Cilostazol

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By: B. Pyran, M.A., M.D., M.P.H.

Associate Professor, New York University Long Island School of Medicine

Not until 1846 Genetic studies have demonstrated several inheritable gene did doctors discover the anesthetic properties of ether spasms below rib cage buy cilostazol with amex, first in abnormalities in certain families muscle relaxant injections neck cheap cilostazol amex, but the vast majority of cases animals and then in humans spasms in stomach cheap 50 mg cilostazol free shipping. Soon afterwards, the usefulness of Parkinson’s occur sporadically. It is believed that heredity fac- of chloroform and nitrous oxide became known and heralded a tors may render some individuals more vulnerable to environ- new era in surgery. The dozens of drugs used today during mental factors such as pesticides. The discovery in the late 1970s surgery abolish pain, relax muscles and induce unconsciousness. MPTP was accidently synthesized by illicit drug to prevent pain during examinations, diagnostic procedures, designers seeking to produce a heroin-like compound. The most famous of these was found to be converted in the brain to a substance that agents, which temporarily interrupt the action of pain-carrying destroys dopamine neurons. Parkinson’s is now being inten- nerve fibers, is Novocain. Until recently, Novocain was used as sively studied in a primate MPTP model. In the past several decades, scientists have shown in a pri- Analgesia produces loss of pain sensation without loss of sen- mate model of Parkinson’s that specific regions in the basal gan- sitivity to touch. The two main types of analgesics are nonopioids glia, the collections of cell bodies deep in the brain, are abnor- (aspirin and related non-steroidal anti-inflammatory drugs such mally overactive. Most importantly, they found that surgical as ibuprofen, naproxen and acetaminophen) and opioids (mor- destruction of these overactive nuclei—the pallidum and sub- phine, codeine). Nonopioid analgesics are useful for treating thalamic nucleus—can greatly reduce symptoms. The past mild or moderate pain, such as headache or toothache. Mod- decade has witnessed a resurgence in this surgical procedure, erate pain also can be treated by combining a mild opioid, such pallidotomy, and more recently chronic deep brain stimulation. Opioids are the most potent pain- These techniques are highly successful for treating patients who killers and are used for severe pain, such as that occurring after have experienced significant worsening of symptoms and are major chest or abdominal surgery. At the site of injury, the body produces prostaglandins that increase pain sensitivity. Aspirin, which acts primarily in the periphery, prevents the pro- duction of prostaglandins. Acetaminophen is believed to Aspirin acts here Cerebral cortex block pain impulses in the brain itself. Local anesthetics inter- Thalamus cept pain signals traveling up Opiate drugs the nerve. Opiate drugs, which act here act primarily in the central ner- vous system, block the transfer of pain signals from the spinal cord to the brain. Local anesthetics act here Spinal cord Insights into the body’s own pain-control system mediated Many di∑erent forms of epilepsy have been recognized. It also can result from a wide variety of diseases brospinal fluid in which the spinal cord is bathed without caus- or injuries (including head injury), birth trauma, brain infec- ing paralysis, numbness or other severe side e∑ects. This tech- tion (such as meningitis), brain tumors, stroke, drug intoxica- nique came about through experiments with animals that first tion, drug or alcohol withdrawal states and metabolic disorders. This technique is now commonly have been identified during the past decade. In 70 percent of used in humans to treat pain after surgery. New knowledge about other receptors and chemical medi- Seizures are of two types. Generalized seizures, which result ators involved in the transmission of pain are leading to the in loss of consciousness, can cause several behavioral changes development of new approaches to managing pain. These including convulsions or sudden changes in muscle tone and include drugs that intercept pain messages at receptors that arise when there is excessive electrical activity over a wide area bind glutamate, the major excitatory neurotransmitter in pain of the brain. Partial seizures may occur in full consciousness or pathways.

Carragheenan (Carrageenan). Cilostazol.

• How does Carrageenan work?
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Source: http://www.rxlist.com/script/main/art.asp?articlekey=96696

He has difficulty writing and has begun to notice wavering in his voice when dictating letters (now his preferred method of correspondence) spasms when falling asleep generic 50 mg cilostazol amex. He denies having any his- tory of regular alcohol consumption but keeps a bottle of scotch in his desk because it “steadies his nerves” before important meetings spasms spinal cord injury buy 50 mg cilostazol with mastercard. On examination muscle relaxants knee pain generic cilostazol 100 mg without a prescription, he has a relatively fast tremor of the right hand that is enhanced significantly with finger-to-nose testing. His gait is normal, but his handwriting is very difficult to read because of shaking when he writes. Propranolol Key Concept/Objective: To be able to distinguish the clinical presentation and treatment of essential tremor from those of other movement disorders This patient’s fast tremor that increases with intention and involves his voice is most like- ly caused by essential tremor. Parkinson symptoms typically decrease with intention, and although it can involve facial and jaw muscles, the disease usually spares phonation. Alcohol consumption often briefly suppresses symptoms of essential tremor, and beta blockers can prove to be helpful in long-term therapy. Essential tremor does not typically respond to antiparkinsonian agents, and tricyclic antidepressants or valproate can worsen the problem. A 27-year-old patient of yours comes in because her 48-year-old father has been diagnosed with Huntington disease. She wants to know what this means for her risk of getting the disease. She is a carrier of the gene for Huntington disease, but she is unlikely to get the disease herself unless it runs in her mother’s family B. There is a 50% chance that she has inherited the gene for Huntington disease, but if she has, she is unlikely to show symptoms until she is in her 50s or 60s C. There is a 50% chance that she has inherited the gene for Huntington disease, but fewer than half of the people with the gene develop the disease, so her odds are not too bad D. There is a 50% chance that she has inherited the gene for Huntington disease; if she has, she is likely to show symptoms at a younger age than did her father E. She may have inherited the gene for Huntington disease, but it usually only manifests in men because it is on the X chromosome Key Concept/Objective: To understand the genetics of Huntington disease and the implications for families of affected patients Huntington disease is an autosomal dominant disorder that manifests anticipation (i. The genotype manifests when an area of glutamine (CAG) repeats on chromosome 4 exceeds 40 repetitions of the CAG codon. These repeats tend to increase in subsequent generations, a phenomenon that cor- relates with onset of the disease. It is a disease characterized by very high penetrance: almost all patients with the genotype develop Huntington disease. For this reason, genet- ic testing of asymptomatic family members is an ethically complex and difficult proposi- tion. With regard to the alternative answers to this question, choice A characterizes auto- somal recessive inheritance; choice B characterizes autosomal dominant inheritance with negative anticipation; choice C characterizes autosomal dominant inheritance with low penetrance; and choice E characterizes X-linked recessive inheritance. A 26-year-old elementary schoolteacher presents to the emergency department for evaluation of headache and neck stiffness. On physical examination, the patient is noted to have an erythematous, maculopapular rash. The remainder of the physical examina- tion, including neurologic examination, is unremarkable. A lumbar puncture is performed to evaluate for meningitis. Which of the following cerebrospinal fluid findings is NOT characteristic of viral meningitis? Clear cerebrospinal fluid (CSF) Key Concept/Objective: To know the typical CSF findings of viral meningitis Careful examination of the CSF is the mainstay of diagnosis of viral meningitis or encephalitis. Characteristically, the CSF is clear and features a predominantly mononu- clear pleocytosis and normal glucose content. Initially, the CSF may contain polymor- phonuclear leukocytes. The CSF cell count is usually below 100 cells/mm3; it may be high- er with enteroviral infections, however, and the CSF may contain thousands of mononu- clear cells after mumps and lymphocytic choriomeningitis (LCM) virus infections. The CSF protein concentration is usually normal or mildly elevated (not markedly elevated, as seen in this patient). Bacteria are not found on Gram stain, and CSF cultures are sterile.

Linum catharticum (Mountain Flax). Cilostazol.

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Source: http://www.rxlist.com/script/main/art.asp?articlekey=96347

Methotrexate is best given in a single weekly oral dose of up to 30 mg or in three divided doses at 12- hour intervals during a 24-hour period (e muscle relaxant drugs cyclobenzaprine order cilostazol with visa. Side effects of methotrexate therapy include bone marrow suppression muscle relaxant without aspirin cheap cilostazol 100mg mastercard, nausea muscle relaxant medication over the counter cilostazol 100 mg otc, diar- rhea, stomatitis, and hepatotoxicity. Methotrexate is teratogenic and can cause reversible oligospermia. Evaluation by tests of liver function, renal function, and blood elements must be made before and throughout the course of methotrexate therapy. Cases of pancy- topenia after low-dose methotrexate therapy underscore the hazards of use of the drug in patients with renal insufficiency or in patients who are concomitantly receiving drugs that increase methotrexate toxicity. The use of liver biopsy to monitor patients on methotrexate has been a source of great controversy. Liver biopsies are not routinely performed in patients with rheumatoid arthritis who are undergoing treatment with methotrexate, but liver biopsy has been advo- cated in patients with psoriasis. Patients with psoriasis who are treated with methotrexate are more prone to hepatic fibrosis, possibly because of their underlying disease or because of the concomitant treatments they are given. Current guidelines call for the use of liver biopsy in patients with psoriasis who have received a cumulative dose of 1 to 1. Biopsy should be performed early in the course of treatment in patients with a history of hepatitis C, alco- holism, or other liver disease. Risk factors for hepatotoxicity include heavy alcohol intake, obesity, a history of diabetes or hepatitis, and abnormal results on liver function testing. Although methotrexate causes bone marrow suppression, routine bone marrow biop- sies are not indicated. A 32-year-old high school teacher reports a mildly itchy new rash over the past week. He has been gen- erally healthy, although he did take a course of penicillin for culture-positive streptococcal pharyngitis several weeks ago. He does not smoke, drinks alcohol only occasionally, and has been monogamous with his wife over the 5 years they have been married. He has had no fever, chills, eye symptoms, anorexia, nausea, diarrhea, bloody stool, abdominal pain, penile sores or discharge, dysuria, or joint pains. On examination, the patient is afebrile, with multiple sharply demarcated scaly papules 3 to 10 mm in diam- eter distributed symmetrically on his trunk, arms, palms, and penis. There are no target lesions or oral lesions, and no lymphadenopathy is found. What is the most likely cause of this patient’s rash? Drug reaction Key Concept/Objective: To be able to recognize guttate psoriasis This is a classic presentation of guttate psoriasis, with onset after a recent streptococcal infection; a symmetrical distribution involving trunk, extremities, palms, and penis; and 8 BOARD REVIEW well-demarcated, small, scaly, erythematous papules. In contrast, the rash of primary HIV infection is a maculopapular, diffuse eruption, with poorly defined borders and no scal- ing, usually accompanied by low-grade fever, malaise, lymphadenopathy, and other flu- like symptoms. Secondary syphilis can cause a scaly rash that may include the palms and soles, but the rash is not itchy and is usually accompanied by lymphadenopathy and/or oral lesions. Secondary syphilis is also accompanied by a positive rapid plasma reagin test. Reiter syndrome usually presents as a tetrad of arthritis, urethritis, conjunctivitis/uveitis, and mucocutaneous lesions. The skin and nail lesions of Reiter syndrome can be difficult to distinguish clinically from psoriasis. For example, the balanitis of Reiter syndrome can look scaly or pustular as in psoriasis; the keratoderma blennorrhagicum can cause a scaly or pustular rash on the palms or soles that can be indistinguishable from psoriasis; and Reiter syndrome nail changes (ridging, pitting, onycholysis) can mimic psoriasis. Though this patient does have penile lesions that could be confused with balanitis, he does not have the rest of the tetrad of symptoms. Most patients with Reiter syndrome also describe a preceding diarrheal illness or sexually transmitted infection, which this patient did not report. Drug reactions usually occur sooner after use of antibiotics than was seen in this patient, who took penicillin several weeks before his rash developed. Additionally, though drug reactions are often symmetrical, they are usually more diffuse, maculopapular erup- tions and are worse on the trunk than on the extremities.