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Retinal Detachment: Retinal detachment is a pathological condition of the retina where there is a separation of the two layers of the retina, the retina proper and the pigmentary epithelium by sub-retinal fluid. Classification            1. Primary or simple detachment, also known as Rhegmatogenous detachment            2. Secondary detachment, also known as non-rhegmatogenous detachment. Symptoms Signs and Diagnosis Complications and Treatment of Retinal Detachment. Retinal detachment is an ophthalmological emergency and the patient who is suspected to have a retinal detachment should be referred to an ophthalmologist urgently.  Visit Home page

Primary or Simple or Rhegmatogenous Retinal Detachment It is due to a break in the retina in the form of a hole or tear. Fluid from the vitreous seep through the hole or tear and raise the retina from its bud. Mechanism Of Detachment:  Retinal degeneration or trauma creates a hole or tears in the retina, fluid seeps through it and cause retinal separation. A strong traumatic force can separate the retina, presence of degenerated vitreous fluid aid to separation. Visit Home page

Secondary or Non-Rhegmatogenous Retinal Detachment. It is always secondary to retinal disease or pathology, unlike primary retinal detachment which is caused by trauma or mechanical force. Mechanism Of Detachment. 1. Retina being pushed away from its bed by the accumulation of blood for example as in case of choroidal haemorrhage or exudate as in case of exudative choroiditis or retinopathy. Neoplasms or tumours of the choroid may also push the retina away from its bed. 2. The retina is pulled away from its bed for example as in case of contraction of fibrous tissue bands in the vitreous for example as in plastic cyclitis, proliferative retinopathy or retrolental fibroplasia... Visit Home Page

Complications Of Detached Retina. 1. Total Retinal Detachment may occur 2. Proliferative vitreoretinopathy 3. Complicated Cataract 4. Chronic Uveitis 5. Phthisis bulbi may occur. Treatment of Detached Retina. The mainstay of treatment is to approximate and adhere to the torn part of the retina to the area of choroid by exciting aseptic inflammation of choroid. following methods are used. 1. Photocoagulation : 2. Cryosurgery : It is done to seal the retinal breaks by causing tissue necrosis. 3. Scleral Buckling 4. Drainage of subretinal fluid 5. Pars Plana Vitrectomy: It breaks the tractional fibrous band in the vitreous, thus releasing the pull on the retina in cases of tractional retinal detachment.  6. Pneumoretinopexy : Air or other suitable gas such as SF6 or silicon oil is used as a vitreous substitute to produce internal tamponade which pushes the retina back to its position. Visit Home Page

Symptoms, Signs and Diagnosis Of Retinal Detachment - Separation Of Retina Symptoms : 1. Transient flashes of light (photopsia) 2. Muscae Volitantes 3. Distortion of objects 4. Shadow or cloud is seen in front of the eye 5. dimness of vision. Signs and Diagnosis: 1. Plan mirror examination : There is defective or no red glow was seen 2. Fundus examination: The detached retina looks greyish white and raised above the surface, the retinal vessels are dark with no central light reflex, the detached retina oscillates with the movement of the eye, one or more holes are commonly seen in the upper temporal region, in total retinal detachment the retina is funnel-shaped being attached to the disc and ora serrata, it is grey in colour. 3. Visual fields : Scotomas (dark spots) appear corresponding to the area of detached retina 4. Electroretinography (ERG) It is subnormal or absent 5. Ultrasonography (B scan): it confirms the diagnosis of retinal detachment in cases when retina

Causes Of Sudden Loss of Vision Eye sight Sudden loss of vision commonly occurs in  1. Central Retinal Artery Occlusion 2. Central Retinal Vein Occlusion. 3. Retinal Detachment 4. Papillitis 5. Acute Congestive Glaucoma 6. Vitreous Haemorrhage Causes Of gradual Loss Of Vision / Eye sight The gradual loss of vision commonly occurs in  1. Cataract  2. Open-angle glaucoma 3. Uveitis maculopathy (Uveitis is defined as inflammation of the uveal tract of which the anatomy includes the    iris, ciliary body, and choroid and  A maculopathy is any pathological condition of the macula, an area at the centre of the retina that is associated with highly sensitive, accurate vision . , ) 4. Toxic amblyopia (Toxic amblyopia is a condition where a toxic reaction in the optic nerve results in visual loss. Various poisonous substances may cause the condition as well as nutritional factors. Tobacco amblyopia is a form of toxic amblyopia caused by tobacco containing cyanide. Tobacco ambly

Complications Of Infective Endocarditis. A) Cardiac Complications. 1. Valvular Insufficiency. Valvular insufficiency results from incomplete closure of leaflets of valves. 2. Ring abscesses with the possibility of perforation. 3. Suppurative pericarditis. Suppurative pericarditis is a rare life-threatening disease, difficult to treat. B) Embolic Complications. Vegetations may break loose, and give rise to emboli in brain, spleen, kidneys, and heart itself (in left side infective endocarditis) and to lungs ( in right side infective endocarditis.) C) Renal Complications:    1. Embolic infarcts    2. Focal and diffuse glomerulonephritis    3. Multiple abscesses.

following are the predisposing factors for Infective Endocarditis. 1.` Mitral Prolapse 2. Degenerative Calcified stenosis. 3. Prosthetic valves 4. Neutropenia 5. Immunodeficiency 6. Diabetes Mellitus 7. Intravenous drug abuse. 8. Vascular grafts. 9. Alcoholism

Dietary or pharmacological reduction of elevated plasma cholesterol levels can reduce the risk of atherosclerosis and subsequent cardiovascular disease. the association between elevated plasma triglyceride levels is less dramatic, but it is becoming more recognized. In addition, elevated plasma Triglycerides can produce life-threatening pancreatitis. Drugs useful in treating hyperlipidemias ( Increased conc. of lipids in the blood) 1. Inhibitors of Cholesterol Biosynthesis. following drugs inhibit cholesterol synthesis: Lovastatin (mevinolin, Mevacor)  Simvastatin (Zocor) Pravastatin (Pravachol) Fluvastatin (Lescol) Atorvastatin (Lipitor) Rosuvastatin (Crestor) Drugs that inhibit cholesterol synthesis are effective at lowering plasma LDL cholesterol and total cholesterol 2. Nicotinic acid ( Niacin ) (brand names: Nicobid, Nicolar) Nicotinic acid Fibric Acid Analogues. Finofibrate ( Antara, Triglide, Lofibra) Gemfibrozil (Lopid) Bile acid Absorption

Colesevelam (WelChol) Mechanism of action: colesevelam (WelChol)  bind with bile acids and impair their absorption and reduce enterohepatic circulation and re-utilization of bile acids. colesevelam (WelChol) also decreases the absorption of dietary cholesterol. In this way, colesevelam (WelChol) decrease the absorption of cholesterol and blood level of cholesterol is decreased. Therapeutic Uses: colesevelam (WelChol) is effective in reducing plasma cholesterol level (to about 10 - 20 % ) in patients with some normal LDL receptors. colesevelam (WelChol) is ineffective in the treatment of patients who completely lack LDL receptors due to a genetic defect ( homozygous familial hypercholesterolemia). Adverse Effects: colesevelam (WelChol) is generally safe because are not absorbed in the small intestine. common side effects are; colesevelam (WelChol) has lesser GI side effects (constipation, nausea and diarrhoea) than other drugs like Colestipol and Cholestyramine these drugs interfer

Colestipol (Colestid) Mechanism of action: Colestipol (Colestid) bind with bile acids and impair their absorption and reduce enterohepatic circulation and re-utilization of bile acids. Colestipol (Colestid) also decreases the absorption of dietary cholesterol. In this way, Colestipol (Colestid) decrease the absorption of cholesterol and blood level of cholesterol is decreased. Therapeutic Uses: Colestipol (Colestid) is effective in reducing plasma cholesterol level (to about 10 - 20 % ) in patients with some normal LDL receptors. Colestipol (Colestid) is ineffective in the treatment of patients who completely lack LDL receptors due to a genetic defect ( homozygous familial hypercholesterolemia). Adverse Effects: Colestipol (Colestid) is generally safe because are not absorbed in the small intestine. common side effects are; 1. constipation 2. nausea 3. discomfort 4. these drugs interfere with the absorption of anionic drugs ( e.g digitalis and warfarin)

Cholestyramine (Questran) Mechanism of action: Cholestyramine (Questran) bind with bile acids and impair their absorption and reduce enterohepatic circulation and re-utilization of bile acids. cholestyramine (Questran) also decreases the absorption of dietary cholesterol. In this way, cholestyramine (Questran) decrease the absorption of cholesterol and blood level of cholesterol is decreased. Therapeutic Uses: cholestyramine (Questran) is effective in reducing plasma cholesterol level (to about 10 - 20 % ) in patients with some normal LDL receptors. cholestyramine (Questran) is ineffective in the treatment of patients who completely lack LDL receptors due to a genetic defect ( homozygous familial hypercholesterolemia). Adverse Effects: cholestyramine (Questran) is generally safe because are not absorbed in the small intestine. common side effects are; 1. constipation 2. nausea 3. discomfort 4. these drugs interfere with the absorption of anionic drugs ( e.g

Ezetimibe (Zetia)  Mechanism Of Action. Ezetimibe acts within the intestine to reduce cholesterol absorption. Cholesterol is absorbed from the small intestine by a process that includes specific transporters that have not been completely characterized. Ezetimibe appears to block one or more of these cholesterol transporters, reducing cholesterol absorption. Therapeutic Uses: Ezetimibe used alone produces a reduction in plasma cholesterol of about 18 per cent and about 10 per cent decline in plasma triglycerides levels. When combined with a statin, reduction in plasma cholesterol as high as 72 per cent has been reported.  Adverse effects. Although well tolerated. Adverse effects include; 1. fatigue  2. abdominal pain 3. diarrhoea

Gemfibrozil (Lopid) Mechanism Of Action: Gemfibrozil (Lopid) stimulates the activity of peroxisome proliferating activating receptors (PPAR alpha), a class of nuclear receptor. Activation of these receptors alters the transcription of a number of genes involved in triglyceride metabolism including lipoprotein lipase and apolipoprotein CIII. This increases the peripheral catabolism (breakdown) of VLDL and chylomicrons, resulting in a reduction in the plasma concentration of VLDL, most notably in triglycerides, moreover, Gemfibrozil (Lopid) also reduce the synthesis of cholesterol, which further reduces plasma triglycerides. Clinical and therapeutic uses: a) Gemfibrozil (Lopid) can be used to treat hyperlipidemia of several etiologies, especially hypertriglyceridemia due to dysbetalipoproteinemia, a defect in apolipoprotein E that impairs clearance of chylomicron remnants and VLDL. b) it is ineffective in primary chylomicronemia (caused by a deficiency in lipoprotein lipase). c

Fenofibrate ( Antara, Triglide, Lofibra) Mechanism Of Action: Fibrates stimulate the activity of peroxisome proliferating activating receptors (PPAR alpha), a class of nuclear receptor. Activation of these receptors alters the transcription of a number of genes involved in triglyceride metabolism including lipoprotein lipase and apolipoprotein CIII. This increases the peripheral catabolism (breakdown) of VLDL and chylomicrons, resulting in a reduction in the plasma concentration of VLDL, most notably in triglycerides, moreover, fibrates also reduce the synthesis of cholesterol, which further reduces plasma triglycerides. Clinical and therapeutic uses: a) Fenofibrate can be used to treat hyperlipidemia of several etiologies, especially hypertriglyceridemia due to dysbetalipoproteinemia, a defect in apolipoprotein E that impairs clearance of chylomicron remnants and VLDL. b) it is ineffective in primary chylomicronemia (caused by a deficiency in lipoprotein lipase). c) it has an

Nicotinic acid ( Niacin ) (brand names: Nicobid, Nicolar) Mechanism Of Action At higher doses, Nicotinic acid decrease lipolysis in the peripheral tissues, it also inhibits synthesis and esterification of fatty acids in the liver. and therefore it decreases lipid level in blood. Therapeutic Uses: At higher doses, it is used in hyperlipidemia at lower doses, it used as a vitamin and in the treatment of Pellagra Adverse Effects: flushing, itching or burning sensation in the skin can be decreased by taking aspirin 30 minutes before taking nicotinic acid because it is mediated by prostaglandins and histamine and aspirin inhibit prostaglandin synthesis.  it also disturbs hepatic metabolism and may result in hyperglycemia, increased transaminases activity. It may cause GIT disturbances and peptic ulcer. Its renal side effects include elevated uric acid and macular oedema.

Rosuvastatin (Crestor) is effective in treating plasma LDL cholesterol and total cholesterol. Mechanism Of Action: Rosuvastatin (Crestor) competitively inhibit HMG coenzyme A reductase, a rate-limiting step in cholesterol synthesis. Reduce cholesterol synthesis results in a compensatory increase in uptake of plasma cholesterol mediated by an increase in the number of LDL receptors. therefore LDL level in plasma reduces. Therapeutic Uses: Rosuvastatin (Crestor) reduces cholesterol levels in familial and non-familial hypercholesterolemias. Recent studies suggest that statins decrease osteoclast-mediated bone resorption and may reduce osteoporosis moreover statins also decrease the incidence of some cancers Adverse effects: Myositis, rhabdomyolysis, anxiety, irritability, hepatotoxicity, and elevation in aminotransferases.

Atorvastatin (Lipitor) is effective in treating plasma LDL cholesterol and total cholesterol. Mechanism Of Action: Atorvastatin (Lipitor) competitively inhibit HMG coenzyme A reductase, a rate-limiting step in cholesterol synthesis. Reduce cholesterol synthesis results in a compensatory increase in uptake of plasma cholesterol mediated by an increase in the number of LDL receptors. therefore LDL level in plasma reduces. Therapeutic Uses: Atorvastatin (Lipitor)reduces cholesterol levels in familial and non-familial hypercholesterolemias. Recent studies suggest that statins decrease osteoclast-mediated bone resorption and may reduce osteoporosis moreover statins also decrease the incidence of some cancers Adverse effects: Myositis, rhabdomyolysis, anxiety, irritability, hepatotoxicity, and elevation in aminotransferases.

Fluvastatin (Lescol) is effective in treating plasma LDL cholesterol and total cholesterol. Mechanism Of Action: Fluvastatin (Lescol) competitively inhibit HMG coenzyme A reductase, a rate-limiting step in cholesterol synthesis. Reduce cholesterol synthesis results in a compensatory increase in uptake of plasma cholesterol mediated by an increase in the number of LDL receptors. therefore LDL level in plasma reduces. Therapeutic Uses: Fluvastatin (Lescol)reduces cholesterol levels in familial and non-familial hypercholesterolemias. Recent studies suggest that statins decrease osteoclast-mediated bone resorption and may reduce osteoporosis moreover statins also decrease the incidence of some cancers Adverse effects: Myositis, rhabdomyolysis, anxiety, irritability, hepatotoxicity, and elevation in aminotransferases.

Pravastatin (Pravachol)  is effective in treating plasma LDL cholesterol and total cholesterol. Mechanism Of Action: Pravastatin (Pravachol) competitively inhibit HMG coenzyme A reductase, a rate-limiting step in cholesterol synthesis. Reduce cholesterol synthesis results in a compensatory increase in uptake of plasma cholesterol mediated by an increase in the number of LDL receptors. therefore LDL level in plasma reduces. Therapeutic Uses: Pravastatin (Pravachol) reduces cholesterol levels in familial and non-familial hypercholesterolemias. Recent studies suggest that statins decrease osteoclast-mediated bone resorption and may reduce osteoporosis moreover statins also decrease the incidence of some cancers Adverse effects: Myositis, rhabdomyolysis, anxiety, irritability, hepatotoxicity, and elevation in aminotransferases.

Simvastatin (Zocor) is effective in treating plasma LDL cholesterol and total cholesterol. Mechanism Of Action: Simvastatin (Zocor) competitively inhibit HMG coenzyme A reductase, a rate-limiting step in cholesterol synthesis. Reduce cholesterol synthesis results in a compensatory increase in uptake of plasma cholesterol mediated by an increase in the number of LDL receptors. therefore LDL level in plasma reduces. Therapeutic Uses: Simvastatin (Zocor) reduces cholesterol levels in familial and non-familial hypercholesterolemias. Recent studies suggest that statins decrease osteoclast-mediated bone resorption and may reduce osteoporosis moreover statins also decrease the incidence of some cancers Adverse effects: Myositis, rhabdomyolysis, anxiety, irritability, hepatotoxicity, and elevation in aminotransferases.

Lovastatin is effective in treating plasma LDL cholesterol and total cholesterol. Mechanism Of Action: Lovastatin competitively inhibits HMG coenzyme A reductase, a rate-limiting step in cholesterol synthesis. Reduce cholesterol synthesis results in a compensatory increase in uptake of plasma cholesterol mediated by an increase in the number of LDL receptors. therefore LDL level in plasma reduces. Therapeutic Uses: Lovastatin reduces cholesterol levels in familial and non-familial hypercholesterolemias. Recent studies suggest that statins decrease osteoclast-mediated bone resorption and may reduce osteoporosis moreover statins also decrease the incidence of some cancers Adverse effects: Myositis, rhabdomyolysis, anxiety, irritability, hepatotoxicity, and elevation in aminotransferases.