• Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

Card Range To Study

through

image

Play button

image

Play button

image

Progress

1/278

Click to flip

Use LEFT and RIGHT arrow keys to navigate between flashcards;

Use UP and DOWN arrow keys to flip the card;

H to show hint;

A reads text to speech;

278 Cards in this Set

  • Front
  • Back
What drug should be given if patients continue to seize after administration of lorazepam, phenytoin and Phenobarbital?
Midazolam or propofol anesthesia.
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.
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.
What are the side effects of valproic acid?
Side effects include ataxia, tremor, hepatotoxicity, thrombocytopenia, gastrointestinal irritation, and hyponatremia.
What is the mechanism of action of lamotrigine?
Lamotrigine decreases glutamate release. Side effects: Stevens-Johnson syndrome.
What is the treatment of absence seizures?
Ethosuximide. Valproic acid is an acceptable option.
What is the treatment for myoclonic and atonic seizures?
Valproic acid.
What is the treatment for partial seizures?
Carbamazepine and phenytoin are first-line therapy. Valproic acid, lamotrigine, and levetiracetam are alternatives.
What is vertigo?
False sensation of movement.
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.
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.
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.
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.
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.
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.
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.
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.
What is the treatment of peripheral vertigo?
Meclizine or diazepam.
What is the treatment of Mèniére disease?
Low-salt diet and diuretics. Surgical decompression.
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).
What is the treatment of vertigo caused by labyrinthitis?
Meclizine and diazepam.
28-year-old woman with throbbing, right-side headache; nausea; worsened by walking, loud noise, bright light. What is the diagnosis?
Migraine
What are the primary headache syndromes?
Migraine, cluster, and tension headache. Migraine affects 15% of the population.
What are the secondary causes of headache?
Intracranial hemorrhage, brain tumor, meningitis, temporal arteritis, and glaucoma.
What type of headache is characterized by fever and nuchal rigidity?
Meningitis.
"The worst headache of my life" or a "thunderclap" at onset with nuchal rigidity without fever, suggests what type of headache?
Intracranial hemorrhage.
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.
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.
What are the laboratory abnormalities associated with temporal arteritis?
Increased sedimentation rate; diagnosed with biopsy of the temporal artery. Initiate therapy with steroid immediately.
What cause of headache syndrome is associated with eye pain?
Glaucoma
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.
What are the triggers of migraine?
Alcohol, chocolate, cheeses, monosodium glutamate, hunger, or irregular sleep patterns.
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.
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.
What are complicated migraines?
Migraines with severe neurologic deficits that persist after the resolution of pain.
What are basilar migraines?
Migraine headaches associated with vertigo, diplopia, ataxia, or dysarthria.
What are the characteristics of tension-type headaches?
Tension-type headaches are tight, band-like headaches are bilateral.
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).
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.
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.
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.
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.
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.
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.
What is the treatment for pseudotumor cerebri?
Weight loss, discontinue oral contraceptives, acetazolamide, furosemide, prednisone. Repeated lumbar punctures; placement of ventriculoperitoneal shunt.
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.
What is the treatment of trigeminal neuralgia?
Carbamazepine. Phenytoin, baclofen, or gabapentin. Surgery or alcohol injection into the affected nerve.
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
What is Guillain-Barre syndrome?
Acute, often severe polyradiculopathy caused by autoimmune destruction of myelin by an immune response.
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.
What autonomic instabilities are associated with Guillain-Barre syndrome?
Profuse sweating, postural hypotension, labile blood pressure, cardiac dysrhythmia occurs in severe GBS.
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.
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.
What is the treatment for Guillain-Barre syndrome?
Intravenous immunoglobulin or plasmapheresis; monitor the vital capacity and initiate early respiratory support if respiratory weakness.
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.
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.
What is the presentation of myasthenia gravis?
Weakness, fatigability. Initially, diplopia, ptosis, dysphagia. Speech nasal; "snarling." Asymmetric proximal muscle weakness. Normal reflexes, pupillary responses, sensory. Impaired respiration.
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.
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).
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%.
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.
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.
What is amyotrophic lateral sclerosis?
Idiopathic weakness with upper and lower motor neuron loss, CN palsies, respiratory involvement; preserved bowel, bladder sensory, cognitive, sexual.
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.
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.
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.
What is the confirmatory test for amyotrophic lateral sclerosis?
Confirmatory test is the electromyogram. Cerebrospinal fluid and MRI are normal.
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.
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.
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 (< 50 cells/mcL), total protein mildly elevated.
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.
What is the treatment of bladder hyperactivity in multiple sclerosis?
Bladder hyperactivity is treated with oxybutynin; urinary retention is treated with bethanechol.
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.
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.
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%.
What is the prevalence of dementia?
1-5% between ages 65-69; 45% by age 100. Only 5% of Alzheimer disease is inherited.
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.
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.
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.
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.
What are the characteristics of normal pressure hydrocephalus?
Prominent gait abnormalities before the onset of cognitive impairment, urinary incontinence.
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.
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.
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
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.
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.
How is Huntington disease diagnosed?
Genetic testing. CT scanning shows cerebral atrophy or atrophy of caudate nucleus.
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.)
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
What is Parkinson disease?
Neurologic syndrome resulting from the deficiency of the neurotransmitter dopamine; degenerative, vascular, or inflammatory changes in the basal ganglia.
What are the causes of Parkinson disease?
Neuroleptics (haloperidol, chlorpromazine), metoclopramide, alpha-methyldopa, reserpine. MPTP, carbon monoxide, cyanide, manganese. Encephalitis. Basal ganglia lesions.
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.
What is Shy-Drager syndrome?
Parkinsonism with prominent orthostatic hypotension.
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.
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.
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).
Which medications block acetylcholine stimulation of the basal ganglia?
Benztropine and trihexyphenidyl.
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.
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.
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.
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.
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.
What is the treatment of benign essential tremor?
Propranolol. Alternatives are primidone, alprazolam, and clozapine. If no medical therapy is effective, thalamotomy is indicated.
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.
What is the treatment of restless leg syndrome?
Treatment is with dopamine agonists, such as pramipexole or ropinirole; levodopa/carbidopa, benzodiazepines.
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.
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.
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.
How is pemphigus vulgaris diagnosed?
Biopsy the skin with immunofluorescent stains.
What is the treatment for pemphigus vulgaris?
Systemic glucocorticoids, such as prednisone; azathioprine, mycophenolate, or cyclophosphamide. Rituximab and IVIg are also effective.
What is pemphigus foliaceus?
Blistering disease often associated with other autoimmune diseases, or it can be induced by ACE inhibitors or NSAIDs.
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.
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.
How is bullous pemphigoid diagnosed?
Biopsy with immunofluorescent antibodies.
What is the treatment of bullous pemphigoid?
Systemic steroids, such as prednisone; topical steroids only if no oral lesions.
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.
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.
How is porphyria cutanea tarda diagnosed?
Uroporphyrins are elevated two to five times above the coproporphyrins.
What is the treatment for porphyria cutanea tarda?
Stop alcohol and discontinue estrogen, and iron. Chloroquine increases the excretion of porphyrins.
What is acute urticaria?
Hypersensitivity reaction with IgE, mast cell activation; wheals, hives, without hypotension.
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.
What is the presentation of acute urticaria?
Lasts <6 weeks and self-limited: onset of wheals and hives within 30 min, lasts for <24 h. Itching. Chronic urticaria lasts >6 weeks and is associated with pressure on the skin, cold, or vibration.
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.
What is a morbilliform rash?
Milder hypersensitivity reaction than urticaria. Typical type of drug reaction and lymphocyte mediated.
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.
What is the treatment of morbilliform rash?
Antihistamines and steroids.
What is erythema multiforme?
Caused by penicillins, phenytoin, NSAIDs, sulfa drugs. Majority of cases follow infection with herpes simplex or Mycoplasma.
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.
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.
What is the presentation of Stevens-Johnson syndrome?
SJS involves <10-15% of the total body surface area; the overall mortality rate is <5-10%. Mucous-membrane involvement of oral and conjunctivae, respiratory tract.
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.
What is toxic epidermal necrolysis?
Toxic epidermal necrolysis is the most serious cutaneous hypersensitivity reaction. Mortality 40-50%.
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.
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.
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.
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.
What is erythema nodosum?
Localized inflammatory condition, occurring after infections inflammatory conditions, pregnancy, strep infections, coccidioidomycoses, histoplasmosis, sarcoidosis, IBD, syphilis, hepatitis, Yersinia.
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.
What is the treatment for erythema nodosum?
Analgesics and NSAIDs. Potassium iodide solution; usually self-limiting.
What are the superficial fungal infections?
Tinea pedis, cruris, corporis, versicolor, capitis, and onychomycosis
What is the appearance of tinea versicolor on KOH?
Malassezia furfur organism appears as "spaghetti and meatballs" on KOH. The most accurate test is fungus culture, but this is not practical because dermatophytes take up to 6 weeks to grow.
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.
What is the treatment of dermatophyte infection of the hair?
Griseofulvin for 6-8 weeks for tinea capitis. Terbinafine for 2-4 weeks.
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.
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.
What are the most common bacterial organisms that cause skin infections?
Staphylococcus and Streptococcus.
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. <5% cross-reactivity between penicillin and cephalosporins.
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.
What is impetigo?
Superficial bacterial infection of the skin; usually caused by Staphylococcus, but is sometimes caused by Streptococcus pyogenes.
What is the presentation of impetigo?
Weeping, oozing, honey colored crusts; warm, humid conditions. Contagious and autoinoculable. Impetigo may cause glomerulonephritis, but not fever.
What is the treatment of impetigo?
Topical mupirocin or retapamulin; antistaphylococcal oral antibiotics, such as dicloxacillin or cephalexin (Keflex).
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.
What is the treatment for erysipelas?
Oral dicloxacillin or intravenous nafcillin or cefazolin.
What is cellulitis?
Bacterial infection of the dermis and subcutaneous tissues with Staphylococcus and Streptococcus.
What is the presentation of cellulitis?
Redness, swelling, and warmth and tenderness of the skin; no oozing, crusting, weeping, or draining.
What is the treatment for cellulitis?
Dicloxacillin or intravenous oxacillin, nafcillin, or cefazolin.
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.
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.
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.
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.
What is the presentation of necrotizing fasciitis?
High fever, portal of entry into the skin, pain, bullae, palpable crepitus.
How is necrotizing fasciitis diagnosed?
Elevated creatine phosphokinase; x-ray, CT scan or MRI show air in the tissue or necrosis.
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).
What is paronychia?
Infection under the skin surrounding a nail.
What is the treatment of paronychia?
Treatment: drainage, dicloxacillin, cefadroxil or cephalexin orally, or oxacillin, nafcillin, or cefazolin intravenously.
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.
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.
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.
How is varicella diagnosed?
Tzanck prep and viral culture
What is the treatment for varicella?
If immunocompromised child or primary infection in adult, then acyclovir, valacyclovir, or famciclovir.
What is the treatment of zoster?
Acyclovir decreases risk of postherpetic neuralgia. Steroids in elderly with zoster. Postherpetic neuralgia is treated with gabapentin.
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.
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.
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.
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.
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.
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.
What is scabies?
Vesicular eruptions resulting from Sarcoptes scabiei (hominis) mites burrowing into the skin.
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.
How is scabies diagnosed?
Scraping out the organism after mineral oil is applied to a burrow (not routinely done).
What is the treatment for scabies?
Permethrin. Lindane has equal efficacy, but greater toxicity. Norwegian scabies can be treated with ivermectin orally.
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.
What is the treatment for pediculosis?
Over-the-counter pyrethrins, Lindane.
What is the cause of Lyme disease?
Borrelia burgdorferi spirochete, transmitted by the deer tick (Ixodes scapularis).
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.
How is Lyme disease diagnosed?
This rash is more important than serologic testing for diagnosis.
What is the treatment for Lyme disease?
Doxycycline, amoxicillin, or cefuroxime. Without therapy, two-thirds develop joint disease. Some develop neurologic or cardiac disorders.
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.
What is the clinical presentation of toxic shock syndrome?
Presence of 3 or more or of the following: fever >102, SBP <90, desquamative rash, vomiting, involvement of mucous membranes of the eyes, mouth, or genitals, elevated bilirubin, platelets <100,000.
What is the treatment for toxic shock syndrome?
Remove the source of the infection; fluid resuscitation, dopamine, and clindamycin plus vancomycin.
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.
What is the treatment for staphylococcal scalded skin syndrome?
Managed in a burn unit and nafcillin.
What is anthrax?
Bacillus anthracis cutaneous infection acquired from contact with infected livestock; woolsorters, bioterrorism.
What is the presentation of anthrax?
Papule appears that later becomes inflamed and develops with central necrosis, which is black in color.
How is anthrax diagnosed?
Gram stain and culture.
What is the treatment of anthrax?
In lesions due to occupational exposure, penicillin V or doxycycline. Bioterrorism: ciprofloxacin.
What are the characteristics of benign skin lesions?
Benign lesions do not grow in size and have smooth, regular borders with a diameter usually <1 cm. Homogenous in color.
What is seborrheic keratosis?
Benign hyperpigmented lesions in the elderly with a "stuck on" appearance; most common on the face shoulders, chest, and back.
What is the treatment for seborrheic keratosis?
Liquid nitrogen or curettage.
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.
What is the presentation of melanoma?
Grow in size, irregular borders shape, inconsistent color.
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.
What is the treatment for melanoma?
Melanoma is removed by excision. Interferon reduces the recurrence rates of melanoma.
What is squamous cell carcinoma?
Develops on sun-exposed skin surfaces in elderly patients. Ulceration. Metastases are rare.
What is basal cell carcinoma?
Sixty-five to eighty percent of all skin cancers are basal cell. Shiny or "pearly" appearance. Rate of metastases is <0.1%.
What is the treatment of basal cell carcinoma?
Mohs microsurgery. 5-FU for superficial lesions.
What is Kaposi sarcoma?
Purplish lesions found on the skin predominantly of patients with HIV and CD4 counts <100/mm3. Human herpes virus 8 is the causative organism.
What is the treatment for Kaposi sarcoma?
Antiretroviral therapy to raise the CD4 count. Cryotherapy liposomal doxorubicin hydrochloride or vinblastine.
What is the presentation of psoriasis?
Silvery scales on extensor surfaces. Local or extensive. Nail pitting. Koebner phenomenon.
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.
What is atopic dermatitis?
Pruritic disorder with high IgE levels. Red, itchy plaques appear on the flexor surfaces, cheeks, lichenification.
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.
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.
What is the treatment for seborrheic dermatitis?
Low-potency hydrocortisone, or topical antifungals in the form of shampoos, such as ketoconazole or sulfide.
What is contact dermatitis?
Hypersensitivity reaction to soaps, detergents, latex, sunscreens, or neomycin, jewelry, nickel.
What is the presentation of contact dermatitis?
Linear, vesicles, particularly when it is from poison ivy.
What is the treatment of contact dermatitis?
Antihistamines and topical steroids.
What is pityriasis rosea?
Pruritic eruption that begins with a "herald patch". Mild, self-limited, and usually resolves in 8 weeks without scarring.
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.
What is alopecia areata?
Autoimmune disease in which antibodies attack the hair follicles.
What is telogen effluvium?
Loss of hair in response to physiologic stress, such as cancer or malnutrition.
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).
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.
What are the chest x-ray signs of chronic obstructive pulmonary disease and emphysema?
Hyperinflation of the lung causes darkening of the lung fields; flat the diaphragm and tubular-shaped heart. Increased anterior/posterior diameter, or "barrel chest," bullae are thin, white lines.
What are the chest x-ray signs of pneumonia?
Whitening of lobe. "Silhouette" sign: border between the affected lobe and a structure is obscured. Lower lobe pneumonia causes a silhouette of diaphragm. Right middle-lobe pneumonia obscures right heart border.
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.
What disorders cause interstitial infiltrates?
Pneumocystis pneumonia, Mycoplasma, viruses, Chlamydia, pulmonary fibrosis caused by silicosis, asbestosis, mercury poisoning, berylliosis, idiopathic pulmonary fibrosis.
What are the chest x-ray signs of congestive heart failure?
Fluid overload causes the blood vessels toward the apices become fuller, which is pulmonary vascular congestion, or "cephalization" of flow. Cardiomegaly, pleural effusions, and Kerley B lines.
What are Kerley B lines?
Kerley B lines are small, horizontal lines at the bases that represent fluid in the interlobular septa.
What is the proper position of the tip of an endotracheal tube on a chest x-ray?
1 to 2 cm above the carina.
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.
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.
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.
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.
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.
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.
What are the best tests for detecting kidney stones?
Kidney stones are best detected by sonography or CT scanning.
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.
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.
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.
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.
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.
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.
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.
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.
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.
What are the indications for using contrast during a head CT scan?
Contrast is indicated for the detection of cancers and infection. When an abscess or neoplastic process is present, extravasation of contrast is visible as "ring"-enhancing lesion.
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%).
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.
What is proliferative retinopathy?
Proliferative retinopathy progresses rapidly to blindness. "Neovascularization," or new blood vessel formation leads to new vessel formation. Intravitreal hemorrhages. Treatment is laser photocoagulation.
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.
What is the presentation of retinal detachment?
Blurry vision developing in one eye without pain or redness. Floaters, flashes, "curtain coming down."
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.
What is the presentation of retinal artery occlusion?
Sudden, painless, unilateral loss of vision. No redness. Pale retina, with diminished perfusion and a "cherry- red" spot at the fovea.
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.
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.
What medications can cause acute angle-closure glaucoma?
Precipitated by anticholinergic medications, such as ipratropium bromide or tricyclic antidepressants.
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.
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).
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.
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.
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.
What are the causes of infectious conjunctivitis?
Bacteria, viruses, and fungi.
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.
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.
What is the treatment of bacterial conjunctivitis?
Erythromycin ointment, sulfacetamide drops, or topical fluoroquinolones.
What is the treatment of viral conjunctivitis?
Topical antihistamine and decongestants.
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.
What is keratitis?
Any infection or inflammation of the cornea.
What is the presentation of herpes simplex keratitis?
Severe pain in the eye and a foreign body sensation under the eyelid.
How is herpes simplex keratitis diagnosed?
Characteristic dendritic pattern over the cornea on fluorescein staining of the eye under a blue light.
What is the treatment for herpes simplex keratitis?
Oral acyclovir, famciclovir, or valacyclovir and topical trifluridine 1% solution or idoxuridine.
What is periorbital cellulitis?
Cellulitis caused by Staphylococcus aureus or Streptococcus infecting the dermis and subcutaneous tissues surrounding the eye.
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).
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.
What is the presentation of uveitis?
Painful, red eye with photophobia. Pain also occurs when shining a light in the unaffected eye.
How is uveitis diagnosed?
Slit lamp examination. Inflammation of the iris, ciliary body, and choroid.
What is the treatment for uveitis?
Topical or systemic steroids.