5 Flashcards
(356 cards)
1
Q
What is the CT–scan appearance of subdural hematomas?
A
Subdural hematomas are crescent–shaped and epidural hematomas are lens–shaped.
2
Q
What are the indications for cervical spine x–rays after head trauma?
A
Cervical spine x–rays should be obtained in head trauma if there are focal findings consistent with a cervical radiculopathy or if spinal tenderness is present.
3
Q
What is the treatment for severe intracranial hemorrhage?
A
Lowering intracranial pressure with hyperventilation to pCO2 of 30–35, mannitol, elevation of head of bed. Surgical evacuation. Maintain the SBP 110–160. Slight degree of HTN maintains cerebral perfusion.
4
Q
A 50–year–old woman with sudden loss of consciousness, severe headache, nuchal rigidity, photophobia, and a temperature of 38.5 C (101.3 F). What is the diagnosis?
A
Subarachnoid hemorrhage
5
Q
What is subarachnoid hemorrhage?
A
Bleeding into caused by aneurysm. Around the circle of Willis. Association with polycystic kidney disease, Ehlers–Danlos syndrome. Occurs spontaneously. Head trauma is a rare cause.
6
Q
What is the presentation of subarachnoid hemorrhage?
A
Sudden, severe headache, loss consciousness 50%. Focal neurologic symptoms 30% from compression of occulomotor nerve. Nuchal rigidity, photophobia, headache, papilledema. Seizures.
7
Q
What are the long–term outcome of subarachnoid hemorrhage?
A
One–year mortality 50%, with half of the people dying immediately. Longer–term manifestations include focal deficits, seizures, rebleeding, hydrocephalus.
8
Q
How is subarachnoid hemorrhage diagnosed?
A
CT of head without contrast has 95% sensitivity. If CT is normal and SAH is suspected, lumbar puncture is done. Lumbar puncture is most sensitive. The absence of red cells in CSF excludes SAH.
9
Q
What is the treatment for subarachnoid hemorrhage?
A
Maintain SBP 110–160. Seizure prophylaxis with phenytoin. Nimodipine is a calcium–channel antagonist that lowers risk of blood vessel spasm.
10
Q
What test should be done after subarachnoid hemorrhage has been diagnosed?
A
Angiography to determine the site of the bleeding. Surgical clipping of the AVM should occur before rebleeding develops.
11
Q
What is the management of hydrocephalus after subarachnoid hemorrhage?
A
If hydrocephalus occurs, then shunting should be done.
12
Q
What is the treatment for spinal headache after lumbar puncture?
A
A spinal headache is treated with a blood patch.
13
Q
What are the signs of respiratory injury in burn injuries?
A
Soot in the mouth or nose, stridor, wheezing, altered mental status, burned nasal hairs, and burns involving closed spaces are signs of impending pulmonary and laryngeal edema.
14
Q
What are the signs of carbon monoxide overdose?
A
Altered mental status, dyspnea, headache, and chest pain are clues to severe carbon monoxide poisoning.
15
Q
What are the signs of pulmonary thermal injury?
A
Laryngeal edema can result in stridor, hoarseness, and dyspnea. Soot in the nose and mouth can imply impending airway compromise.
16
Q
How is the severity of burn injury assessed?
A
Carboxyhemoglobin elevated in severe burns. Severe burns are defined as combined second– and third–degree burns >20% in adults or >10% in the old or very young or third–degree burns >5% of body surface area.
17
Q
What is the management of severe respiratory injury?
A
If there are signs of severe respiratory injury, intubate the patient. If the carboxyhemoglobin level is significantly elevated (>5–10%), give 100% oxygen.
18
Q
How is the fluid resuscitation requirement determined for burns?
A
Fluid resuscitation over first 24 hours is 4 ml per % BSA/kg. Ringer’s to provide half fluid in first 8 h, with 1/4 in second 8 h, and 1/4 in final 8 h (Parkland formula). Maintain a urine output >0.5–1 mL/kg/h.
19
Q
What is the treatment for burns?
A
Stress ulcer prophylaxis with H2 blockers. Silver sulfadiazine. Do not break blisters. Escharotomy for circumferential burns. Skin grafting.
20
Q
What are heat cramps?
A
Mild fluid and electrolyte depletion. Painful muscular contractions lasting a few minutes. Body temperature normal. Treatment is oral rehydration and salt replacement.
21
Q
What is heat exhaustion?
A
Weakness; body temperature slightly elevated; headache, anxiety. The patient is still able to sweat. Treatment with oral fluid and electrolyte replacement; may need intravenous hydration.
22
Q
What is heat stroke?
A
Loss of ability to lose heat, inability to sweat. T >40 C, confusion, disorientation, nausea, blurred vision, seizures; hemoconcentration, rhabdomyolysis, elevation BUN, creatinine, WBC. Anuria, DIC, lactic acidosis.
23
Q
What is the treatment of heat stroke?
A
Treatment with intravenous fluid replacement and rapid cooling. The body should be sprayed with water. Chlorpromazine and diazepam to control shivering.
24
Q
What is malignant hyperthermia?
A
Nonexertional idiosyncratic heat reaction of rhabdomyolysis caused by anesthetic agents such as halothane or succinylcholine. Treatment is dantrolene.
25
What is neuroleptic malignant syndrome?
Idiosyncratic reaction to phenothiazines or butyrophenones, such as haloperidol. Muscular rigidity and rhabdomyolysis.
26
What is the treatment of neuroleptic malignant syndrome?
Treatment is bromocriptine or dantrolene.
27
What is hypothermia?
Core body temperature below 35 C (normal 37 C). Severe hypothermia is a core temperature below 30 C. Hypothermia often occurs with alcohol intoxication.
28
What is the presentation of hypothermia?
Lethargy, confusion, and weakness. Death from arrhythmia. Ventricular fibrillation or ventricular tachycardia. J–wave elevation may mimic ST segment elevation.
29
What is the effect of ionizing radiation on the body?
Ionizing radiation destroys DNA molecules. Lethal and can cause cancer. Nonionizing radiation includes infrared, ultraviolet, microwave radiation, which are less destructive and causes burns.
30
What are the symptoms of radiation exposure?
Nausea and vomiting early; intestinal ulceration, bleeding, infection later. Injury to skin, salivary glands, respiratory epithelium, thyroid, bone marrow.
31
What is the treatment of radiation exposure?
Antiemetics, platelets and RBC transfusions. Colony–stimulating factors (G–CSF, GM–CSF) to restore marrow. Bone marrow transplantation.
32
What is the presentation of near drowning?
Agitation, coma, cyanosis, coughing, and pulmonary edema, tachypnea, tachycardia, and blood–tinged sputum. Rales and rhonchi. Hypothermia. Hypoxia, hypercarbia, metabolic acidosis, hyperkalemia, hemolysis.
33
What is the presentation of anaphylaxis?
Urticaria, dyspnea, stridor, tachycardia, hypotension, and hemodynamic collapse.
34
What is the treatment of anaphylaxis?
Antihistamine (diphenhydramine), epinephrine injections, intravenous fluids, H2 blockers, and systemic corticosteroids.
35
What is the bacteriology of cat and dog bites?
Infections are most often polymicrobial. Cat bites are associated with Pasteurella multocida; dog bites are associated with Pasteurella, Eikenella, and Capnocytophaga canimorsus.
36
What is the treatment of cat and dog bites?
Wound care. Prophylactic antibiotic is amoxicillin/clavulanate (clindamycin and either ciprofloxacin or trimethoprim/ sulfamethoxazole or azithromycin if penicillin allergic).
37
What is the bacteriology of human bites?
Human bites carry an infection rate of 15%. Anaerobic and aerobic bacteria. Hepatitis B and HIV can also be transmitted through bites.
38
What is the treatment for human bite wounds?
Irrigate wound; cultures are not useful. If the bite is
39
Which animals carry rabies?
Raccoons, rats, wild dogs, woodchucks, skunks, foxes. 100% fatal. Less than 10 persons per year are infected in the US.
40
What is the presentation of rabies?
Incubation period up to one year. Prodrome of 2–10 days of fever and paresthesias at the bite site. Aphasia, paralysis, hypersalivation, and myoclonus.
41
How is rabies diagnosed?
Viral cultures from saliva, CSF, or serum
42
What is the treatment for rabies infection?
Ribavirin. Prophylaxis with human rabies immunoglobin provides immediate passive immunity. Human diploid cell vaccine should be given at 0, 3, 7, 14, and 28 days (5 shots total).
43
How many deaths per year are caused by snake bites?
44
What is the treatment of snake bites?
Decrease the spread of venom with compression bandages. Antivenin may cause anaphylactic reactions. Hypotension is managed with fluids. Ventilatory support for laryngeal edema.
45
What are the causes of spinal cord compression?
Commonly caused by lymphoma, multiple myeloma, carcinomas of prostate, lung, breast, kidney, or colon; herniated disk, epidural abscess, hematoma, or trauma.
46
What is the presentation of spinal cord compression?
Sensory loss, lower extremity weakness; sphincter dysfunction or sexual dysfunction. History of cancer, fever, and bowel or bladder incontinence or retention.
47
How is spinal cord compression diagnosed?
Plain x–rays are abnormal. The diagnostic test of choice is an MRI of the spine.
48
What is the treatment for spinal cord compression?
High–dose dexamethasone immediately, then MRI. For lymphoma or multiple myeloma, radiation therapy should be started. Surgical decompression for a herniated disk, epidural abscess, or hematoma.
49
What is syringomyelia?
Cavitation of spinal cord. Communicating with CSF or noncommunicating. Associated with congenital Arnold Chiari; caused by trauma, tumors.
50
What are the signs of syringomyelia?
Impaired pain, temperature; intact sensation to light touch. Loss of pain and temperature occurs in a cape–like distribution. Sparing of tactile sensation, position, and vibratory sense. Areflexia.
51
What is subacute combined degeneration?
B12 deficiency. Distal paresthesias and weakness of extremities followed by spastic paresis and ataxia. Deficit of vibration and proprioception with pyramidal signs (plantar extension, hyperreflexia). Low B12.
52
What is the presentation of anterior spinal artery infarct?
Flaccid paralysis, spastic paresis. Loss pain, temperature; sparing vibration and position. Motor, sensory, autonomic is lost below the level of the infarction with retained vibration and position. Treatment is supportive.
53
What is the Brown–Sequard syndrome?
Hemisection of the cord with ipsilateral spastic paresis. Ipsilateral loss of joint position sense, tactile discrimination, and vibratory sensations. Contralateral loss of pain and temperature.
54
A 60–year–old woman with sudden onset of right upper extremity weakness, aphasia, pronator drift and right facial nerve palsy. What is the most likely cause?
Ischemic stroke
55
What is a stroke?
Sudden onset of a focal neurologic deficit.
56
What are the mechanisms of strokes?
Large artery thrombosis, small artery thrombosis (lacunar), embolic (cardiogenic or artery–to–artery), vascular dissection, systemic hypotension, intracranial bleeding.
57
What is the presentation of ischemic stroke?
Acute onset of a focal neurologic deficit.
58
What is the blood supply to the brain?
Two major systems: carotid (anterior) circulation, and vertebrobasilar (posterior) circulation. The anterior circulation include the anterior cerebral artery and middle cerebral artery.
59
What are the signs of occlusion of the anterior cerebral artery?
Contralateral weakness in arm and sensory loss in leg more than in the upper extremity. Urinary incontinence, confusion, behavioral disturbances. Lower extremity weakness exceeds upper extremity.
60
What are the signs of occlusions of the middle cerebral artery?
Contralateral hemiplegia, hemisensory loss, homonymous hemianopia, eyes deviated toward lesion. Dominant results in aphasia. Nondominant results preserved speech, comprehension with confusion, apraxia.
61
What parts of the brain are supplied by the posterior circulation?
Cerebellum, brain stem, occipital lobe of the cortex, and pons. The major blood vessels of the posterior circulation are the posterior cerebral artery, basilar artery, and vertebral arteries.
62
What are the signs of posterior cerebral artery occlusion?
Contralateral homonymous hemianopia, hallucinations, agnosias. Occlusion of the penetrating branches of the PCA can result in CN III palsy with contralateral hemiplegia (Weber syndrome) or CN III palsy.
63
What is Wallenberg syndrome?
Occlusion of posterior inferior cerebellar artery, which presents as ipsilateral facial sensory loss, contralateral body sensory loss, vertigo, ataxia, dysarthria, dysphagia, and Horner syndrome (ptosis).
64
What are the signs of occlusion of the major cerebellar arteries?
Vertigo, vomiting, nystagmus, and ipsilateral limb ataxia.
65
How is stroke diagnosed?
Noncontrast CT to distinguish between hemorrhagic and ischemic stroke. CT often negative for ischemia within the first 48 hours. Diffusion–weighted MRI is the most accurate test for cerebral ischemia.
66
What tests will find the embolic source after an acute ischemic stroke?
Echocardiogram, carotid duplex, and 24–hour Holter monitor. Evaluation for inherited hypercoagulability.
67
What is the treatment for ischemic stroke?
Tissue plasminogen activator if within 4.5 hours of symptom onset.
68
What are the contraindications to tissue plasminogen activator for ischemic stroke?
Stroke or head trauma within 3 mo, hemorrhage (GI, GU), surgery within 14 d, intracranial hemorrhage, arterial puncture within 7 d, BP \> 185/110, anticoagulants; platelets 15 sec).
69
What is the prognosis for patients who receive tissue plasminogen activator?
39% of all patients treated with tPA have a good functional outcome. Only 26% of untreated have a good outcome. Intracranial hemorrhage occurs in 5.8%. The fatality rate after intracranial hemorrhage is 45%.
70
What is the secondary prevention of ischemic stroke?
Started 24 hours after TPA. When patients have allergy to aspirin or continue to have recurrent cerebrovascular events on aspirin, dipyridamole may be added or the patient may be switched to clopidogrel.
71
When should heparin be given to patients with ischemic stroke?
Heparin in acute ischemic stroke is limited to patients with atrial fibrillation, basilar artery thrombosis, or stroke in evolution.
72
What is the treatment of subarachnoid hemorrhage?
Nimodipine to reduce the risk of ischemic stroke. Early surgical clipping of the aneurysm or embolization of the vessel. Aspirin is contraindicated.
73
What is the management of intracranial aneurysms that are found incidentally?
Unruptured aneurysms found incidentally should be repaired if they exceed 10 mm.
74
What are the indications for carotid endarterectomy?
Carotid endarterectomy for occlusion \> 70% and the lesion is symptomatic. Endarterectomy may benefit those who are asymptomatic if there is \>60% stenosis in men who are
75
What is a seizure?
Paroxysmal event caused by abnormally discharging central nervous system neurons. Epilepsy is a condition of recurrent seizures due to a chronic underlying process.
76
What are the causes of seizures?
Stroke, bleed, AV malformation; meningitis, abscess, encephalitis, trauma, vasculitis, hypoNa, hypoCa, hypoMg, hypoglycemia, hypoxia, drug overdose/withdrawal, idiopathic, neoplasm, psychiatric.
77
What is the presentation of a seizure?
Paroxysmal, involuntary, abnormal movement or change of consciousness. Sudden onset, with or without an aura. Disorientation, sleepiness, muscle aches. Incontinence, tongue biting, headache.
78
How is syncope different from a seizure?
Patients with syncope will not complain of significant postictal symptoms. Syncope patients will recover consciousness within several minutes of the event, and will not have incontinence or tongue biting.
79
How are seizures classified?
Partial or generalized and complex or simple.
80
What are partial seizures?
Partial seizures affect discrete portions of the brain, such as causing involuntary jerking of a finger or hand.
81
What is a simple partial seizure?
Consciousness is maintained for the duration of a simple seizure, and the seizure affects a discrete portion of brain. When there is a change in consciousness, the seizure is termed a complex partial seizure.
82
What are generalized seizures?
Arise from both cerebral hemisphere. Generalized tonic–clonic seizures are tonic contraction of muscles throughout the body followed by intermittent relaxation (clonic phase).
83
What are absence seizures?
Sudden, brief loss of consciousness without loss of postural tone. The ECG shows a generalized, symmetric 3–Hz spike–and–wave discharge pattern.
84
What are atonic seizures?
Atonic seizures are characterized by sudden loss of postural tone, lasting 1 to 2 seconds.
85
What are myoclonic seizures?
Myoclonic seizures are characterized by a sudden, brief muscle contraction.
86
What is status epilepticus?
Recurrent or continuous seizures lasting at least 5–30 min.
87
How are seizures diagnosed?
Electroencephalogram, serum electrolytes, glucose, toxicology, and arterial blood gas to exclude hypoxia. A CT scan or MRI of the head is indicated to exclude a structural lesion as the cause of seizure.
88
What is the treatment for status epilepticus?
Secure airway, breathing, circulation. Evaluate and treat causes. Lorazepam, which potentiates GABA receptor. If seizure continues, phenytoin or fosphenytoin to add phenobarbital.
89
What are the side effects of phenytoin?
Diplopia, dizziness, ataxia. Gum hyperplasia, lymphadenopathy, hirsutism, and rash.
90
What are the side effects of phenobarbital?
Sedation, ataxia, and rash.
91
What drug should be given if patients continue to seize after administration of lorazepam, phenytoin and Phenobarbital?
Midazolam or propofol anesthesia.
92
When should anticonvulsant therapy be started in patients with a first–time seizure?
Anticonvulsants should be started only if the patients has an abnormal neurologic exam, presented with status epilepticus, has a strong family history of seizure, or has an abnormal EEG.
93
What is the treatment for primary generalized tonic–clonic seizures?
Valproic acid. Valproic acid increases the availability of GABA. Lamotrigine, carbamazepine, or phenytoin are alternatives.
94
What are the side effects of valproic acid?
Side effects include ataxia, tremor, hepatotoxicity, thrombocytopenia, gastrointestinal irritation, and hyponatremia.
95
What is the mechanism of action of lamotrigine?
Lamotrigine decreases glutamate release. Side effects: Stevens–Johnson syndrome.
96
What is the treatment of absence seizures?
Ethosuximide. Valproic acid is an acceptable option.
97
What is the treatment for myoclonic and atonic seizures?
Valproic acid.
98
What is the treatment for partial seizures?
Carbamazepine and phenytoin are first–line therapy. Valproic acid, lamotrigine, and levetiracetam are alternatives.
99
What is vertigo?
False sensation of movement.
100
What are the causes of vertigo?
Mèniére, labyrinthitis, positional vertigo, traumatic, perilymphatic fistula, cervical vertigo. Brain stem disease, AV malformations, tumor, multiple sclerosis, drug overdose, vertebrobasilar migraine.
101
What are the characteristics of central vertigo?
No tinnitus or hearing loss is present. There are is often diplopia, cortical blindness, dysarthria, extremity weakness or numbness. Nystagmus is pure, vertical, does not suppress with fixation, and multidirectional.
102
What are the characteristics of peripheral vertigo?
Tinnitus and hearing loss. Absence of diplopia, cortical blindness, dysarthria, extremity weakness or numbness. Nystagmus is mixed, horizontal, suppresses with fixation, and unidirectional.
103
What are the signs of Mèniére disease?
Tinnitus, hearing loss, episodic vertigo of 1 to 8 h. Symptoms wax and wane as the endolymphatic pressure rises and falls. Most common causes of Mèniére disease are syphilis and head trauma.
104
What are the signs of labyrinthitis?
Sudden onset of severe vertigo that lasts for several days with hearing loss and tinnitus. Occurs with an upper respiratory tract infection.
105
What are the signs of benign paroxysmal positional vertigo?
Peripheral vertigo that characteristically is exacerbated by head movement or change in head position. Episodes occur in clusters that persist for several days. The vertigo usually lasts 10 to 60 seconds.
106
What are the causes of perilymphatic fistula?
Form of peripheral vertigo related temporally to head trauma (slap to the ear) or extreme barotrauma during air flight, scuba diving, or vigorous Valsalva maneuver.
107
What are the causes of central vertigo?
Caused by cerebellar or brain–stem tumor, bleed, or ischemia. Drug toxicity or overdoses. In young patient with unexplained central vertigo, consider multiple sclerosis.
108
What is the treatment of peripheral vertigo?
Meclizine or diazepam.
109
What is the treatment of Mèniére disease?
Low–salt diet and diuretics. Surgical decompression.
110
What is the treatment of benign paroxysmal positional vertigo?
Positional maneuvers that attempt to move the otolith out of the circular canals (e.g., Dix Hallpike and Barany maneuvers).
111
What is the treatment of vertigo caused by labyrinthitis?
Meclizine and diazepam.
112
28–year–old woman with throbbing, right–side headache; nausea; worsened by walking, loud noise, bright light. What is the diagnosis?
Migraine
113
What are the primary headache syndromes?
Migraine, cluster, and tension headache. Migraine affects 15% of the population.
114
What are the secondary causes of headache?
Intracranial hemorrhage, brain tumor, meningitis, temporal arteritis, and glaucoma.
115
What type of headache is characterized by fever and nuchal rigidity?
Meningitis.
116
What are the clinical symptoms of brain tumors?
Deep, dull, aching pain that disturbs sleep. Vomiting before the onset of headache, or a history of headache induced by coughing, lifting or bending is typical of posterior fossa brain tumors.
117
What are the characteristics of temporal arteritis?
Unilateral pounding headache with visual changes; dull and boring with lancinating pains. Polymyalgia rheumatica, jaw claudication, fever, weight loss, scalp tenderness; elderly.
118
What are the laboratory abnormalities associated with temporal arteritis?
Increased sedimentation rate; diagnosed with biopsy of the temporal artery. Initiate therapy with steroid immediately.
119
What cause of headache syndrome is associated with eye pain?
Glaucoma
120
What are the characteristics of migraine headaches?
Benign and recurrent syndrome of headache, nausea, vomiting, and focal neurologic deficits. Pulsatile, throbbing, unilateral, aggravated by movement. Photophobia, phonophobia.
121
What are the triggers of migraine?
Alcohol, chocolate, cheeses, monosodium glutamate, hunger, or irregular sleep patterns.
122
What is migraine without aura?
Migraine without a preceding focal neurologic deficit. Migraine with aura is a migraine headache that is accompanied by a preceding motor, sensory, or visual symptoms. Focal neurologic symptoms.
123
What is the pathognomonic aura for migraine?
Scintillating scotoma. Only 20% of migraine has aura. Stars, sparks, and flashes of light. Migraine equivalent is defined as focal neurologic symptoms without headache.
124
What are complicated migraines?
Migraines with severe neurologic deficits that persist after the resolution of pain.
125
What are basilar migraines?
Migraine headaches associated with vertigo, diplopia, ataxia, or dysarthria.
126
What are the characteristics of tension–type headaches?
Tension–type headaches are tight, band–like headaches are bilateral.
127
What are the characteristics of cluster headaches?
Excruciating, unilateral, periorbital headache without warning 30 min–3 hrs; 1–3 times a day for 4–week period. Red eye, lacrimation, nasal stuffiness, nausea, sensitivity to alcohol. Horner syndrome (ptosis).
128
How is migraine headache diagnosed?
Severe, sudden onset of a first–time headache with signs of an underlying cause should have a CT scan of the head.
129
What is the treatment of migraine headache?
Abortive sumatriptan, which is a serotonin receptor agonist. Dihydroergotamine is an alternative. The triptans are contraindicated in cardiovascular disease. Almotriptan, naratriptan, zolmitriptan, and eletriptan.
130
What is the prophylactic treatment for migraine?
Prophylactic treatment for migraine should be initiated when acute migraine headaches occur more than three to four times per month. Propranolol, timolol, valproic acid, and topiramate. Verapamil and tricyclics.
131
What is the treatment of cluster headaches?
The most effective treatment is 100% oxygen. Cluster headaches are treated with prednisone, lithium, ergotamine, and verapamil. Sumatriptan.
132
What is pseudotumor cerebri?
Idiopathic increase in intracranial pressure. 8–10 times more common in women. Association with obesity, chronic lung disease, Addison disease, oral contraceptives, tetracycline, and vitamin A toxicity.
133
What is the presentation of pseudotumor cerebri?
Headache, diplopia, and 6th cranial nerve (abducens) palsy. Papilledema, blind spot on visual field testing. The CT and MRI are normal, CSF is normal except for an increase in pressure.
134
What is the treatment for pseudotumor cerebri?
Weight loss, discontinue oral contraceptives, acetazolamide, furosemide, prednisone. Repeated lumbar punctures; placement of ventriculoperitoneal shunt.
135
What is trigeminal neuralgia?
Idiopathic, sudden, severe, sharp pain side of the mouth and progressing to ear, eye, or nostril. Triggered by touch or movement; pain lasts a few seconds. Compression of the trigeminal nerve root by a vessel, MS, tumor.
136
What is the treatment of trigeminal neuralgia?
Carbamazepine. Phenytoin, baclofen, or gabapentin. Surgery or alcohol injection into the affected nerve.
137
16–year–old boy with leg weakness. 3 weeks ago had diarrhea. Bilateral lower–extremity weakness and a loss of reflexes. What is the diagnosis?
Guillain–Barre syndrome
138
What is Guillain–Barre syndrome?
Acute, often severe polyradiculopathy caused by autoimmune destruction of myelin by an immune response.
139
What is the presentation of Guillain–Barre syndrome?
Sudden weakness begins lower extremities and moves upward. Loss of reflexes. Legs are more affected than arms and face. Pain, tingling. Loss of large sensory fibers, loss of reflexes and proprioception.
140
What autonomic instabilities are associated with Guillain–Barre syndrome?
Profuse sweating, postural hypotension, labile blood pressure, cardiac dysrhythmia occurs in severe GBS.
141
What is the etiology of Guillain–Barre syndrome?
75% have history of infection 1–3 weeks prior; respiratory or GI © jejuni). GBS may be preceded by HSV, CMV, EBV. Influenza vaccine associated with one case per million. HIV, SLE, lymphoma.
142
How is Guillain–Barre syndrome diagnosed?
A lumbar puncture has an elevated protein without an associated rise in the cell count. Electromyography will show demyelination of the peripheral nerves.
143
What is the treatment for Guillain–Barre syndrome?
Intravenous immunoglobulin or plasmapheresis; monitor the vital capacity and initiate early respiratory support if respiratory weakness.
144
A 32–year–old woman with double vision, difficulty chewing. Symptoms improve following sleep. Snarling appearance when asked to smile, nasal tone in voice; weakness in the upper extremities. What is the diagnosis?
Myasthenia gravis.
145
What is myasthenia gravis?
Disease of the neuromuscular junction characterized by weakness and fatigability. Acetylcholine–receptor antibodies leads to a decreased acetylcholine receptors at the postsynaptic membrane.
146
What is Eaton–Lambert myasthenic syndrome?
Eaton–Lambert myasthenic syndrome is characterized by weakness with increasing muscle strength on repetitive contraction; caused by a malignancy, especially small–cell carcinoma of the lung.
147
What are the signs of botulism?
Botulism may cause myasthenic–like weakness, but pupils are usually dilated and repetitive nerve stimulation shows an incremental increase in muscular fiber contraction (opposite of myasthenia).
148
How is myasthenia gravis diagnosed?
Initial test for myasthenia is acetylcholine–receptor Ab, 80–90% positive. Most accurate test is EMG. Edrophonium (Tension) test is sensitive but not specific. CT performed to detect a thymoma;10%.
149
What is the treatment of myasthenia gravis?
Anticholinesterase (pyridostigmine, neostigmine). If glucocorticoids fail, azathioprine used. Mycophenolate. Plasmapheresis, IV Ig rapidly improve myasthenic crisis with respiratory failure.
150
What are the indications for thymectomy in myasthenia gravis?
Thymectomy is indicated in postpubertal patients and in those younger than 60 before initiation of immunosuppressive therapy. Aminoglycosides exacerbate myasthenia gravis.
151
What is amyotrophic lateral sclerosis?
Idiopathic weakness with upper and lower motor neuron loss, CN palsies, respiratory involvement; preserved bowel, bladder sensory, cognitive, sexual.
152
What are the signs of amyotrophic lateral sclerosis?
Cranial nerve or bulbar palsies result in dysphagia, difficulty chewing, decreased gag, dysarthria; respiratory weakness; aspiration pneumonia is most common cause of death. Weak cough; head ptosis.
153
What is the presentation of amyotrophic lateral sclerosis?
Fully mentally alert patient loses nearly all motor control while still being able to think and perceive.
154
What are the upper motor neuron manifestations of amyotrophic lateral sclerosis?
Weakness with spasticity and hyperreflexia. Lower motor neuron manifestations are weakness with muscle wasting, atrophy, fasciculations. Upper and lower motor neuron weakness is unique to ALS.
155
What is the confirmatory test for amyotrophic lateral sclerosis?
Confirmatory test is the electromyogram. Cerebrospinal fluid and MRI are normal.
156
What is the treatment of amyotrophic lateral sclerosis?
Riluzole shows progression by inhibiting glutamate release. Spasticity is treated with baclofen and tizanidine. Death in 3–5 years.
157
What is the presentation of multiple sclerosis?
Weakness, numbness, tingling, or unsteadiness of a limb. Urinary urgency or retention, blurry vision, double vision. Symptoms persist for weeks; may resolve spontaneously.
158
How is multiple sclerosis diagnosed?
MRI of the brain is the most accurate test (sensitivity 95%); demyelinated plaques in the cerebrum and spine. Enhancement with gadolinium. Mild pleocytosis (
159
What is the treatment for the spasticity of multiple sclerosis?
Baclofen; tizanidine and diazepam for nocturnal spasticity. Pain caused by trigeminal neuralgia and dysesthesias responds to carbamazepine, gabapentin, phenytoin, pregabalin, tricyclic.
160
What is the treatment of bladder hyperactivity in multiple sclerosis?
Bladder hyperactivity is treated with oxybutynin; urinary retention is treated with bethanechol.
161
What is dementia?
Loss of memory with impairment of any other cognitive function (aphasia, agnosia, apraxia, executive) sufficient to interfere with social or occupational functioning.
162
What are the reversible causes of dementia?
Hypothyroidism, B12 deficiency, hepatic or uremic encephalopathy, vasculitis, syphilis, abscess, tumor, anticholinergics, sleep apnea, trauma, subdural hematoma, normal pressure hydrocephalus, depression.
163
What are the irreversible causes of dementia?
Progressive multifocal leukoencephalopathy, Alzheimer, Lewy bodies, Pick disease, multi–infarct dementia, Binswanger disease, Creutzfeldt–Jakob disease. Alzheimer accounts for 80%.
164
What is the prevalence of dementia?
1–5% between ages 65–69; 45% by age 100. Only 5% of Alzheimer disease is inherited.
165
What is the presentation of frontotemporal dementia?
Pick disease presents with personality changes early, with relative sparing of visuospatial function. Social, interpersonal, emotional abnormalities. Frontotemporal dementia lacks insight.
166
What is the presentation of dementia with Lewy bodies?
Dementia with Lewy bodies is characterized by fluctuating cognitive impairment. Dementia caused by Parkinson disease should be accompanied by recurrent visual hallucinations are also characteristic.
167
What are the characteristics of dementia caused by Creutzfeldt–Jakob disease?
Short, aggressive course over weeks. Dementia, myoclonus, ataxia, and 14–3–3 protein in CSF. Variant CJD is bovine spongiform encephalopathy from ingestion of prions from cattle.
168
What are the characteristics of multi–infarct dementia?
Stepwise progression associated with discrete cerebrovascular events. Binswanger disease involves the subcortical white matter and presents with a slowly progressive course.
169
What are the characteristics of normal pressure hydrocephalus?
Prominent gait abnormalities before the onset of cognitive impairment, urinary incontinence.
170
What is the diagnostic evaluation for dementia?
Rule out reversible causes of the dementia. CBC, electrolytes, calcium, creatinine, LFTs, glucose, TSH, v B12, RPR, HIV. MRI or CT with contrast.
171
What is the treatment for dementia?
Memantine is a disease–modifying drug used in advanced disease either alone or with a cholinesterase inhibitor. Memantine is neuroprotective and reduces the rate of progression.
172
A 35–year–old man with spontaneous movements, grimacing with grunting. Father died at the age of 41 from dementia. What is the diagnosis?
Huntington disease
173
What is the cause of Huntington disease?
Degenerative brain disorder. HD gene contains a CAG trinucleotide repeat that codes for huntingtin. Abnormal cleavage of huntingtin protein interferes with nuclear mechanisms, cell death; autosomal dominant.
174
What is the presentation of Huntington disease?
Chorea in 4th–5th decade. Irritability, anger, paranoia, depression. Antisocial. Fidgeting that progresses to sudden movements of the trunk or limbs. Choreic gait. Memory is preserved until late.
175
How is Huntington disease diagnosed?
Genetic testing. CT scanning shows cerebral atrophy or atrophy of caudate nucleus.
176
What is the treatment for Huntington disease?
Haloperidol or clozapine control behavioral changes. Death occurs 15–20 years after diagnosis. Children should receive genetic testing.)
177
58–year–old man with resting tremor; slow moving. Stooped forward, small steps. Cogwheel rigidity in arms; positive Myerson sign. What is the diagnosis?
Parkinson disease
178
What is Parkinson disease?
Neurologic syndrome resulting from the deficiency of the neurotransmitter dopamine; degenerative, vascular, or inflammatory changes in the basal ganglia.
179
What are the causes of Parkinson disease?
Neuroleptics (haloperidol, chlorpromazine), metoclopramide, alpha–methyldopa, reserpine. MPTP, carbon monoxide, cyanide, manganese. Encephalitis. Basal ganglia lesions.
180
What is the presentation of Parkinson disease?
Bradykinesia (mask facies, reduction of automatic movements), cogwheel rigidity, postural instability, resting tremor. Myerson sign is inability to resist blinking when trapped on the glabella.
181
What is Shy–Drager syndrome?
Parkinsonism with prominent orthostatic hypotension.
182
How is Shy–Drager syndrome diagnosed?
Diagnosis of Parkinson disease is clinical. Identify any secondary causes of Parkinsonism that are reversible. There is no diagnostic test that can identify Parkinson disease.
183
What is the treatment for Parkinson disease?
Parkinson disease is caused by low dopaminergic and excessive cholinergic tone on the basal ganglia. Medical treatment increases dopaminergic tone or decreases cholinergic tone on the basal ganglia.
184
What medications are used to stimulate dopamine receptors in patients with Parkinson disease?
Carbidopa/levodopa, dopamine agonists, indirectly increase the amount of dopamine (COMT inhibitors, selegiline, amantadine).
185
Which medications block acetylcholine stimulation of the basal ganglia?
Benztropine and trihexyphenidyl.
186
What direct–acting dopamine agonists are used to treat Parkinson disease?
Pramipexole or ropinirole alone as initial therapy or with levodopa/carbidopa. Other dopamine agonists are bromocriptine, pergolide, tolcapone, entacapone.
187
How does the efficacy of pramipexole and ropinirole compare to levodopa for the treatment of Parkinson disease?
Dopamine agonists are less efficacious than levodopa. Dopamine agonists have less dyskinetic side effects.
188
What is the mechanism of the catechol–O–methyl transferase inhibitors?
COMT inhibitors decrease the metabolism of the levodopa. They are an adjunct to levodopa for the treatment of Parkinson disease.
189
What is the role of selegiline in Parkinson disease?
Selegiline can be used in those with a declining or fluctuating response to levodopa. Selegiline offers mild symptomatic benefit in early disease. Rasagiline is a newer version.
190
What is benign essential tremor?
Idiopathic disorder of isolated tremor of the hands, head. Worsened by caffeine or beta agonists. Interferes with ability to write. Improvement with the use of alcohol.
191
What is the treatment of benign essential tremor?
Propranolol. Alternatives are primidone, alprazolam, and clozapine. If no medical therapy is effective, thalamotomy is indicated.
192
What is restless leg syndrome?
Idiopathic sensation of creeping and crawling dysesthesia within legs; involuntary movements during sleep; familial; exacerbated by sleep deprivation, caffeine, pregnancy.
193
What is the treatment of restless leg syndrome?
Treatment is with dopamine agonists, such as pramipexole or ropinirole; levodopa/carbidopa, benzodiazepines.
194
What is pemphigus vulgaris?
Autoimmune disease of allergy to own skin. Pemphigus vulgaris is most often idiopathic, but ACE inhibitors or penicillamine can cause it.
195
What is the presentation of pemphigus vulgaris?
Vulgaris occurs in thirties and forties, whereas bullous pemphigoid occurs in those in their seventies and eighties. Pemphigus vulgaris is a potentially life–threatening disease. Vulgaris has oral erosions.
196
What is Nikolsky sign?
Removal of skin by a little pressure from the examiner's finger, pulling skin off like a sheet in pemphigus vulgaris, staph scalded skin syndrome, toxic epidermal necrolysis. Lesions of pemphigus vulgaris are painful.
197
How is pemphigus vulgaris diagnosed?
Biopsy the skin with immunofluorescent stains.
198
What is the treatment for pemphigus vulgaris?
Systemic glucocorticoids, such as prednisone; azathioprine, mycophenolate, or cyclophosphamide. Rituximab and IVIg are also effective.
199
What is pemphigus foliaceus?
Blistering disease often associated with other autoimmune diseases, or it can be induced by ACE inhibitors or NSAIDs.
200
What is the presentation of pemphigus foliaceus?
Foliaceus is much more superficial, and intact bullae are not seen because they break. There are no oral lesions. Treatment of pemphigus foliaceus is steroids.
201
What is bullous pemphigoid?
Pemphigoid is twice as common as pemphigus vulgaris and occurs in elderly persons in their seventies and eighties. May be induced with sulfa drugs, furosemide; penicillamine.
202
How is bullous pemphigoid diagnosed?
Biopsy with immunofluorescent antibodies.
203
What is the treatment of bullous pemphigoid?
Systemic steroids, such as prednisone; topical steroids only if no oral lesions.
204
What is porphyria cutanea tarda?
Deficiency of uroporphyrinogen decarboxylase results in accumulation of porphyrins, which leads to photosensitivity; HIV, alcoholism, liver disease, hepatitis C, oral contraceptives.
205
What is the presentation of porphyria cutanea tarda?
Fragile, nonhealing blisters on sun–exposed backs of the hands and the face. Hyperpigmentation of the skin and hypertrichosis of face.
206
How is porphyria cutanea tarda diagnosed?
Uroporphyrins are elevated two to five times above the coproporphyrins.
207
What is the treatment for porphyria cutanea tarda?
Stop alcohol and discontinue estrogen, and iron. Chloroquine increases the excretion of porphyrins.
208
What is acute urticaria?
Hypersensitivity reaction with IgE, mast cell activation; wheals, hives, without hypotension.
209
What are the causes of acute urticaria?
Allergic reaction to insect bites, foods, emotions, aspirin, NSAIDs, morphine, codeine, penicillin, phenytoin, quinolones, ACEI. peanuts, shellfish, tomatoes, strawberries, latex.
210
What is the presentation of acute urticaria?
Lasts 6 weeks and is associated with pressure on the skin, cold, or vibration.
211
What is the treatment of acute urticaria?
H1 antihistamines. Severe, urticaria is treated with diphenhydramine, hydroxyzine, or cyproheptadine. H2 antihistamines, systemic steroids. Chronic therapy is with nonsedating antihistamines, such as loratadine.
212
What is a morbilliform rash?
Milder hypersensitivity reaction than urticaria. Typical type of drug reaction and lymphocyte mediated.
213
What is the presentation of morbilliform rash?
Usually caused by medications allergy, such as penicillin, sulfa drugs, allopurinol, or phenytoin. Generalized, maculopapular eruption that blanches with pressure.
214
What is the treatment of morbilliform rash?
Antihistamines and steroids.
215
What is erythema multiforme?
Caused by penicillins, phenytoin, NSAIDs, sulfa drugs. Majority of cases follow infection with herpes simplex or Mycoplasma.
216
What is the presentation of erythema multiforme?
Target–like lesions that occur on the palms and soles. Bullae are not found, and it does not involve mucous membranes. Treatment is antihistamines.
217
What is Stevens–Johnson syndrome?
Stevens–Johnson syndrome is erythema multiforme major. SJS and toxic epidermal necrolysis are considered to be degrees of same disorder. Penicillin, sulfa drugs, NSAIDs, phenytoin or phenobarbital.
218
What is the presentation of Stevens–Johnson syndrome?
SJS involves
219
What is the treatment for Stevens–Johnson syndrome?
Admission to a burn unit, withdrawal of offending drug, mechanical ventilation. Death occurs from infection, dehydration, malnutrition. No benefit from steroids.
220
What is toxic epidermal necrolysis?
Toxic epidermal necrolysis is the most serious cutaneous hypersensitivity reaction. Mortality 40–50%.
221
What is the presentation of toxic epidermal necrolysis?
Skin sloughing involving a body surface area (BSA) 30 to 100%. Nikolsky sign, and the skin easily sloughs off. TEN is drug induced.
222
How is toxic epidermal necrolysis diagnosed?
Skin biopsy reveal full thickness epidermal necrosis in which the epidermis separates from the dermis. A skin biopsy is usually not necessary.
223
What is the treatment for toxic epidermal necrolysis?
Topical anesthetics, cover denuded skin with saline or Burow solution compresses. Sepsis is the most common cause of death. Systemic steroids are not effective.
224
What is a fixed drug reaction?
Recurrent localized allergic reaction to aspirin, NSAIDs, tetracycline, barbiturates. Round, sharply demarcated, and leave a hyperpigmented spot. Treated with topical steroids.
225
What is erythema nodosum?
Localized inflammatory condition, occurring after infections inflammatory conditions, pregnancy, strep infections, coccidioidomycoses, histoplasmosis, sarcoidosis, IBD, syphilis, hepatitis, Yersinia.
226
What is the presentation of erythema nodosum?
Multiple painful, red, raised nodules on anterior lower extremities; tender, do not ulcerate, last 6 weeks. ASLO titers can reveal a streptococcal infection.
227
What is the treatment for erythema nodosum?
Analgesics and NSAIDs. Potassium iodide solution; usually self–limiting.
228
What are the superficial fungal infections?
Tinea pedis, cruris, corporis, versicolor, capitis, and onychomycosis
229
What is the treatment for onychomycosis or hair infection (tinea capitis)?
Terbinafine or itraconazole for 6 weeks for fingernails and 12 weeks for toenails. Terbinafine is hepatotoxic. Griseofulvin must be used for 6–12 months and has much less antifungal efficacy than terbinafine.
230
What is the treatment of dermatophyte infection of the hair?
Griseofulvin for 6–8 weeks for tinea capitis. Terbinafine for 2–4 weeks.
231
What is the treatment of fungal infections of the skin that do not involve the hair or nails?
Topical ketoconazole, clotrimazole, econazole, terbinafine, miconazole, sertaconazole, sulconazole, tolnaftate, or naftifine.
232
What is tinea versicolor?
Tan to pink lesions. KOH and fungal culture reveals dermatophytes. Topical selenium sulfide every 2 to 3 weeks or oral therapy with itraconazole or fluconazole.
233
What are the most common bacterial organisms that cause skin infections?
Staphylococcus and Streptococcus.
234
What antibiotics are used to treat Staphylococcus?
Dicloxacillin, cephalexin, cefadroxil, cefazolin, nafcillin, oxacillin. If allergic to penicillin was a rash, then cephalosporins can be safely used.
235
What is the treatment of staphylococcal skin infections if the patient is allergic to penicillin?
Cephalosporins cannot be used if anaphylaxis. Alternatives for skin are macrolides, or extended fluoroquinolones (levofloxacin, gatifloxacin, moxifloxacin). Ciprofloxacin will not cover skin.
236
What is impetigo?
Superficial bacterial infection of the skin; usually caused by Staphylococcus, but is sometimes caused by Streptococcus pyogenes.
237
What is the presentation of impetigo?
Weeping, oozing, honey colored crusts; warm, humid conditions. Contagious and autoinoculable. Impetigo may cause glomerulonephritis, but not fever.
238
What is the treatment of impetigo?
Topical mupirocin or retapamulin; antistaphylococcal oral antibiotics, such as dicloxacillin or cephalexin (Keflex).
239
What is erysipelas?
Dermis and epidermis infection by group A Streptococcus (pyogenes). Fever, chills, and bacteremia; involves the face, giving a bright–red, swollen appearance.
240
What is the treatment for erysipelas?
Oral dicloxacillin or intravenous nafcillin or cefazolin.
241
What is cellulitis?
Bacterial infection of the dermis and subcutaneous tissues with Staphylococcus and Streptococcus.
242
What is the presentation of cellulitis?
Redness, swelling, and warmth and tenderness of the skin; no oozing, crusting, weeping, or draining.
243
What is the treatment for cellulitis?
Dicloxacillin or intravenous oxacillin, nafcillin, or cefazolin.
244
What are folliculitis, furuncles, and carbuncles?
Folliculitis, furuncles, and carbuncles represent three different degrees of severity of staphylococcal infections occurring around hair follicle. Folliculitis can be caused by Pseudomonas from a whirlpool or hot tub.
245
What is the presentation of a folliculus?
Folliculitis starts as a superficial infection around a hair follicle progressing to a small collection of infected material known as a furuncle. Several furuncles merge into a single carbuncle, which is a skin abscess.
246
What is the treatment for folliculitis?
Warm compresses; mupirocin. Furuncles and carbuncles require systemic antistaphylococcal antibiotics. Carbuncles require dicloxacillin or cefadroxil or IV nafcillin and surgical drainage.
247
What is necrotizing fasciitis?
Severe, life–threatening infection that starts as a cellulitis that dissects into the fascial planes of the skin. Streptococcus and Clostridium produce a toxin. Diabetes increases risk of fasciitis.
248
What is the presentation of necrotizing fasciitis?
High fever, portal of entry into the skin, pain, bullae, palpable crepitus.
249
How is necrotizing fasciitis diagnosed?
Elevated creatine phosphokinase; x–ray, CT scan or MRI show air in the tissue or necrosis.
250
What is the treatment for necrotizing fasciitis?
Surgery. beta–Lactam/beta–lactamase combination medications, such as ampicillin/sulbactam (Unasyn), ticarcillin/clavulanate (Timentin), or piperacillin/tazobactam (Zosyn).
251
What is paronychia?
Infection under the skin surrounding a nail.
252
What is the treatment of paronychia?
Treatment: drainage, dicloxacillin, cefadroxil or cephalexin orally, or oxacillin, nafcillin, or cefazolin intravenously.
253
What is herpes simplex?
Infection of the genitals, multiple, painful vesicles. Most accurate diagnostic test is a viral culture, which will grow in 24 to 48 hours. Serology is not useful.
254
What is the treatment for herpes simplex?
Acyclovir, famciclovir, or valacyclovir. Topical acyclovir has little efficacy in primary lesions and will not prevent recurrent lesions. Acyclovir–resistant herpes is treated with foscarnet.
255
What are the complications of varicella?
Pneumonia, hepatitis, dissemination. Dermatomal herpes zoster occur more frequently in elderly and with immune defects. The vesicles are 2 to 3 mm in size on an erythematous base.
256
How is varicella diagnosed?
Tzanck prep and viral culture
257
What is the treatment for varicella?
If immunocompromised child or primary infection in adult, then acyclovir, valacyclovir, or famciclovir.
258
What is the treatment of zoster?
Acyclovir decreases risk of postherpetic neuralgia. Steroids in elderly with zoster. Postherpetic neuralgia is treated with gabapentin.
259
What is human papilloma virus?
Responsible for sexually transmitted anogenital and oral warts (condylomata acuminata). Lesions, are translucent, white, or flesh, and are located on skin and mucosal surfaces.
260
What is the treatment for condyloma acuminata?
Cryotherapy with liquid nitrogen, laser removal, and trichloroacetic acid or podophyllin (teratogenic). Imiquimod is a local immunostimulant that takes 14 weeks to result in sloughing off of the wart.
261
What is the presentation of primary syphilis?
The chancre of primary syphilis is an ulceration with heaped–up, indurated edges that is painless. Causative organism is Treponema pallidum.
262
What is secondary syphilis?
Generalized copper–colored, maculopapular rash that is more intense on the palms and soles of the feet. The other manifestations of secondary syphilis are mucous patch, alopecia areata, and condylomata lata.
263
How is primary syphilis diagnosed?
Initial test darkfield. False–neg rate 25% for VDRL/RPR. Serologic tests need several weeks to become positive, and only 75% sensitive in primary. For secondary syphilis, VDRL/RPR tests are 100% sensitive.
264
What is the treatment of syphilis?
Primary and secondary syphilis are treated with a single, intramuscular dose of penicillin; penicillin allergic patients are treated with doxycycline orally for 2 weeks.
265
What is scabies?
Vesicular eruptions resulting from Sarcoptes scabiei (hominis) mites burrowing into the skin.
266
What is the presentation of scabies?
Web spaces of hands, feet, pruritic lesions around penis, breasts. Itching, burrows and excoriations around small pruritic vesicles. Spares head. Patients with HIV have severe crusting, known as Norwegian scabies.
267
How is scabies diagnosed?
Scraping out the organism after mineral oil is applied to a burrow (not routinely done).
268
What is the treatment for scabies?
Permethrin. Lindane has equal efficacy, but greater toxicity. Norwegian scabies can be treated with ivermectin orally.
269
What is pediculosis?
Pediculosis (lice and crabs from the genus Pediculus) tends to involve the head. Both P. humanus (lice) and P. pubis (crabs) can be sexually transmitted.
270
What is the treatment for pediculosis?
Over–the–counter pyrethrins, Lindane.
271
What is the cause of Lyme disease?
Borrelia burgdorferi spirochete, transmitted by the deer tick (Ixodes scapularis).
272
What is the presentation of Lyme disease?
Erythematous with central clearing at least 5 cm in diameter. 7 to 10 days after the tick bite.
273
How is Lyme disease diagnosed?
This rash is more important than serologic testing for diagnosis.
274
What is the treatment for Lyme disease?
Doxycycline, amoxicillin, or cefuroxime. Without therapy, two–thirds develop joint disease. Some develop neurologic or cardiac disorders.
275
What is toxic shock syndrome?
Systemic reaction to a toxin produced by Staphylococci in a tampon, vaginal packing, nasal packing, retained sutures, or other surgical material.
276
What is the clinical presentation of toxic shock syndrome?
Presence of 3 or more or of the following: fever \>102, SBP
277
What is the treatment for toxic shock syndrome?
Remove the source of the infection; fluid resuscitation, dopamine, and clindamycin plus vancomycin.
278
What is staphylococcal scalded skin syndrome?
Occurs in infants and young children and in the immunocompromised. Mediated by a toxin from Staphylococcus, loss of the superficial layers of the epidermis in sheets.
279
What is the treatment for staphylococcal scalded skin syndrome?
Managed in a burn unit and nafcillin.
280
What is anthrax?
Bacillus anthracis cutaneous infection acquired from contact with infected livestock; woolsorters, bioterrorism.
281
What is the presentation of anthrax?
Papule appears that later becomes inflamed and develops with central necrosis, which is black in color.
282
How is anthrax diagnosed?
Gram stain and culture.
283
What is the treatment of anthrax?
In lesions due to occupational exposure, penicillin V or doxycycline. Bioterrorism: ciprofloxacin.
284
What are the characteristics of benign skin lesions?
Benign lesions do not grow in size and have smooth, regular borders with a diameter usually
285
What is the treatment for seborrheic keratosis?
Liquid nitrogen or curettage.
286
What are actinic keratoses?
Precancerous lesion on sun–exposed areas of the body in older persons. 1:1,000 progresses to squamous cell cancer. Light in color. Removed with cryotherapy, 5FU, imiquimod.
287
What is the presentation of melanoma?
Grow in size, irregular borders shape, inconsistent color.
288
What is lentigo maligna melanoma?
Lentigo maligna melanoma arises on sun–exposed body parts in the elderly. Acral–lentiginous melanoma arises on the palms, soles of feet, and nail beds.
289
What is the treatment for melanoma?
Melanoma is removed by excision. Interferon reduces the recurrence rates of melanoma.
290
What is squamous cell carcinoma?
Develops on sun–exposed skin surfaces in elderly patients. Ulceration. Metastases are rare.
291
What is the treatment of basal cell carcinoma?
Mohs microsurgery. 5–FU for superficial lesions.
292
What is Kaposi sarcoma?
Purplish lesions found on the skin predominantly of patients with HIV and CD4 counts
293
What is the treatment for Kaposi sarcoma?
Antiretroviral therapy to raise the CD4 count. Cryotherapy liposomal doxorubicin hydrochloride or vinblastine.
294
What is the presentation of psoriasis?
Silvery scales on extensor surfaces. Local or extensive. Nail pitting. Koebner phenomenon.
295
What is the treatment for psoriasis?
Salicylic acid, coal tar or anthralin derivatives. Biologic agents, such alefacept, efalizumab, etanercept, and infliximab, which are monoclonal antibodies.
296
What is atopic dermatitis?
Pruritic disorder with high IgE levels. Red, itchy plaques appear on the flexor surfaces, cheeks, lichenification.
297
What is the treatment for atopic dermatitis?
Emollients, avoid hot water and drying soaps; wear cotton clothes. Topical steroids, antihistamines, coal tars, phototherapy. Antistaphylococcal antibiotics. Topical doxepin.
298
What is seborrheic dermatitis?
Oversecretion of sebaceous material and a hypersensitivity reaction to a superficial fungus, Pityrosporum ovale. Scaly, greasy, flaky skin is found on a red base on the scalp, eyebrows, and in the nasolabial fold.
299
What is the treatment for seborrheic dermatitis?
Low–potency hydrocortisone, or topical antifungals in the form of shampoos, such as ketoconazole or sulfide.
300
What is contact dermatitis?
Hypersensitivity reaction to soaps, detergents, latex, sunscreens, or neomycin, jewelry, nickel.
301
What is the presentation of contact dermatitis?
Linear, vesicles, particularly when it is from poison ivy.
302
What is the treatment of contact dermatitis?
Antihistamines and topical steroids.
303
What is the presentation of pityriasis rosea?
Salmon colored patches that are similar to secondary syphilis, except spares the palms and soles and has a herald patch. Lesions on the back appear in a pattern like a Christmas tree. VDRL negative.
304
What is alopecia areata?
Autoimmune disease in which antibodies attack the hair follicles.
305
What is telogen effluvium?
Loss of hair in response to physiologic stress, such as cancer or malnutrition.
306
What is the treatment for acne?
Topical clindamycin or erythromycin. Benzoyl peroxide. Retinoids: tazarotene, tretinoin, and adapalene. Severe cystic acne is treated with minocycline, tetracycline, clindamycin, oral isotretinoin (teratogenic).
307
What are the steps in assessing the technical quality of a chest x–ray?
Determine if rotated by determining if trachea and spinous apophysis are midway between the clavicles. Ten ribs visible. Underexposed film appear too white. Overexposure is too dark.
308
What are the signs of interstitial pneumonia?
Disease of the lung in the interstitial space produces a fine, lacy appearance visible in most of the lobes.
309
What disorders cause interstitial infiltrates?
Pneumocystis pneumonia, Mycoplasma, viruses, Chlamydia, pulmonary fibrosis caused by silicosis, asbestosis, mercury poisoning, berylliosis, idiopathic pulmonary fibrosis.
310
What are Kerley B lines?
Kerley B lines are small, horizontal lines at the bases that represent fluid in the interlobular septa.
311
What is the proper position of the tip of an endotracheal tube on a chest x–ray?
1 to 2 cm above the carina.
312
What is the correct position of a central line on a chest x–ray?
Tip at junction of the superior vena cava and the right atrium, at right main stem bronchus. The tip of the line should not be inside the atrium because it can irritate the heart and provoke an arrhythmia.
313
What conditions can cause air under the diaphragm on a chest x–ray?
Perforation of esophagus or ulcer. In the upright position. Air is also visible after surgery or laparoscopy.
314
What are the indications for high resolution CT scan?
Symptomatic patients with a normal chest x–ray to detect metastatic lesions, solitary nodules, bullae, bronchiectasis, and diffuse parenchymal disease. CT is used as a guide to determine the site of biopsy.
315
What conditions are detected by abdominal x–rays?
Abdominal x–rays are useful only in the detection of an abdominal obstruction, such as an ileus or a volvulus.
316
What is the best method of detecting mass lesions of the abdomen?
Mass lesions in all abdominal organs are best detected with CT scanning or an MRI of the abdomen. Polyps are detected by colonoscopy. Ascites is visualized by ultrasound or CT scanning.
317
What is the best test for detecting inflammatory bowel disease, diverticulitis, or colon cancer?
Inflammatory bowel disease, diverticulosis, and cancer are detected by either endoscopy or barium studies of the bowel.
318
What are the best tests for detecting kidney stones?
Kidney stones are best detected by sonography or CT scanning.
319
What are the best tests for detecting gallstones?
Only 10 to 15% of gallstones can be detected on an abdominal film; the best tests for gallstones are sonography and CT scanning.
320
What is the role of sonography in detecting abdominal lithiasis?
Sonograms should be used first for evaluation of the biliary tract for cholelithiasis. Nephrolithiasis is visible by sonography, although there is less accuracy because retroperitoneal location.
321
What is the role of sonography in evaluating the abdomen?
Sonography is useful in the evaluation of masses in the liver, spleen, pancreas, pelvis, and for evaluating the presence of ascites. CT has a greater sensitivity and specificity for the abdomen and pelvis.
322
What is endoscopic retrograde cholangiopancreatography?
Contrast is injected to visualize the biliary tract and pancreatic structures for detecting strictures, stones, and neoplasms. ERCP can remove stones and dilate strictures and biopsy.
323
What is capsule endoscopy?
Allows direct visualization of the small bowel by swallowing a camera. If a patient has serious bleeding and both upper and lower endoscopy do not reveal the source, capsule endoscopy is indicated.
324
What is HIDA scanning?
Nuclear scan useful only in the detection of acute cholecystitis. Useful in patients in whom the diagnosis of cholecystitis is not clear. An abnormal or positive test is lack of visualization of the gallbladder.
325
What is positron emission tomography?
Useful to determine if lesions are malignant or benign. Cancer is associated with increased uptake of fluorodeoxyglucose. Used after chemotherapy to assess the presence of residual cancer.
326
What is the most accurate test for evaluating central nervous system lesions?
Magnetic resonance imaging is superior for the detection of stroke, cancer, multiple sclerosis, infections, and in the evaluation of the posterior fossa, such as the cerebellum and brainstem.
327
What is the sensitivity of MRI in detecting ischemic strokes?
\>90% within the 24 h after onset, whereas the CT needs 3 days before \>90% of ischemic strokes are visible. CT is superior to MRI in detection of blood. CT is the best for trauma and to exclude hemorrhagic stroke.
328
What tests are useful for diagnosing osteomyelitis?
X–ray is done first. Plain x–rays lack sensitivity; the specificity for osteomyelitis is excellent. Earliest finding of osteomyelitis is elevation of the periosteum. The MRI has high sensitivity (95%) and specificity (95%).
329
What is diabetic retinopathy?
Caused by damage to the endothelial lining of small blood vessels, leading to occlusion. The earliest form is nonproliferative retinopathy, characterized by dilation of veins, microaneurysms, edema, hemorrhages.
330
What are the predisposing factors to retinal detachment?
Spontaneous, but may result from trauma. Predisposing factors are myopia and surgical extraction of cataracts; proliferative retinopathy, retinal vein occlusion, and age–related macular degeneration.
331
What is the presentation of retinal detachment?
Blurry vision developing in one eye without pain or redness. Floaters, flashes, curtain coming down.
332
What are the causes of central retinal artery occlusion?
Carotid artery embolic disease, temporal arteritis, cardiac thrombi or myxoma, or thrombophilia, such as factor V Leiden mutation.
333
What is the treatment of central retinal artery occlusion?
Lay the patient flat and give oxygen; ocular massage in an attempt to unobstruct the vessel. Acetazolamide and thrombolytics.
334
What is the presentation of central retinal vein occlusion?
Sudden loss of vision without pain, redness, or abnormality in pupillary dilation. Ocular examination by funduscopy reveals disk swelling, venous dilation, tortuosity, and retinal hemorrhages.
335
What medications can cause acute angle–closure glaucoma?
Precipitated by anticholinergic medications, such as ipratropium bromide or tricyclic antidepressants.
336
How is open–angle glaucoma diagnosed?
Cup–to–disk ratio of \>0.3; confirmed by an elevation in intraocular pressure by tonometry. This disorder accounts for \>90% of cases of glaucoma; asymptomatic.
337
What medications are useful for decreasing the production of the aqueous humor in glaucoma?
Beta–blockers (timolol, betaxolol, levobunolol), alpha–adrenergic agonists (apraclonidine, brimonidine), and carbonic anhydrase inhibitors (dorzolamide and brinzolamide).
338
What treatments increase the outflow of aqueous humor in the treatment of glaucoma?
Prostaglandin analogs, such as latanoprost, travoprost, bimatoprost. Can change the color of the eyes and darken eyelid. Pilocarpine is a miotic agent that increases outflow of aqueous humor. Laser trabeculoplasty or surgical trabeculectomy.
339
What is the presentation of closed–angle glaucoma?
Eye is red, painful, hard, fixed midpoint pupil. The cornea has a hazy cloudiness, diminished visual acuity. Precipitated by anticholinergic medications.
340
What is the treatment of closed–angle glaucoma?
IV acetazolamide, urea, osmotic diuretics (mannitol or glycerol). Pilocarpine can be used to open the canal of Schlemm; beta–blockers decrease humor production. Laser trabeculoplasty.
341
What are the causes of infectious conjunctivitis?
Bacteria, viruses, and fungi.
342
What is the presentation of bacterial conjunctivitis?
Unilateral, purulent discharge. Crusting overnight. Less itching compared with viral conjunctivitis. Red eye, normally reactive pupil, normal ocular pressure, and no visual impairment.
343
What is the presentation of viral conjunctivitis?
Viral conjunctivitis is more often bilateral in nature, with much more severe ocular itching and enlarged preauricular adenopathy. The eyes are also red, the pupil reacts normally, and there is no photophobia.
344
What is the treatment of bacterial conjunctivitis?
Erythromycin ointment, sulfacetamide drops, or topical fluoroquinolones.
345
What is the treatment of viral conjunctivitis?
Topical antihistamine and decongestants.
346
What is subconjunctival hemorrhage?
Most commonly caused by trauma. The hematoma stops at the limbus, which is the junction between the conjunctiva and the cornea. There is no impairment of vision.
347
What is keratitis?
Any infection or inflammation of the cornea.
348
What is the presentation of herpes simplex keratitis?
Severe pain in the eye and a foreign body sensation under the eyelid.
349
How is herpes simplex keratitis diagnosed?
Characteristic dendritic pattern over the cornea on fluorescein staining of the eye under a blue light.
350
What is the treatment for herpes simplex keratitis?
Oral acyclovir, famciclovir, or valacyclovir and topical trifluridine 1% solution or idoxuridine.
351
What is periorbital cellulitis?
Cellulitis caused by Staphylococcus aureus or Streptococcus infecting the dermis and subcutaneous tissues surrounding the eye.
352
What is the treatment for periorbital cellulitis?
Antistaphylococcal penicillins, such as oxacillin or nafcillin. If there is an allergic rash to penicillins, then first–generation cephalosporins can be used (cefazolin).
353
What is uveitis?
Uveitis is inflammation of the iris, ciliary body, and choroid. Uveitis is caused by psoriasis, sarcoidosis, syphilis, reactive arthritis, and inflammatory bowel disease.
354
What is the presentation of uveitis?
Painful, red eye with photophobia. Pain also occurs when shining a light in the unaffected eye.
355
How is uveitis diagnosed?
Slit lamp examination. Inflammation of the iris, ciliary body, and choroid.
356
What is the treatment for uveitis?
Topical or systemic steroids.
