186.ZONKER'S DEGENERATION SEEN IN

A.STARVATION
B.ELECTROCUTION
C.HYDROCUTION
D.SYRINGOMYELIA

ANS:STARVATION

185.UNILATERAL ASTEREXIS SEEN IN

A.HEPATIC FAILURE
B.RENAL FAILURE
C.PARIETAL LESION
D.TEMPORAL LESION

ANS:PARIETAL LESION

These are most commonly due to focal brain lesions in the genu and anterior portion of the internal capsule or ventrolateral thalamus. Lesions in the midbrain, parietal cortex, and medial frontal cortex may also cause unilateral asterixis

184.THYROID TUMOR SECRETING ACTH CAUSING CUSHING SYNDROME

A.ANAPALSTIC
B.PAPILLARY
C.MEDULLARY
D.FOLLICULAR

ANS:MEDULLARY

Ectopic ACTH Syndrome

Some benign or, more often, cancerous tumors that arise outside the pituitary can produce ACTH. This condition is known as ectopic ACTH syndrome. Lung tumors cause more than half of these cases, and men are affected three times more often than women. The most common forms of ACTH-producing tumors are small cell lung cancer, which accounts for about 13 percent of all lung cancer cases, and carcinoid tumors-small, slow-growing tumors that arise from hormone-producing cells in various parts of the body. Other less common types of tumors that can produce ACTH are thymomas, pancreatic islet cell tumors, and medullary carcinomas of the thyroid.

183.BIRBECK GRANULES ARE SEEN IN

A. LANGERHANS CELLS
B.HISTIOCYTES
C.MAST CELLS
D.PHAGOCYTES

ANS: LANGERHANS CELLS

BIRBECK GRANULES - Tennis racket shaped structures found in Langerhan's cells in histiocytosis X (Langerhan's cell histiocytosis) which includes eosinophilic granuloma, Letterer-Siwe disease and Hand-Schuller-Christian disease.

182.AUTONOMIC INSTABILITY ALL EXCEPT

A.SCHIZOPRENIA
B.KORSAKOFF'S PSYCHOSIS
C.DELERIUM TREMENS
D.WERNICKES ENCEPHALOPATHY

ANS:WERNICKE'S ENCEPHALOPATHY

181.RIVASTIGMINE AND DONEPEZIL ARE USED IN

A.DEPRESSION
B.DYSPHONIA
C.DELERIUM
D.DEMENTIA

ANS:DEMENTIA

Psychoanaleptics: Antidementia agents (N06D)
Anticholinesterases	Cymserine   Donepezil Galantamine   Huperzine A (Huperzia serrata)   Ladostigil   Rivastigmine   Tacrine
Others	Bifemelane   Bilobalide (Ginkgo biloba)   Cerlapirdine   Ensaculin   Latrepirdine   Lecozotan   Leteprinim   Memantine   Semagacestat

180.HLA B27 RELATED TO

A.ANKYLOSING SPONDYLITIS
B.BEHCETS SYNDROME
C.CERVICAL RIB
D.DARIERS DISEASE

ANS:ANKYLOSING SPONDYLITIS

A positive test means HLA-B27 is present. It suggests a greater-than-average risk for developing or having certain autoimmune disorders. An autoimmune disorder is a condition that occurs when the immune system mistakenly attacks and destroys healthy body tissue.

An abnormal result may be caused by:

• Ankylosing spondylitis
• Arthritis related to Crohn's disease
• Reactive arthritis
• Sacroiliitis (inflammation of the sacroiliac joint)
• Uveitis

179.ST ELEVATION IN LEAD II,III,aVF

A.AWMI
B.IWMI
C.PWMI
D.ALWMI

ANS:IWMI

INFARCT LOCATION:	ST ELEVATION FOUND IN:
Anterior - Septal	V1, V2, V3, and V4 -- 0.2mV or more in leads
Posterior	V1, and V2 -- 0.2mV or more in leads
Inferior	II, III, and aVF -- 0.1mV or more in 2 leads
High Lateral	I, and aVL -- 0.1mV or more in 2 leads
Low Lateral	V5, and V6 -- 0.1mV or more in 2 leads

178.BROWN SEQUARD SYNDROME

A.C/L SPINOTHALAMIC INVOLVEMENT
B.C/L POSTERIOR COLUMN INVOLVEMENT
C.C/L LOSS OF MOTOR POWER
D.IPSILATERAL SENSORY LOSS

ANS:C/L SPINOTHALAMIC INVOLVEMENT


Pure Brown-Séquard syndrome is associated with the following:

Interruption of the lateral corticospinal tracts
Ipsilateral spastic paralysis below the level of the lesion
Babinski sign ipsilateral to lesion
Abnormal reflexes and Babinski sign may not be present in acute injury.
Interruption of posterior white column - Ipsilateral loss of tactile discrimination, vibratory, and position sensation below the level of the lesion
Interruption of lateral spinothalamic tracts: Contralateral loss of pain and temperature sensation. This usually occurs 2-3 segments below the level of the lesion.

177.COLD INDUCED SHOCK REFRACTORY TO DOPAMINE,DOBUTAMINE

A.NOR EPINEPHRINE
B.EPINEPHRINE
C.STEROID
D.PDE INHIBITOR

ANS:EPINEPHRINE

176.METABOLIC SYNDROME ALL EXCEPT

A.INCREASED TGL
B.HDL
C.LDL
D.INCRESED BP

ANS:LDL


According to the American Heart Association and the National Heart, Lung, and Blood Institute, metabolic syndrome is present if you have three or more of the following signs:

• Blood pressure equal to or higher than 130/85 mmHg
• Fasting blood sugar (glucose) equal to or higher than 100 mg/dL
• Large waist circumference (length around the waist):

1. Men - 40 inches or more
2. Women - 35 inches or more

• Low HDL cholesterol:

1. Men - under 40 mg/dL
2. Women - under 50 mg/dL

• Triglycerides equal to or higher than 150 mg/dL

175.METFORMIN

A.CAUSES INSULIN RELEASE
B.INCREASE INSULIN SENSITIVITY
C.ACTS AS INSULIN SECRETAGOGUE
D.INHIBITS GLUCOSE ABSORPTION

ANS:INCREASE INSULIN SENSITIVITY


Metformin improves hyperglycemia primarily by suppressing glucose production by the liver (hepatic gluconeogenesis). The "average" person with type 2 diabetes has three times the normal rate of gluconeogenesis; metformin treatment reduces this by over one third.Metformin activates AMP-activated protein kinase (AMPK), an enzyme that plays an important role in insulin signaling, whole body energy balance, and the metabolism of glucose and fats;activation of AMPK is required for metformin's inhibitory effect on the production of glucose by liver cells.Research published in 2008 further elucidated metformin's mechanism of action, showing activation of AMPK is required for an increase in the expression of SHP, which in turn inhibits the expression of the hepatic gluconeogenic genes PEPCK and Glc-6-Pase.Metformin is frequently used in research along with AICAR as an AMPK agonist. The mechanism by which biguanides increase the activity of AMPK remains uncertain; however, research suggests that metformin increases the amount of cytosolic AMP (as opposed to a change in total AMP or total AMP/ATP).

In addition to suppressing hepatic glucose production, metformin increases insulin sensitivity, enhances peripheral glucose uptake (by phosphorylating GLUT-4 enhancer factor), increases fatty acid oxidation,and decreases absorption of glucose from the gastrointestinal tract. Increased peripheral utilization of glucose may be due to improved insulin binding to insulin receptors.AMPK probably also plays a role, as metformin administration increases AMPK activity in skeletal muscle. AMPK is known to cause GLUT4 deployment to the plasma membrane, resulting in insulin-independent glucose uptake. Some metabolic actions of metformin do appear to occur by AMPK-independent mechanisms; a 2008 study found "the metabolic actions of metformin in the heart muscle can occur independent of changes in AMPK activity and may be mediated by p38 MAPK- and PKC-dependent mechanisms."

174.ANGIOGNESIS FACTOR INVOLVED ALL EXCEPT

A.PDGF
B.HGF
C.FGF
D.VEGF

ANS:HGF

173.BLOCK AT NEUROMUSCULAR JUNCTION

A.FATIGUE
B.FASCICULATION
C.FLACCIDITY
D.

ANS:FLACCIDITY


A block or decrease in the transmission across the neuromuscular junction can cause a complete or relative loss of muscle function. It can result from neuromuscular junction diseases or be intentionally induced with neuromuscular blocking drugs. It can also be a side effect of other drugs that are generally not classified as neuromuscular blocking drugs, such as some anesthetic drugs

The degree of neuromuscular block may be estimated by Bromage score, which originally had four grades designate with the Roman numerals I until IV, but later complemented by Breen et al. with an inverse grading with Hindu-Arabic numerals:

Bromage score
       Grade                                         Criteria                                       Approximatedegree of block
IV              1       Complete block, inability to move feet or knees                                            100%
III              2       Almost complete block, ability to move feet only, with inability to flex knees     66%
II              3       Partial block, ability to flex knees                                                                     33%
                     4       Detectable weakness of hip flexion while supine, ability of full flexion of knees
                     5       No detectable weakness of hip flexion while supine
I              6       Free movement of legs and feet, ability to perform partial knee bend                 0%


In unconscious patients, such as during anesthesia, neural block can be assessed by a "train-of-four" by stimulating muscles from surface electrodes.

172.IN BOTULINISM IT BLOCKS

A.POST SYNAPTIC INHIBITION
B.INHIBIT ACETYL CHOLINE RELEASE
C.INHIBITS ACETYL CHOLINE ESTERASE
D.

ANS:INHIBIT RELEASE OF ACETYL CHOLINE

There are seven serologically distinct toxin types, designated A through G. Additionally, six of the seven toxin types have subtypes with five subtypes of BoNT A having been described. The toxin is a two-chain polypeptide with a 100-kDa heavy chain joined by a disulfide bond to a 50-kDa light chain. This light chain is an enzyme (a protease) that attacks one of the fusion proteins (SNAP-25, syntaxin or synaptobrevin) at a neuromuscular junction, preventing vesicles from anchoring to the membrane to release acetylcholine. By inhibiting acetylcholine release, the toxin interferes with nerve impulses and causes flaccid (sagging) paralysis of muscles in botulism, as opposed to the spastic paralysis seen in tetanus.

171.PTH RELEASING TUMOR IS

A.SMALL CELL CA OF LUNG
B.SQUAMOUS CELL CA OF LUNG
C.CLEAR CELL CA
D.

ANS:SQUAMOUS CELL CA OF LUNG


Squamous Cell Lung Cancer
This type of lung cancer commonly develops from the bronchus -- a branch of the main airway to the lungs, and with further growth, this cancer invades the lungs; it releases PTHrP, a protein that behaves like the parathyroid hormone. The parathyroid hormone is released by the parathyroid glands; they promote the increased breakdown of bone to release calcium into the blood. Increase PTHrP release from squamous cell cancer of the lungs, results in hypercalcemia, or high blood calcium.

Small Cell Lung Cancer
Small cell lung cancer is the most aggressive type of lung cancer; It commonly originates within the lungs. The cancer releases antidiuretic hormone, or ADH, which acts in the kidneys. ADH is normally released when blood volume is low, but with small cell lung cancer, ADH is constantly released. The action of ADH results in the direct reabsorption of water from the kidneys. Increased water reabsorption from the kidneys results in water retention.

170.LEONINE FACIES IS SEEN IN

A.EARLY CHRONIC LEPROMATOUS LEPROSY
B.LATE CHRONIC LEPROMATOUS LEPROSY
C.LATE CHRONIC TUBERCULOID LEPROSY
D.EARLY CHRONIC TUBERCULOID LEPROSY

ANS: LATE CHRONIC LEPROMATOUS LEPROSY



Lepromatous

Early nerve involvement may go unnoticed
Numerous lesions of all kinds, plaques, macules, papules and nodules
Early symptoms include nasal stuffiness, discharge and bleeding, and swelling of the legs and ankles
Left untreated, the following problems may occur:

• Skin thickens over forehead (leonine facies), eyebrows and eyelashes are lost, nose becomes misshapen or collapses, ear lobes thicken, upper incisor teeth fall out
• Eye involvement causing photophobia (light sensitivity), glaucoma and blindness
• Skin on legs thickens and forms ulcers when nodules break down
• Testicles shrivel causing sterility and enlarged breasts (males)
• Internal organ infection causing enlarged liver and lymph nodes
• Voice becomes hoarse due to involvement of the larynx
• Slow scarring of peripheral nerves resulting in nerve thickening and sensory loss. Fingers and toes become deformed due to painless repeated trauma.

169.MELD SCORE,ALL ARE PRESENT EXCEPT

A.ALBUMIN
B.BILIRUBIN
C.INR
D.CREATININE

ANS:ALBUMIN


MELD uses the patient's values for serum bilirubin, serum creatinine, and the international normalized ratio for prothrombin time (INR) to predict survival. It is calculated according to the following formula:

MELD = 3.78[Ln serum bilirubin (mg/dL)] + 11.2[Ln INR] + 9.57[Ln serum creatinine (mg/dL)] + 6.43

168.ACTIVATION OF PROCARCINOGENS DONE BY

A.OXIDOREDUCTASE
B.CYP450
C.XANTHINE OXIDASE
D.

ANS:CYP450

Enzymatic transformation of most chemical carcinogens is requisite to the formation of electrophiles that cause genotoxicity, and the cytochrome P450 (P450) enzymes are the most prominent enzymes involved in such activation reactions.

167.AROMATASE CONVERTS

A.TESTOSTERONE TO ESTRADIAL
B.ESTROGEN TO TERSTOSTERONE
C.
D.

ANS:TESTOSTERONE TO ESTRADIAL

166.ALL ARE PRESENT IN ADDISON DISEASE EXCEPT

A.HYPERTENSION
B.PIGMENTATION
C.LOW SODIUM
D.HIGH POTASSIUM

ANS:HYPERTENSION


Clinical signs

• Low blood pressure that falls further when standing (orthostatic hypotension)
• Most people with primary Addison's have darkening (hyperpigmentation) of the skin, including areas not exposed to the sun; characteristic sites are skin creases (e.g. of the hands), nipple, and the inside of the cheek (buccal mucosa); also, old scars may darken. This occurs because melanocyte-stimulating hormone (MSH) and adrenocorticotropic hormone (ACTH) share the same precursor molecule, pro-opiomelanocortin (POMC). After production in anterior pituitary gland, POMC gets cleaved into gamma-MSH, ACTH and beta-lipotropin. The subunit ACTH undergoes further cleavage to produce alpha-MSH, the most important MSH for skin pigmentation. In secondary and tertiary forms of Addison's, skin darkening does not occur.
• Medical conditions, such as type I diabetes, autoimmune thyroid disease (Hashimoto's thyroiditis and goiter) and vitiligo often occur together with Addison's (often in the setting of autoimmune polyendocrine syndrome). Hence, symptoms and signs of any of the former conditions may also be present in the individual with Addison's.
• The occurrence of Addison's disease in someone who also has Hashimoto's thyroiditis is called Schmidt syndrome.

Addisonian crisis

An "Addisonian crisis" or "adrenal crisis" is a constellation of symptoms that indicate severe adrenal insufficiency. This may be the result of either previously undiagnosed Addison's disease, a disease process suddenly affecting adrenal function (such as adrenal hemorrhage), or an intercurrent problem (e.g. infection, trauma) in someone known to have Addison's disease. It is a medical emergency and potentially life-threatening situation requiring immediate emergency treatment.

Characteristic symptoms are:

Sudden penetrating pain in the legs, lower back or abdomen
Severe vomiting and diarrhea, resulting in dehydration
Low blood pressure
Syncope (loss of consciousness and ability to stand)
Hypoglycemia (reduced level of blood glucose)
Confusion, psychosis, slurred speech
Severe lethargy
Hyponatremia (low sodium level in the blood)
Hyperkalemia (elevated potassium level in the blood)
Hypercalcemia (elevated calcium level in the blood)
Convulsions
Fever

165.CONN'S SYNDROME ALL ARE ABSENT EXCEPT

A.LOW POTASSIUM
B.LOW SODIUM
C.ACIDOSIS
D.HIGH RENIN

ANS:LOW POTASSIUM


Aldosterone enhances exchange of sodium for potassium in the kidney, so increased aldosteronism will lead to hypernatremia (elevated sodium level) and low blood potassium known as hypokalemia. Once the potassium has been significantly reduced by aldosterone, a sodium/hydrogen pump in the nephron becomes more active, leading to increased excretion of hydrogen ions and further exacerbating the elevated sodium level resulting in a further increase in hypernatremia. The hydrogen ions exchanged for sodium are generated by carbonic anhydrase in the renal tubule epithelium, causing increased production of bicarbonate. The increased bicarbonate and the excreted hydrogen combine to generate a metabolic alkalosis.

The high pH of the blood makes calcium less available to the tissues and causes symptoms of hypocalcemia (low calcium levels).

The sodium retention leads to plasma volume expansion and elevated blood pressure. The increased blood pressure will lead to an increased glomerular filtration rate and cause a decrease in renin release from the granular cells of the juxtaglomerular apparatus in the kidney. If a patient is thought to suffer from primary hyperaldosteronism, the aldosterone:renin activity ratio is used to assess this. The decreased renin levels and in turn the reactive down-regulation of angiotensin II are thought to be unable to down-regulate the constitutively formed aldosterone, thus leading to an elevated [plasma aldosterone:plasma renin activity] ratio (lending the assay to be a clinical tool for diagnostic purposes).

Aside from hypertension, other manifesting problems include myalgias, weakness, and chronic headaches. The muscle cramps are due to neuron hyperexcitability seen in the setting of hypocalcemia, muscle weakness secondary to hypoexcitability of skeletal muscles in the setting of low blood potassium (hypokalemia), and headaches which are thought to be due to both electrolyte imbalance (hypokalemia) and hypertension.

Secondary hyperaldosteronism is often related to decreased cardiac output, which is associated with elevated renin levels.

164.PURE RIGHT VENTRICULAR FAILURE SEEN IN

A.COR PULMONALE
B.VSD
C.ASD
D.TOF

ANS:COR PULMONALE


Cor pulmonale or pulmonary heart disease is enlargement of the right ventricle of the heart as a response to increased resistance or high blood pressure in the lungs (pulmonary hypertension).
Chronic cor pulmonale usually results in right ventricular hypertrophy (RVH), whereas acute cor pulmonale usually results in dilatation.
Hypertrophy is an adaptive response to a long-term increase in pressure. Individual muscle cells grow larger (in thickness) and change to drive the increased contractile force required to move the blood against greater resistance.
Dilatation is a stretching (in length) of the ventricle in response to acute increased pressure, such as when caused by a pulmonary embolism.
To be classified as cor pulmonale, the cause must originate in the pulmonary circulation system. Two major causes are vascular changes as a result of tissue damage (e.g. disease, hypoxic injury, chemical agents, etc.), and chronic hypoxic pulmonary vasoconstriction. RVH due to a systemic defect is not classified as cor pulmonale.
If left untreated, cor pulmonale can lead to right-heart failure and death.

163.BREATH HOLDING SPELLS PRESENT IN ALL EXCEPT

A.SEIZURE
B.ARRYTHMIA
C.TOF
D.BRAIN MALFORMATION

ANS:BRAIN MALFORMATION

Most spells are a response to strong emotions (like being angry, scared, or frustrated), but some are caused by more serious medical conditions, like a seizure disorder, syncope, cardiac malformation (TOF),heart arrhythmia, or iron deficiency anemia. Treating these conditions may help reduce the frequency of breath-holding spells.

MEDICINE

162.TREE BARK APPEARENCE SEEN IN

A.SYPHILITIC ANEURYSM
B.ATHEROSCLEROTIC ANEURYSM
C.BERRY ANEURYSM
D.AORTIC ANEURYSM

ANS:SYPHILITIC ANEURYSM

SYPHILITIC

Before the advent of antibiotics, syphilis was the most common cause of aneurysms of the ascending aorta. Syphilitic infection produces aortitis and an obliterative endarteritis. Destruction of the vasa vasorum causes degeneration of the medial elastic fibers.  The intima in syphilitic aortas classically is described as having a “tree-bark” appearance, with wrinkles, ridges, and pearly plaques. The disease most commonly affects the ascending aorta and aortic arch . There may be patchy or diffuse involvement of the aorta, and both saccular and fusiform aneurysms are observed. Inflammatory changes surrounding the coronary ostia may lead to clinically significant coronary arterial obstruction. Anti-syphilitic drug therapy does not reverse the vascular lesions or consequences. Patients with syphilis commonly have other risk factors associated with aneurysm formation; thus, aneurysms in patients who are seropositive for syphilis may not be caused by infection with Treponema pallidum.

161.WORM INFESTATION INDEX IS

A.CHANDLERS INDEX
B.SULLIVANS INDEX
C.BROCAS INDEX
D.WORM INDEX

ANS:CHANDLERS INDEX

Chandler’s index is used to identify the importance of hookworm infestation as a public health problem in a community. It is calculated based on average number of hookworm eggs / gram of stool.

Average no. of hookworm eggs/gm of stool	Significance of hookworm infestation
<200	Not much significance
200-250	Potential danger
250-300	Minor public health problem
>300	Major public health problem

160."ROAD TO HEALTH" CHART DESIGNED BY

A.JOHN SNOW
B.FRIEDMAN
C.DAVID MORLEY
D.SIGMEND FREUD

ANS:DAVID MORLEY

159.INCUBATION PERIOD OF PRIMARY SYPHILIS

A.7-28 DAYS
B.3-10 DAYS
C.7-21 DAYS
D.9-90 DAYS

ANS:9-90 DAYS

After becoming infected with syphilis, there is an incubation period between of 9 to 90 days (the average being around 21 days) before the first signs and symptoms of the disease appear. Each stage of syphilis has characteristic symptoms, but any particular sign may or may not be present.

158.BMI = HEIGHT-100 IS

A.BROCA'S INDEX
B.QUETLET INDEX
C.PONDERAL INDEX
D.SULLIVAN'S INDEX

ANS:BROCAS INDEX

BROCA’S INDEX:


IBW FOR ADULT MALES = Height in Centimeters minus 100 


IBW FOR ADULT FEMALES = (Height in Centimeters minus 100) minus 10 % of (Height in centimeters.

157.LIQUID WASTE DISCARDED BY

A.INERTIZATION
B.DUMPING
C.AUTOCLAVE
D.NEUTRALIZE WITH HYPOCHLORITE AND DISPOSE VIA SEWAGE

ANS:NEUTRALIZE WITH HYPOCHLORITE AND DISPOSE VIA SEWAGE

156.ICDS STARTED IN YEAR

A.1975
B.1984
C.1992
D.2000

ANS:1975

ICDS was first launched in 1975 in accordance to the National Policy for Children in India. Over the years it has grown into one of the largest integrated family and community welfare schemes in the world. Given its effectiveness over the last few decades, Government of India has committed towards ensuring universal availability of the programme

155.AGE OF MIDDLE ADOLESENCE

A.10-12 YRS
B.12-14 YRS
C.14-16 YRS
D.16-18 YRS

ANS:14-16 YRS

Middle Adolescence Approximately 14 – 18 years of age

Puberty is completed Physical growth slows for girls, continues for boys

Continued growth of capacity for abstract thought Greater capacity for setting goals Interest in moral reasoning Thinking about the meaning of life

Intense self-involvement, changing between high expectations and poor self-concept Continued adjustment to changing body, worries about being normal Tendency to distance selves from parents, continued drive for independence Driven to make friends and greater reliance on them, popularity can be an important issue Feelings of love and passion Increased sexual interest

154.INCUBATION PERIOD OF TYPHOID

A.3-30 DAYS
B.17-18 DAYS
C.2-4WKS
D.10-24 DAYS

ANS:3-30 DAYS

CLINICAL PRESENTATION

The incubation period of typhoid and paratyphoid infections is 6–30 days. The onset of illness is insidious, with gradually increasing fatigue and a fever that increases daily from low-grade to as high as 102°F–104°F (38°C–40°C) by the third to fourth day of illness. Headache, malaise, and anorexia are nearly universal. Hepatosplenomegaly can often be detected. A transient, macular rash of rose-colored spots can occasionally be seen on the trunk. Fever is commonly lowest in the morning, reaching a peak in late afternoon or evening. Untreated, the disease can last for a month. The serious complications of typhoid fever generally occur after 2–3 weeks of illness and may include intestinal hemorrhage or perforation, which can be life threatening.

153.CHLORINATION OF WATER DOESN'T KILLS

A.POLIO
B.HEPATITIS A
C.VIBRIO CHOLERA
D.SALMONELLA TYPHI

ANS:HEPATITIS A

Chlorination is the application of chlorine to wastewater to accomplish some definite purpose.  In this lesson, we will be concerned with the application of chlorine for the purpose of disinfection, but you should be aware that chlorination can also be used for odor control and for other purposes.  

Chlorine is a well known and economical form of disinfection.  However, chlorination has numerous disadvantages.  Chlorination can produce trihalomethanes, can slow the nervous system in people, can produce chlorinated hydrocarbons which are considered health hazards, and can be corrosive.  

The main types of chlorine used to disinfect wastewater are explained below.  All types of chlorine will kill bacteria and some viruses, E-coli, Salmonella, Typhoid, Cholera, Shingella, and Polio.  But only chlorine dioxide will effectively kill Cryptosporidium, Giardia, protozoans, and some viruses

152.TEMPORAL ASSOCIATION BETWEEN CAUSE AND EFFECT IDENTIFIED BY

A.RELATIVE RISK
B.SPECIFICITY OF ASSOCIATION
C.SENSITIVITY OF ASSOCIATION
D.ATTRIBUTABLE RISK

ANS:RELATIVE RISK

151.MOST HEAT SENSITIVE VACCINE

A.BCG
B.DPT
C.OPV
D.MEASLES

ANS:OPV

150.STATE MOST PREVALENT WITH HIV

A.TAMILNADU
B.NAGALAND
C.MAHARASTRA
D.MANIPUR

ANS:MANIPUR


ndia has a population of one billion, around half of whom are adults in the sexually active age group. The first AIDS case in India was detected in 1986 and since then HIV infection has been reported in all states and union territories.

The spread of HIV in India has been uneven. Although much of India has a low rate of infection, certain places have been more affected than others. HIV epidemics are more severe in the southern half of the country and the far north-east. The highest estimated adult HIV prevalence is found in Manipur (1.40%), followed by Andhra Pradesh (0.90%), Mizoram (0.81%), Nagaland (0.78%), Karnataka (0.63%) and Maharashtra (0.55%).

In the southern states, HIV is primarily spread through heterosexual contact. Infections in the north-east are mainly found amongst injecting drug users (IDUs) and sex workers.

149.PATHOGENECITY OF DISEASE DETERMINED BY

A.SPREADING OF DISEASE
B.ARISING OF COMPLICATION
C.INDUCE CLINICAL DISEASE
D.INDUCE INFECTION IN CONTRACTS

ANS:INDUCE CLINICAL DISEASE

A pathogen is a microorganism that is able to cause disease in a plant, animal or insect. Pathogenicity is the ability to produce disease in a host organism. Microbes express their pathogenicity by means of their virulence, a term which refers to the degree of pathogenicity of the microbe. Hence, the determinants of virulence of a pathogen are any of its genetic or biochemical or structural features that enable it to produce disease in a host.

SOCIAL AND PREVENTIVE MEDICINE

148.LIMITING AMINO ACID IN BENGAL GRAM
A.METHIONINE
B.LYSINE
C.LEUCINE
D.TRYPTOPHAN

ANS:TRYPTOPHAN

147.WALDENSTORM MACROGLOBULINEMIA ASSOCIATED WITH

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

ANS:IgM


Waldenström's macroglobulinaemia (WM) is a rare chronic B-cell lymphoproliferative disorder characterised by a monoclonal immunoglobulin M (IgM) paraprotein and morphological evidence of lymphoplasmacytic lymphoma. The clinical manifestations are caused by direct organ tumour infiltration and hyperviscosity.1 It is regarded as a low-grade non-Hodgkin's lymphoma. The overproduction of IgM causes hyperviscosity of blood, interfering with circulation through small blood vessels.

Diagnostic criteria for WM are:

IgM monoclonal gammopathy of any concentration.
Bone marrow infiltration by small lymphocytes showing plasmacytoid or plasma cell differentiation.
Intertrabecular pattern of bone marrow infiltration.
Surface IgM+ CD5- CD10- CD19+ CD20+ CD22+ CD23- CD25+ CD27+ FMC7+ CD103- CD138- immunophenotype.

146.CD MARKER FOR HAIRY CELL LEUKEMIA

A.CD11A,103
B.CD11A,113
C.CD11C,103
D.CD11C,113

ANS:CD11C,103

It is also possible to definitively diagnose hairy cell leukemia through flow cytometry on blood or bone marrow. The hairy cells are larger than normal and positive for CD19, CD20, CD22, CD11c, CD25, CD103, and FMC7.(CD103, CD22, and CD11c are strongly expressed.)

145.PAROXYSMAL NOCTURNAL HEMOGLOBINURIA RELATED TO DEFECIENCY OF

A.CD 59

B.CD5

C.CD8

D.CD36

ANS:CD59

Blood tests in PNH show changes consistent with intravascular hemolytic anemia: low hemoglobin, raised lactate dehydrogenase, raised reticulocytes (immature red cells released by the bone marrow to replace the destroyed cells), raised bilirubin (a breakdown product of hemoglobin), and decreased levels of haptoglobin. The direct antiglobulin test (DAT, or direct Coombs' test) is negative, as the hemolysis of PNH is not caused by antibodies.

Historically, the sucrose lysis test, in which a patient's red blood cells are placed in low-ionic-strength solution and observed for hemolysis, was used for screening. If this was positive, the Ham's acid hemolysis test was performed for confirmation. 

Today, many labs use flow cytometry for CD55 and CD59 on white and red blood cells. Based on the levels of these cell proteins, erythrocytes may be classified as type I, II, or III PNH cells. Type I cells have normal levels of CD55 and CD59; type II have reduced levels; and type III have absent levels. The fluorescein-labeled proaerolysin (FLAER) test is being used more frequently to diagnose PNH. FLAER binds selectively to the glycophosphatidylinositol anchor and is more accurate in demonstrating a deficit than flow cytometry for CD59 or CD55. 

144.TRINUCLEOTIDE REPEAT IN FRAGILE X SYNDROME

A.CAG
B.CGA
C.CGG
D.CTG

ANS:CGG

The first triplet disease to be identified was fragile X syndrome, which has since been mapped to the long arm of the X chromosome. At this point, there are from 230 to 4000 CGG repeats in the gene that causes fragile X syndrome in these patients, as compared with 60 to 230 repeats in carriers and 5 to 54 repeats in unaffected individuals. The chromosomal instability resulting from this trinucleotide expansion presents clinically as mental retardation, distinctive facial features, and macroorchidism in males.

143.AMYLOID RELATED WITH LONG TERM HEMODIALYSIS

A.TRANSTHYRETIN
B.APP
C.ISLET AMYLOID
D.BETA 2 MICROGLOBULIN

ANS:BETA 2 MICROGLOBULIN

Long-term haemodialysis results in a gradual accumulation of β2 microglobulin, a serum protein, in the blood. It accumulates because it is unable to cross the dialysis filter.

142.DIGEORGE SYNDROME

A.B-CELL DEFECT

B.T-CELL DEFECT

C.PRE B CELL DEFECT

D.COMPLEMENT DEFECT

ANS:T CELL DEFECT

T-cells, which originate in the bone marrow, are responsible for fighting off viruses and fungi. A lack of T-cells can lead to frequent infections. One PI disease caused by a T-cell deficiency is DiGeorge syndrome, a disorder that begins during fetal development and can affect various parts of the body, including the head, neck, face, parts of the brain, heart, and thymus. Symptoms of DiGeorge syndrome can be mild to severe, and treatments will vary depending on whether the immune defect is partial or complete.

141.DIGEORGE SYNDROME

A.B-CELL DEFECT

B.T-CELL DEFECT

C.PRE B CELL DEFECT

D.COMPLEMENT DEFECT

ANS:T CELL DEFECT

T-cells, which originate in the bone marrow, are responsible for fighting off viruses and fungi. A lack of T-cells can lead to frequent infections. One PI disease caused by a T-cell deficiency is DiGeorge syndrome, a disorder that begins during fetal development and can affect various parts of the body, including the head, neck, face, parts of the brain, heart, and thymus. Symptoms of DiGeorge syndrome can be mild to severe, and treatments will vary depending on whether the immune defect is partial or complete.

140.ALL ARE FEATURE OF NECROSIS EXCEPT

A.PYKNOSIS
B.KARYOLYSIS
C.KARYOHEXIS'
D.HYPERCHROMASIA

ANS:KARYOHEXXIS

139.HEMOSIDERIN STAINED BY

A.CONGO RED STAIN
B.PRUSSIAN BLUE STAIN
C.EOSIN HEMOTOXYLIN STAIN
D.PAS STAIN

ANS:PRUSSIAN BLUE STAIN

138.ACUTE PHASE REACTANTS ARE ALL EXCEPT

A.FIBRINOGEN
B.HAPTOGLOBULIN
C.ALBUMIN
D.BENCE JONES PROTEIN

ANS:BENCE JONES PROTEIN


NEGATIVE APR

"Negative" acute-phase proteins decrease in inflammation. Examples include albumin, transferrin,transthyretin, retinol-binding protein, antithrombin, transcortin

POSITIVE APR

PATHOLOGY

137.ACUTE PHASE REACTANTS ARE ALL EXCEPT
A.FIBRINOGEN
B.HEPCIDIN
C.PLASMINOGEN
D.MYELIN

ANS:MYELIN

NEGATIVE APR

"Negative" acute-phase proteins decrease in inflammation. Examples include albumin, transferrin,transthyretin, retinol-binding protein, antithrombin, transcortin


POSITIVE APR