate next step? Answer Choices 1 Intravenous phenytoin 2 Intravenous empirical antibiotics 3 MRI of the head 4 Lumbar puncture 5 Intravenous glucose ANS: intravenous emiprical antibiotics The infant in the vignette appears to have bacterial meningitis. The initial

approach to the patient should be the "ABCs." After assessing and stabilizing the patient's airway and obtaining IV access, intravenous antibiotics should be given immediately. As bacterial meningitis is associated with high morbidity and mortality, prompt initiation of empirical antibiotics is crucial for better prognosis. The choice of antibiotics is dependent on the patient's age and specific predisposing conditions. Use of broad-spectrum cephalosporins, such as ceftriaxone or cefotaxime with vancomycin, may be used in infants more than 1 month old. Ideally, serum glucose, blood culture, complete blood count, and serum chemistries should be drawn when IV access is obtained; however, drawing labs should not delay beginning antibiotics.

Intravenous glucose is necessary if the patient is found to be hypoglycemic; bedside serum glucose is mandatory in any patient that presents with a seizure. Intravenous phenytoin and an MRI of the head might also be necessary for a patient such as the one in the vignette, but would not emergently precede antibiotics. The diagnosis of bacterial meningitis rests on CSF examination performed after lumbar puncture. However, LP is deferred in patients with evidence of increased intracranial pressure, new onset seizure, cardiorespiratory compromise, or focal neurological deficits. Antibiotics should be given, and CT scan of the head should be performed. If CT scan is negative, LP can be performed. A 12-year-old girl presents with a 3-day history of progressive dysarthria, dysphagia, and weakness. The patient was well until 3 days prior to admission to the hospital; at that time, she developed the onset and subsequent gradual worsening of dysarthria. She attributed the dysarthria to a sore throat that she had had about 2 weeks earlier. 3 days prior to admission, she also had the onset of mild dysphagia; it mostly occurred with liquids. 24 hours prior to admission, she developed weakness in both upper extremities, which increased and began to involve the lower extremities. This limb weakness was neither worsened by activity nor improved by rest. She also developed tingling in her toes 24 hours prior to presentation. When she became unable to walk without assistance on the day of admission, she decided to seek medical attention and was admitted to the hospital. Past medical history is significant for measles and mumps. Because of family religious beliefs, she has not had any immunizations. She is very athletic, and frequently plays soccer with friends and siblings in the fields on her grandfather's horse farm. Physical examination reveals a well-developed, well- nourished girl. She is awake, alert, cooperative, and in no acute distress. Temperature is 98.7 F by mouth, blood pressure of 140/80 mm Hg, heart rate is 84/min and regular, and respirations are 22/min and unlabored. There are multiple scratches and abrasions in varying stages of healing over most of her extremities. Her speech is moderately dysarthric. She experiences some mild choking when she tries to drink a glass of water. She can smile weakly, but she cannot raise her eyebrows against resistance. She shows mild bilateral

weakness of eye adduction. Pupillary responses are normal. There is mild to moderate upper extremity and mild lower extremity weakness, greater distally than proximally. Her motor strength is sustained over at least 30 seconds without fatigue. Her gait is ataxic, and she cannot walk without assistance. Reflexes are hypoactive to absent, and the response to plantar stimulation is downgoing bilaterally. Sensation is intact, except for mildly impaired position and vibratory sensation in both feet. A complete blood count, chemistry profile, chest X-ray, and EKG are all normal. Computed tomography of the brain, with and without contrast, is negative. A nerve conduction study reveals a moderate degree of mostly motor demyelinating peripheral neuropathy, highly suggestive of Guillain- Barre. Question What statement best describes the patient's prognosis? Answer Choices 1 With a predominantly demyelinating rather than axonal neuropathy, her prognosis is especially bad

2 Mortality is 25 - 30% 3 Full functional recovery is expected in 45% in several months to a year 4 Whether recovery is full or partial, relapses do not occur during the recovery phase 5 Her rapidly evolving clinical course indicates a poor prognosis ANS: 5 Her rapidly evolving clinical course indicates a poor prognosis This patient must be watched very closely for the very real possibility of respiratory failure and the need for ventilatory support (2). Mortality is expected to be less than 5% with good medical support (1). With a demyelinating pattern on EMG, her prognosis is better. A consistent indicator of residual muscle weakness is an EMG pattern of axonal damage, with the more severe degrees of damage suggesting the worse prognosis (1). About 85% of patients with GBS have a full functional recovery within a year; however, some may be left with minor residuals such as areflexia on exam (2). Between 5-10% of patients with Guillain-Barre have 1 or more relapses; these cases are referred to as chronic inflammatory demyelinating peripheral neuropathy (CIDP) (1). A 45-year-old African-American man with no significant past medical history presents with a 1-hour history of left retroorbital headache. The headache was of a sudden onset and began upon waking that morning. It is described as excruciating, stabbing, sharp, and lancinating; it is rated as severe in intensity. He denies any preceding infections, nausea, vomiting, photophobia, or osmophobia; he also denies fever, chills, stiff neck, focal weakness, numbness, tingling, vision, hearing, gait, or speech changes. He recalls a similar episode several months ago; it lasted about a week, and it dissipated without complications. His physical exam is remarkable for painful distress, lacrimation with conjunctival injection, nasal congestion, rhinorrhea, left ocular miosis, and left forehead diaphoretic flushing. Question What pharmacologic agent is the most beneficial for this patient at this time?

Answer Choices 1 Sumatripta n 2 Verapamil 3 Lithium 4 Topiramate 5 Prednisone ANS: 1

Sumatriptan The correct response is sumatriptan. This patient's most likely diagnosis is most likely a cluster headache. Pharmacologic management of cluster headache may be divided into abortive/symptomatic and preventive/prophylactic strategies. Abortive agents are used to stop or reduce the severity of an acute attack, and include oxygen, triptans, ergot alkaloids, and anesthetics. Inhalation of high-flow concentrated oxygen is extremely effective for aborting attacks. 5- Hydroxytryptamine-1 (5-HT1) receptor agonists, such as triptans or ergot alkaloids with metoclopramide, are often the first line of treatment. Stimulation of 5-HT1 receptors produces a direct vasoconstrictive effect and may abort the attack. Subcutaneous injection of sumatriptan can be effective, in large part because of the rapidity of onset. Studies have indicated that intranasal administration is more effective than placebo but not as effective as injections. Prophylactic agents are used to reduce the frequency and intensity of individual headache exacerbations. Preventive and prophylactic medications include calcium channel blockers, mood stabilizers, and anticonvulsants. Verpamil is the most effective calcium channel blocker for prophylaxis. It inhibits calcium ions from entering slow channels, select voltage-sensitive areas, or vascular smooth muscle, thereby producing vasodilation and preventing the initial vasoconstrictive phase of cluster headaches. It can be combined with ergotamine or lithium. Preliminary evidence suggests that prophylactic lithium may interfere with substance P and vasoactive intestinal peptide (VIP)-induced arterial relaxation. Anticonvulsants such as Divalproex and Topiramate are preventative medications whose mechanism of action may involve regulation of central sensitization. Prednisone is very effective for aborting the cluster headache cycle or providing intermediate prophylaxis as bridging therapy between acute and