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Lacrimal Puncta these are two small openings situated on a small elevation called lacrimal papilla medications known to cause pancreatitis proven 100mg trazodone, about 6 mm from the inner canthus on each lid margin medications ending in zine buy discount trazodone 100 mg online. Lacrimal Canaliculi these are narrow tubular passages which lie one above the other being separated by a small body medications hypothyroidism cheap trazodone 100 mg, the caruncle treatment xyy generic 100 mg trazodone fast delivery. The two canaliculi may open separately in the lacrimal sac or may join to form a common canaliculi. It is situated in the lacrimal fossa formed by the lacrimal bone and the frontal process of the maxilla. The portion of the sac above the opening of the canaliculi is known as the fundus. Nasolacrimal Duct It is a membranous canal approximately 2 cm long extending from lower part of the sac to the inferior meatus of the nose. Blood Supply of the Lacrimal Gland the arterial supply is by the lacrimal branch of the ophthalmic artery and infraorbital branch of the maxillary artery. The venous drainage is by the lacrimal vein which opens into the superior ophthalmic vein. Lymphatic Drainage the lymph vessels join the conjunctival and palpebral lymphatics and pass to the preauricular nodes. Secretomotor fibres—These are derived from the facial nerve via the sphenopalatine ganglion. It is slightly alkaline and consists mainly of water, small quantities of salts, such as sodium chloride, sugar, urea, protein and lysozyme, a bactericidal enzyme. The Tear Film the fluid which fills the conjunctival sac consists of 3 layers namely: 1. Mucous layer—A hydrated layer of mucoproteins secreted by the goblet cells, crypts of Henle and glands of Manz. Aqueous layer—It consists of tears secreted by the lacrimal gland and accessory lacrimal glands. Lipid layer—It consists mainly of cholesterol, esters and lipid being secreted by the meibomian glands and Zeis glands. Functions the surface of the eyeball must remain wet for comfort and normal functioning. The tear film spreads over the surface of corneal epithelium by gravity, capillary action and blinking of the eyelids. It contains protective substances such as lysozyme, immunoglobulin, lactoferrin, compliments. The oiliness of this mixed fluid delays evaporation and prevents drying of the conjunctiva and cornea. When a foreign body or other irritant enters the eye, the secretion of tears is greatly increased and the conjunctival vessels dilate. Etiology It is a rare condition occurring in association with mumps, influenza, infectious mononucleosis, etc. Symptom There is marked pain, redness and swelling in the upper and outer angle of the orbit along with excessive watering of the eye. A tender swelling is present at the outer part of the upper lid spreading towards the temple and cheeks. Acute dacryo-adenitis – Both eyes Differential Diagnosis It should be differentiated from lid abscess, stye, suppurative chalazion, acute purulent conjunctivitis, orbital cellulitis and osteomyeliltis of frontal bone. Etiology There is failure in canalization of the nasolacrimal duct, the lumen being blocked by epithelial debris. There is epiphora or continuous watering of the eyes usually evident in 2nd week of life. This constitutes the treatment of congenital nasolacrimal duct block up to 6-8 weeks of age. Then bring the thumb Massage with thumb downward pressing towards the ala of the nose. Massage increases the hydrostatic pressure in the sac and helps to open up the membranous occlusions. It should be carried out at least 3 times a day to be followed by instillation of antibiotic drops. Broad-spectrum antibiotic eyedrops are instilled frequently after expressing the contents of the sac by pressure over the sac area. Intubation with silicone tube—This may be performed if repeated probing is a failure. Probing of Nasolacrimal Duct If there is no improvement after three months, probing of the nasolacrimal duct is performed through the upper punctum under general anesthesia. Great care is taken to avoid injury to the walls of the duct as it may cause fibrosis or infection. The probe is then rotated towards the middle line and pushed down the nasal duct till it reaches the floor of the nose. This procedure will Lacrimal probe in correct position cure most congenital cases. Etiology It usually occurs as an acute exacerbation of the chronic dacryocystitis. It is caused by pyogenic pathogens such as Pneumococcus, Staphylococcus, Streptococcus, etc. There is marked swelling, redness and tenderness of the skin over the sac and adjacent area. Fluctuation is present on palpation over the sac area when there is abscess formation. Hot compresses, systemic antibiotics, analgesics and anti-inflammatory are effective. In case of lacrimal abscess, a vertical incision is given over the sac area in the lower part to facilitate the drainage by gravity. In case of lacrimal fistula, excision of the fistulous tract and removal of sac is done. It is of clinical importance as hypopyon or even panophthalmitis may occur after intraocular surgery. Etiology It is usually due to stricture of the nasal duct as a result of: • Chronic inflammation of the nasal mucosa. The stagnant sac content gets infected by pyogenic bacterias such as Pneumococcus, Streptococcus, Staphylococcus and rarely by a fungus called rhinosporiodosis. Mucocele—Presence of swelling at the sac region and positive regurgitation test are diagnostic of mucocele. Pathogenesis Chronic dacryocystitis There are two main factors resulting in a vicious cycle: 1. Stasis of sac content—The anatomical factors responsible for stasis are narrow lumen of nasolacrimal duct. Infection—It may ascend from nose, descend from conjunctiva or spread from vicinity. There is constant epiphora or passive overflow of tears over the lid margin which is aggravated by exposure to wind. There is swelling, pain and redness at the site of the sac (mucocele) in cases of acute or recurrent infection. Persistent congestion of the neighbouring conjunctiva, caruncle and skin may be seen. Atonic sac—The contents of the atonic sac can be evacuated by external pressure only. Lacrimal abscess may occur following probing or spontaneously due to pyogenic infection. Radiological examination—The lacrimal passage is visualized radiographically by : i. X-ray is taken immediately and after 10-15 minutes to find out the size of the sac and site of obstruction. Subtraction macrodacryocystography with canalicular catheterization is a more accurate diagnostic technique. Radioactive tracer containing sulphur is instilled into the conjunctival sac and its excretion is visualized by gamma camera. In recent cases Repeating syringing of the nasolacrimal duct and frequent instillation of antibiotic drops is indicated in recent cases. Therapeutic—Syringing is curative in early cases by separating the oedematous mucosal walls sticking together and by clearing the mucosal debris. Principle—It reduces the swelling of the inflamed mucosa and restores the patency of lacrimal excretory passage by clearing the epithelial debris.


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It will not only lessen the pain and suffering of the patient symptoms yeast infection men cheap 100mg trazodone visa, but also allay apprehension and counteract neurogenic shock keratin treatment order 100mg trazodone overnight delivery. The primary reason for no improvement in the state of the patient is that all medicines treatment centers for depression purchase trazodone with a mastercard, including donepezil medications janumet buy trazodone 100 mg with visa, take weeks and months before any perceptible improvement in Alzheimer’s symptoms become apparent. Moreover, donepezil (or any other drug) is not effective in a significant number of patients. However, one week is too short a time to know whether this patient is going to benefit or not. Since this patient has developed intolerable cholinergic side effects, they are due to donepezil which should be discontinued. Therefore, a drug which acts by a different mechanism could be used in this patient. Memantine is the only other drug, with documented efficacy in moderate to severe Alzheimer’s disease, which is not a cholinergic drug, and which probably acts by blocking glutamate excitotoxicity. However, improvement in memory and cognitive function is less likely, and it may only serve to slow the functional decline. The first measure to be taken in this case is to put the patient in 15° head low position. Digoxin should be prescribed concurrently as it is the most effective drug for restoring compensation by increasing cardiac contractility. Enalapril dose of 5 mg twice a day should be increased by 5 mg/day at 1–2 week intervals till hypotension or other side effects appear or 40 mg/day dose is reached. Since the patient is in a decompensated state, a blocker cannot be added at this stage, because chances of deterioration of cardiac status are high. However, after compensation has been restored by digoxin, diuretic and enalapril and the patient is in a stable condition, a suitable blocker may be started at a very low dose, to be upward titrated later, because blockers afford further morbidity and mortality benefits. Therefore, he has been put on anticoagulant medication with warfarin to prevent thromboembolism. His heart (ventricular) rate can be controlled by a drug which depresses A-V conduction. For this purpose verapamil or diltiazem or propranolol should be given orally and dose adjusted to maintain a heart rate between 60–70/min. This patient is having one or more episodes of angina practically every day; therefore, he should be prescribed regular medication to prevent the episodes. Considering the age of the patient (>55 years), diagnosis of isolated systolic hypertension, history of stroke in the past, absence of diabetes/heart failure/ischaemic heart disease/chronic kidney disease, the most suitable antihypertensive drug for this patient is a thiazide diuretic (hydrochlorothiazide/chlorthalidone) or a long-acting dihydropyridine calcium channel blocker (like amlodipine). Therapy may be initiated with either of these classes of drugs and later modified depending on the response and tolerability. Induction of brisk diuresis with furosemide alone is not the appropriate treatment of cirrhotic edema and ascites. It can be supplemented by furosemide, because spironolactone alone is a weak diuretic. In this patient, use of furosemide alone resulted in further hypokalaemia and alkalosis. Because of secondary hyperaldosteronism, the response to furosemide decreased within few days. At this stage, the patient should be managed by temporarily stopping furosemide and instituting spironolactone (50 mg 6 hourly) therapy along with appropriate i. After restoration of the fluid/electrolyte balance and his mental status, the patient should be put on maintenance therapy with spironolactone (100–400 mg/day) and furosemide (40–160 mg/day) with dose adjustment according to response. If hormonal side effects of spironolactone occur, it may be substituted by the other aldosterone antagonist eplerenone. The potassium sparing non aldosterone antagonist diuretic amiloride is an alternative. There are several reasons which could account for failure of this patient of iron deficiency anaemia to respond to the oral iron medication she has been taking: • Taking 160 mg of ferric ammonium citrate (iron content 20%) would provide just 32 mg of elemental iron/day. This is grossly inadequate to treat iron deficiency, for which 200 mg of elemental iron/day is required to yield optimum response. This patient is taking acid suppressant medication (rabeprazole, a proton pump inhibitor). Since there are obvious factors in this case which can be tackled, it would be inappropriate to abandon oral iron therapy at this stage and jump on to injectable iron. Proper selection of oral iron preparation and its dose, and careful management of therapy may yield a response in this patient. A ferrous salt with high iron content like ferrous sulphate or ferrous fumarate (both having ~33% iron) should be prescribed in a dose of 200 mg 3 times a day (total 600 mg or 200 mg elemental iron/day). However, therapy should be initiated with a low dose to be gradually increased as the gastrointestinal tract adjusts to the medication and tolerance to side effects develops. The doses should preferably be taken in empty stomach, but if gastric discomfort occurs, it may be given with food. Selection of ferrous salt would reduce dependence on gastric acid for absorption of iron. The obvious cause in this patient is the additive hypoprothrombinaemic action of inj ceftriaxone given for treatment of pelvic infection. This complication could have been prevented either by selecting an antibiotic that does not cause hypoprothrombinaemia/interact with warfarin or by reducing the dose of warfarin when ceftriaxone was started. Because Hb level is 9 g/dl, blood transfusion is not required at this stage, but must be kept handy in case she bleeds further. Changing the antibiotic to one which does not cause hypoprothrombinaemia or bleeding may be considered on the basis of bacteriological sensitivity of the organism causing pelvic infection. Thus, apart from life style changes to regulate diet, reduce body weight and increase physical exercise, he requires lipid lowering medication. However, it alone cannot prevent recurrences, which most commonly are caused by persistent Contd. Since the same cannot be confirmed in the absence of testing facility, he should be given the benefit of H. This child has developed acute muscular dystonia, an extrapyramidal motor reaction that can be caused by drugs with dopaminergic D2 receptor blocking action. Antiemetics with D2 blocking action are chlorpromazine and related neuroleptics like triflupromazine, prochlorperazine, etc. It is likely that the girl was given injection of one of these drugs by the local doctor, following which the vomiting had subsided and the dystonia had developed within 2–3 hours. Though the dystonic reaction usually passes off within a few hours, it can be rapidly reversed by a parenterally administered centrally acting anticholinergic drug. Since the parents are alarmed and to afford quick relief, she may be given a deep intramuscular injection of 10–15 mg of promethazine or hydroxyzine, which have anticholinergic, antihistaminergic, sedative and antiemetic properties. This patient of diarrhoea seems to have lost only small amount of fluid and there are no signs of dehydration. Thus, there is no need of rehydration therapy, but normal fluid intake and nutrition should be continued. The features of this patient including fever are indicative of moderately severe enteroinvasive infection. A well absorbed fluoroquinolone like ciprofloxacin or ofloxacin would be suitable first line antibiotic for empiric therapy. Antimotility-antidiarrhoeal drug is contraindicated in this patient, because in all likelyhood there is enteroinvasive infection, so that restriction of bowel clearance can favour further bowel wall invasion and systemic spread of the pathogen. Abdominal pain can be dampened by an antispasmodic drug like dicyclomine 20 mg 6–8 hourly. Since this is an elective surgery with no indication of any infection in the operative area, but where the biliary tract is going to be cut, with no/minimal spillage or contact with infected material expected, it may be categorized as ‘clean-contaminated’ surgery. Therefore, prophylaxis covering aerobic as well as anaerobic organisms and both gram-negative as well as gram-positive bacteria would be appropriate. Normally, there is no need to repeat the injection, but if the surgery lasts more than 2 hours, a repeat injection after surgery may be given. Moreover, it has a convenient once a day oral dosing schedule and is generally well tolerated. These could be the considerations on the basis of which the doctor has decided to use moxifloxacin. However, moxifloxacin is not appropirate for this patient because she is receiving amitryptyline, a tricyclic antidepressant which has proarrhythmic potential. Moxifloxacin can prolong Q-T interval and increase the risk of serious cardiac arrhythmias such as Torsades de pointes when given along with amitryptyline. Other antibiotics which are active against gram-positive cocci and suitable for treating sinusitis are amoxicillin alone or with clavulanic acid, a first generation cephalosporin or azithromycin.

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Photoallergic reactions typically develop within days of drug and ultraviolet light exposure chapter 7 medications and older adults discount trazodone 100mg without a prescription. Phototoxic reactions typically present with erythroderma within minutes to medications you cant drink alcohol with purchase trazodone with mastercard hours of sunlight exposure but may present with vesicles with severe reactions symptoms for diabetes generic trazodone 100 mg. Drug-induced cutaneous lupus may also present with eruptions in a photodistribution medications are administered to generic trazodone 100 mg free shipping, typically with erythema, or scaly, annular plaques. Lichenoid eruptions Some drug reactions may manifest as lichenoid reactions with violaceous, polygonal papules. Pustular drug eruptions Several cutaneous drug reactions may present with pustules. Acne can occur with glucocorticoids, androgens, lithium, phenytoin, and iso-niazid and is quite common with the immunosuppressant sirolimus. Implicated drugs include antibiotics, with development of lesions within a few days. Finally, drug-induced Sweet’s syndrome may present with fever, painful nodules, pustules, plaques, and a neutrophilic dermatosis. The onset of drug-induced Sweet’s syndrome is variable over weeks to months after drug initiation. Vesicular/bullous drug eruptions Drug allergic reactions may also present with vesicles or bullae. Drug-induced pemphigus presents with flaccid blisters and is most often caused by drugs containing a thiol group. Drug-induced bullous pemphigoid presents with tense bullae on extremities, the trunk, and occasionally mucous membranes. Linear IgA bullous disease causes a clinically similar eruption, and vancomycin is the most commonly incriminated drug. Vancomycin-induced linear IgA bullous disease is not dose dependent, and the severity does not appear to correlate with serum vancomycin levels. Purpuric/petechial drug reactions the presence of purpura and petechiae are often cutaneous stigmata of vasculitis, which can be drug induced. A number of different types of drug-induced vasculitic reactions have been reported. A wide variety of drugs have been implicated, and the onset of cutaneous symptoms may occur after years of therapy with the offending drug. Fever, neutrophilia, and, in one-third of cases, eosinophilia may also be present. A common classification separates these conditions based on the degree of body involvement. A prodromal phase of fever, cough, and malaise may precede cutaneous findings by a few weeks. Target lesions, which may evolve from three-ringed iris lesions to purpuric two-ringed lesions, often first appear on the trunk, then rapidly spread to the face, neck, and extremities, usually peaking in 4 days. Mucosal lesions develop with painful lesions involving the lip, oral cavity, conjunctiva, nasal cavity, urethra, and vagina. Corneal involvement may result in ulceration, perforation, and sclerotic corneal changes. The terminology describing this syndrome has varied in the literature, with various terms preferred by some authors, and includes terms such as phenytoin hypersensitivity syndrome, drug hypersensitivity syndrome, drug-induced hypersensitivity syndrome, and drug-induced delayed multiorgan hypersensitivity syndrome. Cutaneous manifestations typically include maculopapular exanthems, but vesicles, bullae, pustules, target lesions, and erythroderma may also be seen. Drug-induced vasculitis Vasculitis from drugs may present with cutaneous signs or have systemic involvement. Some drugs are associated with antineutrophil cytoplasmic antibodies including propylthiouracil, hydralazine, allopu-rinol, minocycline, penicillamine, and phenytoin. These medications can induce severe systemic vasculitic syndromes resembling microscopic poly-angiitis, Wegener’s granulomatosis, and polyarteritis nodosa. Churg-Strauss syndrome has also been reported to occur in association with certain asthma medications including leukotriene modifiers, inhaled corticosteroids, and omalizumab. Several theories have been postulated including that the drug causes a steroid-sparing effect with an “unmasking” of the already present but unidentified vasculitis. To date, a cause and effect relationship for asthma medications and Churg-Strauss syndrome remains to be established. Procainamide and hydralazine are the most frequently implicated drugs, but causal evidence is also convincing for isoniazid, methyldopa, quinidine, mino-cycline, and chlorpromazine. Serum sickness Serum sickness is a clinical syndrome mediated by immune complex hypersensitivity. It is characterized by fever, lymphadenopathy, arthralgias, cutaneous eruptions, gastrointestinal disturbances, and may be associated with proteinuria. Symptoms typically appear 1 to 3 weeks after starting an offending drug but may occur more rapidly in previously sensitized individuals. Serum sickness was first described with heterologous antisera such as snake antivenom. Subsequently, many small-molecular-weight drugs have been found to be associated with serum sickness–like symptoms. Monoclonal antibody therapies have also been associated with serum sickness–like reactions to several agents including infliximab, rituximab, omalizumab, and natalizumab. The prognosis for complete recovery is excellent; however, symptoms may last as long as several weeks. Serum sickness–like reactions have also been described with symptoms of erythema multiforme and arthralgias with or without fever, but no evidence for immune complexes, hypocomplementemia, vasculitis, or renal disease. In children, cefaclor is the most common drug associated with serum sickness–like reactions. Serum sickness–like reactions to cefaclor are thought to result from altered metabolism of the parent drug resulting in toxic reactive intermediate compounds. In vitro tests for toxic metabolites have shown a lack of cross-reactivity between cefaclor and loracarbef, but confirmation of lack of clinical cross-reactivity has not been well studied. Immunologic nephropathy the most common type of an immunologic drug-induced nephropathy is acute interstitial nephritis. Eosinophiluria lacks both specificity and sensitivity for a diagnosis of acute interstitial nephritis. Other types of immunologic drug-induced conditions include membranous glomerulone-phritis. Clinically, both hepatocellular injury and cholestasis can occur, and most episodes have a good prognosis with discontinuation of the drug. Resolution of the hepatitis may take 1 to 3 months upon discontinuation but, in some cases, may be associated with fulminant hepatitis, which is associated with high mortality. Amiodarone has been associated with various pulmonary reactions including interstitial pneumonitis, bronchiolitis obliterans, and acute respiratory distress syndrome, with some reactions thought to be immu-nologic in origin. Nitrofurantoin is the most commonly reported antimicrobial causing pulmonary toxicity. The acute form of nitrofurantoin pulmonary toxicity is a hypersensitivity reaction and may develop hours to days after treatment. Symptoms may include fever, dyspnea, cough, and rash, with radiographic findings showing a diffuse reticular pattern with basilar predominance. History A detailed history is the most important diagnostic tool for drug allergy. When available, medical records documenting drug allergic reactions should be reviewed as patient recall is often limited and may be inaccurate. A thorough drug allergy history can be divided into a stepwise fashion (Table 15-3). Are the symptoms and physical findings compatible with an unpredictable (type B) drug reaction Many patients (and some physicians) report other adverse reactions as drug allergy. For example, a history of diarrhea after taking an antibiotic is not consistent with a drug allergic reaction. Can it be classified according to the Gell and Coombs hypersensitivity, an organ based reaction, or a well-defined drug allergic syndrome.

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