Friday, 29 June 2012

136.PYOGENIC LIVER ABCESS CAUSED BY

A.ENTAMEOBA
B.ECHINOCOCCUS
C.ENTEROCOCCUS
D.

ANS:ENTEROCOCCUS


Pyogenic liver abscess is a pus-filled area in the liver.

Causes, incidence, and risk factors

There are many potential causes of liver abscesses, including:


  1. Abdominal infection such as appendicitis, diverticulitis, or a perforated bowel
  2. Infection in the blood
  3. Infection of the bile draining tubes
  4. Recent endoscopy of the bile draining tubes
  5. Trauma that damages the liver


The most common bacteria that cause liver abscesses are:


  • Bacteroides
  • Enterococcus
  • Escherichia coli
  • Klebsiella
  • Staphylococcus
  • Streptococcus


In most cases, more than one type of bacteria is found.



135.INFECTIVE FORM OF MALARIA

A.SCHIZONT
B.SPOROZOITE'
C.MEROZOITE
D.TROPOZOITE

ANS:SPOROZOITE



  • Diploid: Cells containing a full set of chromosomes. 
  • Gametes: Reproductive elements, male and female. 
  • Gametocytes: Precursors of the sexual forms of the malaria parasite, which release either male or female gametes within the stomach of the mosquito. 
  • Haploid: Cells containing a half set of chromosomes.
  • Merozoite: The form of the malaria parasite that invades red blood cells.
  • Oocyst: A stage of the malaria parasite within the mosquito which is produced when male and female gametes combine. 
  • Ookinete: The actively moving zygote of the malarial organism that penetrates the mosquito stomach to form an oocyst under the outer gut lining. 
  • Sporozoite: The infectious form of the malaria parasite, which is injected into people by mosquitoes. 
  • Zygote: The diploid cell resulting from union of a male and a female gamete. 

134.DISEASE CAUSED BY MITE

A.SCRUB TYPHUS
B.ENDEMIC TYPHUS
C.EPIDEMIC TYPHUS
D.TERNCH FEVER

ANS:SCRUB TYPHUS

Scrub typhus fever is not directly spread from person-to-person. Disease is spread to people by the bite of a mite infected with the bacteria that causes scrub typhus fever.

133.ALL ARE DETECTABLE IN PERIPHERAL SMEAR EXCEPT

A.PLASMODIUM
B.LEISHMANIA
C.WUCHERERIA
D.SCHISTOSOMIA

ANS:SCHISTOSMIA


Microscopic identification of eggs in stool or urine is the most practical method for diagnosis. The stool exam is the more common of the two. For the measurement of eggs in the feces of presenting patients the scientific unit used is eggs per gram (epg). Stool examination should be performed when infection with S. mansoni or S. japonicum is suspected, and urine examination should be performed if S. haematobium is suspected.

Eggs can be present in the stool in infections with all Schistosoma species. The examination can be performed on a simple smear (1 to 2 mg of fecal material). Since eggs may be passed intermittently or in small amounts, their detection will be enhanced by repeated examinations and/or concentration procedures (such as the formalin-ethyl acetate technique). In addition, for field surveys and investigational purposes, the egg output can be quantified by using the Kato-Katz technique (20 to 50 mg of fecal material) or the Ritchie technique.

Eggs can be found in the urine in infections with S. japonicum and with S. intercalatum (recommended time for collection: between noon and 3 PM). Detection will be enhanced by centrifugation and examination of the sediment. Quantification is possible by using filtration through a nucleopore membrane of a standard volume of urine followed by egg counts on the membrane. Investigation of S. haematobium should also include a pelvic x-ray as bladder wall calcificaition is highly characteristic of chronic infection.




132.SPECIES OF CLOSTRIDIUM ASSOCIATED WITH COLITIS

A.DIFFICILE
B.PARVUM
C.PERFRINGES A
D.PERFRINGES C

ANS:DIFFICILE


Clostridium consists of around 100 species that include common free-living bacteria as well as important pathogens. There are five main species responsible for disease in humans:

C. botulinum, an organism that produces botulinum toxin in food/wound and can cause botulism.Honey sometimes contains spores of Clostridium botulinum, which may cause infant botulism in humans one year old and younger. The toxin eventually paralyzes the infant's breathing muscles.Adults and older children can eat honey safely, because Clostridium do not compete well with the other rapidly growing bacteria present in the gastrointestinal tract. This same toxin is known as "Botox" and is used cosmetically to paralyze facial muscles to reduce the signs of aging; it also has numerous therapeutic uses.

C. difficile, which can flourish when other bacteria in the gut are killed during antibiotic therapy, leading to pseudomembranous colitis (a cause of antibiotic-associated diarrhea).

C. perfringens, formerly called C. welchii, causes a wide range of symptoms, from food poisoning to gas gangrene. Also responsible for enterotoxemia (also known as "overeating disease" or "pulpy kidney disease") in sheep and goats. C. perfringens also takes the place of yeast in the making of salt rising bread. The name perfringens means 'breaking through' or 'breaking in pieces'.


C. tetani, the causative organism of tetanus. The name derives from "of a tension", referring to the tension (caused by tetanus) in the muscles.


C. sordellii can cause a fatal infection in exceptionally rare cases after medical abortions.Less than one case per year has been reported since 2000.


131.RETROSPECTIVE DIAGNOSIS OF STREPTOCOCCAL SKIN INFECTION

A.ASO TITRE
B.ANTI DNAse B
C.ERYTHROGENIC TOXIN
D.

ANS:ASO TITRE


When the body is infected with streptococci, it produces antibodies against the various antigens that the streptococci produce. ASO is one such antibody. A raised or rising levels can indicate past or present infection. Historically it was one of the first bacterial markers used for diagnosis and follow up of rheumatism or scarlet fever. Its importance in this regard has not diminished.

Since these antibodies are produced as a delayed hypersensitivity reaction to the above mentioned bacteria, there is no normal value. The presence of these antibodies indicates an exposure to these bacteria. However, as many people are exposed to these bacteria and remain asymptomatic, the mere presence of ASO does not indicate disease.

Acceptable values, where there is no clinical suspicion of rheumatism are as follows:

Adults: less than 200 units
Children: less than 300 units
This titre has a significance only if it is greatly elevated, or if a rise in titre can be demonstrated in paired blood samples taken days apart.The antibody levels begin to rise after 1 to 3 weeks of strep infection,peaks in 3 to 5 weeks and falls back to insignificant levels in 6 months.
130.ASYMPTOMATIC BACTERIURIA CAN BE SAID IF THERE IS ____________ BACTERIA

A.MORE THAN 10^5
B.10^2
C.10^3
D.10^6

ANS:MORE THAN 10^5


DEFINITION AND DIAGNOSIS

The term asymptomatic bacteriuria refers to the presence of high quantities of a uropathogen in the urine of an asymptomatic person. Initial studies showed that colony counts ≥10(5) cfu/mL more often predicted persistently high levels of bacteriuria compared with lower colony counts

The 2005 IDSA guidelines for the diagnosis and treatment of asymptomatic bacteriuria in adults recommend the following criteria for the diagnosis of asymptomatic bacteriuria :


  • For asymptomatic women, bacteriuria is defined as two consecutive clean-catch voided urine specimens with isolation of the same bacterial strain in counts ≥10(5) cfu/mL.
  • For any asymptomatic patient, bacteriuria is defined as a single catheterized urine specimen with one bacterial species isolated in counts ≥10(2) cfu/mL. Although a count of ≥10(2) cfu/mL has been validated in research settings to be significant, many clinical laboratories do not routinely quantify counts in this range



129.STREPTOCOCCUS PNEUMONIA 

A.ALPHA HEMOLYTIC
B.BETA HEMOLYTIC
C.GAMMA HEMOLYTIC
D.DELTA HEMOLYTIC

ANS:ALPHA HEMOLYTIC




128.EVALUATION FUNCTION OF GENE BY INTRODUCING GENETIC MATERIAL

A.GENE THERAPHY
B.CLONING
C.HUMAN GENOME PROJECT
D.

ANS:HUMAN GENOME PROJECT

127.MOST COMMON ORGANISM CAUSING OTOMYCOSIS

A.MUCOR
B.ASPERGILLUS
C.CANDIDA
D.PENCILLIUM

ANS:ASPERGILLUS

Otomycosis is fungal infection of the external auditory canal.

The incidence of otomycosis is not known but it is more common in hot climates and in those who indulge in aquatic sports. About 1 in 8 of otitis external infections is fungal in origin. 90% of fungal infections involve Aspergillus spp. and the rest Candida spp. The prevalence rate has been quoted as 9% of patients presenting with signs and symptoms of otitis externa. The fraction of otitis externa that is otomycosis may be higher in hot climates and much of the literature originates from tropical and subtropical countries. the diagnosis of otitis externa is made most often in late summer when swimming is most common.


126.ORIENTAL SPOTTED FEVER CAUSED BY

A.R.AKARI
B.R.JAPONICA
C.R.TSUTSUGAMUSHI
D.ORIENTALA

ANS:R.JAPONICA


Japanese spotted fever (or oriental spotted fever) is a condition characterized by a rash that has early macules, and later, in some patients, petechiae.It is caused by Rickettsia japonica
125.INFECTIOUS MONONUCLEOSIS CAUSED BY

A.EBV
B.HSV
C.CMV
D.HIV

ANS:EBV

Infectious mononucleosis (IM; also known as EBV infectious mononucleosis, Pfeiffer's disease, Filatov's disease and sometimes colloquially as the kissing disease from its oral transmission or simply as mono in North America and as glandular fever in other English-speaking countries) is an infectious, widespread viral disease caused by the Epstein–Barr virus (EBV), one type of herpes virus, to which more than 90% of adults have been exposed


124.ERYTHEMA INFECTIOSUM CAUSED BY

A.EBV
B.HPV
C.CMV
D.PARVOVIRUS B

ANS:PARVOVIRUS B



Erythema infectiosum or fifth disease is one of several possible manifestations of infection by erythrovirus, previously called parvovirus B19.The disease is also referred to as slapped cheek syndrome, slapcheek, slap face or slapped face.In Japan the disease is called 'apple sickness',in reference to the symptom of facial redness. In Hungary it is called "butterfly pox" as the red cheeks look like the wings of a butterfly.
123.HIV IS

A.ENVELOPED RNA VIRUS
B.NON ENVELOPED RNA VIRUS
C.ENVELOPED DNA VIRUS
D.NON ENVELOPED DNA VIRUS

ANS:ENVELOPED RNA VIRUS

HIV is a member of the genus Lentivirus, part of the family of Retroviridae. Lentiviruses have many morphologies and biological properties in common. Many species are infected by lentiviruses, which are characteristically responsible for long-duration illnesses with a long incubation period. Lentiviruses are transmitted as single-stranded, positive-sense, enveloped RNA viruses. Upon entry into the target cell, the viral RNA genome is converted (reverse transcribed) into double-stranded DNA by a virally encoded reverse transcriptase that is transported along with the viral genome in the virus particle. The resulting viral DNA is then imported into the cell nucleus and integrated into the cellular DNA by a virally encoded integrase and host co-factors. Once integrated, the virus may become latent, allowing the virus and its host cell to avoid detection by the immune system. Alternatively, the virus may be transcribed, producing new RNA genomes and viral proteins that are packaged and released from the cell as new virus particles that begin the replication cycle anew.


122.HERPES GENITALIS COMMONLY CAUSED BY

A.HSV 1
B.HHV 8
C.CMV
D.HSV 2

ANS:HSV 2


Genital herpes is a sexually transmitted disease (STD) caused by the herpes simplex viruses type 1 (HSV-1) or type 2 (HSV-2). Most genital herpes is caused by HSV-2. Most individuals have no or only minimal signs or symptoms from HSV-1 or HSV-2 infection. When signs do occur, they typically appear as one or more blisters on or around the genitals or rectum. The blisters break, leaving tender ulcers (sores) that may take two to four weeks to heal the first time they occur. Typically, another outbreak can appear weeks or months after the first, but it almost always is less severe and shorter than the first outbreak.  Although the infection can stay in the body indefinitely, the number of outbreaks tends to decrease over a period of years.


Genital HSV-2 infection is more common in women (approximately one out of five women 14 to 49 years of age) than in men (about one out of nine men 14 to 49 years of age). Transmission from an infected male to his female partner is more likely than from an infected female to her male partner




121.ENTERO VIRUS 72 IS

A.HEPATITIS A
B.HEPATITIS B
C.HSV
D.HIV

ANS:HEPATITIS A


120.SERUM SICKNESS

A.TYPE 1
B.TYPE 2
C.TYPE 3
D.TYPE 4

ANS:TYPE 3


Type III hypersensitivity is also known as immune complex hypersensitivity. The reaction may be general (e.g., serum sickness) or may involve individual organs including skin (e.g., systemic lupus erythematosus, Arthus reaction), kidneys (e.g., lupus nephritis), lungs (e.g., aspergillosis), blood vessels (e.g., polyarteritis), joints (e.g., rheumatoid arthritis) or other organs. This reaction may be the pathogenic mechanism of diseases caused by many microorganisms.

The reaction may take 3 - 10 hours after exposure to the antigen (as in Arthus reaction). It is mediated by soluble immune complexes. They are mostly of the IgG class, although IgM may also be involved. The antigen may be exogenous (chronic bacterial, viral or parasitic infections), or endogenous (non-organ specific autoimmunity: e.g., systemic lupus erythematosus, SLE). The antigen is soluble and not attached to the organ involved. Primary components are soluble immune complexes and complement (C3a, 4a and 5a). The damage is caused by platelets and neutrophils . The lesion contains primarily neutrophils and deposits of immune complexes and complement. Macrophages infiltrating in later stages may be involved in the healing process.

The affinity of antibody and size of immune complexes are important in production of disease and determining the tissue involved. Diagnosis involves examination of tissue biopsies for deposits of immunoglobulin and complement by immunofluorescence microscopy. The immunofluorescent staining in type III hypersensitivity is granular (as opposed to linear in type II such as seen in  Goodpasture's syndrome). The presence of immune complexes in serum and depletion in the level of complement are also diagnostic. Polyethylene glycol-mediated turbidity (nephelometry) binding of C1q and Raji cell test are utilized to detect immune complexes. Treatment includes anti-inflammatory agents.
119.CONTACT DERMATITIS

A.TYPE 1
B.TYPE 2
C.TYPE 3
D.TYPE 4

ANS:TYPE 4

Type IV hypersensitivity is involved in the pathogenesis of many autoimmune and infectious diseases (tuberculosis, leprosy, blastomycosis, histoplasmosis, toxoplasmosis, leishmaniasis, etc.) and granulomas due to infections and foreign antigens. Another form of delayed hypersensitivity is contact dermatitis (poison ivy , chemicals, heavy metals, etc.) in which the lesions are more papular. Type IV hypersensitivity can be classified into three categories depending on the time of onset and clinical and histological presentation.
118.IgE SEEN IN WHICH TYPE OF HYPERSENSITIVITY

A.TYPE 1
B.TYPE 2
C,TYPE 3
D.TYPE 4

ANS:TYPE 1



  • Type I reactions (ie, immediate hypersensitivity reactions) involve immunoglobulin E (IgE)–mediated release of histamine and other mediators from mast cells and basophils.
  • Type II reactions (ie, cytotoxic hypersensitivity reactions) involve immunoglobulin G or immunoglobulin M antibodies bound to cell surface antigens, with subsequent complement fixation.
  • Type III reactions (ie, immune-complex reactions) involve circulating antigen-antibody immune complexes that deposit in postcapillary venules, with subsequent complement fixation.
  • Type IV reactions (ie, delayed hypersensitivity reactions, cell-mediated immunity) are mediated by T cells rather than by antibodies.

Thursday, 28 June 2012

117.SINGLE DOSE SUFFICIENT IN WHICH TYPE OF HYPERSENSITIVITY

A.TYPE 1
B.TYPE 2
C.TYPE 3
D.TYPE 4

ANS:TYPE 2


In type II hypersensitivity (or cytotoxic hypersensitivity)the antibodies produced by the immune response bind to antigens on the patient's own cell surfaces. The antigens recognized in this way may either be intrinsic ("self" antigen, innately part of the patient's cells) or extrinsic (adsorbed onto the cells during exposure to some foreign antigen, possibly as part of infection with a pathogen). These cells are recognized by macrophages or dendritic cells, which act as antigen-presenting cells. This causes a B cell response, wherein antibodies are produced against the foreign antigen.

116.T CELL IMMUNITY DUE TO

A.PHAGOCYTE
B.LEUKOCYTE
C.STEM CELL
D.BASOPHIL

ANS:PHAGOCYTE


Cell-mediated immunity is an immune response that does not involve antibodies but rather involves the activation of phagocytes, natural killer cells (NK), antigen-specific cytotoxic T-lymphocytes, and the release of various cytokines in response to an antigen. Historically, the immune system was separated into two branches: humoral immunity, for which the protective function of immunization could be found in the humor (cell-free bodily fluid or serum) and cellular immunity, for which the protective function of immunization was associated with cells. CD4 cells or helper T cells provide protection against different pathogens. Cytotoxic T cells cause death by apoptosis without using cytokines, therefore in cell mediated immunity cytokines are not always present.

Cellular immunity protects the body by:

activating antigen-specific cytotoxic T-lymphocytes that are able to induce apoptosis in body cells displaying epitopes of foreign antigen on their surface, such as virus-infected cells, cells with intracellular bacteria, and cancer cells displaying tumor antigens;
activating macrophages and natural killer cells, enabling them to destroy pathogens; and
stimulating cells to secrete a variety of cytokines that influence the function of other cells involved in adaptive immune responses and innate immune responses.
Cell-mediated immunity is directed primarily at microbes that survive in phagocytes and microbes that infect non-phagocytic cells. It is most effective in removing virus-infected cells, but also participates in defending against fungi, protozoans, cancers, and intracellular bacteria. It also plays a major role in transplant rejection
115.FRISH BACILLUS

A.RHINOSCLEROMATIS
B.RHINOSPORIDIUM SEEBERI
C.MYCOPLASMA
D.PSEUDOMONAS

ANS:RHINOSCLEROMATIS

RHINOSCLEROMA

It is caused by Klebsiella rhinoscleromatis—subspecies of Klebsiella pneumoniae— a gram-negative, encapsulated, nonmotile, rod-shaped bacillus (diplobacillus), member of the Enterobacteriaceae family. It is sometimes referred to as the "Frisch bacillus," named for Anton von Frisch who identified the organism in 1882



114.DELTA HEAVY CHAIN PRESENT IN

A.IgG
B.IgD
C.IgM
D.IgA

ANS:IgD

Immunoglobulin D (IgD) is an antibody isotype that makes up about 1% of proteins in the plasma membranes of immature B-lymphocytes where it is usually coexpressed with another cell surface antibody called IgM. IgD is also produced in a secreted form that is found in very small amounts in blood serum. Secreted IgD is produced as a monomeric antibody with two heavy chains of the delta (δ) class, and two Ig light chains.


MICROBIOLOGY

113.C5-C9 DEFECIENCY

A.ANGIONERITIC EDEMA
B.SEPTIC PYOGENIC INFECTION
C.SLE
D.MENINGITIS

ANS:MENINGITIS

Terminal pathway (C5-C9): The lack of MAC formation results in severe recurrent infection by Neisseria gonorrhoeae or Neisseria meningitidis.
112.CALCIUM CHANNEL BLOCKER USED IN SUB ARACHNOID H'GHE

A.NIFEDIPINE
B.NICARDIPINE
C.NIMODIPINE
D.VERAPAMIL

ANS:NIMODIPINE


Vasospasm, in which the blood vessels constrict and thus restrict blood flow, is a serious complication of SAH. It can cause ischemic brain injury (referred to as "delayed ischemia") and permanent brain damage due to lack of oxygen in parts of the brain. It can be fatal if severe. Delayed ischemia is characterized by new neurological symptoms, and can be confirmed by transcranial doppler or cerebral angiography. About one third of all people admitted with subarachnoid hemorrhage will have delayed ischemia, and half of those suffer permanent damage as a result. It is possible to screen for the development of vasospasm with transcranial doppler every 24–48 hours. A blood flow velocity of more than 120 centimeters per second is suggestive of vasospasm.

The use of calcium channel blockers, thought to be able to prevent the spasm of blood vessels by preventing calcium from entering smooth muscle cells, has been proposed for the prevention of vasospasm. The oral calcium channel blocker nimodipine improves outcome if administered between the fourth and twenty-first day after the hemorrhage, even if it does not significantly reduce the amount of vasospasm detected on angiography.Other calcium channel blockers and magnesium sulfate have been studied, but are not presently recommended; neither is there any evidence that shows benefit if nimodipine is given intravenously


111.WHICH NSAID HAS LEAST COX 1 AND SELECTIVE COX 2 ACTIVITY LIKE CELECOXIB

A.INDOMETHACIN
B.IBUPROFEN
C.MEFENAMIC ACID
D.DICLOFENAC

ANS:DICLOFENAC


 the primary mechanism responsible for its anti-inflammatory, antipyretic, and analgesic action is inhibition of prostaglandin synthesis by inhibition of cyclooxygenase (COX). It also appears to exhibit bacteriostatic activity by inhibiting bacterial DNA synthesis.

Inhibition of COX also decreases prostaglandins in the epithelium of the stomach, making it more sensitive to corrosion by gastric acid.[citation needed] This is also the main side-effect of diclofenac. Diclofenac has a low to moderate preference to block the COX2-isoenzyme (approximately 10-fold) and is said to have, therefore, a somewhat lower incidence of gastrointestinal complaints than noted with indomethacin and aspirin.

The action of one single dose is much longer (6 to 8 hours) than the very short half-life that the drug indicates.This could be partly because it persists for over 11 hours in synovial fluids.

Diclofenac may also be a unique member of the NSAIDs. There is some evidence that diclofenac inhibits the lipoxygenase pathways,thus reducing formation of the leukotrienes (also pro-inflammatory autacoids). There is also speculation.that diclofenac may inhibit phospholipase A2 as part of its mechanism of action. These additional actions may explain the high potency of diclofenac – it is the most potent NSAID on a broad basis.

There are marked differences among NSAIDs in their selective inhibition of the two subtypes of cyclo-oxygenase, COX-1 and COX-2 Much pharmaceutical drug design has attempted to focus on selective COX-2 inhibition as a way to minimize the gastrointestinal side-effects of NSAIDs like aspirin. In practice, use of some COX-2 inhibitors with their adverse effects has led to massive numbers of patient family lawsuits alleging wrongful death by heart attack, yet other significantly COX-selective NSAIDs such as diclofenac have been well-tolerated by most of the population
110.SHORT ACTING DEPOLARISING MUSCLE RELAXENT

A.SUCCINYL CHOLINE
B.PANCURONIUM
C.ATRACURIUM
D.VENCURONIUM

ANS:SUCCINYL CHOLINE


109.SHORTEST ACTING BETA BLOCKER

A.ESMOLOL
B.SOTALAL
C.BETAXALOL
D.PROPRANOLOL

ANS:ESMOLOL

It is a cardioselective, ultra-short-acting beta blocker that is rapidly metabolized by an esterase in the erythrocyte cytosol to an inactive metabolite. Its half-life is only nine minutes; therefore, one can minimize side effects simply by stopping infusion of the drug.
108.FIRST CHOICE OF ANTIPLATELET

A.ASPIRIN
B.CLOPIDOGREL
C.DYPYRIDAMOLE
D.TICLOPIDINE

ANS:ASPIRIN


Antiplatelet drugs

First choice: ASPIRIN

Aspirin (dispersible tablets) should be used after myocardial infarction, in unstable and stable angina, for primary prevention in high-risk individuals, in patients with a strong family history of bowel cancer, in "low-risk" patients in atrial fibrillation and in thrombotic cerebrovascular disease. There is no conclusive evidence that enteric-coated preparations in general are better tolerated. In acute myocardial infarction, a loading dose of 300mg of dispersible or crushed (if enteric-coated) aspirin is given as early as possible after the onset of symptoms, followed by a daily maintenance dose of 150mg daily for at least one month. Thereafter, a daily maintenance dose of 75 - 150mg dispersible is suggested.

SPECIAL INDICATIONS

Abciximab (IV injection) is a monoclonal antibody, which inhibits platelet aggregation and thrombus formation. It is used by specialists as an adjunct to heparin and aspirin for the prevention of ischaemic complications in high-risk patients undergoing percutaneous transluminal coronary angioplasty (PTCA).

Dipyridamole (m/r capsules) in the modified-release formulation is used for secondary prevention of ischaemic stroke. An injectable form is used for certain diagnostic purposes such as myocardial perfusion imaging.

Clopidogrel (75mg tablets) is a prodrug. One of its metabolites inhibits platelet aggregation by irreversibly and selectively blocking adenosine diphosphate (ADP) at its platelet receptor. It is used in the treatment of ischaemic heart disease. Its use is restricted to patients who are truly intolerant to aspirin. It is contra-indicated in patients at high risk of GI bleeds. It can also be used in combination with aspirin in stented angioplasty, administered for 2 days before and for 4 weeks after the procedure. It is used in combination with aspirin for up to one year for unstable angina or acute coronary syndrome and four weeks in patients with ST segment elevation acute myocardial infarction.
107.BRUCELLOSIS TREATMENT ALL EXCEPT

A.RIFAMPICIN
B.STREPTOMYCIN
C.DOXYCYCLINE 
D.PYRAZINAMIDE

ANS:PYRAZINAMIDE

Brucellosis, also called Bang's disease, Crimean fever, Gibraltar fever, Malta fever, Maltese fever, Mediterranean fever, rock fever, or undulant fever,is a highly contagious zoonosis caused by ingestion of unsterilized milk or meat from infected animals or close contact with their secretions. Transmission from human to human, through sexual contact or from mother to child, is rare but possible.Brucella spp. are small, Gram-negative, non-motile, non-spore-forming, rod shaped (coccobacilli) bacteria. They function as facultative intracellular parasites causing chronic disease, which usually persists for life. Symptoms include profuse sweating and joint and muscle pain


Treatment and prevention
Antibiotics like tetracyclines, rifampicin, and the aminoglycosides streptomycin and gentamicin are effective against Brucella bacteria. However, the use of more than one antibiotic is needed for several weeks, because the bacteria incubate within cells.

The gold standard treatment for adults is daily intramuscular injections of streptomycin 1 g for 14 days and oral doxycycline 100 mg twice daily for 45 days (concurrently). Gentamicin 5 mg/kg by intramuscular injection once daily for seven days is an acceptable substitute when streptomycin is not available or difficult to obtain.Another widely used regimen is doxycycline plus rifampin twice daily for at least six weeks. This regimen has the advantage of oral administration. A triple therapy of doxycycline, with rifampin and cotrimoxazole, has been used successfully to treat neurobrucellosis. Doxycycline is able to cross the blood–brain barrier, but requires the addition of two other drugs to prevent relapse. Ciprofloxacin and cotrimoxazole therapy is associated with an unacceptably high rate of relapse. In brucellic endocarditis, surgery is required for an optimal outcome. Even with optimal antibrucellic therapy, relapses still occur in 5–10 percent of patients with Malta fever.

The main way of preventing brucellosis is by using fastidious hygiene in producing raw milk products, or by pasteurizing all milk that is to be ingested by human beings, either in its unaltered form or as a derivate, such as cheese. Experiments have shown that cotrimoxazol and rifampin are both safe drugs to use in treatment of pregnant women who have brucellosis.

Tuesday, 26 June 2012

106.SSRI ARE ALL EXCEPT

A.FLUVOXAMINE
B.DOSULEPIN
C.PAROXETINE
D.CITALOPRAM

ANS:DOSULEPIN

DOSULEPIN - AN SSNRI

Dosulepin (INN), formerly known as dothiepin (BAN), is a tricyclic antidepressant (TCA). It is sold under the brand names Prothiaden, Dothep, Thaden and Dopress. Dosulepin blocks the reuptake of serotonin and norepinephrine in the brain, thereby increasing their levels. It is believed that this action is responsible for its mood-elevating effects.

105.INTERFERON MOST COMMONLY USED IN TREATMENT OF VIRAL INFECTION

A.ALPHA 2B
B.BETA 2A
C.BETA 2B
D,GAMMA 2A

ANS:ALPHA 2B


Since interferons enhance the immune system in many ways, they are used for many diseases that involve the immune system. For example:

Interferon alfa-2a  is FDA-approved to treat hairy cell leukemia, AIDS-related Kaposi's sarcoma, and chronic myelogenous leukemia.
Interferon alfa-2b is approved for the treatment of hairy cell leukemia, malignant melanoma, condylomata acuminata, AIDS-related Kaposi's sarcoma, chronic hepatitis C, and chronic hepatitis B.
Ribavirin combined with interferon alfa-2b, interferon alfacon-1 , pegylated interferon alfa-2b, or pegylated interferon alpha-2a, all are approved for the treatment of chronic hepatitis C.
Interferon beta-1b  and interferon beta-1a  are approved for the treatment of multiple sclerosis.
Interferon alfa-n3  is approved for the treatment of genital and perianal warts caused by human papillomavirus (HPV).
Interferon gamma-1B is approved for the treatment of chronic granulomatous disease, and severe, malignant osteopetrosis.

Monday, 25 June 2012

104.DMARD MODIFYING DRUG PRIMARILY USED IN RA

A.METHOTREXATE
B.ALLOPURINAL
C.SULFASALAZINE
D.HYDROXY CHLOROQUINE

ANS:METHOTREXARE


Disease-modifying drugs act on the immune system to slow the progression of rheumatoid arthritis. This is why they are called "disease-modifying." Many different medicines can be used as DMARDs in the treatment of rheumatoid arthritis, but some are used more often than others:

Methotrexate is the most commonly used DMARD. This is because it has been shown to work as well or better than any other single medicine. It is also relatively inexpensive and generally safe. Like other DMARDs, methotrexate has side effects; it can cause rash and stomach upset, can be toxic to the liver or bone marrow, and can cause birth defects. In rare cases, it can also cause shortness of breath. Regular blood work is necessary when taking methotrexate. Taking folic acid helps reduce some of the side effects. Methotrexate's biggest advantage could be that it has been shown to be safe to take for long periods of time and can even be used in children.
Plaquenil (hydroxychloroquine) and Azulfidine(sulfasalazine) are used for mild rheumatoid arthritis. They are not as powerful as other DMARDs, but they usually cause fewer side effects. In rare cases, Plaquenil can adversely affect the eyes, and patients taking this medicine should be seen by an ophthalmologist at least once a year.
Minocin (minocycline) is an antibiotic. But it may help RA by stopping inflammation. It can take several months to start working and up to a year before the full effects are known. When taken for long periods, minocycline can cause discoloration of the skin.
Arava (leflunomide) works about as well as methotrexate and can work even better in combination with it. The side effects are similar to methotrexate. Sometimes Arava causes diarrhea and can't be used. Since Arava is known to cause harm to a fetus, women must take special precautions to not get pregnant while on it.

103.MITOTIC INHIBITOR THAT BINDS WITH TUBULIN AND INHIBITS CELL CYCLE

A.VINKA ALKALOIDS
B.ANTIMETABOLITES
C.ANTIBIOTICS
D,

ANS:VINKA ALKALOIDS


Vinca alkaloids are a set of anti-mitotic and anti-microtubule agents that were originally derived from the Periwinkle plant Catharanthus roseus.

Vinca alkaloids are used in the treatment of cancer. They are a class of cell-cycle-specific cytotoxic drugs that work by inhibiting the ability of cancer cells to divide: Acting upon tubulin, they prevent it from forming into microtubules, a necessary component for cellular division.

Vinca alkaloids are now produced synthetically and used as drugs in cancer therapy and as immunosuppressive drugs. These compounds include vinblastine, vincristine, vindesine, and vinorelbine.
102.METHOTREXATE INHIBITS

A.DYHYDROFOLATE REDUCTASE
B.
C.
D.

ANS:DHFR


Methotrexate is thought to affect cancer and rheumatoid arthritis by two different pathways. For cancer, methotrexate allosterically inhibits dihydrofolate reductase (DHFR), an enzyme that participates in the tetrahydrofolate synthesis.The affinity of methotrexate for DHFR is about one thousand-fold that of folate. DHFR catalyses the conversion of dihydrofolate to the active tetrahydrofolate. Folic acid is needed for the de novo synthesis of the nucleoside thymidine, required for DNA synthesis. Also, folate is needed for purine base synthesis, so all purine synthesis will be inhibited. Methotrexate, therefore, inhibits the synthesis of DNA, RNA, thymidylates, and proteins.

Methotrexate acts specifically during DNA and RNA synthesis, and thus it is cytotoxic during the S-phase of the cell cycle. It therefore has a greater toxic effect on rapidly dividing cells (such as malignant and myeloid cells, and gastrointestinal and oral mucosa), which replicate their DNA more frequently, and thus inhibits the growth and proliferation of these noncancerous cells, as well as causing the listed side effects. Facing a scarcity of dTMP, rapidly dividing cancerous cells undergo cell death via thymineless death.
101.IDAZOXAN IS A

A.ALPHA 1 AGONIST
B.ALPHA 2 BLOCKER
C.BETA 3 AGONIST
D,ALPHA 1 BLOCKER

ANS:ALPHA 2 BLOCKER

Idazoxan (INN) is a drug which is used in scientific research. It acts as both a selective α2 adrenergic receptor antagonist, and an antagonist for the imidazoline receptor.Idazoxan has been under investigation as an antidepressant, but it did not reach the market as such. More recently, it is under investigation as an adjunctive treatment in schizophrenia. Due to its alpha-2 receptor antagonism it is capable of enhancing therapeutic effects of antipsychotics, possibly by enhancing dopamine neurotransmission in the prefrontal cortex of the brain, a brain area thought to be involved in the pathogenesis of schizophrenia

PHARMACOLOGY

100.YOHIMBINE IS A

A.ALPHA 1 BLOCKER
B.ALPHA 2 BLOCKER
C.BETA 1 BLOCKER
D.NONE

ANS:ALPHA 2 BLOCKER

Yohimbine blocks the pre- and post-synaptic alpha-2 adrenoceptors. Blockade of post-synaptic alpha-2 adrenoceptors leads to minor corpora cavernosa smooth muscle relaxation. In fact the majority of adrenoceptors in the corpora cavernosa are alpha-1. Blockade of pre-synaptic alpha-2 adrenoceptors leads to increased release of neurotransmitters in the central nervous system and in the corpora cavernosa penis such as nitric oxide, noradrenaline, and dopamine. Whether nitric oxide released in the corpora cavernosa has a relaxing effect, noradrenaline has a much powerful constricting effect by stimulating the unblocked alpha-1 adrenoceptors. Concomitant use of an alpha-1 blocking agent will prevent constriction caused by the increased adrenergic stimulation.

Sunday, 24 June 2012

99.REGARDING LIPOPROTEIN LIPASE ALL ARE TRUE EXCEPT

A.LOCATED ON ENDOTHELIAL CELLS OF CAPILLARIES
B.HYDROLYSE CHYLOMICRONS AND VLDL
C.APO-CII ACTS AS CO FACTOR
D. RELEASED BY ADMINISTRATION OF HEPARIN

ANS:RELEASED BY ADMINISTRATION OF HEPARIN


LPL isozymes are regulated differently depending on the tissue. For example, insulin is known to activate LPL in adipocytes and its placement in the capillary endothelium.The form that is in adipocytes is activated by insulin, whereas that in muscle and myocardium is activated by glucagon and adrenaline. This helps to explain why during fasting, LPL activity increases in muscle tissue and decreases in adipose tissue. After feasting, the opposite occurs


Lipoprotein lipase (LPL) is a member of the lipase gene family, which includes pancreatic lipase, hepatic lipase, and endothelial lipase. It is a water soluble enzyme that hydrolyzes triglycerides in lipoproteins, such as those found in chylomicrons and very low-density lipoproteins (VLDL), into two free fatty acids and one monoacylglycerol molecule. It is also involved in promoting the cellular uptake of chylomicron remnants, cholesterol-rich lipoproteins, and free fatty acids. LPL requires Apo-CII as a cofactor.

LPL is attached to the luminal surface of endothelial cells in capillaries. It is most widely distributed in adipose, heart, and skeletal muscle tissue, as well as in lactating mammary glands.

98.SERATONIN SYNTHESISED FROM

A.DOPAMINE
B.DOBUTAMINE
C.TRYPTOPHAN
D.TYROSINE

ANS:TRYPTOPHAN


97.MICRO RNA IS USEFUL IN

A.DNA SEQUENCING
B.GENE REGULATION
C.RNA SPLICING
D.

ANS:GENE REGULATION


The function of miRNAs appears to be in gene regulation. For that purpose, a miRNA is complementary to a part of one or more messenger RNAs (mRNAs). Animal miRNAs are usually complementary to a site in the 3' UTR whereas plant miRNAs are usually complementary to coding regions of mRNAs. Perfect or near perfect base pairing with the target RNA promotes cleavage of the RNA.This is the primary mode of plant miRNAs. In animals miRNAs more often have only partly the right sequence of nucleotides to bond with the target mRNA. The match-ups are imperfect. For partially complementary microRNAs to recognise their targets, nucleotides 2–7 of the miRNA (its 'seed region'[5][9]) still have to be perfectly complementary. Animal miRNAs inhibit protein translation of the target mRNA(this exists in plants as well but is less Common). MicroRNAs that are partially complementary to a target can also speed up deadenylation, causing mRNAs to be degraded sooner. While degradation of miRNA-targeted mRNA is well documented, whether or not translational repression is accomplished through mRNA degradation, translational inhibition, or a combination of the two is hotly debated. Recent work on miR-430 shows that translational repression is caused by the disruption of translation initiation, independent of mRNA deadenylation.

miRNAs occasionally also cause histone modification and DNA methylation of promoter sites, which affects the expression of target genes
96.INULIN IS A

A.GLUCAN
B.FRUCTAN
C.XYLAN
D.GLYCAN

ANS:FRUCTAN

Inulins are a group of naturally occurring polysaccharides produced by many types of plants. They belong to a class of dietary fibers known as fructans. Inulin is used by some plants as a means of storing energy and is typically found in roots or rhizomes. Most plants that synthesize and store inulin do not store other forms of carbohydrate such as starch.


95.FERRIC CHLORIDE TEST POSITIVE IN

A.ALKAPTONIRIA
B.PHENYL KETONURIA
C.HOMOCYSTINURIA
D.ALBINISM

ANS:PHENYL KETONURIA

a qualitative test for the detection of phenylketonuria; the addition of ferric chloride to urine gives rise to a blue-green color in the presence of phenylketonuria.
94.DNA SEQUENCING DONE BY WHICH METHOD

A.SANGERS
B.EDMONTON
C.
D.

ANS:SANGERS


Chain-termination methods

Because the chain-terminator method (or Sanger method after its developer Frederick Sanger) is more efficient and uses fewer toxic chemicals and lower amounts of radioactivity than the method of Maxam and Gilbert, it rapidly became the method of choice. The key principle of the Sanger method was the use of dideoxynucleotide triphosphates (ddNTPs) as DNA chain terminators.


93.AMINOACIDURIA ASSOCIATED WITH MENTAL RETARDATION ALL EXCEPT

A.PHENYL KETONURIA
B.ALKAPTONURIA
C.HOMOCYSTINURIA
D.MAPPLE SYRUP URINE DISEASE

ANS:ALKAPTONURIA
92.CARDIOMYOPATHY DUE TO DEFECIENCY OF

A.LEAD
B.MOLYBDENUM
C.SELENIUM
D.IRON

ANS:SELENIUM


Selenium deficiency in combination with Coxsackievirus infection can lead to Keshan disease, which is potentially fatal. Selenium deficiency also contributes (along with iodine deficiency) to Kashin-Beck disease.The primary symptom of Keshan disease is myocardial necrosis, leading to weakening of the heart. Kashin-Beck disease results in atrophy, degeneration and necrosis of cartilage tissue causing cardiomyopathy.Keshan disease also makes the body more susceptible to illness caused by other nutritional, biochemical, or infectious diseases.

Selenium is also necessary for the conversion of the thyroid hormone thyroxine into its more active counterpart, triiodothyronine , and as such a deficiency can cause symptoms of hypothyroidism, including extreme fatigue, mental slowing, goiter, cretinism and recurrent miscarriage.
91.LEAD INHIBITS ALL EXCEPT

A.ALA SYNTHASE
B.ALA DEHYDRATASE
C.FERROCHELATASE
D.CO-PORPHYRINOGEN OXIDASE

ANS:ALA SYNTHASE



90.TAY SACHS DISEASE DUE TO DEFECIENCY OF

A.GLUCOCEREBROSIDASE
B.HEXOSAMINIDASE
C.SPHINGOMYELINASE
D.ARYL SULPHATASE

ANS:HEXOSAMINIDASE


Tay–Sachs disease (also known as GM2 gangliosidosis or hexosaminidase A deficiency) is an autosomal recessive genetic disorder. In its most common variant (known as infantile Tay–Sachs disease), it causes a progressive deterioration of mental and physical abilities that commences around six months of age and usually results in death by the age of four. The disease occurs when harmful quantities of cell membrane components known as gangliosides accumulate in the brain's nerve cells, eventually leading to the premature death of the cells. A ganglioside is a form of sphingolipid, which makes Tay–Sachs disease a member of the sphingolipidoses. There is no known cure or treatment.


Tay–Sachs disease is classified into several forms, which are differentiated based on the onset age of neurological symptoms.

Infantile Tay–Sachs disease. Infants with Tay–Sachs disease appear to develop normally for the first six months after birth. Then, as neurons become distended with gangliosides, a relentless deterioration of mental and physical abilities begins. The child becomes blind, deaf, unable to swallow, atrophied, and paralytic. Death usually occurs before the age of four.

Juvenile Tay–Sachs disease. Juvenile Tay–Sachs disease is rarer than other forms of Tay–Sachs, and usually is initially seen in children between two and ten years old. People with Tay–Sachs disease develop cognitive and motor skill deterioration, dysarthria, dysphagia, ataxia, and spasticity; they typically die between five and fifteen years old.

Adult/Late-Onset Tay–Sachs disease. A rare form of this disease, known as Adult-Onset or Late-Onset Tay–Sachs disease, usually has its first symptoms during the 30s or 40s. In contrast to the other forms, late-onset Tay–Sachs disease is usually not fatal as the effects can stop progressing. It is frequently misdiagnosed. It is characterized by unsteadiness of gait and progressive neurological deterioration. Symptoms of late-onset Tay–Sachs - which typically begin to be seen in adolescence or early adulthood – include speech and swallowing difficulties, unsteadiness of gait, spasticity, cognitive decline, and psychiatric illness, particularly a schizophrenia-like psychosis.People with late-onset Tay–Sachs frequently become full-time wheelchair users in adulthood.



Saturday, 23 June 2012

89.HERS DISEASE DUE TO DEFECIENCY OF

A.MUSCLE PHOSPHORYLASE
B.LIVER PHOSPHORYLASE
C.DEBRANCHING ENZYME
D.GLUCOSE  PHOSPHATASE

ANS:LIVER PHOSPHORYLASE


SYNONYMS OF HERS DISEASE
Glycogenosis Type VI
Glycogen Storage Disease VI
Hepatophosphorylase Deficiency Glycogenosis
Liver Phosphorylase Deficiency
Phosphorylase Deficiency Glycogen Storage Disease

Hers disease is a genetic metabolic disorder caused by a deficiency of the enzyme, liver phosphorylase. This enzyme is necessary to break down (metabolize) glycogen, a carbohydrate that is stored in the liver and muscle and used for energy. Deficiency of this enzyme results in the abnormal accumulation of glycogen in the body. Hers disease is one of a group of disorders known as the glycogen storage disorders. It is characterized by enlargement of the liver (hepatomegaly), moderately low blood sugar (hypoglycemia), elevated levels of acetone and other ketone bodies in the blood (ketosis), and moderate growth retardation. Symptoms are not always evident during childhood, and children are usually able to lead normal lives.


88.PYRUVATE DEHYDROGENASE REQUIRES ALL EXCEPT

A.VITAMIN B1
B.VITAMIN B6
C.LIPOIC ACID
D.PANTOTHENIC ACID

ANS:VIT B6


Lipoic acid (LA) is a prosthetic group, which is covalently attached to a specific lysine residue in the lipoyl domains of the of the pyruvate dehydrogenase (PDH) multienzyme complex. Lipoyl-lysine's function consists of two parts: one is allowing the reactant to access three different catalytic sites (swinging arm), and the other one is carrying the substrate.
Chemical properties
Lipoic acid is a sulphur-containing carboxylic acids. The two sulphur atoms are located in a five-membered ring in adjacent positions. In enzymes it is covalently attached to the epsilon-amino group of a lysine residue, where it provides substrate binding and mobility (swinging arm, range about 14Ã…). The five-membered hererocycle can open between the two S-atoms (dihydrolipoyllysine)
Pathways
The best-known enzyme, which depends on lipoic acid is the PDH (pyruvate dehydrogenase) complex, which forms part of the centre of aerobic metabolism: the citrate cycle. [KEGG PATHWAYS]


Pyruvate dehydrogenase requires:
Vitamin B1: Thiamine/TPP, transaldolase.
Vitamin B5: Pantothenic acid, CoA
Vitamin B2: Riboflavin, FADH2
Vitamin B3: Niacin, NAD+






BIOCHEMISTRY

87.ACONITASE WHICH ACTS IN CONVERSION OF CITRATE TO ISOCITRATE CONTAINS

A.IRON
B.MAGANESE
C.ZINC
D.CALCIUM

ANS:IRON

The cytosolic form of aconitase also acts as iron regulatory protein 1. The lower structure, from PDB entry 2ipy, shows how it performs this entirely different function. The iron-sulfur cluster in aconitase is unstable and must be replaced occasionally when it falls out. When iron levels in the cell get low, there isn't enough iron to regenerate the cluster, and the protein shifts to its second function. The protein opens up and grips hairpin loops in a few specific messenger RNA molecules. These include a hairpin at the start of the messenger RNA for ferritin, and five similar hairpins at the end of messenger RNA for the transferrin receptor. When the iron regulatory protein 1 binds, it inhibits the formation of ferritin, so that less iron is locked up in storage, and it enhances construction of the transferrin receptor, so the cell can pick up more transferrin out of the blood, and with it, more iron.
86.TREATMENT OF REFRACTIVE ERROR -THE BEST

A.KERATOPLASTY
B.EXCIMER LASER
C.PRK
D.LASIK

ANS:LASIK
85.SUNFLOWER CATARACT SEEN IN

A.WILSON DISEASE
B.DIABETES MELLITUS
C.ABETALIPOPROTEINEMIA
D.

ANS:WILSON DISEASE




Sunflower Cataract in Wilson's disease
Deposits of copper under the central anterior capsule of the lens have a yellow, brown or red sheen. These changes are reversible with therapy of Penicillamine.


84.BERLINS EDEMA SEEN IN

A.CONCISSION TRAUMA OF EYE
B.INFECTION TO EYE
C.
D

ANS:CONCUSSION TRAUMA OF EYE


Berlin's edema (Commotio Retinae) is a condition caused by blunt injury to the eye.It is characterized by decreased vision in the injured eye a few hours after the injury. Under examination the retina appears opaque and white in colour in the periphery but the blood vessels are normally seen. Usually there is no leakage of fluid and therefore it is not considered a true edema. The choroidal fluorescence in fluorescent angiography is absent. Visual acuity ranges from 20/20 to 20/400.

The prognosis is excellent except in case of complications of choroidal rupture, hemorrhage or pigment epithelial damage. The outcome can be worsened in the case of retinal detachment, atrophy or hyperplasia. Visual field defects can occur. In late cases cystoid macular edema sometimes develops which can further lead to macular destruction. Commotio retinae is usually self limiting and there is no treatment as such. It usually resolves without any complications and sequelae.


83.PUPILLARY REFLEX NOT AFFECTED IN INJURY TO

A.LATERAL GENICULATE BODY
B.CENTRAL CHIASMA
C.CAUDAL CHIASMA
D.OPTIC TRACT

ANS:LATERAL GENICULATE BODY


82.ROUTE OF ADMINISTRATION OF ANTIBIOTICS IN ENDOPHTHALMITIS

A.INTRAVENOUS
B.INTRAVITREAL
C.TOPICAL
D.ORAL

ANS:INTRAVITREAL




81.FIRST SIGN OF PAPILLOEDEMA IN OPTHALMOSCOPE

A.BLURRING OF DISC MARGIN
B.HYPEREMIA OF DISC
C.SPLINTER HEMMORHAGE
D.VENOUS ENGORGEMENT

ANS:VENOUS ENGORGEMENT



The signs of papilledema that are seen using an ophthalmoscope include

venous engorgement (usually the first signs)
loss of venous pulsation
hemorrhages over and / or adjacent to the optic disc
blurring of optic margins
elevation of optic disc
Paton's lines = radial retinal lines cascading from the optic disc
On visual field examination, the physician may elicit an enlarged blind spot; the visual acuity may remain relatively intact until papilledema is severe or prolonged.

80,SIZE OF INCISION IN CATARACT  DEPENDS UPON

A.SIZE OF IOL
B.TYPE OF IOL
C,TYPE OF NUCLEAR INVOLVEMENT
D.

C.TYPE OF NUCLEAR INVOLVEMENT


OPHTHALMOLOGY

79.EFFECT OF PAPILLOEDEMA DEPENTS UPON

A.SIZE
B.SITE
C.RATE OF GROWTH
D.INTRACRANIAL SPREAD

ANS:SIZE

 Papilledema (or papilloedema) is optic disc swelling that is caused by increased intracranial pressure. The swelling is usually bilateral and can occur over a period of hours to weeks. Unilateral presentation is extremely rare. Papilledema is mostly seen as a symptom resulting from another pathophysiological process.

In intracranial hypertension, papilledema most commonly occurs bilaterally. When papilledema is found on fundoscopy, further evaluation is warranted as vision loss can result if the underlying condition is not treated. Further evaluation with a CT or MRI of the brain and/or spine is usually performed. Unilateral papilledema can suggest orbital pathology, such as an optic nerve glioma.

Papilledema may be asymptomatic or present with headache in the early stages. However it may progress to enlargement of the blind spot, blurring of vision, visual obscurations (inability to see in a particular part of the visual field for a period of time) and ultimately total loss of vision may occur.

The signs of papilledema that are seen using an ophthalmoscope include

venous engorgement (usually the first signs)
loss of venous pulsation
hemorrhages over and / or adjacent to the optic disc
blurring of optic margins
elevation of optic disc
Paton's lines = radial retinal lines cascading from the optic disc
On visual field examination, the physician may elicit an enlarged blind spot; the visual acuity may remain relatively intact until papilledema is severe or prolonged.

Diagnosis

Checking the eyes for signs of papilledema should be carried out whenever there is a clinical suspicion of raised intracranial pressure, and is recommended in newly onset headaches. This may be done by ophthalmoscopy or fundus photography, and possibly slit lamp examination.

Causes

Raised intracranial pressure: brain tumor, pseudotumor cerebri or cerebral venous sinus thrombosis, Intracerebral hemorrhage
Respiratory failure
Hypotonia
Accutane (Isotretinoin), which is a powerful derivative of Vitamin A, rarely causes Papilledema.
Hypervitaminosis A, in some people who take megadoses of nutritional supplements and vitamins.
Hyperammonemia, elevated level of ammonia in blood (including cerebral edema/intracranial pressure)
Guillain-Barré syndrome due to elevated protein levels
Foster Kennedy syndrome (FKS)
Chiari Malformation
Tumors of the frontal lobe
Acute Mountain Sickness and High Altitude Cerebral Oedema
Lyme disease (Lyme meningitis specifically, when the bacterial infection is in the central nervous system, causing increased intracranial pressure).
Malignant Hypertension
Medulloblastoma
Orbital A.Ocular venous drainage block:central retinal venous block, cavernous sinus trombosis B.Local lesion:optic neuritis, ischemia of the nerve head, toxin (methanol), infiltration of the disc by glioma,sarcoidosis and lymphoma
Acute Lymphocytic Leukemia (caused by infiltration of the retinal vessels by immature leukocytes)
Long periods of weightlessness (microgravity) for males


Pathophysiology
As the optic nerve sheath is continuous with the subarachnoid space of the brain (and is regarded as an extension of the central nervous system), increased pressure is transmitted through to the optic nerve. The brain itself is relatively spared from pathological consequences of high pressure. However, the anterior end of the optic nerve stops abruptly at the eye. Hence the pressure is asymmetrical and this causes a pinching and protrusion of the optic nerve at its head. The fibers of the retinal ganglion cells of the optic disc become engorged and bulge anteriorly. Persistent and extensive optic nerve head swelling, or optic disc edema, can lead to loss of these fibers and permanent visual impairment.

Treatment

The treatment depends largely on the underlying cause. However, the root cause of papilledema is the increased intracranial pressure (ICP). This is a dangerous sign, indicative of a brain tumor, CNS inflammation or idiopathic intracranial hypertension (IIH) that may become manifest in the near future.

Thus, a biopsy is routinely performed prior to the treatment in the initial stages of papilledema to detect whether a brain tumor is present. If detected, laser treatment, radiation and surgeries can be used to treat the tumor.

To decrease ICP, medications can be administered by increasing the absorption of Cerebrospinal fluid (CSF), or decreasing its production. Such medicines include diuretics like acetazolamide and lasix. These diuretics, along with surgical interventions, can also treat IIH. In IIH, weight loss (even a loss of 10-15%) can lead to normalization of ICP.

Meanwhile, steroids can reduce inflammation (if this is a contributing factor to increased ICP), and may help to prevent vision loss. However, steroids have also been known to cause increased ICP, especially with a change in dosage. However, if a severe inflammatory condition exist, such as multiple sclerosis, steroids with anti-inflammatory effects such as Methylprednisolone and prednisone can help.

Other treatments include repeated lumbar punctures to remove excess spinal fluid in the cranium. The removal of potentially causative medicines including tetracyclines and vitamin A analogues may help decrease ICP, however this is only necessary if the medication is truly felt to contribute to ICP increase.


78.NERVE COMMONLY INVOLVED IN MALIGNANT OTITIS EXTERNA

A.FACIAL
B.TRIGEMINAL
C.ABDUCENT
D.VESTIBULO COCHLEAR

ANS:FACIAL


Malignant otitis externa is  a inflammatory disorder involving the external auditory canal caused by psuedomonas organism.  Majority of these patients are elderly diabetics.  This condition is termed as malignant otitis externa because of its propensity to cause complications.  Hence the term malignant must not be constured in a histological sense.


Pseudomonas aeruginosa is a gram negative aerobe with polar flagella.  It is found on the skin.  It invariably behaves like an opportunistic pathogen.  The pathogenicity of this organism is due to ability to secrete exotoxin and various enzymes like lecithinase, lipase, esterase, protease etc.  Since this organism is cloathed by a mucoid layer it is resistant to digestion by macrophages.


Clinical features:
The patient gives history of trivial trauma to the ear often by ear buds, followed by pain and swelling involving the external auditory canal.  Pain is often the common initial presentation.  It is often severe, throbbing and worse during nights.  It needs increasing doses of analgesics.  On examination granulation tissue may be seen occupying the external canal. It often begins at the bony cartilagenous junction of the external canal.  Discharge eminating from the external canal is scanty and foul smelling in nature.  When the discharge is foul smelling it indicates the onset of osteomyelitis.  Ironically the patient does not have fever or other constitutional symptoms.

Otoscopy: Reveals granulation tissue at the bony cartilagenous junction.  The ear drum is usually normal.  The external auditory canal skin is soggy and edematous.
Cranial nerve palsies are common when the disease affects the skull base.  The facial nerve is the most common nerve affected.  As the disease progresses the lower three cranial nerves are affected close to the jugular foramen.
Intracranial complications like meningitis and brain abscess are also known to occur.


77.CART WHEEL APPEARENCE ON TYMPANIC MEMBRANE

A.ASOM
B.CSOM
C.SUPPURATIVE OTITIS MEDIA
D.OTOSCELOSIS

ANS:ASOM


Stages of A.S.O.M.

1. Stage of Hyperaemia 

Synonym: Stage of tubal occlusion
Mild earache
T.M. retracted in early stage
T.M. congested later stage
Cartwheel appearance: radiating blood vessels from handle of malleus

2. Stage of Exudation 

High fever
Severe earache
Deafness
Marked congestion + bulging of T.M.
Mastoid tenderness
P.T.A.: high frequency conductive deafness
               due to mass effect of pus

Nipple sign (impending perforation)

Localized protrusion of tympanic membrane due to destruction of fibrous layer by continuous pressure of pus

3. Stage of Suppuration 

Symptoms:

Ear discharge (blood-stained  purulent)
Increased deafness
Decreased fever
Decreased earache
Blood stained otorrhoea

Signs & Investigations

Pinhole perforation + otorrhoea
Light house sign: intermittent reflection of light
Decreased mastoid tenderness
High (mass effect) + low frequency (stiffness effect of thick periosteum) Conductive deafness
Clouding of air cells in mastoid X-ray
Light House sign

4. Stage of Coalescent Mastoiditis 


Otorrhoea > 2 weeks, otalgia & deafness
Mastoid reservoir sign: pus fills up on mopping
Sagging of postero-superior canal wall caused by peri-osteitis due to pus in adjacent mastoid antrum
Ironed out appearance of skin over mastoid due to thickened periosteum
Mastoid cavity in X-ray & CT scan

ENT

76.SNHL.SYNCOPE,ARRYTHMIA SEEN IN

A.PENDRED SYNDROME
B.USHER'S SYNDROME
C.JERVELL LANGE NIELSON SYNDROME
D.

ANS:JERVELL LANGE NIELSON SYNDROME

Jervell and Lange-Nielsen syndrome is a condition that causes profound hearing loss from birth and a disruption of the heart's normal rhythm (arrhythmia). This disorder is a form of long QT syndrome, which is a heart condition that causes the heart (cardiac) muscle to take longer than usual to recharge between beats. Beginning in early childhood, the irregular heartbeats increase the risk of fainting (syncope) and sudden death.

Friday, 22 June 2012

75.GENERAL ANESTHETIC WITH LEAST EFFECT ON HEART

A.ETOMIDATE
B.KETAMINE
C.THIOPENTONE
D.

ANS:ETOMIDATE


Heart Rate
Heart Rhythm
Contractility
Propofol
no significant change to decreases at higher doses
little effect, potential benefit in slowing heart rate in some fast arrythmias
little effect to ability to decrease cardiac output at higher doses
Pentothal
increases by 10-40%
potential disruption, prolong QT interval
decreases cardiac output
Etomidate
mimimal effect
minimal effect
minimal effect
Ketamine
increases
no specific changes
increases
Fentanyl
decreases
variable, but overall may prevent some arrhythmias
little change to mild increase
Morphine
decreases
variable, but overall may prevent some arrhythmias
uncertain, may be similar to fentanyl
Succinylcholine
variable, usually decreases especially at usual doses and after a second dose
increases likelihood of several kinds of arrhythmias
decreases at usual doses
Halothane
no change to little change
increases likelihood of arrythmias
decreases
Isofllurane
decreases
potential changes, but of unknown significance
decreases
Sevoflurane
decreases
potential changes, but of unknown significance
decreases