2005 GEN MED 40. Ans:D: autonomic dysfunction. Ref: harrison 17/ e- pg1009.

Exp: vit E is a fat soluble vitamin , acts as an antioxidant. Dietary Vit E deficiency is not known and is seen in only severe and prolonged malabsorption diseases. Vit E deficiency causes hemolytic anemia, cerebellar ataxia, neuropathy, myopathy, retinopathy and posterior column abnormalities . Autonomic dysfunction is not mentioned as a manifestation of vit E deficiency.hence the choice of answer. Additional info: DEFICIENCY OF VITAMINS-TABLE IN ROBINS PATHOLOGY 8/ E- PG 314 VITAMIN E: Vitamin E/ antisterility vitamin: refers to a group of eight fat-soluble compounds that include both tocopherols and tocotrienols. Sources: -Tocopherol can be found in corn oil, soybean oil, wheat germ oil, sunflower, and safflower oils margarine, and dressings. -tocopherol, the most biologically active form of vitamin E, is the second-most common form of vitamin E in the diet. Vitamin E is antioxidant, it stops the production of reactive oxygen species formed when fat undergoes oxidation. Daily requirement: 10-30 mg Function: Vitamin E has many biological functions, the antioxidant function being the most important and/or best known.

Other functions include enzymatic activities, gene expression, and neurological function(s). The most important function of vitamin E has been suggested to be in cell signaling (and it may not have a significant role in antioxidant metabolism). As an antioxidant, vitamin E acts as a peroxyl radical scavenger, preventing the propagation of free radicals in tissues, by reacting with them to form a tocopheryl radical, which will then be reduced by a hydrogen donor (such as vitamin C) and thus return to its reduced state. As it is fat-soluble, it is incorporated into cell membranes, which protects them from oxidative damage. Vitamin E has also found use as a commercial antioxidant in ultra high molecular weight polyethylene (UHMWPE) used in hip and knee replacements, to help resist oxidation. As an enzymatic activity regulator, for instance, protein kinase C (PKC), which plays a role in smooth muscle growth, can be inhibited by -tocopherol. Vitamin E also has an effect on gene expression. Macrophages rich in cholesterol are found in the atherogenetic tissue. Scavenger receptor CD36 is a class B scavenger receptor found to be up-regulated by oxidized low density lipoprotein (LDL) and binds it. Treatment with -tocopherol was found to downregulate the expression of the CD36 scavenger receptor gene and the scavenger receptor class A (SR-A) and modulates expression of the connective tissue growth factor (CTGF). The CTGF gene, when expressed, is responsible for the repair of wounds and regeneration of the extracellular tissue lost or damaged during atherosclerosis.

Vitamin E also plays a role in neurological functions, and inhibition of platelet aggregation. Vitamin E also protects lipids and prevents the oxidation of polyunsaturated fatty acids.

Deficiency Vitamin E deficiency can cause:

spinocerebellar ataxia myopathies peripheral neuropathy

ataxia skeletal myopathy retinopathy impairment of the immune response red blood cell destruction

Supplementation While vitamin E supplementation was initially hoped to have a positive effect on health, research has not supported this hope. Vitamin E does not decrease mortality in adults, even at large doses, and highdosage supplementation may slightly increase it. It does not improve blood sugar control in an unselected group of people with diabetes mellitusor decrease the risk of stroke. Daily supplementation of vitamin E does not decrease the risk of prostate cancer and may increase it. Dietary supplements are indicated in macular degeneration. Lets have a review of other vitamins in brief Fat soluble vitamins: Vitamin A : VIT A/ A1- retinol found in marine fishes. Vit A2- present in fresh water fishes. Carotenoids: pigmented and found in green plants most important carotene. Vit A is found in 2 natural forms viz cis and trans and naturally occuring vit A is trans isomer. Daily requirement-750g Function:

rhodopsin is formed by vit A ( 11 cis retinal)+ opsin ( in the rods of retinaconcerned with low vision. In light and split from protein, electric impulse resulting from this splits in visual sensation. In dark all trans retinal is isomerised back to 11 cis transretinal and binds to opsin completing the cycle. Deficiency: xeropthalmia, keratomalacia,night blindness,toad skin,bitots spots Respiratory infection and diarrhoea Vit A has anticancer effect , also anti infective vitamin Hypervitaminosis A can occur if excess VIT A intake usually theapeutic doses. Vit D: Sunshine vitamin. It behaves more like harmone. It plays an important role in calcium metabolism vitamin D3 (also known as cholecalciferol) and vitamin D2 (ergocalciferol). Cholecalciferol and ergocalciferol can be ingested from the diet and from supplements. Sources: meat , fish ,eggs. Etc.The body can also synthesize vitamin D (specifically cholecalciferol) in the skin, from cholesterol, when sun exposure is adequate (hence its nickname, the "sunshine vitamin"). .In the liver, cholecalciferol (vitamin D3) is converted to calcidiol, which is also known as calcifediol (INN), 25-hydroxycholecalciferol, or 25-hydroxyvitamin D3 abbreviated 25(OH)D3. Ergocalciferol (vitamin D2) is converted in the liver to 25-hydroxyergocalciferol, also known as 25-hydroxyvitamin D2 abbreviated 25(OH)D2. These are the two specific vitamin D metabolites that are measured in serum to determine a person's vitamin D status. Part of the calcidiol is converted by the kidneys to calcitriol, the biologically active form of vitamin D.

Calcitriol circulates as a hormone in the blood, regulating the concentration of calcium and phosphate in the bloodstream and promoting the healthy growth and remodeling of bone. Calcitriol also affects neuromuscular and immune function. Deficiency: rickets in children and osteomalacia in adults: retarded growth, bowed legs, rickety rosary, pigeon chest, bending of spine, bone fragility, muscle weakness and increased risk of fractures, hypocalcified dentin, malaigned teeth. VIT E- aldready discussed above VIT KCoagulation factor 3 forms- vit K1- phylloqiunone- green vegetable, cabbage Vit K2- intestinal bacteria- menaquinone Vit k3 synthetic form menadione It has arole in synthesis of clooting factor II, VII, IX AND X Dietary deficiency alone cannot produce vit k deficiency Deficiency seen in 1. obstructive jaundice- here lack of bile causes reduced absorption of vit K. 2. comatose patient- massive antibiotic therapy destroys intestinal bacteria. 3. Newborn- intestinal bacteria is yet to develop Signs; bleeding disorder. Water soluble vitamins: Vitamin B1(Thiamine) a) Richest source : polishing of rice, whole wheat flour and yeast. Function:

After absorption converted to thiamine pyrophosphate ( co enzyme for decarboxylation of keto acids.) Daily requirement: 1mg.day Deficiency: Beri Beri, Wernicke encephalopathy Beri Beri: polyneuropathy : loss of motor and sensory functions Cardiac enlargement: edema, oligouria and breathlessness( due to cardiac insufficiency) Wet Beri Beri: when there is excess edema. VIT B2( riboflavin) 2 forms Riboflavin phosphate ( flavin mononucleotide) (FMN) Flavin adenine dinucleotide( FAD) Thus riboflavin is a nucleoside. Sources:germinating seeds , yeast , eggs Daily requirement: 0.3mg/1000kcal consumed. Function: acts as a hydrogen carrier Deficiency:common in children who do not consume milk Oral: cheilosis, paleness of lips is the earliest sign of deficiency. Magenta tongue: stomatitis .in riboflavin deficiency filiform papillae become atrophic while fungiform papillae persist.in advanced deficiency the tongue becomes smooth.the lesion begins at the tip or lateral border. Affects nasolabial fold . Ocular: corneal vascularisation Skin: dermatitis

Normocytic anemia NIACIN / NICOTINIC ACID: Nicotinic acid converted to NAD and NADP in the body. Amino acid Tryptophan can be converted to niacin by intestinal flora. 60 mg of tryptophan =1mg of niacin. Sources: liver,yeast, wheat rice Daily requirement:15-20mg/day. Function: co enzymes( NAD and NADP) Deficiency: pellagra( dermatitis,diarrhoea, dementia) The word pellagra means rough skin Burning swollen tongue Oral mucositis VITAMIN B6/ PYRIDOXINE Widely present in food and synthesized by intestinal flora. Daily requirement: 1.5mg

Function: 1.coenzyme in transamination. 2. conversion of tryptophan to niacin. 3.Synthesis of heme.

Deficiency: dermatitis, anemia and neurological signs. Patients on antitubercular drugs isoniazid may develop peripheral neuritis due to pyridoxine deficiency. Finding of xanthurenic acid in the urine is suggested as biologic test for pyridoxine deficiency. Panthotenic acid: Need for synthesis of coenzyme A Biotin: Excess raw egg feeding leads to biotin deficiency which causes lack of muscular control. VIT B12/ CYANOCOBALAMINE Circulates in blood as methyl cobalamine. Cobalamine compound contains corrin and cobalt in the center. Deficiency causes inhibition of DNA synthesis but RNA synthesis is unaffected so the latter accmulates within the cell forming bigger but immature cells( megaloblastic anemia) FOLIC ACID: Deficiency interfers with DNA synthesis. Megaloblastic anemia caused by folic acid deficiency was reported by Wills in 1930 the factor was called as wills factor. Daily requirement: 30mcg. Pregnant women should double their intake . VITAMIN C Active form is folinic acid. Sources: citrus fruits, gauva, amla,

Daily requirement: 15mg/ day Function: Antioxidant : hydrogen ion transfer and maintenance of intracellular redox potential facilitated iron uptake in intestine. Normal development of ground substance of dentine and bone. Deficiency : Scurvy: ulcerated boggy, bleeding swollen gingiva, loss of bone, and peridontal inflammation Delayed wound healing. It helps in post translation modification of clotting factors along with vit K. H/F: Osteoblast fail to form osteoid on calcified spicules of the cartilage , thus wide zone of calcified but non ossified matrix. Scorbutic lattice is formed. Lattice may increase in size and fracture: trummerfeld zones Area beneath this zone is free of hemopoetic cells made up of connective tissue and is callled gerustmark 41. Ans: B: ADRENALINE Ref: harrison 17/ e pg 117, KDT,6/E- Pg 130 Exp: adrenaline is a life saving drug in anaphylaxis and given 0. 2 0.5 mg SC/ IM . It not only increases BP but also counteracts bronchospasm or laryngeal edema and hence the choice of drug in anaphylaxis( Type I hypersensitivity reaction). Additional info:

anaphylaxis
Definition A life-threatening systemic hypersensitivity reaction ( type I) to contact with an allergen; it may appear within minutes of exposure to the offending substance. Clinical presentation Time to onset is variable, but symptoms usually occur within seconds to minutes of exposure to the offending antigen: Respiratory: mucous membrane swelling, hoarseness, stridor, wheezing Cardiovascular: tachycardia, hypotension Cutaneous: pruritus, urticaria, angioedema ,mucous membrane swelling, gastrointestinal disturbances (including nausea, vomiting, pain, and diarrhea), and vascular collapse. Virtually any allergen may incite an anaphylactic reaction, but among the more common agents are proteins such as antisera, hormones, pollen extracts, Hymenoptera venom, foods; drugs (especially antibiotics); and diagnostic agents. Atopy does not seem to predispose to anaphylaxis from penicillin or venom exposures. Typical progression of generalized anaphylaxis- table 18-7 pg -326 malamed handbook local anaesthesia Diagnosis: Made by obtaining history of exposure to offending substance with subsequent development of characteristic complex of symptoms. With prompt and appropriate treatment the entire reaction may be terminated rapidly however hypotension and laryngeal edema may persist for hours to days despite intensive therapy. Death may occur at any time during the reaction , usually secondary to upper airway obstruction produced by laryngeal edema. Treatment: Mild symptoms such as pruritus and urticaria can be controlled by administrationof 0.3 0.5 mL of 1:1000 (1.0 mg/mL) epinephrine SC or IM, with repeated doses as required at 5- to 20-min intervals for a severe reaction. An IV infusion should be initiated for administration of 2.5 mL of 1:10,000

epinephrine solution at 5- to 10-min intervals, volume expanders such as normal saline, and vasopressor agents, e.g., dopamine, if intractable hypotension occurs. Epinephrine provides both - and -adrenergic effects, resulting in vasoconstriction and bronchial smooth-muscle relaxation. Beta blockers are relatively contraindicated in persons at risk for anaphylactic reactions. The following should also be used as necessary: Antihistamines such as diphenhydramine 50100 mg IM or IV Aminophylline 0.250.5 g IV for bronchospasm Oxygen Glucocorticoids (medrol 0.51.0 mg/kg IV); not useful for acute manifestations but may help control persistent hypotension or bronchospasm For antigenic material injected into an extremity consider: use of a tourniquet proximal to the site, 0.2 mL of 1:1000 epinephrine into the site, removal of an insect stinger if present. 42. Ans: a: ephinephrine Ref: : harrison 17/ e pg 117, KDT,6/E- Pg 130

Exp and additional info: same as above question 43. Ans: c: flourosis Ref:harrison 17/e pg -966 Exp and additional info Q 34- 2006 GEN MED PAPER 44 ANS:D: albumin Ref: robins pathology 8/e pg 633-634 Exp:Only minimal changes in serum albumin are seen in acute liver conditions. Hypoalbumenianis common in chronic liver diseases such as cirrhosis.

ADDITIONAL INFO: The most severe clinical consequence of liver disease is hepatic failure. It generally develops as the end point of progressive damage to the liver, either by insidious destruction of hepatocytes or by repetitive discrete waves of parenchymal damage. Less commonly, hepatic failure is the result of sudden and massive destruction of hepatic tissue. Whatever the sequence, 80% to 90% of hepatic function must be lost before hepatic failure ensues. In many cases, the balance is tipped toward decompensation by intercurrent diseases that place demands on the liver like systemic infections, electrolyte disturbances, stress (major surgery, heart failure), and gastrointestinal bleeding. The alterations that cause liver failure fall into three categories: 1. Acute liver failure with massive hepatic necrosis. This is most often caused by drugs or fulminant viral hepatitis. Acute liver failure denotes clinical hepatic insufficiency that progresses from onset of symptoms to hepatic encephalopathy within 2 to 3 weeks. A course extending as long as 3 months is called subacute failure. The histologic correlate of acute liver failure is massive hepatic necrosis. It is an uncommon but life-threatening condition that often requires liver transplantation.. 2. Chronic liver disease. This is the most common route to hepatic failure and is the end point of relentless chronic liver damage ending in cirrhosis. 3. Hepatic dysfunction without overt necrosis. Hepatocytes may be viable but unable to perform normal metabolic function, as in acute fatty liver of pregnancy (which can lead to acute liver failure a few days after onset), tetracycline toxicity, and Reye syndrome (a rare syndrome of fatty liver and encephalopathy in children, associated with aspirin intake and virus infection.: Causes : The list of conditions associated with chronic liver disease is extensive and can be categorised in the following way:

Viral causes

Hepatitis B Hepatitis C Cytomegalovirus (CMV) Epstein Barr Virus (EBV)

Toxic and drugs

Alcoholic liver disease Amiodarone Methotrexate Nitrofurantoin

Metabolic

Non-alcoholic fatty liver disease Haemochromatosis Wilson's Disease

Autoimmune

Autoimmune Chronic Hepatitis Primary Biliary Cirrhosis Primary Sclerosing Cholangitis

Other

Right heart failure

Clinical Features : Regardless of cause, the clinical signs of hepatic failure occurring in individuals with chronic liver disease are much the same. Jaundice is an almost invariable finding. Impaired hepatic synthesis and secretion of albumin leads to hypoalbuminemia, which predisposes to peripheral edema. Hyperammonemia is attributable to defective hepatic urea cycle function. On a longer term basis, impaired estrogen metabolism and consequent hyperestrogenemia are the putative causes of palmar erythema (a reflection of

local vasodilatation) and spider angiomas of the skin. Each angioma is a central, pulsating, dilated arteriole from which small vessels radiate. In the male, hyperestrogenemia also leads to hypogonadism and gynecomastia Acute liver failure may present as jaundice or encephalopathy, but notably absent on physical examination are stigmata of chronic liver disease (e.g., gynecomastia, spider angiomas). Diagnosis and lab features: Table in robins path 8/e- pg 634

Complications: Hepatic failure is life-threatening for several reasons. The accumulation of toxic metabolites may have widespread effects. With severely impaired liver function, patients are highly susceptible to failure of multiple organ systems. Thus, respiratory failure with pneumonia and sepsis combines with renal failure to claim the lives of many individuals with hepatic failure A coagulopathy develops, attributable to impaired hepatic synthesis of blood clotting factors. The resultant bleeding tendency may lead to massive gastrointestinal hemorrhage as well as bleeding elsewhere. Intestinal absorption of blood places a metabolic load on the liver that worsens the severity of hepatic failure. Two particular complications merit separate consideration, because they herald the most grave stages of hepatic failure: hepatic encephalopathy and hepatorenal syndrome.

Treatment and Prognosis: About 40% of individuals with liver failure may recover spontaneously.

The treatment of chronic liver disease depends on the cause. While some conditions may be treated with medications, others may require surgery or a transplant. Transplant is required when the liver fails and there is no other alternative The outlook of full-blown hepatic failure is particularly grave for persons with chronic liver disease. A rapid downhill course is usual, with death occurring within weeks to a few months in about 80% of cases. 45. Ans:A: EXPOSURE AND RESPONSE PREVENTION. REF: net sources Exp:The patient is a case of obsessive compulsive neurosis and is not responding to the drug treatment.The treatment of choice is behavioural therapy. Exposure and response prevention is the first line technique of behavioural therapy in Obsessive compulsive neurosis patients. Additional info:

Obsessive-compulsive disorder (OCD) is an anxiety disorder characterized by uncontrollable, unwanted thoughts and repetitive, ritualized behaviors you feel compelled to perform. Obsessions are involuntary, seemingly uncontrollable thoughts, images, or impulses that occur over and over again in your mind. Compulsions are behaviors or rituals that you feel driven to act out again and again. Usually, compulsions are performed in an attempt to make obsessions go away. Most people with obsessive-compulsive disorder (OCD) fall into one of the

following categories:

Washers are afraid of contamination. They usually have cleaning or handwashing compulsions. Checkers repeatedly check things (oven turned off, door locked, etc.) that they associate with harm or danger. Doubters and sinners are afraid that if everything isnt perfect or done just right something terrible will happen or they will be punished. Counters and arrangers are obsessed with order and symmetry. They may have superstitions about certain numbers, colors, or arrangements. Hoarders fear that something bad will happen if they throw anything away. They compulsively hoard things that they dont need or use.

Signs and symptoms: Common obsessive thoughts in obsessive-compulsive disorder (OCD) include:

Fear of being contaminated by germs or dirt or contaminating others. Fear of causing harm to yourself or others. Intrusive sexually explicit or violent thoughts and images. Excessive focus on religious or moral ideas. Fear of losing or not having things you might need. Order and symmetry: the idea that everything must line up just right. Superstitions; excessive attention to something considered lucky or unlucky Excessive double-checking of things, such as locks, appliances, and switches. Repeatedly checking in on loved ones to make sure theyre safe. Counting, tapping, repeating certain words, or doing other senseless things to reduce anxiety. Spending a lot of time washing or cleaning. Ordering or arranging things just so. Praying excessively or engaging in rituals triggered by religious fear.

Diganosis: Proper History taking and assessment. Treatment: Behavioral therapy (BT), cognitive behavioral therapy (CBT), and

medications are first-line treatments for OCD. Psychodynamic psychotherapy may help in managing some aspects of the disorder.

Behavioral therapy The specific technique used in BT/CBT is called exposure and ritual prevention (also known as "exposure and response prevention") or ERP; this involves gradually learning to tolerate the anxiety associated with not performing the ritual behavior. At first, for example, someone might touch something only very mildly "contaminated" (such as a tissue that has been touched by another tissue that has been touched by the end of a toothpick that has touched a book that came from a "contaminated" location, such as a school.) That is the "exposure". The "ritual prevention" is not washing. Another example might be leaving the house and checking the lock only once (exposure) without going back and checking again (ritual prevention). The person fairly quickly habituates to the anxiety-producing situation and discovers that their anxiety level has dropped considerably; they can then progress to touching something more "contaminated" or not checking the lock at allagain, without performing the ritual behavior of washing or checking. Exposure ritual/response prevention (ERP) has a strong evidence base. It is considered the most effective treatment for OCD. . It has generally been accepted that psychotherapy, in combination with psychiatric medication, is more effective than either option alone. However, more recent studies have shown no difference in outcomes for those treated with the combination of medicine and CBT versus CBT alone. Medication Medications as treatment include selective serotonin reuptake inhibitors (SSRIs) and the tricyclic antidepressants, in particular clomipramine.

Treatment of OCD is an area needing significant improvement in prescribing regimens. Benzodiazepines are sometimes used, although they are generally believed to be ineffective for treating OCD; . In most cases antidepressant therapy alone provides only a partial reduction in symptoms, even in cases that are not deemed treatment resistant current research is devoted to the therapeutic potential of the agents that affect the release of the neurotransmitter glutamate or the binding to its receptors. These include riluzole, memantine, gabapentin, N-Acetylcysteine, and lamotrigine. The atypical antipsychotics such as quetiapine have also been found to be useful as adjuncts to an SSRI in treatment-resistant OCD. However, these drugs are often poorly tolerated, and have metabolic side effects that limit their use. None of the atypical antipsychotics appear to be useful when used alone. Electroconvulsive therapy Electroconvulsive therapy (ECT) has been found to have effectiveness in some severe and refractory cases. Psychosurgery For some, medication, support groups and psychological treatments fail to alleviate obsessivecompulsive symptoms. These patients may choose to undergo psychosurgery as a last resort. In this procedure, a surgical lesion is made in an area of the brain (the cingulate cortex. Deep-brain stimulation and vagus nerve stimulation are possible surgical options that do not require destruction of brain tissue. psychosurgery for OCD is a treatment of last resort and will not be performed until the patient has failed several attempts at medication (at the full dosage) with augmentation, and many months of intensive cognitivebehavioral therapy with exposure and ritual/response prevention

46. Ans : B: an overall score of less than 9 indicates a poor prognosis. Ref:: bailey and love surgery 25 /E pg-301 Exp: GCS score shows a prognostic value about the eventual outcome of the injury. It permits a reliable and reproducible assessment of neurological status but this assessment is not accurate. It is only a rough estimate of the neurological status of the patient. A GCS of 8 or less is generally accepted as coma. A GCS score of 11 in 1st 24 hrs sugeest a guarded prognosis as these patients can improve or deteriorate . a score of 9-12 means moderate level skull injury to the patient and the patient is confused but is able to follow commands such patients show improvement in 90 % of cases but 10% can deteriorate. Hence although prognosis is favourable , its not good. Hence continued observation of the patient is needed. So option A is partially correct.GCS can be assessed in both conscious and unconscious patients. Hence from all of these we infer that ,B the choice of answer. Additional info: Glassgow coma score: The Glasgow Coma Scale or GCS is a neurological scale that aims to give a reliable, objective way of recording the conscious state of a person for initial as well as subsequent assessment. It is shown to have prognostic value. A patient is assessed against the criteria of the scale, and the resulting points give a patient score between 3 (indicating deep unconsciousness) and either 14 (original scale) or 15 (the more widely used modified or revised scale). GCS was initially used to assess level of consciousness after head injury, and the

scale is now used in hospitals in monitoring chronic patients in intensive care. The scale was published in 1974 by Graham Teasdale and Bryan J. Jennett,.
Severity of head injury is classified according to the Glasgow Coma Score (GCS) , as the GCS and in particular the motor score is the best predictor of neurological outcome: 3 variables used are: Motor response: to assess the level of CNS function. Verbal response: show ability of CNS to integrate information. Eye opening: demonstrates brainstem activity. The score ranges from 3 (worst) -15 (best) Outcome: minor head injury: GCS 15 with no loss of consciousness (LOC); mild head injury: GCS 14 or 15 with LOC; moderate head injury: GCS 913; severe head injury: GCS 38. Note: GCS score:TABLE- 23.1 , PG 301 BAILEY AND LOVE SURGERY 25/ E GCS is shown to have prognostic outcome in neurological assessment in head injury patients.

47. Ans: C: immediately stich wound under antibiotic coverage. Ref: net sources Exp:Dog bites are a major source of morbidity and mortalityworldwide,
accounting for up to 1.5% of all visits to emergency medicine units .They are associated with various disease transmission like rabies and hence prompt care earlier is advisable after exposure. Dog bites are graded as 1, 2 or 3, depending on severity .This grading is important because it guides therapy: only grade 3 bites require immunoglobulin; only grade 2 or 3 bites require

vaccine; and grade 1 bites require no treatment. And rabies can only be prevented through the use of immunoglobulin, which is effective against the rabies virus for the first 10 days after exposure. Immediate stitch of the wound and antibiotic coverage is usually not recommended and hence the choice of answer. Additional info: Dog bites are a major source of morbidity and mortality worldwide, accounting for up to 1.5% of all visits to emergency medicine units. They are associated with various disease transmission like rabies and hence prompt care earlier is advisable after exposure. Since rabies is almost universally fatal, its control is of paramount importance . Dog bites are graded as 1, 2 or 3, depending on severity .This grading is important because it guides therapy. Post exposure treatment is is given according to the WHO guidelines.

Type of contact with a suspect or Category confirmed rabid domestic or wild animals or animal unavailable for observation. I

Recommended treatment

None , if reliable case history Touching or feeding of animals. is available. Licks on intact skin. Administer vaccine immediately . Stop treatrment if animal remains healthy throughout an observation period of 10 days or if animal is euthanised and found to be negative for rabies by appropriate laboratory techniques. Administer rabies immunoglobulin and vaccine immediately .Stop treatement if animals remains healthy throughout an observation period of 10 days or if animal is euthanised and

II

Nibbling of uncovered skin.Minor scratches or abrasions without bleeding. licks on broken skin.

III

Single or multiple transdermal bites or scratches Contamination of mucous membrane with saliva(i.e.,licks).

found to be negative for rabies by appropriate laboratory techniques.

only grade 3 bites require immunoglobulin; only grade 2 or 3 bites require vaccine; and grade 1 bites require no treatment. And rabies can only be prevented through the use of immunoglobulin, which is effective against the rabies virus for the first 10 days after exposure. Post exposure prophylaxis: All wounds potentially exposed to rabies must be aggressively and thoroughly cleaned and irrigated. Immediate stitch of the wound and antibiotic coverage is usually not recommended .Prophylactic antimicrobials for low risk lacerations have not been shown to reduce the incidence of infection. Hence not recommended except those with high risk. Patients suspected of being exposed to a rabid animal should begin post -exposure treatment immediately. If a patient delays seeking evaluation, treatment should not be withheld, because incubation periods >1 yr have been reported. The recommendation for previously unvaccinated individuals is a regimen of rabies immune globulin (RIG) 20 IU/kg and a series of rabies vaccines, 1.0 ml IM in the deltoid area, to be given on day 0, 3, 7, 14, and 28. If anatomically feasible, the full dose of RIG should be infiltrated around the wound, with the remainder given IM at another anatomical site distant from the wound and the vaccine site. If the patient is previously vaccinated, then RIG is not given, and the passive vaccine is administered, 1.0 ml IM in the deltoid area, on days 0 and 3 only.