Instant Cure for Hyperhidrosis
Etiology Excessive sweating, either generalized or focal (e.g., palmar, palmoplantar, axillae), and affecting 2 3 of general population most common in adolescence and young adults. Generalized hyperhidrosis can be associated with underlying systemic disorder, e.g., infectious (e.g., TB), endocrine, or neurologic focal hyperhidrosis often idiopathic. Diagnostic criteria for primary focal idiopathic hyperhidrosis. Focal, visible, excessive sweating of at least 6 mo duration without apparent cause with at least 2 of the following characteristics Bilateral and relatively symmetrical sweating. Cessation of sweating during sleep. of excessive sweating. DDx Thyrotoxicosis, medication-induced hyperhydrosis, pheochromocytoma.
The course of acromegaly is slow, with very gradual changes over 7 to 10 years. Reviewing a patient's old photographs may reveal the progressive changes in facial features. Determine if the patient has had a change in hat, glove, ring, or shoe size because of an overgrowth of the hands and feet. Ask the patient if he or she has had headaches or visual disturbances, which in acromegaly are caused by the growth of the adenoma, which exerts pressure on brain tissue and cranial nerves III, IV, and VI. Establish a history of altered sexual function, which may be an indicator of decreased gonadotropin production. Ask about the presence of pain in the hands, feet, and spine, which is probably caused by bone growths also ask about problems with chewing, swallowing, or talking, which may be caused by tongue, jaw, and teeth enlargement. Note the presence of a deepening of the voice, recurrent bronchitis, excessive sweating, heat intolerance, fatigue, and muscle weakness. Check for a...
Frey's syndrome Baillarger's syndrome Dupuy's syndrome salivosudoriparous syndrome sweating gustatory syndrome gustatory sweating Gustatory sweating secondary to auriculotemporal nerve injury Flushing or sweating on one side of the face when certain foods are eaten Gustatory sweating from diabetic neuropathy or post-herpetic neuralgia Horner's syndrome lacrimal sweating harlequin syndrome Gustatory sweating
SLUDE Muscarinic features Salivation, Lacrimation, Urination, Defecation, Emesis, plus miosis, bronchorrhea and broncho-spasm DUMBBELS Diarrhea, Urination, Miosis, Bronchorrhea, Bronchospasm, Emesis, Lacrimation, and Salivation. Nicotinic features Weakness, fascicula-tions, sweating, tachycardia, hypertension.
Anterior hypothalamus, which act as temperature sensors. Efferent responses cutaneous vasoconstriction or vasodilatation allowing shunting of blood to the core or the periphery opening or closure of thermoregulatory arterio-venous shunts non-shivering thermogenesis shivering sweating. Behavioural responses include heat avoidance and external cooling.
Horner syndrome is produced by a lesion at any site along the sympathetic pathway to the eye and is characterized by unilateral miosis (with sluggish dilatation) and ptosis anhidrosis (absence of sweating) and enophthalmos are part of the syndrome but are of no practical diagnostic value. The affected pupil will fail to dilate in response to the instillation of 5 cocaine eyedrops. Preganglionic lesions (i.e., those proximal to the superior cervical ganglion) can be distinguished from postganglionic lesions by the instillation of 5 pholedrine eyedrops (at least three days after the cocaine test) the miotic pupil dilates more than the normal pupil if the lesion is preganglionic, symmetrically if it is postganglionic. Central Horner syndrome (first preganglionic neuron) may be due to lesions of hypothalamus, brain stem, or cervicothoracic spinal cord the second preganglionic neuron may be affected by lesions of the brachial plexus, apical thorax, mediastinum, or neck the postganglionic...
Features Fight or flight hypertension, tachycardia, sweating, fever, excitation-psychomotor agitation, tremor, seizures, dilated pupils. Causes Amphetamines diet drugs, cocaine, theophylline, caffeine, methylphenidate, mono-amine oxidase inhibitors over-the-counter cold medications, especially those containing phenylpropanolamine (PPA), ephedrine, and pseudoephedrine.
GI Nausea, diarrhea. CNS Somnolence, mania, hypomania, seizures, tremor. GU Delayed ejaculation. Miscellaneous Increased sweating, hyponatre-mia, syndrome of inappropriate anit-diuretic hormone secretion. Drug Interactions No drug interactions reported.
Epidural use causes analgesia at presynaptic and postjunctional al-pha-2-adrenergic receptors in the spinal cord due to prevention of pain signal transmission to the brain. tv2, distribution, epidural 19 min elimination 22 hr. Uses Oral, Transdermal Mild to moderate hypertension. A diuretic or other antihypertensive drugs, or both, are often used concomitantly. Non-FDA Approved Uses Alcohol withdrawal, atrial fibrillation, attention deficit hyperactivity disorder, constitutional growth delay in children, cyclosporine-associated nephro-toxicity, diabetic diarrhea, Gilles de la Tourette's syndrome, hyperhidrosis, hypertensive emergencies, mania, menopausal flushing, opiate detoxification, diagnosis of pheochromocy-toma, postherpetic neuralgia, psychosis in schizophrenia, reduce allergen-induced inflammatory reactions in extrinsic asthma, restless leg syndrome, facilitate smoking cessation, ulcerative colitis. ziness, headache, fatigue, malaise, nightmares, nervousness, restlessness,...
Attacks of severe, strictly unilateral pain, orbital, supraorbital, and or temporal, usually lasting 15-180 minutes and occurring from at least once every other day up to eight times per day. Associated with one or more of the following conjunctival injection, lacrimation, nasal congestion, rhinorrhea, forehead and facial sweating, miosis, ptosis, eyelid edema. Attacks occur in series for weeks or months ( cluster periods), separated by remissions of usually months or years.
Vectors All pufferfish (balloonfish, blowfish, fugu fish, globefish, swellfish, toadfish), porcupine fish, marine sunfish xanthid crabs, marine worms blue-ringed octopus bites skin secretions of some newts, frogs, and toads. Incubation 10-20 minutes. Symptoms Initial paresthesias, perioral burning, then salivation, headache, nausea and vomiting (diarrhea rare), sweating, glove and stocking paresthesias then numbness, tremor, ataxia, dysarthria, dysphagia, respiratory depression then paralysis, cardiovascular instability, stupor, and coma. Diagnosis Mouse bioassay, TLC, HPLC, gas chromatography mass spectrometry. Treatment Supportive protect airway, gastric lavage then AC-MDAC, IV fluids, vasopressors, and mechanical ventilation. Prognosis CFR 62 survivors will recover within 1 week of ICU care (not universally available, especially in developing world).
Hyponatremia can occur in any age group, in all races and ethnicities, and in both sexes. It is more common, however, in infants, young children, elderly people, and debilitated patients because these groups are more likely to experience variation in the TBW. It is most common in the very young and in the very old, because these individuals cannot express thirst and may be less able to regulate fluid intake as contrasted with other individuals. Hyponatremia can occur in healthy individuals, such as athletes or outdoor laborers, as a result of sodium loss through excessive perspiration.
The clinical course begins (stage I) with a slowly progressive dementia, often affecting behavior and associated with school performance decline. Stage II features include spasticity, weakness, and myoclonic jerks, and seizures occur. Optic manifestations are common and include a macular chorioretinitis and optic atrophy. There may be cerebellar ataxia and dystonia. Stage III is marked by stupor and coma, often with autonomic instability leading to marked fluctuations in body temperature and abnormal sweating. Diagnosis may be made with the presence of one major and one minor criterion.
The parkinsonian features are usually unresponsive to levodopa therapy. There may be gait and limb ataxia, orthostatic hypotension, erectile dysfunction, constipation, and decreased sweating. Whereas multiple-system atrophy is a distinct neuropathological entity, the consensus diagnostic criteria depend on specific clinical features. Pathologically, glial cytoplasmic inclusions and degeneration are found throughout the basal ganglia, substantia nigra, brainstem autonomic nuclei, and Purkinje cells of the cerebellum.
Lucinations, restlessness, suggestibility, and au-tonomic disturbances (tachycardia, blood pressure fluctuations, hyperhidrosis). Somnolence is a mild reduction of the level of consciousness (drowsiness, reduced spontaneous movement, psychomotor sluggishness, and delayed response to verbal stimuli) while the patient remains arousable he or she is easily awakened by a stimulus, but falls back asleep once it is removed. The patient responds to noxious stimuli with direct and goal-directed defensive behavior. Orientation and attention are mildly impaired but improve on stimulation. Stupor is a significant reduction of the level of consciousness. These patients require vigorous and repeated stimulation before they open their eyes and look at the examiner. They answer questions slowly and inadequately, or not at all. They may lie motionless or display restless or stereotyped movements. Confusion reflects concomitant impairment of the content of consciousness.
Clinical problems associated with the parasympathetic division of the ANS usually arise as a result of side effects or toxic-ity produced by chemical agents that act as either as agonists or antagonists at the muscarinic receptor. Excessive use of the muscarinic agonist pilocarpine, for example, results in decreased blood pressure, bronchoconstriction, GIT discomfort, and excessive sweating (although the last effect is due to stimulation of sympathetic cholinergic muscarinic receptors, see p. 242). Muscarinic antagonists, on the other hand, may produce urinary retention, mydriasis, tachycardia, and hypertension.
The clinical suspicion of hyperthyroidism may not be obvious as symptoms of tachycardia, sweating, dyspnoea and nervousness are seen in normal pregnancy as are cardiac systolic flow murmurs. The diagnosis should always be confirmed by estimation of circulating thyroid hormone concentrations. It should be noted that serum thyroxine (both total and free) varies during normal gestation. Recent national and internationally agreed guidelines suggest that laboratories should be encouraged to develop normal ranges for total but more particularly free T4 and T3, as well as TSH after the 1st trimester during pregnancy, all of which may change during the course of gestation. Normally the TSH is suppressed in hyperthyroidism but in early pregnancy (approx. 9-12 weeks) TSH is usually suppressed by human chorionic gonadotrophin and may also be lowered due to non-specific illness such as vomiting as well as multiple pregnancy. This may lead to uncertainty in differentiating Graves' hyperthyroidism...
Tic worry or dread about the circumstances of daily life. The excessive worries often pertain to many areas of the affected person's life, including work, relationships, finances, personal health, the well-being of one's family, perceived misfortunes, and impending deadlines. Affected people can experience a variety of symptoms, including feelings of fear and dread, restlessness, muscle tension, a rapid heart rate, light-headedness, poor concentration, insomnia, increased perspiration, cold hands and feet, and shortness of breath. Symptoms typically worsen during stressful periods.
Skin areas of hyperpigmentation alternating with hypopigmentation overall appearance of tanned skin persists long after sun exposure telangiectasias on face, neck, and periungual areas skin of the hands sometimes edematous or indurated early, later sclerotic stage where skin is tight and shiny, with a loss of hair, decreased sweating, and loss of ability to make a skin fold starts distally on the fingers any area of the body ultimately may be involved calcinosis on the fingers and extremities reduced oral aperture (microstomia) from perioral involvement
HIV infection may cause no symptoms in the early stages or can produce flulike symptoms, including fever, chills, fatigue, sweating at night, and a dry cough. Other symptoms include sudden unexplained weight loss and chronic diarrhea. Although some infected people may have no symptoms, they still can transmit the virus to others.
Lethal infantile (hepatic) form. The first mutation associated with the hepatic form was the before mentioned R631C mutation found homozygously in a boy with an acute episode with seizures, coma and respiratory distress after a history of recurrent episodes of vomiting, sweating and lethargy. Three more mutations associated with the lethal infantile form were identified subsequently either homozygously or compound het-erozygously, namely F383Y, Q174L and Y628S.2 28 All patients displayed the above mentioned metabolic features and died within a few month.
The clinical use of stimulants in narcolepsy has been the object of an American Sleep Disorders Association (ASDA) Standards of Practice publication. Typically, the patient is started at a low dose, which is then increased progressively to obtain satisfactory results. This final dose varies widely from patient to patient. In adults, methylphenidate and amphetamines at dosages of more than 60 mg day do not significantly improve EDS without the appearance of long-term side effects, including frequent worsening of the nocturnal sleep disruption. The drug is usually administered in three divided doses with a maximum of 20 mg in the morning, 20 mg at lunchtime, and 20 mg at 3 pm - never later. Therefore, short naps are necessary. The combination of pharmacological agents and two short naps provides the best daily response to EDS, with no stimulant drug taken after 3 pm. The slow-release form may provide gradual and delayed response during the daytime. Side effects such as headaches,...
It is a rheumatic disorder of clinical importance and academic interest. Involvement is usually regional and diffuse, but can be segmental and small in rare cases (Helms et al. 1980). The condition is also referred to as causalgia, Sudeck's atrophy, posttraumatic osteoporosis and angiospasm, reflex neurovascular dystrophy, and the shoulder-hand syndrome. Common symptoms include pain, swelling, stiffness, tenderness, vasomotor and sensory disturbances, hyperesthesia, disability, and skin atrophy, and other trophic skin alterations such as hypertrichosis and hyperhidrosis. The pathogenesis is yet not clarified, although the theory of internuncial pool proposed by Lorente (1938) is widely supported. The theory assumes that painful impulses created by a peripheral injury travel via the afferent pathways to the spinal cord, where a series of reflexes originate. Reflex-
Accompanying hyperhidrosis are common, producing a great deal of discomfort (Costner et al. 2003). Ulceration is frequent in digital pulp lesions, and they easily become necrotic on the soles (Mascaro et al. 1997). When located in the periungual zone, the nail plate may develop mild to severe dystrophy.
Important types of information (1) information about the feared stimuli or situation (2) information about the person's response to the feared stimuli or situation and (3) information about the meaning of the feared stimuli and the consequent response. Foa and Kozak (1986) posited that the fear networks of individuals with PTSD differ from the fear networks of individuals with other anxiety disorders in three ways. First, the fear network of individuals with PTSD is larger because it contains a greater number of erroneous or inaccurate connections between stimulus, response, and meaning elements. Second, the network is more easily activated by stimulus, response, or meaning elements. Third, the affective and physiological response elements of the networks are more intense. Accordingly, for individuals with PTSD, stimuli reminiscent of the traumatic experience activate the fear network and prompt states of high sympathetic arousal (e.g., increased heart rate and blood pressure,...
Portions of the OMPC are also closely connected with the hypothalamus, which controls the autonomic nervous system and portions of the endocrine system. Bechara et al. (2000) measured changes in skin conductance induced by sweating (galvanic skin responses) while participants played the card game that measures risk-taking behaviors. These investigators found that before normal participants made a decision to perform a high-risk move, their palms sweated, suggesting that the participants activated their autonomic nervous system. In contrast, their patients with OMPC injury, who repeatedly performed high-risk behaviors in this card game, did not develop a robust skin response before they performed a high-risk behavior.
The sudden, but not instantaneous, death is illustrated by the individual who begins to complain of chest pain, difficulty in breathing, weakness, sweating, nausea, and vomiting, and then collapses. He is then transported to the hospital. On the way to the hospital, he goes into cardiac arrest and by the time he reaches the emergency room he is not resuscitatable. Another individual with the same initial symptoms may arrive conscious at the hospital only to experience his fatal cardiac arrhythmia 2 h after admission. Is this still a sudden death This depends upon one's definition of sudden death. Many, if not most, medical examiners limit classification of sudden deaths as those occurring instantaneously or within 1 h of the onset of symptoms.
If you frequently experience indigestion, see your doctor so that he or she can examine you, determine the cause of your symptoms, and provide treatment. Contact your doctor promptly if your indigestion is accompanied by vomiting, weight loss, lack of appetite, blood in vomit or stool, pain when you eat, or severe pain in the upper abdomen. Symptoms of indigestion accompanied by shortness of breath, sweating, or pain radiating to the jaw, neck, or left arm can be warning signs of heart disease or a heart attack (see page 207).
Asthma affects the lining of the bronchi and the bronchioles. These airways become inflamed and produce extra mucus. Smooth muscle tissue in the airways contracts, narrowing the passageways even further. Common symptoms of asthma include wheezing (a faint whistling noise that occurs with each breath), shortness of breath, chest tightness (feeling as if someone is squeezing your chest), and coughing. Signs of an asthma emergency include extreme difficulty breathing, bluish tinge (cyanosis) to the lips and face, severe anxiety, rapid pulse, and sweating.
Acne where sweating is an aggravating factor aluminium chloride solution Severe nodulocystic acne unresponsive to other therapies isotretinoin* Acne surgery comedone expression incision and drainage of fluctuant cysts and abscesses chemical peel microdermabra-sion intralesional triamcinolone 2-4 mg ml
An immature sweat gland apparatus in infants and individual genetic susceptibility play a role. Rapid change in ambient temperature, high humidity, occlusive clothing, friction from garments, and any factor that favors skin surface bacterial colonization predisposes to miliaria. A recent study implicates certain strains of S. epidermidis as the source of the polysaccharide plug that can be demonstrated microscopically in the eccrine duct orifice. Once occlusion has occurred, any stimulus that initiates sweating will cause a short-lived exacerbation.
Danazol (Danocrine) has been highly effective in relieving the symptoms of endometriosis, but adverse effects may preclude its use. Adverse effects include headache, flushing, sweating and atrophic vaginitis. Androgenic side effects include acne, edema, hirsutism, deepening of the voice and weight gain. The initial dosage should be 800 mg per day, given in two divided oral doses. The overall response rate is 84 to 92 percent.
CLINICAL SYMPTOMS Muller's sympathetic eyelid muscles contribute to retraction of both the upper and lower eyelids. In Horner's syndrome there is a minimal ptosis of the upper lid of about 1 to 2 mm, associated with elevation of the lower eyelid. Thus, the interpalpebral fissure is narrowed. The pupil is mildly constricted and there may be loss of sweating on the ipsilateral face and dryness of the mouth. In congenital Horner's syndrome the affected iris is lighter in color resulting in heterochromia. Diagnosis is facilitated by pharmacologic testing with 4 cocaine where the affected pupil does not dilate but he normal pupil does. If the denervation involves the third order neurons between the superior cervical ganglion and the eye, the pupil is supersensitive to epinephrine and will dilate with 1 1000 dilution of epinephrine, a concentration that does not affect the normal pupil.
Ness, drowsiness, fatigue, hallucinations, insomnia, lethargy, mental changes, memory loss, strange dreams. GI Diarrhea, ischemic colitis, nausea, mesenteric arterial thrombosis, vomiting. Hematologic Agranulocytosis, thrombocytopenia. Allergic Fever, sore throat, respiratory distress, rash, pharyngitis, laryngos-pasm, anaphylaxis. Skin Pruritus, rash, increased skin pigmentation, sweating, dry skin, alopecia, skin irritation, psoriasis. Ophthalmic Dry, burning eyes. GU Dysuria, impotence, nocturia. Other Hypoglycemia or hyperglycemia. Respiratory Bronchospasm, dyspnea, wheezing. Drug Interactions See also Drug Interactions for Beta-Adrenergic Blocking Agents and Antihypertensive Agents.
DTs are most likely to develop if the patient has had an alcohol withdrawal seizure or a concomitant medical disorder, such as an infection, hepatic insufficiency, pancreatitis, subdural hematoma, or a bone fracture. Onset is usually 2-3 days after cessation of alcohol use and usually lasts 3-7 days, but can be prolonged. DTs must be considered a medical emergency (Goforth, Primeau, & Fernandez, 2003) and are characterized by visual, auditory, and or tactile hallucinations, gross tremor, tachycardia, sweating, and, possibly, fever, as well as the disturbances of consciousness described earlier.
Disturbances of thermoregulatory sweating. Examination Useful tests include palpation of the skin to appreciate its moisture and temperature, the quantitative sudomotor axon reflex test (QSART), the sympathetic skin response (SSR), iodine-starch test (Minor test), and the ninhy-drin test. Generalized anhidrosis (which confers a risk of hyperthermia) may be idiopathic or may be due to lesions in the hypothalamus or in the spinal cord above T3 4 . Monoradicular lesions or cervical or lumbosacral polyradicular lesions do not impair sweating. Lesions of the sympathetic trunk cause segmental anhidrosis. Plexus lesions and isolated or combined neuropathies produce anhidrosis in the area of a sensory deficit. Lesions from the level of the stellate ganglion upward cause anhidrosis as a component of Horner syndrome. Sweating of the palms and soles is not influenced by thermoregulatory mechanisms but rather by the emotional state (fear, nervousness). Fever. The symptoms include malaise,...
CLINICAL PRESENTATION Such lesions present as solitary or multiple, small translucent 1 to 5 mm fluid filled cysts. The lesions are typically flesh-colored to bluish, tense shiny vesicles usually near the eyelid margins. They are located in the dermis and the overlying epidermis is uninvolved. They tend to increase in size in hot, humid weather associated with increased perspiration. When the cyst wall is punctured the cyst collapses and exudes a clear thin fluid and there is no evidence of layered debris from cellular decapitation as with apocrine cysts.
1 Spinal cord level (not the same as vertebral level). 2 See p. 32ff. 3 Disturbance of bladder, bowel, rectal, and erectile function, sweating, and blood pressure regulation p. 140ff. 4 High cervical cord lesion. 5 Low cervical cord lesion. 6 Epiconus. 7 Conus medullaris.
Well demarcated, brown-red, minimally scaly plaques, commonly occurring over inner thighs, crural region, scrotum, and toe webs other intertriginous sites such as axillae, submammary area, periumbilical region, and intergluteal fold less commonly involved toe web lesions appear macerated predisposing factors excessive sweating and hyperhidrosis, disrupted cutaneous barrier, obesity, diabetes mellitus, and immunocompromised state
Special Concerns Use with caution, if at all, during lactation. Give a lower initial dose in liver impairment. Safety and efficacy have not been determined in children less than 2 years of age. Side Effects Most commonly, headache, somnolence, fatigue, and dry mouth. GI Altered salivation, gastritis, dyspepsia, stomatitis, tooth ache, thirst, altered taste, flatulence. CNS Hypoesthesia, hyperkinesia, migraine, anxiety, depression, agitation, paroniria, amnesia, impaired concentration. Ophthalmologic Altered lacrimation, conjunctivitis, blurred vision, eye pain, blepharo-spasm. Respiratory Upper respiratory infection, epistaxis, pharyngitis, dyspnea, coughing, rhinitis, sinusitis, sneezing, bronchitis, bronchospasm, hemoptysis, laryngitis. Body as a whole Asthenia, increased sweating, flushing, malaise, rigors, fever, dry skin, aggravated allergy, pruritus, purpura. Musculoskeletal Back chest pain, leg cramps, arthralgia, myalgia. GU Breast pain, menorrha-gia, dysmenorrhea, vaginitis....
Acute alcohol intoxication (drunkenness, inebriation) may be mild (blood alcohol 0.1-1.5 dysarthria, incoordination, disinhibition, increased self-confidence, uncritical self-assessment), moderate (blood alcohol 1.5-2.5 ataxia, nystagmus, explosive reactions, aggressiveness, euphoria, suggestibility), or severe (blood alcohol 2.5 loss of judgment, severe ataxia, impairment of consciousness, au-tonomic symptoms such as hypothermia, hypotension, or respiratory arrest). Concomitant intoxication with other substances (sedatives, hypnotics, illicit drugs) is not uncommon. The possibility of a traumatic brain injury (subdural or epidural hematoma, intracerebral hemorrhage) must also be considered. Pathological intoxication after the intake of relatively small quantities of alcohol is a rare disorder characterized by intense outbursts of emotion and destructive behavior, followed by deep sleep. The patient has no memory of these events. Alcohol withdrawal syndrome. Reduction of...
Fear is the driving force behind anxiety disorders. Each of us experiences fear throughout the course of our lives. But instead of feeling the reasonable fear that helps us recognize and respond to immediate danger, such as narrowly avoiding a traffic accident, people with an anxiety disorder experience fear that occurs in response to dangers that are either imagined or not immediately threatening. Such people experience almost constant feelings of worry or dread that interfere with their daily activities, along with symptoms of anxiety such as rapid heartbeat and increased perspiration.
Primary lesion a perifollicular papule or pustule often appears as grid-like pattern of multiple red papules and or pustules on hair-bearing areas, such as the face, scalp, thighs, axilla, and inguinal area predisposing factors friction perspiration occlusion shaving hyperhidrosis diabetes melli-tus or immunologic disorders Staphylococcal nasal carriage skin injuries abrasions surgical wounds draining abscesses skin occlusion for topical corticosteroid therapy
People who have atopic eczema seem to have easily irritated skin, so anything that dries or irritates the skin may trigger a flare-up. They are often sensitive to low levels of humidity, and their skin condition may worsen in the winter. If this is true for you, try to bathe no more than once a day, avoid using very hot water, and use the mildest soap you can find. After bathing, pat your skin dry do not rub it. Immediately apply a moisturizing lotion or oil to your skin, before it has completely dried. Avoid dressing in clothes made of rough or scratchy fabrics, which can aggravate the condition. Sweating also can make the condition worse.
Athlete's foot (known medically as tinea pedis) is a common fungal infection of the foot. It affects mainly adolescent and adult males. The tinea fungus readily grows in moist, damp areas such as shower stalls and floors. Sweating and inadequate ventilation of the feet provide ideal conditions for growth of the fungus.
Functional activity in skull base paragangliomas is 1 to 2 .8,17-19 In these cases, the continuous or episodic secretion of catecholamines may produce clinical symptoms mimicking a pheochromocytoma. These features include persistent or paroxysmal hypertension, tachycardia, excessive perspiration, and anx-iousness. When manipulated surgically, catecholamine-secreting paragangliomomas can potentially initiate a life-threatening hypertensive crisis, constituting an anesthetic emergency.
Trichinella spiralis may cause symptoms ranging from apparent infection to fulminating and fatal disease depending on the number of larvae ingested. During the initial phase, corresponding to the development of the larvae into adults in the epithelium the infection manifests itself with nausea, vomiting, diarrhoea and fever. The female worm produces larvae, which migrate in the body through the lymphatic and blood system. The larvae encapsulate in the skeletal muscle. At this stage, other symptoms such as rheumatic conditions, muscle soreness and pain, together with oedema of the upper eyelids, followed by retinal haemorrhages, pain and photophobia may appear. Thirst, profuse sweating, chills, weakness and prostration follow the ocular symptoms. Cardiac and neurological complications appear 3-6 weeks later. In most severe cases death may result from myocardial failure.
Locked-in syndrome (p. 359) is a de-efferented state in which the patient is fully conscious but can make no spontaneous movements except lid and vertical eye movements. There may be reflex extension of the arms and legs in response to mild stimuli such as repositioning in bed or tracheal suction. Physicians and nurses must remember that these patients can perceive themselves and their surroundings fully even though they may be unable to communicate. Possible causes include basilar artery occlusion, head trauma, pontine hemorrhage, central pontine myelinolysis, and brain stem encephalitis a similar clinical picture may be produced by my-asthenia gravis, Guillain-Barre syndrome, or periodic paralysis (see pp.326, 338). Persistent vegetative state (apallic syndrome) is caused by extensive injury to the cerebral cortex, subcortical white matter, or thalamus. The patients are awake but unconscious (loss of cortical function). Periods in which the eyes are open and move spontaneously, in...
Side Effects Serious side effects are uncommon with PO dosage but more common following SC use. Oral Salivation. GI Nausea, diarrhea, GI upset, involuntary defecation, cramps, colic, belching, rumbling gurgling of stomach. CV Hypotension with reflex tachycardia, vasomotor response. CNS Headache, malaise. Other Flushing, sensation of heat about the face, sweating, urinary urgency, attacks of asthma, bronchial constriction, miosis, lacrimation.
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