Questions FMGE -2008(Part-1,11; Set-A)

Discussion in 'FMGE' started by Guest, Oct 4, 2008.

  1. Guest

    Guest Guest

    Questions FMGE -2008(Part-1,11; Set-A)


    1) Trendelenberg test is positive due to…..?
    2) Notochord exists as….?
    3) Neuroglia….?
    4) Hyaline Arteriosclerosis seen in …..?
    5) Which Ig crosses through placenta …..?
    6) M.C cardiac lesion seen in pregnancy ……?
    7) M.C valve disease due to M.I ? (Sorry, I forgot the question. It was asked in similarly)
    8) Herd Immunity?
    9) Koplik’s spots seen in ……?
    10) A ♀ patient with hypertension & suffering from Thyroiditis, DOC ……?
    11) Hypocalcemia is seen with the following?
    12) Most common position of Uterus?
    13) Shortest ø of pelvis is……?
    14) Right base of the heart is formed by …..?
    15) Right side Mid calvicle the lung ends at which rib?
    16) Water supply in hilly areas?
    17) Prophylaxis DOC for Meningitis?
    18) Anaemia is seen with all except?
    19) Dose of Folic acid during pregnancy? (prophylaxis dose)
    20) Vitamin “A†dosage is given in….? (№. of doses.)
    21) What is Apoptosis?
    22) Extrinsic factor in blood coagulation? (PT/PTT)
    23) Curschmann’s spirals are due to?
    24) Bell’s palsy?
    25) In Dialysis which toxicity is seen commonly?
    26) TOC for Gastric ulcer?
    27) Squamous non-keratinizing is seen in….? a) Tongue b) Trachea c) Oesophagus d) Vagina
    28) Tumour marker CA-125 is related to pancreatic Ca &…….?
    29) Bilaterally kidneys are shrunken in …….?
    30) Poisoning due to ______________preserved are hair, Etc..etc….?
    31) The hormone helps in milk secretion?
    32) Most abundant ICF is …….?
    33) Features like-Hypogonadism, Loss of Hair, Pigmentation of skin Etc..etc Deficiency due to?
    34) Most common features of alcohol withdrawl?
    35) Negri bodies are characteristic of ?
    36) M.C opportunistic Infection in immuno compromised patient?
    37) Mallory-weiss syndrome? (Mallory bodies seen with….?)
    38) Sickness benefit under ESI Act is given for the following illness?
    39) Glucose is reabsorbed at?
    40) M.C pemphigus seen in India?

    41) India ia at which stage of Demographic?
    42) Urinary incontinence in Older people is due to……?
    43) Breast cancer is due to all, Except?
    44) Black & white colour vision is due to ………?
    45) Grey colour……? ( Extremely sorry I forgot what was asked ,{Ophthalmology Q} if any one can remember please ADD)
    46) Kussmaul breathing is due to or seen in ………?
    47) Cellulitis is caused by…….?
    48) Auer rods are seen in ……?
    49) Gynaecomastia is due to drugs……..?
    50) In a new born Jaundice occurs on 3-5days;its not due to ……….?
    51) Transmitted by faeco-orally, Except ?
    52) β-Thalassemia inherited as ……..?
    53) Foreign body inhaled usually lodges in which lung?
    54) Change in blood viscosity causes ………?
    55) * Question regarding Dentition? “Eruptionâ€
    56) Food poisoning 4-6 hrs organism responsible ……..?
    57) Dreaming is common in which type of sleep?
    58) Second heart sound is due to ……..?
    59) “SAFE†; ‘S’-stands for ……..?
    60) Long term status of blood sugar explained by …….? (Ans: HbA1c ; The way the question was formed is different, any way the matter is most Important.)
    61) Hyperglycemic drugs reduces weight ………..?
    62) Surfactant is formed from which type of cells?
    63) Spleenectomy is helpful in ……..?
    64) Incineration done for which of the following?
    65) Anti-gliadin antibodies are seen in?
  2. fiks.

    fiks. Guest

    ) The following are example of Apootosis Except-
    a) Graft versus host disease
    b) Menstrual cycle
    c) Pathological atrophy following duct obstruction
    d) Tumour necrosis

    2) The normal tensile strength of tissue at the site of wound is gained after:
    a) 1 week of wound healing
    b) 2 weeks of wound healing
    c) 2 months of wound healing
    d) 2 years of wound healing
  3. khoshla.

    khoshla. Guest

    Ths best test for BEST Disrase

    Best disease is characterized by a striking accumulation of lipofuscin-like material in the macula that often results in an "egg-yolk-like" appearance. In addition, patients affected with Best's disease display an abnormal electrophysiologic sign known as a depressed Arden ratio. The electro-oculogram (EOG) is a measurement of the electric potential that normally exists across the retinal pigment epithelium. This potential normally doubles in response to bright light. However, in Best's disease, this increase does not exist. This test can be used to diagnose patients without classic macular lesions, as well as identifying patients that are unlikely to have the disease.
  4. Kite.

    Kite. Guest

    qs of sept 2008 paper

    21 trisomy asso. with
    ALL
    CLL
    AML
    CML

    2) esophagus length
    40
    25
    15
    30

    3)pre malignant cond. of esophagus
    barrets

    4)length of external aud. canal cartilagenous part
    8
    16
    24
    12

    5)max. Na absorption at
    PCT
    DCT
    LOH
    CT

    6)SUNRAY apearance on x ray
    osteoclastoma
    osteoblastoma
    osteosarcoma
    chondroblastoma

    7)m\c tumor in spine
    sec.
    ewings sarcoma
    oteosarcoma
    m. myeloma

    8) punched out lesion in skull
    ewings sarcoma
    m.myeloma
    sec.
    oteosarcoma
  5. Kite.

    Kite. Guest

    9)m\c reason for bradycardia in MI
    septal MI
    right vent. MI
    left ventricular MI

    10) S1 split seen in
    RBBB
    ?
    ?
    ?

    11)snow flake cat. (from prev.papers)

    12)after injury to one eye other aslo worsen
    glucoma
    cat.
    sym. opthalmia
    ?

    13)qs from placenta abroptia ...bleeding per vagina tender and hard

    very few qs from Obs

    14) 60 year old man with left hydroceal + ???

    ans. nephroma

    15)lateral epicondyal fac.
    non union
    tardy ulnar nerve palsy
    ?
    all

    16)m\c parasitic infection in AIDS
    strongiloids

    17)toxin responsibel for TSS in femals
    exo toxin

    !8) in stap. aures food poisoning diarrhea occur due 2
    endotoxin
    vagus
    exotoxin
    ?

    19)pheochromocytoma diagnosis
    24 hours urine metabolites VMA+ CA
    MIBG
    CT scan
    surgery

    20) what we use for thyroid scan
    I 131
  6. crm

    crm Guest

    Q)DRUG WHICH CAUSES REVERSIBLE GYNECOMASTIA
    -CIMETEDINE
    -OMEPRAZOLE
    Q)DOC FOR PROPHYLAXIS OF MENINGOCOCCAL MENINGITIS--RIFAMPIN
    Q)A PT WITH THROMBOCYTOPENIA.1ST IOC
    *-BLEEDING TIME
    -PLATELET COUNT
    -PROTHROMBIN TIME
    Q)MC CAUSE OF SOLITARY THYROID NODULE
    -FOLLICULAR ADENOMA
    Q)TUMOR MARKER4BOTH PANCREATIC &COLON CA
    -CA125
    -CA19
    Q)A PT VID AN INFERIOR WALL MI IN SHOCK.REASON?
    ANS-RIGHT VENTRICULAR INFARCTION
    Q)ALL R FEATURES OF ATRIAL MYXOMA EXCEPT
    -FEVER
    -CLUBBING
    -EMBOLI
    *HYPERTENSION
    Q)DOC IN SVT--ADENOSINE
    Q)A FEMALE PT HAS CHEST PAIN (NON EXERTIONAL)
    AUSCULTATION--MULTIPLE NON EJECTION ? ..IOC?
    *ECHO
    Q)A PT PESENTS WITH MI.EARLEST MARKER?
    CK-MB
    TROP-T
    MYOGLOBIN
    Q)STAPH AUREUS FOOD POISONING-CAUSE OF NAUSEA?
    ANS--DIRECT VAGAL STIMULATION
    Q)A Q ON WEGENERS GRANULOMATOSIS
    Q)A PT ON TPN.WHAT COULD BE THE CAUSE OF MORTALITY IN THAT PT?
    OPTIONS CANT RECALL,BUT I MARKED INFECTIONS DUE2CENTRAL LINE
    Q)A Q ON APGAR SCORE
    Q)A Q ON ARDS--DIAGNOSTIC CRITERIA
  7. Senior.

    Senior. Guest

    some more recalls!

    Q)A PT WITH BULBAR URETRAL RUPTURE.UR 1ST MN: WUD BE
    --SUPRAPUBIC CYSTOSTOMY
    --FOLEY'S
    --CONSERVATIVE MN
    --REFER2UROLOGIST

    Q)MJ MUSCLE FOR EYE INTORSION?

    Q)ERYTHRODERMA IS ASSOCIATED WID A/E
    --LEPROMATOUS LEPROSY
    --AIR BORNE DERMATITIS

    Q)DERMATITIS HERPETIFORMIS IS A/W
    *ULCERATIVE COLITIS

    Q)MC TYPE OF PEMPHIGUS IN INDIA?
    *P.VULGARIS

    Q)LA SAFE IN RF?
    GALLAMINE

    Q)A PT WID MYASTHENIA GRAVIS IS RESISTANT2
    --*DEPOLARISING MR
    --NON DEPOLARISING MR
    --BOTH
    --NONE

    Q)A PSM Q 2FIND OUT RELATIVE RISK

    Q)ANOTHER PSM Q ON PANEL DISCUSSION..Q WAS AS2VAT WAS IT ABOUT

    Q)A Q ON SARCOIDOSIS(PATHO)

    Q)WHICH ANTIBODY HAS BEST4 CELIAC DISEASE(SENSITIVE &SPECIFIC)?
    *ANTI ENDOMYSIAL AB


    Q)BEST PROGNOSTIC FACTOR 4 A/C PANCREATITIS
    -*S.LIPASE

    Q)A Q ON ZES--WHICH IS NOT TRUE
    ONE OF THE OPTION READ--REDUCED BAO:MAO WHICH S D ANS


    Q)AN OHA WHICH IS USED 2TREAT OBESITY
    ANS WAS SUM BIGUANIDE GIVEN IN THE OPTIONS

    Q)ANOTHER Q ON DIAB DRUG
    WHICH ONE DOES'NT CAUSE HYPOGLYCEMIA
    (SORRY,CANT RECALL OPTIONS)



    BUT FRIENDS,,NEXT TIME DO READ A BIT ABOUT ORAL HYPOGLYCEMICS AS WELL AS SOME IMP BITS ABOUT ANTI-OBESITY DRUGS
    (SEEMS NAT BOARD HAS LOST IT'S LONG LASTED LOVE 4 MALARIA,TB,N OTHER PARASITIC INFECTIONS!NOT A SINGLE Q WAS ASKED!!))


    Q)DRUG USED4TREMORS IN HYPERTHYROIDISM?
    --PROPRANOLOL


    Q)AN EASY Q--WHICH CAUSES HYPOCALCEMIA?
    ANS WAS CALCITONIN

    Q)A PT ON TPN FOR A WEEK DEVELOPS FEATURES((WHICH WAS SUGGESTIVE OF ZN DEFICIENCY))..DEFICIENCY OF VAT?


    Q)A Q ON NEPHROTIC SYNDROME IN CHILDREN....


    Q)HYALINE ARTERIOSCLEROSIS IS SEEN IN
    *BENIGN HTN
  8. Liza.

    Liza. Guest

    some more questions frm FMGE sept 2008

    1-ring shaped ulcers seen in?
    2-neurotrophic keratitis-nerve involved
    3-question on sympathetic ophthalmia
    4-extra capsular cataract surgery-parts of lens which are excised?
    5- SAFE strategy for trachoma-S stands for?
    6-rubro iridis is not seen in?
    7-questions on cost benefit and cost accounting in PSM
    8-central tendancy seen in-(refer biostats PSM )
    9-question on odds ratio
    10-complication of measles virus -encephalomelyitis
  9. Liza.

    Liza. Guest

    some more-
    NNN Media used for- Ans-leshmania donavani
    Treatment of first degree testicular cancer
    Fourniers (sorry for d spelling,I don remember exactly!) gangrene seen in- Ans scrotum
    Treatment Regimen for hodkgins lymphoma
    Shape of tracheal cartilage-ans-horse shoe shape
    Comonest congenital anomaly of trachea
    Erythoderma is not seen in-?
    Commonest lupus in india-
    Fate of notochord-?
    Mysanthia gravis is not inhibited by-depolarizing agents,non depolarizing agents,both,?
    Rarest form of opportunistic fungal infection seen in AIDS-
    White line of frenkel seen in-ans Scurvy
    Xray sign of rickets
    Splenomegaly not seen in-?
    The first clinical presentation of acoustic neuroma-ans-facial nerve involvement
    Stones r seen most commonly in submandibular salivary gland
    The calories required by one year old child
    4-5 questions on Tracheostomy
    Sunray sign on xray seen in-?osteosarcoma
    Tardy ulnar palsy seen in-?
    Rigor mortis is due to-?
    Vitreous hemorrhage on autopsy seen in poisoning of-?
    One question on [bleep]-Refer Forensic Medicin
    Most specific method of diagnosis of kalazar
  10. Neesha

    Neesha Guest

    questions

    questions

    Q.a patient with tb had decrease SERUM level of Na and k....... and has hyperpigmentation of crease of hand??...
    ans.. secondary hyperaldeosteroism.
    Q.MC. CAUSE OF DEATH IN INDIA?
    ANS. CORONAY HEART DISEASE.
    Q.CXR AP VIEWON RIGHT SIDE OF CARDIAC SILHOUTE U CAN SEE ALL EXCEPT?
    ANS. SUPERIOR VENA CAVA
    Q.NORMAL TO INCREASE SIZE OF KIDNEY IS SEEN ALL EXCEPT?
    ANS. *CHRONOC GN
    DIABETIC NEPHROPATHY
    AIDS REALTED NEPHROPATHY
    PKD
    Q.SPLEEN IS SUPPORT BY WHICH LIGAMNET FROM UPPER SIDE?
    ANS. GASTROSPLENIC LIGAMENT.
    Q.STAIN FOR AMLYDOSIS
    ANS. CONGO RED
    Q.AUER RODS ARE SEEN IN?
    AN. AML
    Q.WHICH TUMOR IS MC IN DOWN SYNDROME?\
    ANS MAY BE RETINOBLASTOMA (PLZ MAKE SURE FROM BOOK)
  11. shri.

    shri. Guest

    1.Trendelenburg's test

    Also known as:
    Brodie-Trendelenburg test
    Trendelenburg-Brodie test

    Associated persons:
    Sir Benjamin Collins Brodie
    Friedrich Trendelenburg

    Description:

    Test for varicose veins. Patient lies on his back and raises his leg to empty the veins. A tourniquet is applied just below the saphenous opening. The patient is then stood up and the tourniquet removed in 60 seconds. Normally the vein should fill from below within 35 seconds with the tourniquet in situ. Earlier filling indicates incompetence of a communicating vein. If on release the veins fill rapidly from above it is due to incompetent sapheno-femoral valves.


    2. Trendelenburg's test


    Trendelenburg's test is a test of the saphenous and other veins.[1]
    It is named for Friedrich Trendelenburg.[2][3]
    It should not be confused with Trendelenburg's sign, which involves the muscles of the hip.


    Trendelenburg's sign:


    Trendelenburg's sign is found in people with weak abductor muscles of the hip. It is named after the German surgeon Friedrich Trendelenburg.
    The Trendelenburg sign is said to be positive if, when standing on one leg, the pelvis drops on the side opposite to the stance leg. The weakness is present on the side of the stance leg. The body is not able to maintain the center of gravity on the side of the stance leg. Normally, the body shifts the weight to the stance leg, allowing the shift of the center of gravity and consequently stabilizing or balancing the body. However, in this scenario, when the patient/person lifts the opposing leg, the shift is not created and the patient/person cannot maintain balance leading to instability.

    Essentially, Trendelenburg sign is caused by paralysis of the gluteus medius and minimus muscles.

    Paralysis may arise due to nerve damage, namely, the superior gluteal nerve
  12. Guest

    Guest Guest

    1.
    Trendelenburg test is a standard clinical assessment of hip stability.

    A positive test indicates gluteus medius weaknessand is observed when weight is supported by the affected limband the pelvis on the healthy side falls instead of rises.

    This test was used in this study to compare the two approaches. Incases of minimal abductor weakness there may be a delayedpositive test. It is for this reason that an element of musclefatigue was taken into account by considering the pelvicposition at 30 seconds of single leg stance. Since gait analysisallows subtle differences to be detected compared to clinicalanalysis, it was hoped this test would be an effective measureto compare the two approaches

    -------------------------------------------------------------------------------------

    2.

    The notochord exists transiently during the life of most vertebrates.

    A notochord is the defining characteristic of members of the phylum Chordata, a large and diverse biological group which includes all animals with spines, or backbones, along with more primitive chordates. The notochord has very large cells which are densely arranged within a protective sheath. Chordates are divided into three subphyla, depending on what form their notochords take and when they appear. At any developmental stage, a notochord acts as a form of support for the animal that possesses it, giving animals the ability to do things such as walking upright.

    The most primitive group of chordates, urochordates, also called tunicates, only have a notochord in the larval stages of development. The animals in this group are pelagic, meaning that they are found in the world's oceans, and there are a number of representative species, most of whom are only known to biologists. These animals do provide an insight into the development of chordates, however, showing the notochord at an early stage of development.

    The next group of chordates, cephalochordates, also called lancelets, possess a notochord into adulthood, and also live in the ocean. The notochord runs all the way along the body, even up into the head, and the animals lack a protective layer of bone such as a spine. The notochord acts as an axial support, providing a strong core for the animal. The notochord is highly flexible, but not compressible, allowing the animal to move freely without damaging the notochord.

    In the highest class of chordates, the vertebrates, the notochord only exists when the animal is in an embryonic form. As the vertebrate develops, the notochord is first ensheathed in and then replaced by spinal vertebrae, protective cases of bone which cover the delicate spinal cord. The spinal column is able to support a much larger and more complex organism, and is much stronger than the notochord. This allowed early vertebrates to make the leap to the land and develop into well known species such as humans.

    In all chordates, the notochord exists in some form when the animal is in a larval or embryonic stage[/size]. The development of the notochord from there helps shape what sort of animal it will turn into, whether it be a sac like tunicate or a pure bred Norwegian Fjord horse. The development of the notochord represents a major advance in evolution, as it allowed animals to get much larger and more complex, a drastic departure from simpler orders of animals which existed previously.

    ------------------------------------------------------------------------------------

    3. NeuroGLIA

    Glial cells, commonly called neuroglia or simply glia (Greek for "glue"), are non-neuronal cells that provide support and nutrition, maintain homeostasis, form myelin, and participate in signal transmission in the nervous system. In the human brain, glia are estimated to outnumber neurons by about 10 to 1.

    Glial cells provide support and protection for neurons, the other main type of cell in the nervous system. They are thus known as the "glue" of the nervous system. The four main functions of glial cells are to surround neurons and hold them in place, to supply nutrients and oxygen to neurons, to insulate one neuron from another, and to destroy pathogens and remove dead neurons. They also modulate neurotransmission.


    The supportive tissue of the nervous system, including the network of branched cells in the central nervous system (astrocytes, microglia, and oligodendrocytes) and the supporting cells of the peripheral nervous system (Schwann cells and satellite cells). Also called glia, reticulum.
    ------------------------------------------------------------------------------

    4. Hyaline arteriolosclerosis:

    Hyaline arteriolosclerosis can be seen in patients with diabetes mellitus and with hypertension. Hyaline arteriolosclerosis are more common in diabetic sufferers.


    5. M.C cardiac lesion seen in pregnancy -->

    Mitral stenosis is the most common rheumatic valvular lesion seen in pregnancy due to its prevalence in young women.


    6. M.C valve disease due to ----

    Mitral valve prolapse (MVP) : is the most common forms of valve disease, affecting 6 percent of all women. In this condition one or both of the valve leaflets is enlarged or floppy, preventing the valve from closing evenly. When the valve shuts, the leaflets bulge into the left atrium. You may have heard mitral valve prolapse referred to as click-murmur syndrome from the sound the valve makes when it closes.

    7. Herd Immunity:

    In immunology, herd immunity refers to a situation in which a high percentage of a population is immune to a disease, essentially stopping the disease in its tracks because it cannot find new hosts. You may also hear this concept referred to as “community immunity.†The threshold for herd immunity varies, depending on the disease, with more virulent agents requiring vaccination of a higher percentage of the population to crate the desired herd immunity. In addition to being used in disease prevention, community immunity is also utilized to fight ongoing outbreaks.

    Most vaccination policies are focused on creating herd immunity. Many countries require vaccinations in childhood, for example, protecting children from common diseases and ensuring that when these diseases enter the population, they cannot prey on children or adults, who have been previously vaccinated or exposed to the disease. The creation of herd immunity is especially important in crowded environments which facilitate the spread of disease, like schools.

    Immunologists try to prevent the outbreak of diseases by creating herd immunity, but they are not always successful. Sometimes a disease mutates or is entirely new, or a batch of vaccinations is faulty, or a large percentage of the population fails to get vaccinated, creating a situation in which an outbreak can occur, because much of the population is vulnerable. In the event of an outbreak of a major disease, agencies like the World Health Organization can dispatch teams within days to figure out the cause of the outbreak and develop a vaccine, in the hopes of creating herd immunity to halt the outbreak in its tracks.

    For some diseases, herd immunity thresholds are as low as 50%, especially when combined with good hygiene. In other instances, up to 90% of the population may need to be vaccinated to create the desired herd immunity. It is also extremely important to receive regular boosters, as some vaccines lose their efficacy over time, leaving people vulnerable to an outbreak. Herd immunity led to the eradication of smallpox, and it explains why diseases such as polio and diphtheria are rare in developed nations with established vaccination policies.

    The concept of herd immunity is often used to encourage reluctant parents to vaccinate their children. In addition to ensuring that their children are protected from fully preventable diseases, childhood vaccinations also benefit society at large by creating herd immunity. Likewise, adults may be reminded to receive boosters to help protect their communities.

    ---------------------------------------
    9. Koplik’s spots seen in ---

    Also known as: Filatov’s spots, Flindt’s spots Maculae Koplik.

    Associated persons:
    Nil Feodorovich Filatov
    Nikolaj Flindt
    Henry Koplik

    Description:
    Small, grain-of-sand sized, irregular, bright red spots with blue-white centres, occurring on the inside of the cheek (buccal mucosa). Seen only on measles (rubeolae) they are, by themselves, a diagnostic sign in measles. The spots usually occur briefly after the fever begins and a couple of days before the generalized rash appears. Not infrequently, the spots disappear as the eruption develops.

    --------------

    Koplik's spots are bluish-white spots seen on the mucous membranes of the mouth and are pathognomonic of measles.

    They often appear a few days before the rash arrives and can be a useful sign to look for in children known to be exposed to the measles virus.

    --------------

    10. A ♀ patient with hypertension & suffering from Thyroiditis, DOC --

    L-Thyroxine has long been the treatment drug of choice

    Goals of
    therapy (Rx) To bring free T4 (L-thyroxine) and TSH levels into normal range and improve symptoms. 1st choice therapy L-thyroxine.


    11. Hypocalcemia is seen with the following-->

    Hypocalcemia can be seen in chronic renal insufficiency.


    Hypocalcemia may be seen in a number of disorders affecting the synthesis or action of PTH or vitamin D or following sequestration of calcium into a functionally inaccessible compartment.

    Many of these represent chronic illnesses where hypocalcemic symptoms develop insidiously or where the complication of hypocalcemia is anticipated early and appropriate treatment initiated prior to acute decompensation.


    Hypocalcemia occurs in the setting of acute systemic illness (eg, toxic shock syndrome), a finding that has been linked to elevated free fatty acids levels in this setting. It has also been associated with specific drugs, including antineoplastic agents such as doxorubicin and cytarabine and other agents such as ketoconazole, pentamidine, and foscarnet.

    12.Most common position of Uterus?
    The most common position is for the long axis of the uterus to lie in approximately the same axis as the pelvis, that is, with the upper part tilted forward and the lower end, the cervix, inserted into the top of the vagina. There is therefore an angle between the uterus and the vagina, the long axis of which corresponds to the lower part of the pelvis.

    13. Shortest ø of pelvis is-->
    The interspinous diameter is the shortest in the pelvis.

    Obstetrical Pelvic Diameters
    The shape and size of the bony pelvis are important factors determining the outcome of labour. The pelvic inlet is the entrance to the true pelvis. The plane of the pelvic inlet is almost circular in a normal female or gynaecoid pelvis with a slightly greater transverse than anterior-posterior diameter. The true diameter of the pelvic inlet is difficult to assess clinically. An estimate can be made from the diagonal conjugate diameter which is measured between the midpoint of the sacral promontory and the nearest point on the posterior surface of the pubic symphysis. This measure is about 1.5cm greater than the obstetrical conjugate diameter. In practice it is rarely possible to reach the promontory on clinical examination. The pelvic outlet is narrower than the pelvic inlet. The anterior-posterior diameter of the pelvic outlet is measured from the inferior border of the pubic symphysis to the sacrococcygeal joint, and is usually about 12.5cm. The transverse diameter of the pelvic outlet is measured between the ischial tuberosities and is usually about 10cm. The plane of least pelvic dimensions represents the narrowest part of the birth canal. The anteroposterior diameter extends from the inferior margin of the pubic symphysis posteriorly through a line which connects the ischial spines, the transverse diameter. Both diameters can be assessed clinically, and the interspinous diameter is the shortest in the pelvis.

    14. Right base of the heart is formed by --->

    The base of the heart is opposite to that of the apex is mainly formed by the left atria, but getting some contribution from the right atrium.

    15. Right side Mid calvicle the lung ends at which rib --10 Rib?

    The border of the right lung lies immediately inside the pleural margin from the cupola down to about the 6th costal cartilages.

    It then lies about two spaces above the pleural margin:
    it crosses the 6th rib in the midclavicular line and the 8th rib in the midaxillary line, and reaches the vertebral column at the level of the 10th rib.

    16. Water supply in hilly areas---?


    Developing springs as a source for rural water supply is ideally suited for the following situations: (a). The springs are perennial (at least discharge at the rate of 20 lpcd during peak summer) and of good water quality (to be tested for chemical and bacteriological) contamination); (b) Chance of polluting the catchment is minimum; (c) The beneficiary population lives within close proximity of the springs preferably in the down stream areas of the springs.

    In the era of decentralized planning, community mobilization, resource mobilization, cost sharing, community management, cost recovery and operation and maintenance plays a significant role in the water supply schemes. In 1989, the Pazhakulam Social Service Society (PASSS) has taken the initiative for the development of natural springs as alternative safe drinking water to the communities in the remote hilly areas of Southern Kerala. The main objective of the spring development programme was to demonstrate to the Government, Non-Governmental Organizations and the people of Kerala, that it is possible to design and develop alternate delivery of drinking water through private sector initiatives. The concept of rejuvenation of springs is an alternative mechanism to increase the coverage and accessibility of safe water supply in the remote areas. PASSS has taken the leadership in demonstrating the programme since 1991 and more than 1150 springs have already been developed with the active participation of the community. The salient features of the programme is as follows:

    Established water committees as the nucleus of community organization, participation and management of the programme; Capacity building and empowerment; Capital cost sharing mechanism has become mandatory;
    Full O & M by water committees/community; Low cost participatory design; Panchayat institutions as a partner; Integration of water, sanitation and hygiene; Water quality monitoring; Community monitoring and follow up.


    17. Prophylaxis DOC for Meningitis -->

    Meningitis is an inflammation of the leptomeninges and underlying subarachnoid cerebrospinal fluid


    Cephalexin/Cefazolin


    PO/IV
    Stable vs Staph penicillinase
    Spectrum: MSSA, PSSP, most E. coli, and some Klebs
    Can be dose thrice weekly in HD pts
    [1.5 grams IV TIW]
    DoC: surgical prophylaxis, bacterial peritonitis in CAPD pts [1 gm in the dwell bag]

    --------------------

    Ampicillin/Amoxicillin


    Amp (IV, PO) Amox (PO)
    Spectrum: PenG + H. flu and some E. coli
    DoC: Listeria monocytogenes and
    Enterococcus [Amp 2g IV q4h]

    Dental Prophylaxis
    Amox 1 gram PO x 1 prior to appt.
    Integral in H. pylori regimens
    ADRs
    Non-allergic rashes (9%) – esp. when associated with a viral illness (mononucleosis - EBV)
    Amox better tolerated PO and better absorbed (Amp must be taken on empty stomach)
    -----------------------------
  13. libera.

    libera. Guest

    more qns from FMGE sept 08

    more qns from FMGE sept 08

    who discovered xrays?
    roentgen

    which disease is X linked recessive?
    Hemophlia

    most common cause of death in people older than 70 yrs?
    cardiovascular disease, cancer,respiratory disease?

    in retinal detachment?? options were red colour, blue colour, green colour? i cant remember exactly.

    in which poisoning shud the vitrous humor be preserved?

    malignant pustule?
    anthrax

    a qn from varicocele frm surgery, i cant remember..


    frnds, there were over 20 questions frm Ophthalmology and Biochemistry and many from parasitology in Microbiology ..
    few questions were simple and thats all we can recollect! there were many confusing questions too...
    all da best for 2009....
  14. trimurtulu.

    trimurtulu. Guest

    Prophylaxis DOC for Meningitis?


    PRESCRIPTIONS FOR PROPHYLAXIS OF MENINGITIS :
    PROCEDURES FOR GGHB COMMUNITY PHARMACISTS

    · Identify a prescription for meningitis prophylaxis:

    Rifampicin 600mg (or 10mg/kg for children) twice daily for 2 days

    or

    Ciprofloxacin 500mg as a single dose (although not yet licensed for this purpose).

    Establish the patient’s eligibility for exemption from prescription charge.

    If not exempt via NHS, reassure the patient that a special GGHB exemption will apply.

    Dispense the prescription.

    Please do not collect the prescription charge.

    Please submit an invoice for the prescription charge on headed notepaper to myself at GGHB Headquarters, noting patient name and date.

    Submit the prescription in the non-exempt category to the PPD.


    -------------------------------------------------

    PRESCRIPTIONS FOR PROPHYLAXIS OF MENINGOCOCCAL SEPTICAEMIA

    You will be aware of the increased incidence of meningitis in recent weeks. All cases are notified to the GGHB Public Health Department. Treatment of the individual case in an acute hospital is accompanied by management of the public health implications in primary care. Typically, specialists in Communicable Disease will identify close family and friends of the patient who may require prophylactic treatment. The treatment options currently are:

    Rifampicin 600mg (or 10mg/kg for children) twice daily for 2 days

    or

    Ciprofloxacin 500mg as a single dose (although not yet licensed for this purpose)

    The options for supply of these prescriptions are as follows:

    community administration programme (e.g. school, church)

    hospital supply

    supply through the local GEMS centre

    prescription on HBP forms by the Public Health Consultant on call

    prescription on GP10

    The last of these is frequently the preferred option. Treatment needs to be started quickly but not urgently and both drugs need to be used cautiously in combination with other therapies. Community pharmacists can reinforce these points.
  15. tarjan.

    tarjan. Guest

    18) Anaemia is seen with all except?

    Anemia
    Definition
    If you have anemia, people may say you have tired blood. That's because anemia — a condition in which there aren't enough healthy red blood cells to carry adequate oxygen to your tissues — can make you feel tired.

    There are many forms of anemia, each with its own cause. Anemia can be temporary or long term, and it can range from mild to severe.

    Anemia is a common blood disorder. Women and people with chronic diseases are at increased risk of the condition.

    If you suspect you have anemia, see your doctor. Anemia can be a sign of serious illnesses. Treatments for anemia range from taking supplements to undergoing medical procedures. You may be able to prevent some types of anemia by eating a healthy, varied diet.

    Symptoms
    The main symptom of most types of anemia is fatigue. Other anemia symptoms include:

    •Weakness
    •Pale skin
    •A fast or irregular heartbeat
    •Shortness of breath
    •Chest pain
    •Dizziness
    •Cognitive problems
    •Numbness or coldness in your extremities
    •Headache
    Initially, anemia can be so mild it goes unnoticed. But signs and symptoms increase as the condition worsens.

    Causes
    Blood consists of both a liquid called plasma and cells. Floating within the plasma are three types of blood cells:

    •White blood cells. These blood cells fight infection.
    •Platelets. These blood cells help your blood clot after a cut.
    •Red blood cells (erythrocytes). These blood cells carry oxygen from your lungs, via your bloodstream, to your brain and the other organs and tissues. Your body needs a supply of oxygenated blood to function. Oxygenated blood helps give your body its energy and your skin a healthy glow.
    Red blood cells contain hemoglobin — a red, iron-rich protein that gives blood its red color. Hemoglobin enables red blood cells to carry oxygen from your lungs to all parts of your body, and to carry carbon dioxide from other parts of the body to the lungs so that it can be exhaled.

    Most blood cells, including red blood cells, are produced regularly in your bone marrow — a red, spongy material found within the cavities of many of your large bones. To produce hemoglobin and red blood cells, your body needs iron, protein and vitamins from the foods you eat.

    Anemia is a state in which the number of red blood cells or the hemoglobin in them is below normal. When you're anemic, your body produces too few healthy red blood cells, loses too many of them or destroys them faster than they can be replaced. As a result, your blood is low on red blood cells to carry oxygen to your tissues — leaving you fatigued. Common types of anemia and their causes include:

    •Iron deficiency anemia. This most common form of anemia affects about one in five women, half of pregnant women and 3 percent of men in the United States. The cause is a shortage of the element iron in your body. Your bone marrow needs iron to make hemoglobin. Without adequate iron, your body can't produce enough hemoglobin for red blood cells. The result is iron deficiency anemia.

    One way your body gets needed iron is when blood cells die — the iron in them is recycled and used to produce new blood cells. So, if you lose blood, you lose iron. Women with heavy periods who lose a lot of blood each month during menstruation are at risk of iron deficiency anemia. Slow, chronic blood loss from a source within the body — such as an ulcer, a colon polyp or even colon cancer — also can lead to iron loss and iron deficiency anemia.

    Your body also gets iron from the foods you eat. An iron-poor diet can lead to this anemia. In pregnant women, a growing fetus can deplete the mother's store of iron, leading to iron deficiency anemia.

    •Vitamin deficiency anemias. In addition to iron, your body needs folate and vitamin B-12 to produce sufficient numbers of healthy red blood cells. A diet lacking in these and other key nutrients can cause decreased red blood cell production. People who have an intestinal disorder that affects the absorption of nutrients are prone to this type of anemia. Some people are unable to absorb vitamin B-12 for a variety of reasons and develop vitamin B-12 deficiency anemia, which is sometimes called pernicious anemia. Vitamin deficiency anemias fall into a group of anemias called megaloblastic anemias, in which the bone marrow produces large, abnormal red blood cells.
    •Anemia of chronic disease. Certain chronic diseases — such as cancer, rheumatoid arthritis, Crohn's disease and other chronic inflammatory diseases — can interfere with the production of red blood cells, resulting in chronic anemia. Kidney failure also can be a cause of anemia. The kidneys produce a hormone called erythropoietin, which stimulates your bone marrow to produce red blood cells. A shortage of erythropoietin, which can result from kidney failure or be a side effect of chemotherapy, can result in a shortage of red blood cells.
    •Aplastic anemia. This is a life-threatening anemia caused by a decrease in the bone marrow's ability to produce all three types of blood cells — red blood cells, white blood cells and platelets. Many times, the cause of aplastic anemia is unknown, but it's believed to often be an autoimmune disease. Some factors that can be responsible for this type of anemia include chemotherapy, radiation therapy, environmental toxins, pregnancy and lupus.
    •Anemias associated with bone marrow disease. A variety of diseases, such as leukemia and myelodysplasia, a pre-leukemic condition, can cause anemia by affecting blood production in the bone marrow. The effects of these types of cancer and cancer-like disorders vary from a mild alteration in blood production to a complete, life-threatening shutdown of the blood-making process. Additionally, other cancers of the blood or bone marrow, such as multiple myeloma, myeloproliferative disorders and lymphoma, can cause anemia.
    •Hemolytic anemias. This group of anemias develops when red blood cells are destroyed faster than bone marrow can replace them. Certain blood diseases can cause increased red blood cell destruction. Autoimmune disorders can cause your body to produce antibodies to red blood cells, destroying them prematurely. Certain medications, such as some antibiotics used to treat infections, also can break down red blood cells. Hemolytic anemias may cause yellowing of the skin (jaundice) and an enlarged spleen.
    •Sickle cell anemia. This inherited and sometimes serious anemia, which affects mainly people of African and Arabic descent, is caused by a defective form of hemoglobin that forces red blood cells to assume an abnormal crescent (sickle) shape. These irregular-shaped red blood cells die prematurely, resulting in a chronic shortage of red blood cells. Sickle-shaped red blood cells can also block blood flow through small blood vessels in the body, producing other, often painful, symptoms.
    •Other anemias. There are several other, rarer forms of anemia, such as thalassemia and anemias caused by defective hemoglobin.
    Sometimes, no cause of anemia can be identified.

    Risk factors
    These factors place you at increased risk of anemia:

    •Poor diet. Anyone — young or old — whose diet is consistently low in iron and vitamins, especially folate, is at risk of anemia. Your body needs iron, protein and vitamins to produce sufficient numbers of red blood cells.
    •Intestinal disorders. Having an intestinal disorder that affects the absorption of nutrients in the small intestine — such as Crohn's disease and celiac disease — puts you at risk of anemia. Surgical removal of or surgery to the parts of the small intestine where nutrients are absorbed can lead to nutrient deficiencies and anemia.
    •Menstruation. In general, women are at greater risk of iron deficiency anemia than are men. That's because women lose blood — and with it, iron — each month during menstruation.
    •Pregnancy. Pregnant women are at an increased risk of iron deficiency anemia because their iron stores have to serve the increased blood volume of the mother as well as be a source of hemoglobin for the growing fetus.
    •Chronic conditions. For example, if you have cancer, kidney or liver failure, or another chronic condition, you may be at risk of what's called anemia of chronic disease. These conditions can lead to a shortage of red blood cells. Slow, chronic blood loss from an ulcer or other source within the body can deplete your body's store of iron, leading to iron deficiency anemia.
    •Family history. If your family has a history of an inherited anemia, you also may be at increased risk of the condition.
    Certain infections, blood diseases and autoimmune disorders, exposure to toxic chemicals, and the use of some medications can affect red blood cell production and lead to anemia. Other people at risk of anemia are people with diabetes, people who are dependent on alcohol (alcohol interferes with the absorption of folic acid) and people who adhere to a strict vegetarian diet, who may not get enough iron or vitamin B-12 in their diet.

    When to seek medical advice
    See your doctor if you're feeling fatigued for unexplained reasons, especially if you're at risk of anemia. Some anemias, such as iron deficiency anemia, are common. But don't assume that if you're tired, you must be anemic. Fatigue has many causes besides anemia.

    Some people learn that their hemoglobin is low, which indicates anemia, when they go to donate blood. Low hemoglobin may be a temporary problem remedied by eating more iron-rich foods or taking a multivitamin containing iron. However, it may also be a warning sign of blood loss in your body that may be causing you to be deficient in iron. If you're told that you can't donate blood because of low hemoglobin, ask your doctor if you should be concerned.

    If you have a family history of an inherited anemia, such as sickle cell anemia, talk to your doctor and possibly a genetic counselor about your risk and what risks you may pass on to your children.

    Tests and diagnosis
    Doctors diagnose anemia with the help of a medical history, a physical exam and blood tests, including a complete blood count (CBC). This blood test measures levels of red blood cells and hemoglobin in your blood. Some of your blood may also be examined under a microscope to study the size, shape and color of your red blood cells, which may indicate a diagnosis. For example, in iron deficiency anemia, red blood cells are smaller and paler in color than normal. In vitamin deficiency anemias, red blood cells are enlarged and fewer in number.

    If you receive a diagnosis of anemia, your doctor may order additional tests to determine the underlying cause. For example, iron deficiency anemia can result from chronic bleeding of known or unknown ulcers, benign polyps in the colon, colon cancer, tumors, or kidney failure. Your doctor may test for these and other conditions that may underlie the anemia.

    Occasionally, it may be necessary to study a sample of your bone marrow to diagnose anemia.

    Complications
    When anemia is severe enough, it may interfere with your ability to do everyday tasks. You may be too exhausted to work or play. Although anemia is often treatable, it may take several weeks to months for red blood cell levels to return to normal after treatment. Ask your doctor what to expect from treatment.

    If you've been diagnosed with anemia — it's often detected during routine blood tests — ask your doctor what treatment is necessary. Then be sure to follow through on treatment, even if you quickly start to feel better. Left unchecked, anemia can lead to a rapid or irregular heartbeat — an arrhythmia. Your heart must pump more blood to compensate for the lack of oxygen in the blood when you're anemic. This can even lead to congestive heart failure. Untreated pernicious anemia can lead to nerve damage and decreased mental function, as vitamin B-12 is important not only for healthy red blood cells but also for optimal nerve and brain function.

    Some inherited anemias, such as sickle cell anemia, can be serious and lead to life-threatening complications. Losing a lot of blood quickly results in acute, severe anemia and can be fatal.

    Treatments and drugs
    Anemia treatment depends on the cause:

    •Iron deficiency anemia. This form of anemia is treated with iron supplements, which you may need to take for several months or longer. If the underlying cause of iron deficiency is loss of blood — other than from menstruation — the source of the bleeding must be located and stopped. This may involve surgery.
    •Vitamin deficiency anemias. Pernicious anemia is treated with injections — often lifetime injections — of vitamin B-12. Folic acid deficiency anemia is treated with folic acid supplements.
    •Anemia of chronic disease. There's no specific treatment for this type of anemia. Doctors focus on treating the underlying disease. Iron supplements and vitamins generally don't help this type of anemia. However, if symptoms become severe, a blood transfusion or injections of synthetic erythropoietin, a hormone normally produced by the kidneys, may help stimulate red blood cell production and ease fatigue.
    •Aplastic anemia. Treatment for this serious anemia may include blood transfusions to boost levels of red blood cells. You may need a bone marrow transplant if your bone marrow is diseased and can't make healthy blood cells. You may need immune-suppressing medications to lessen your immune system's response and give the transplanted bone marrow a chance to start functioning again.
    •Anemias associated with bone marrow disease. Treatment of these various diseases can range from simple medication to chemotherapy to bone marrow transplantation. Treatment of these types of anemia usually involves a consultation from a blood specialist (hematologist).
    •Hemolytic anemias. Managing hemolytic anemias includes avoiding suspect medications, treating related infections and taking drugs that suppress your immune system, which may be attacking your red blood cells. Short courses of treatment with steroids or gamma globulin can help suppress your immune system's attack on your red blood cells. If the condition has caused an enlarged spleen, you may need to have your spleen removed. The spleen — a small organ below your rib cage on the left side — filters out and stores defective red blood cells. Certain hemolytic anemias can cause the spleen to become enlarged with damaged red blood cells.
    •Sickle cell anemia. Treatment for this incurable anemia may include the administration of oxygen, pain-relieving drugs, and oral and intravenous fluids to reduce pain and prevent complications. Doctors also commonly use blood transfusions, folic acid supplements and antibiotics. A bone marrow transplant may be an effective treatment in some circumstances. A cancer drug called hydroxyurea (Droxia, Hydrea) also is used to treat sickle cell anemia in adults.
    Prevention
    Many types of anemia can't be prevented. However, you can help avoid iron deficiency anemia and vitamin deficiency anemias by eating a healthy, varied diet that includes foods rich in iron, folate and vitamin B-12.

    The best sources of iron are beef and other meats. Other foods rich in iron include beans, lentils, iron-fortified cereals, dark green leafy vegetables, dried fruit, nuts and seeds. Folate, and its synthetic form, folic acid, can be found in citrus juices and fruits, dark green leafy vegetables, legumes and fortified breakfast cereals. Vitamin B-12 is plentiful in meat and dairy products. Foods containing vitamin C, such as citrus fruits, help increase iron absorption.

    Eating plenty of iron-containing foods is particularly important for people who have high iron requirements, such as children — iron is needed during growth spurts — and pregnant and menstruating women. Adequate iron intake is also crucial for infants, strict vegetarians and long-distance runners.

    Doctors may prescribe iron supplements or multivitamins containing iron for people with high iron requirements. But iron supplements are appropriate only when you need more iron than a balanced diet can provide. Don't assume that if you're tired that you simply need to take iron supplements. Overloading your body with iron can be dangerous.
  16. tarjan.

    tarjan. Guest

    Anaemia is a condition in which the haemoglobin concentration in the blood is below a defined level, resulting in a reduced oxygen-carrying capacity of red blood cells.

    About half of all cases of anaemia can be attributed to iron deficiency; other common causes include infections, such as malaria and schistosomiasis, and genetic factors, which result in thalassaemias and sickle-cell disease.

    In its severe form, anaemia is associated with fatigue, weakness, dizziness and drowsiness. Pregnant women and children are particularly vulnerable.
  17. tarjan.

    tarjan. Guest

    19 ) Dose of Folic acid during pregnancy?


    Taking 400 micrograms of synthetic folic acid daily from fortified foods and/or supplements has been suggested.

    The Recommended Dietary Allowance (RDA) for folate equivalents for pregnant women is 600-800 micrograms, twice the normal RDA of 400 micrograms for women who are not pregnant.
  18. tarjan.

    tarjan. Guest

    Prophylaxis vs Neural Tube Defects (NTD):

    The Society of Obstetricians and Gynaecologists of Canada , in its 1993 Policy Statement, recommended that all women of child bearing potential, whether planning pregnancy or not, should consider maintaining a folic acid intake of at least 0.4 mg daily, either in the diet or as a supplement.

    Pregnant women with no previous history of fetal NTD and no other predisposing factors are advised to maintain an intake of at least 0.4 mg daily until 10 to 12 weeks after last menstrual period.
  19. tarjan.

    tarjan. Guest

    20) Vitamin “A†dosage is given in….? (№. of doses.)

    The World Health Organization recommends single-large-dose vitamin A supplementation for postpartum women in areas of prevalent vitamin A deficiency; neonatal dosing is under consideration.

    It is safe to give fertile women, independentof their vitamin A status, as much as 10,000IU (3000 µg RE) daily at any time duringpregnancy.


    21) What is Apoptosis?

    Apoptosis, by contrast, is a process in which cells play an active role in their own death (which is why apoptosis is often referred to as cell suicide).

    Apoptosis, or programmed cell death, is a normal component of the development and health of multicellular organisms. Cells die in response to a variety of stimuli and during apoptosis they do so in a controlled, regulated fashion.

    This makes apoptosis distinct from another form of cell death called necrosis in which uncontrolled cell death leads to lysis of cells, inflammatory responses and, potentially, to serious health problems.


    22) Extrinsic factor in blood coagulation? (PT/PTT)

    PT, PTT, D-DIMER

    This panel of tests is used to evaluate the extrinsic coagulation system. They may also aid in screening for congenital deficiencies of factors II, V, VII, X as well as deficiencies of prothrombin dysfibrinogenemia, and afibrinogenemia. Levels of PT, PTT and D-dimmer, can determine heparin effect, warfarin anticoagulant therapy, liver failure, disseminated intravascular coagulation (DIC), vitamin K deficiency. This test includes the following: prothrombin time (PT) and partial thromboplastin time (PTT), and D-dimmer.

    Prothrombin time (PT)

    This test is used to evaluate the adequacy of the extrinsic system and common pathway in the clotting mechanism. Prothrombin time (PT) test provides a control for long-term anticoagulant therapy that usually involves the use of a coumarin derivative (eg, Coumadin®).This therapy attempts to impede thrombus formation without the threat of mortality from hemorrhage.

    Partial Thromboplastin Time

    This test is used to evaluate the intrinsic coagulation system. It is also used to monitor heparin therapy, to aid in detecting classical hemophilia A, Christmas disease, and detection of congenital deficiencies of factors II, V, VIII, IX, X, XI, and XII. PTT is used to screen for the presence of dysfibrinogenemia, disseminated intravascular coagulation, liver failure, congenital hypofibrinogenemia, vitamin K deficiency, congenital deficiency of Fitzgerald factor, congenital deficiency of prekallikrein, high molecular weight kininogen, and circulatory anticoagulant.

    D-DIMER

    This test is a very specific confirmatory test for disseminated intravascular coagulation (DIC). This test is also used for the detection of deep vein thrombosis (DVT) and to detect acute myocardial infarction and unstable angina. The Fragment D-dimmer assess both thrombin and plasmin activity.



    23) Curschmann’s spirals are due to?

    Curschmann's spirals have been observed in the sputum of patients affected by lung cancer, asthma, chronic bronchitis, or in asymptomatic smokers.

    Spirally twisted masses of mucus occurring in the sputum in bronchial asthma.

    Curschmann's spirals:

    coiled, basophilic plugs of mucus formed in the lower airways and found in sputum and tracheal washings; indicate chronic obstruction.

    Curschmann's Spirals refer to parts of the desquamated epithelium seen in biopsies from asthmatic patients. They are named after German physician Heinrich Curschmann (1846-1910). They are often seen in association with eosinophilic infiltration and Charcot-Leyden crystals.

    However, to date, their clinical significance and pathogenesis have not been completely explained.


    24) Bell’s palsy?
    WHAT IS BELL'S PALSY?
    Bells palsy is a condition that causes the facial muscles to weaken or become paralyzed. It's caused by trauma to the 7th cranial nerve, and is not permanent.

    WHY IS IT CALLED BELL'S PALSY?
    The condition is named for Sir Charles Bell, a Scottish surgeon who studied the nerve and its innervation of the facial muscles 200 years ago.

    HOW COMMON IS BELL'S PALSY?
    Bells palsy is not as uncommon as is generally believed. Worldwide statistics set the frequency at approximately .02% of the population (with geographical variations). In human terms this is 1 of every 5000 people, and 40,000 Americans every year.

    IS BELL'S PALSY ALWAYS ON THE SAME SIDE?
    The percentage of left or right side cases is approximately equal, and remains equal for recurrences.

    IS THERE ANY DIFFERENCE BECAUSE OF GENDER OR RACE?
    The incidence of Bells palsy in males and females, as well as in the various races is also approximately equal. The chances of the condition being mild or severe, and the rate of recovery is also equal.

    WHAT CONDITIONS CAN INCREASE THE CHANCE OF HAVING BELL'S PALSY?
    Older people are more likely to be afflicted, but children are not immune to it. Children tend to recover well. Diabetics are more than 4 times more likely to develop Bells palsy than the general population. The last trimester of pregnancy is considered to be a time of increased risk for Bell's palsy. Conditions that compromise the immune system such as HIV or sarcoidosis increase the odds of facial paralysis occurring and recurring.

    CAN BELL'S PALSY AFFECT BOTH SIDES OF THE FACE?
    It is possible to have bilateral Bells palsy, but it's rare, accounting for less than 1% of cases. With bilateral facial palsy, it's important to rule out all other possible diagnoses with thorough diagnostic tests.

    CAN BELL'S PALSY AFFECT OTHER PARTS OF THE BODY?
    Bells palsy should not cause any other part of the body to become paralyzed, weak or numb. If any other areas are affected Bell's palsy is not the cause of the symptoms, and further testing must be done.

    HOW DO THE SYMPTOMS OF BELL'S PALSY PROGRESS?
    Very quickly. Most people either wake up to find they have Bells palsy, or have symptoms such as a dry eye or tingling around their lips that progress to classic Bell's palsy during that same day. Occasionally symptoms may take a few days to be recognizable as Bells palsy. The degree of paralysis should peak within several days of onset - never in longer than 2 weeks (3 weeks maximum for Ramsey Hunt syndrome). A warning sign may be neck pain, or pain in or behind the ear prior to palsy, but it is not usually recognized in first-time cases.

    IS BELL'S PALSY CONTAGIOUS?
    No, it is not contagious. People with Bells palsy can return to work and resume normal activity as soon as they feel up to it.

    WHAT ABOUT RECOVERY FROM BELL'S PALSY?
    Approximately 50% of Bells palsy patients will have essentially complete recoveries in a short time. Another 35% will have good recoveries in less than a year.

    Regardless of the trigger, Bell's palsy is best described as an event - trauma to the nerve. As with any other injury, healing follows. The quality and duration of recovery is dependent on the severity of the initial injury. If the nerve has suffered nothing more than a mild trauma, recovery can be very fast, taking several days to several weeks. An "average" recovery is likely to take between a few weeks and a few months. The nerve regenerates at a rate of approximately 1-2 millimeters per day, and can continue to regenerate for 18 months, probably even longer. Improvement of appearance can continue beyond that time frame.

    IS MUSCLE ATROPHY A CONCERN?
    Not as a rule. It takes longer for the muscles to start to atrophy than it takes for most people to fully recover.

    IS BELL'S PALSY LIKELY TO HAPPEN AGAIN?
    The possibility of recurrence had been thought to be as high as 10 - 20%. These figures have been lowered as more has been learned about conditions that are now diagnosed as other types of facial palsies. Estimates of the rate of recurrence still vary widely, from around 4 - 14%. Most recent reports hover at 5 - 9%. The average timespan between recurrences is 10 years.



    25) In Dialysis which toxicity is seen commonly?

    Aluminum toxicity

    Aluminum toxicity, prevalent among individuals with chronic renal failure, is associated with disabling osteomalacia, encephalopathy, and anemia.

    The control of aluminum intake has included standards to limit the amount of aluminum in the dialysis fluid in addition to the use of nonaluminum containing phosphate binders.

    Deferoxamine mesylate, a heavy metal chelating agent, is used to remove aluminum from the tissues of dialysis patients. Chelation therapy has resulted in improvements of clinical symptoms and bone histology. Ocular, auditory, and infectious adverse effects have occurred with the use of deferoxamine.


    26) TOC for Gastric ulcer?

    For people with Helicobacter pylori infection, the main goal is to get rid of the bacteria that causes the infection.

    H2 receptor antagonist such as famotidine (Pepcid) or nizatidine (Axid) or a proton pump inhibitor such as omeprazole (Prilosec) or esomeprazole (Nexium) to suppress acid, combined with two antibiotics.

    Those who do not have an H. pylori infection may be prescribed ulcer-healing medications such as antacids, H2 receptor antagonists, or proton pump inhibitors. Long-term treatment may be needed.

    If the ulcer bleeds, endoscopy can control bleeding in most cases.

    Surgery may be recommended for persons who do not respond to medicines or endoscopy. Surgical procedures for gastric ulcers include:

    Vagotomy -- cuts the vagus nerve, which controls the stomach's production of gastric acid
    Partial gastrectomy -- removes part of the stomach
  20. sujjain.

    sujjain. Guest

    27) Squamous non-keratinizing is seen in….?

    Squamous nonkeratinizing

    Function: barrier, protection.
    Location: wet surfaces: oral cavity, esophagus, and vagina.

    Origin: ectoderm
    • cells of basal layer (stratum germinatinum, stratum basale)

    • cells of stratum spinosum

    • squamous cells


    Stratified squamous keratinizing (epidermis)

    Function: barrier, protection.

    Location: dry surfaces: skin.

    Origin: ectoderm
    • keratinocytes of stratum germinatinum (stratum basale)

    • keratinocytes of stratum spinosum

    • keratinocytes of stratum granulosum

    • keratinocytes of stratum lucidum

    • squames of keratin of stratum corneum

    • melanocytes

    Stratified cuboidal & columnar

    Function: barrier, conduit.

    Location: sweat gland, ducts of exocrine glands, anorectal junction.

    Origin: ectoderm


    Transitional

    Function: barrier, distensible property.

    Location: renal calyces, ureters, bladder, urethra.

    Origin: mesoderm
  21. sujjain.

    sujjain. Guest

    28) Tumour marker CA-125 is related to pancreatic Ca &…….?



    The utility of following CA 125 levels in pancreatic cancer has undergone significant scrutiny in the last decade. Most notably it has been compared with CA19-9, a tumor marker with proven prognostic value in the treatment of pancreatic cancer. In head to head comparisons CA 125 demonstrated both a lower ability to detect a problem (low sensitivity) and a higher likelihood of being abnormal in a healthy patient (low specificity).

    If CA 125 has a present role in the treatment of pancreatic disease it appears to be in the differentiation of pancreatic cancer from pancreatitis. Haga showed that CA 125 level were apt to be elevated in pancreatic cancer but not in pancreatitis. When combined with the relative reliability of CA19-9 levels one may conclude both that a process is of pancreatic origin and is, or is not, malignant.

    Once malignancy is proven there appears no additional benefit in following the CA 125 level. Even this use is presently disputed in patients with chronic pancreatitis.
  22. sujjain.

    sujjain. Guest

    CA 125 is a glycoprotein and a commonly used tumor marker in ovarian carcinoma.

    CA-125.is a tumor marker for ovarian cancer and occasionally cancer of the uterus. It is useful to have this test done when cancer is suspected.

    However, this test is not always reliable. Some women with ovarian cancer may not have high levels of CA-125. High levels are common in women with advanced ovarian cancer. This tumor marker is also used to see how the body is responding to treatment.

    If the level of CA-125 in the blood goes down after treatment, the disease is probably responding. If the level goes up, the disease may be getting worse.
  23. sujjain.

    sujjain. Guest

    31) The hormone helps in milk secretion?


    Anatomy of the female breast


    Each nipple has 15 to 20 openings for milk to flow.

    When your baby nurses, the action of baby’s jaw and tongue pressing down on the milk sinuses creates suction. This causes the milk to flow out of your breast and into your baby’s mouth.


    The let-down reflex

    How your body responds to your baby’s suckling:

    Infant suckling stimulates the nerve endings in the nipple and areola, which signal the pituitary gland in the brain to release two hormones, prolactin and oxytocin.


    How Your Breast Responds to Your Baby’s Suckling:

    •Prolactin causes your alveoli to take nutrients (proteins, sugars) from your blood supply and turn them into breast milk.


    •Oxytocin causes the cells around the alveoli to contract and eject your milk down the milk ducts. This passing of the milk down the ducts is called the “let-down†(milk ejection) reflex.
  24. tarjan.

    tarjan. Guest

    32) Most abundant ICF is
    • Potassium (K+)
    --------------

    o
    • Potassium (K+) creates most of the osmotic pressure in intracellular fluid (ICF), and is the most abundant cation in ICF.


    -------------------------------

    Electrolytes are chemicals that dissolve in water and dissociate into their positive and negative ions (an element that carries an electrical charge).
    Most electrolytes are inorganic salts, acids, and bases found in all body fluids. Organic compounds are usually non-electrolytes, meaning that they do not ionize in a solution.

    Positive ions are called cations (sodium Na+, potassium K+, calcium Ca+2, magnesium Mg+2 , iron Fe+2 , and hydrogen H+ ). In intracellular fluid, the most abundant cation is potassium. In both tissue fluid and plasma, the most abundant cation is sodium.

    Negative ions are called anions (chloride Cl¬, bicarbonate HCO3-, sulfate SO4-2, phosphate HPO4-2, and protein anions). In intracellular fluid, the most abundant anion is HPO4-2, along with protein anions. In both tissue fluid and plasma, the most abundant anion is chloride. Protein anions form a significant part of plasma, but not of tissue fluid.

    Electrolytes help regulate the osmosis of water between water compartments. Some are involved in acid-base regulations. They can also be part of the structural components of tissues or enzymes.

    Major electrolytes and their functions

    Sodium (Na+) creates most of the osmotic pressure of extracellular fluid (ECF), and is the most abundant cation in ECF. It is essential for electrical activity of neurons and muscle cells. The primary mechanism regulating sodium concentration is aldosterone, which stimulates the distal tubule of the nephron unit to reabsorb sodium. Imbalances cause hypo- or hypernaturemia.

    Hyponaturemia is a consequence of excessive sweating, diarrhea, or vomiting causing dizziness, confusion, weakness, low BP, and shock.

    Hypernaturemia is a consequence of excessive water loss or sodium ingestion, causing a loss of ICF characterized by extreme thirst and agitation.


    Potassium (K+) creates most of the osmotic pressure in intracellular fluid (ICF), and is the most abundant cation in ICF. It is essential for electrical activity of neurons and muscle cells. The primary substance regulating potassium concentration is aldosterone, which stimulates the distal tubule of the nephron unit to excrete potassium. Imbalances cause hypo- or hyperkalemia.

    Hypokalemia is a consequence of vomiting, diarrhea, or kidney disease causing fatigue, confusion, and possible cardiac failure.
    Hyperkalemia is a consequence of Addison's disease causing weakness, abnormal sensations, and cardiac arrhythmias with possible arrest.


    Calcium (Ca+2) - [snip]% of the body’s calcium is found in bones and teeth. It maintains normal excitability of neurons and muscle cells and is essential for blood clotting. The primary regulator of plasma levels of calcium stems from the parathyroid hormone. Imbalances cause hypo- or hypercalcemia.

    Hypocalcemia is a consequence of hypoparathyroidism or decreased calcium intake, which results in muscle spasms leading to tetany.
    Hypercalcemia is a consequence of hyperparathyroidism resulting in muscle weakness, bone fragility, and possible kidney stones.

    Magnesium (Mg+2) – 50% of the body’s magnesium is found in bone. It is the most abundant cation in ICF and essential for ATP production as well as activity of neurons and muscle cells, especially the heart.

    Chloride (Cl¬) is the most abundant anion in ECF. It diffuses easily into and out of cells. It helps regulate osmotic pressure. Chloride is a part of HCl (hydrochloric acid) in gastric juices and tends passively to follow sodium.

    Bicarbonate (HCO3-) is an important anion of the bicarbonate buffer system. It is the form used to transport carbon dioxide in the blood. Excretion is controlled by the kidneys and can be reabsorbed, if the need arises.

    Phosphate (HPO4-2) – 85% of the body’s phosphate is found in bones and teeth. It is primarily an ICF anion. Phosphate is part of DNA, RNA, ATP, and phopholipids, as well as the phosphate buffer system.


    Sulfate (SO4-2) is part of some amino acids and proteins.
  25. tarjan.

    tarjan. Guest

    33) Features like-Hypogonadism, Loss of Hair, Pigmentation of skin Etc..etc Deficiency due to?

    Hypogonadism :

    Male hypogonadism refers to an inability of the testes to produce testosterone (male sex hormone), sperm or both. The condition is also referred to as testosterone deficiency. The testicles are oval-shaped sex organs (gonads) that reside in a fold of skin (scrotum) behind the penis.

    The testes produce sperm necessary for reproduction and testosterone which maintains male secondary sex characteristics (such as body hair, facial hair, muscle mass, deep voice), sexual drive and helps spermatogenesis (sperm production).


    Androgen deficiency ?

    Androgen deficiency in men means the body has lower than normal amounts of male hormones, including testosterone.

    This deficiency may be caused by problems in the brain signals to the testes or problems in the testes. Treatment involves testosterone replacement therapy. Androgen deficiency is sometimes called ‘male menopause’ but this is misleading.
  26. tarjan.

    tarjan. Guest

    35) Negri bodies are characteristic of ?

    Description:

    Cytoplasmatic Inclusion bodies found in the purkinje cells of the brain in cases of rabies. Negri's bodies are important becuse their presence make possible a positive diagnosis of rabies.

    Negri bodies as round or oval inclusions within the cytoplasm of nerve cells of animals infected with rabies. Negri bodies may vary in size from 0.25 to 27 µm.

    They are found most frequently in the pyramidal cells of Ammon's horn, and the Purkinje cells of the cerebellum. They are also found in the cells of the medulla and various other ganglia. Negri bodies can also be found in the neurons of the salivary glands, tongue, or other organs. Staining with Mann's, giemsa, or Sellers stains can permit differentiation of rabies inclusions from other intracellular inclusions. With these stains, Negri bodies appear magenta in color and have small (0.2 µm to 0.5 µm), dark-blue interior basophilic granules.
  27. tarjan.

    tarjan. Guest

    36) M.C opportunistic Infection in immuno compromised patient?

    Persons immunocompromised due to human immunodeficiency virus (HIV) infection or cancer can be strongly affected by herpesviruses.

    HUMAN IMMUNODEFICIENCY VIRUS (HIV) AND HERPES SIMPLEX VIRUS (HSV) COINFECTION

    HSV is the most common opportunistic infection in HIV-infected American adults, with 50% to 80% of HIV-seropositive males coinfected with HSV-2, and perhaps 90% or more coinfected with HSV-1.

    Coinfection with HSV-2 is also extremely common in HIV-infected pregnant women, with 75% found to have HSV-2 antibodies compared with 32% of those who are HIV seronegative. This coinfection increases the risk of HIV disease progression, decreases survival rates, and alters the natural history of HSV-2 through the complex interrelationship between the 2 viruses.
    Effect of HIV on HSV Disease
    Although genital herpes may be as unrecognizable in persons with early stage HIV infection as it is in HIV-seronegative individuals, outbreaks of HSV-2 infection are generally more severe, extensive, persistent, and invasive in those with more advanced HIV disease. First-episode genital herpes in this population can be characterized by extensive and progressive anogenital lesions and systemic symptoms, while reactivation of HSV infection can present as multiple necrotic lesions in atypical locations, particularly in the perirectal area. Symptoms can include large sloughing ulcers, rectal spasm with tenesmus, severe pain, obstipation, sacral paresthesias, and bacterial superinfection. Orolabial lesions can also progress to severe disease, such as oral stomatitis or esophagitis. Furthermore, individuals coinfected with HSV-2 and HIV are 3 to 7 times more likely to symptomatically and asymptomatically shed HSV-2 than those who are HIV seronegative. This increased likelihood of shedding puts HIV-infected persons at greater risk of unwittingly transmitting HSV, particularly when such shedding is asymptomatic.
    Effect of HSV on HIV
    Disease Reactivation of HSV-2 accelerates the progression of HIV disease toward and beyond AIDS. Acute HSV infection has been shown to result in a significant increase in levels of HIV RNA. Reactivation of HSV in the prior year was reported to be significantly associated with the rapid onset of AIDS.
    Diagnosis of HSV Infection in HIV-Seropositive Persons
    HSV antibody status can be easily determined by type-specific serological testing, while the causative agent of ulcers can be confirmed by viral culture. Once HSV status is known, patients can be counseled about virus transmission and, if HSV seropositive, appropriately managed. For example, HIV-seropositive pregnant women may require cesarean section delivery if HSV reactivates at delivery, while HIV-seropositive individuals in HSV-discordant relationships may need to desist from oral sex and use condoms during sexual activities.
    Treatment of HSV Infection in HIV-Seropositive Persons
    Because of the complex molecular interaction between HIV and HSV, coinfected patients need to be managed far more aggressively than patients infected with HSV alone. By optimizing control of HIV disease with highly active antiretroviral therapy (HAART), the reactivation of HSV-2 will be reduced. In addition, antiherpes therapy may help to control HIV disease and reduce HIV transmission and acquisition. Although the antiherpes drugs, acyclovir, famciclovir, foscarnet, and valacyclovir, are effective in the HIV-infected patient, in coinfected patients they often work more slowly and higher doses may be required (eg, acyclovir 400 mg 3-5 times daily for 10 or more days for episodic therapy). Furthermore, HSV is likely to be more resistant to antiviral therapy in individuals coinfected with HIV, though the level of resistance remains fairly low. Nonetheless, aggressive antiherpes therapy will usually limit and resolve HSV disease in the HIV-infected individual, even when HSV manifestations are severe.
  28. Shubham.

    Shubham. Guest

    37) Mallory-weiss syndrome? (Mallory bodies seen with….?)

    Mallory-Weiss tears occur more commonly in patients with hiatal hernias.


    Mallory-Weiss tear

    In 1929, Kenneth Mallory and Soma Weiss first described a syndrome characterized by esophageal bleeding from a mucosal tear in the esophagus as a result of forceful vomiting or retching. The initial description was associated with alcoholic bingeing; however, with the advent of endoscopy, Mallory-Weiss tears have been diagnosed in many patients with no history of alcohol intake.


    Any disorder that initiates vomiting may also result in the development of a Mallory-Weiss tear, which occurs as a linear laceration at the gastroesophageal junction. At this point, the esophagus and stomach are cylindrical; the cylindrical shape makes longitudinal tears occur more easily than circumferential tears.

    Two mechanisms are postulated to play a part in the development of Mallory-Weiss tears:

    1. A rapid increase in intragastric pressure that increases forceful fluid ejection through the esophagus.


    2. A significant change in transgastric pressure (ie, a difference in pressure across the gastric wall) caused by negative intrathoracic pressure and positive intragastric pressure, which leads to distortion of the gastric cardia and results in a gastric or esophageal tear.


    Because of these factors, Mallory-Weiss tears occur more commonly in patients with hiatal hernias.
  29. Shubham.

    Shubham. Guest

    Mallory-Weiss Syndrome

    Mallory-Weiss syndrome is a condition in which the inner lining of the esophagus tears at or near where it connects to the stomach.


    Symptoms

    A person with this condition will vomit blood or pass black, sticky stools after periods of vomiting, retching or coughing. Immediate medical attention should be sought if these symptoms are present.


    Causes and Risk Factors

    Mallory-Weiss syndrome can be caused by severe coughing, retching or vomiting.


    Diagnosis

    For a diagnosis, a doctor usually performs an upper GI endoscopy to see the site of bleeding.


    Treatment

    In most cases, this condition stops bleeding and heals with no specific therapy. If the bleeding does not stop, the following can be used to treat it:

    •Injection therapy is done by inserting a needle through an endoscope to a point near the site of bleeding. Epinephrine, which makes blood vessels close off, is injected to stop the bleeding.

    •Coagulation therapy is done by passing a special probe that heats up through an endoscope to the site to stop the bleeding.

    •Arteriography is a special X-ray test that allows doctors to see arteries. A thin catheter is placed in the artery, where the bleeding is thought to be. A special dye is injected into it while X-rays are taken. After the bleeding artery is identified, the bleeding is stopped. This is done by injecting either vaopressin, a drug that makes blood vessels close off, or a substance that plugs the artery.
  30. Shubham.

    Shubham. Guest

    39) Glucose is reabsorbed at?

    The Proximal Tubule: Reabsorption and Secretion

    Glucose and amino acids are reabsorbed across the luminal face of the proximal tubule by sodium-coupled secondary active transport.

    The inwardly directed Na+ gradient that energises glucose and amino acid uptake is created and maintained by primary (ATP dependent) active transport of Na+ out of the cells.

    The proximal tubule is composed of polarised epithelial cells and the Na+ pump is found only on the basolateral (blood side) membrane.

    Thus the Na+ that enters along with the glucose at the luminal membrane is also reabsorbed. Chloride and bicarbonate are the main anions that follow Na+ to preserve electroneutrality.
  31. Shubham.

    Shubham. Guest

    40) M.C pemphigus seen in India?
    PV is most common in Tamil Hindus. The fact that PV is the commonest variant of pemphigus seen in Indians


    PV patients share features in common with patients from their land of origin (India), suggesting a genetic link.

    Pemphigus
    Pemphigus is a group of rare autoimmune blistering diseases of the skin and/or mucous membranes. Pemphigus is not contagious - not even blood to blood.

    The term pemphigus refers to a group of autoimmune blistering diseases of the skin and mucous membranes characterized histologically by intradermal blister and immunopathologically by the finding of in vivo bound and circulating immunoglobulin G (IgG) antibody directed against the cell surface of keratinocytes.

    The 3 primary subsets of pemphigus include pemphigus vulgaris (PV), pemphigus foliaceus, and paraneoplastic pemphigus.

    Each type of pemphigus has distinct clinical and immunopathologic features.

    PV accounts for approximately 70% of pemphigus cases.
  32. harsha.

    harsha. Guest

    41) India ia at which stage of Demographic?

    India's national savings have risen over the last two decades from 19 per cent to 23.5 per cent of national income. But the composition is revealing.

    Household savings have risen sharply from 14 per cent to 22 per cent and corporate savings from 1.5 per cent to 4 per cent; public savings, however, have fallen from 3.5 per cent to minus 2.5 per cent.

    The expected demographic trends suggest, in the light of experience elsewhere, that over the next decade India's national savings rate could rise to around 30 per cent if public savings do not fall further, and to about 32 per cent if public dissaving is eliminated.
  33. harsha.

    harsha. Guest

    42) Urinary incontinence in Older people is due to……?


    Urinary and faecal (rectal urgency) incontinence can be considered a risk factor for falls in
    two ways.

    Firstly, there is the incontinence episode and associated potential for a slip on the
    soiled or wet floor surface.

    Secondly, in the presence of urge incontinence, the risk of
    falling may increase when a person hurries to the toilet to avoid soiling themselves and the
    subsequent difficulties in cleaning their undergarments.

    Limited ambulatory ability, poor
    balance and a tendency to fall make it difficult to reach the toilet and thereby increase the risk
    of incontinence.
  34. harsha.

    harsha. Guest

    46) Kussmaul breathing is due to or seen in ………?


    Kussmaul breathing is the rapid, deep, and labored breathing of people who have acidosis.

    Kussmaul breathing is named for Adolph Kussmaul , the 19th century German doctor who first noted it.

    It is also called "air hunger".
    The cause of Kussmaul breathing is respiratory compensation for a metabolic acidosis , most commonly occurring in diabetics in diabetic ketoacidosis.

    Blood gases on a patient with Kussmaul breathing will show a low p CO2 because of a forced increased respiratory rate (blowing off the carbon dioxide).

    The patient feels an urge to breathe deeply, and it appears almost involuntary.
  35. harsha.

    harsha. Guest

    Kussmaul breathing: deep, regular breathing due to metabolic acidosis (diabetic acidosis & coma), and the rate may be fast, normal or slow

    Apnea: cessation of respiration lasting from 2 to 60 second. Seen in Primary Respiratory disorders:Respiratory Distress syndrome, Bronchopulmonary dysplasia; Infection/Inflammation: Pertussis, Pneumonia, Septicemia, Meningitis, Bronchioloitis; Drug related: Drug withdrawal (maternal addiction), Early cessation of theophylline/aminophylline, Analgesic or anaesthetic drugs in labor; CNS: Convulsions, Intracranial haemorrhage: tentorial tear, intraventricular haemorrhage, subdural haemorrhage, cerebral edema; Gastrointestinal disorders: Gastroesophageal reflux; Cardiac disorders: congenital heart disease, cardiac conduction disorders (rare); Sleep apnea: enlarged tonsils and adenoids, extreme obesity (rare), narcolepsy (rare), primary alveolar hypoventilation (rare); Other: Hypoglycemia/Hypocalcaemia, Obstruction of the nasal airway by vomitus, milk, mucus, nasogastric feeding tube, meconium, choanal atresisa (rare), Other airway obstructions: transient obstruction at level of larynx, excessive flexion of neck, mandibular hypoplasia (Pierre-Robin syndrome), Preterm, Introduction of milk feed in preterm infants, Hypoxia: birth asphyxia, acute hypoxia, anaemia
    Unpleasant stimulus, Low or high body temperature, Arnold-Chiari malformation/hydrocephalus/Inborn errors of metabolism (rare), Munchausen syndrome by proxy (rare)/Joubert syndrome (rare)


    Biots’ Breathing: Characterized by several short breaths followed by long irregular periods of apnea. It is seen in increase intracranial pressure

    Cheyne-Stokes respiration: periods of apnea of 10-20 sec separated by approximately equal periods of hyperventilation.

    This may be a normal pattern for children during sleep. Seen in Severe heart disease; congestive heart failure, Brain damage (typically on both sides of the cerebral hemispheres of diencephalon), Uremia, Drug-induced respiratory depression, Increased intracranial pressure
  36. harsha.

    harsha. Guest

    47) Cellulitis is caused by…….?


    Cellulitis is an infection of the dermis and subcutaneous tissue that has poorly demarcated borders and is usually caused by Streptococcus or Staphylococcus but can be caused by a wide range of both aerobic and anaerobic bacteria.

    Epidemiology

    • Cellulits is a common problem and a common presentation in primary care.

    • Cellulitis is more common and more serious in individuals with underlying diseases such as diabetes, cancer, or immunodeficiency.1
    Causes

    • The most common bacteria that cause cellulitis in patients with a healthy immune system are Group A Beta Haemolytic Streptococcus (Streptococcus pyogenes) and Staphylococcus aureus.

    • Rarely, gram-negative organisms, anaerobes, or fungi may cause cellulitis. However these organisms are more common causes in children, people with diabetes and immunocompromised individuals.2

    • Cellulitis in infants is usually caused by bloodborne spread of group B Streptococcus (urgent admission is required).

    • In children, Haemophilus influenzae was a frequent cause prior to the introduction of the HiB vaccination.

    • Cellulitis occurring around surgical wounds less than 24 hours post-operatively may result from Group A Beta Haemolytic Streptococcus or Clostridium perfringens. C. perfringens produces gas, leading to crepitus on examination.

    • Cellulitis is being seen with increasing frequency in HIV-infected patients.
  37. harsha.

    harsha. Guest

    What is cellulitis?

    Cellulitis is a skin infection caused by bacteria. Normally, your skin helps protect you from infection. But if you have a cut, sore, or insect bite, bacteria can get into the skin and spread to deeper tissues. If it is not treated with antibiotics, the infection can spread to the blood or lymph nodes. This can be deadly.

    Some people can get cellulitis without having a break in the skin. These include older adults and people who have diabetes or a weak immune system. These people are also more likely to develop dangerous problems from cellulitis. And they are more likely to get cellulitis again.

    What causes cellulitis?

    Cellulitis is caused by bacteria (usually strep or staph). Some people are at risk for infection by other types of bacteria. They include people with weak immune systems and those who handle fish, meat, poultry, or soil without using gloves.

    What are the symptoms?

    At first, the infected area will be warm, red, swollen, and tender. As the infection spreads, you may have a fever, chills, and swollen glands.

    Cellulitis can occur anywhere on the body. In adults, it often occurs on the legs, face, or arms. In children, it is most common on the face or around the anus. An infection on the face could lead to a dangerous eye infection.

    See a doctor right away if you have an infected area of skin and:

    The infected area is getting redder, more painful, or larger, or it has red streaks extending from it.
    You have a fever or chills.
    The infected area is on your face or your groin.

    How do you get cellulitis?

    There are many ways to get cellulitis. You can get it if you have:

    An injury to your skin, such as a cut, surgical wound, burn, or animal or insect bite.

    Skin problems, such as ulcers, eczema, psoriasis, or a fungal infection like athlete's foot.

    Certain medical conditions. These include diabetes, peripheral arterial disease, or a weak immune system.
    Fluid buildup (edema) in the legs or arms.
    Had liposuction to remove excess fat.
    Injected illegal drugs under your skin.

    How is it treated?

    Doctors use antibiotics to treat cellulitis. If the infection is mild, you may be able to take antibiotic pills at home. If the infection is severe, you may need to be treated in the hospital with antibiotics that go right into your bloodstream.

    If your doctor prescribes antibiotics, it is important to take them as directed. Do not stop taking them just because you feel better. You need to take the full course of antibiotics.

    It is very important to get treatment right away for cellulitis. If it is not treated, the bacteria can spread quickly through the body and cause sepsis, an extreme response by the body’s defense system. This can be deadly. Cellulitis on the face can spread to the brain and cause a dangerous infection (meningitis). Cellulitis can also cause other serious problems, such as blood clots in the legs (thrombophlebitis).

    You are more likely to have these problems if you are an older adult, have a medical condition such as diabetes or peripheral arterial disease, or have a weak immune system. Your chances of the cellulitis coming back may be higher too.

    How can you prevent cellulitis?

    If you are at risk for cellulitis, you can take steps to help prevent it.

    Take good care of your skin. Keep it clean, and use lotion to prevent drying and cracking.

    Check your feet and legs often. This is especially important if you have diabetes.

    Treat any skin infection, such as athlete’s foot, right away.
    Ask your doctor if you need to take antibiotics on a regular basis to prevent cellulitis.
  38. harsha.

    harsha. Guest

    49) Gynaecomastia is due to drugs……..?
    It may occur at any time and there are a number of causes, some physiological and others pathological. Pathological causes involve an imbalance between the activity of androgens and oestrogens - the former is decreased compared to the latter.2

    Epidemiology
    •Gynaecomastia is common and is thought to be present in more than 30% of men, with much higher rates in men over the age of 70 years (e.g. up to 55% at autopsy).1,2 In comparison breast cancer is only detected in 1% of cases of male breast enlargement.
    •65-90% of neonates have gynaecomastia due to the transfer of maternal oestrogen and progesterone.1
    Pathophysiology
    Oestrogen stimulates breast tissue growth whilst androgens inhibit it. The important factor is the ratio of active androgens to oestrogens. The ratio can be altered as a result of reduced testosterone production/action or enhanced oestrogen production/action or both. Once this ratio falls breast tissue is stimulated to grow. This leads to proliferation of breast ducts and fibroblastic stroma. If the stimulus to proliferation continues then the ducts and fibroblastic stroma are replaced by fibrosis and gynaecomastia becomes well established and irreversible.

    Aromatase is one of the cytochrome P450 enzymes and is involved in the aromatisation of androgens to oestrogens e.g. changing androstenedione to estrone and testosterone to oestradiol. This enzyme is found in many tissues e.g. brain, adipose tissue, blood vessels and the gonads. Enhanced adipose tissue, as in obesity, provides increased levels of the enzyme and hence, increased production of oestrogens leading to gynaecomastia


    Drugs:
    Drugs account for 20% of all cases in adult men:

    ◦Oestrogen e.g. OCP, digoxin, diethylstilbestrol

    ◦Gonadotrophins

    ◦Antipsychotics (blocks dopamine - leading to increased prolactin release from the pituitary)

    ◦Flutamide - blocks androgen receptors2

    ◦Inhibitors of testosterone e.g. finasteride, metronidazole, spironolactone, alkylating agents

    ◦Anabolic steroid abuse

    ◦Others e.g. amiodarone, isoniazid, cimetidine, methyldopa, tricyclic antidepressants, diazepam, calcium channel blockers, heroin

    Cosmetics e.g. lavender and tea tree oil products (stops once offending cosmetic removed)
  39. harsha.

    harsha. Guest

    50) In a new born Jaundice occurs on 3-5days;its not due to ……….?

    A common condition in newborns, jaundice refers to the yellow color of the skin and whites of the eyes caused by excess bilirubin in the blood. Bilirubin is produced by the normal breakdown of red blood cells.

    Normally, bilirubin passes through the liver and is excreted as bile through the intestines. Jaundice occurs when bilirubin builds up faster than a newborn's liver can break it down and pass it from the body. Reasons for this include:

    •Newborns make more bilirubin than adults do since they have more turnover of red blood cells.
    •A newborn baby's still-developing liver may not yet be able to remove adequate bilirubin from the blood.
    •Too large an amount of bilirubin is reabsorbed from the intestines before the baby gets rid of it in the stool.
    High levels of bilirubin — usually above 25 mg — can cause deafness, cerebral palsy, or other forms of brain damage in some babies. In less common cases, jaundice may indicate the presence of another condition, such as an infection or a thyroid problem. The American Academy of Pediatrics (AAP) recommends that all infants should be examined for jaundice within a few days of birth.

    Types of Jaundice
    The most common types of jaundice are:

    Physiological (normal) jaundice:
    occurring in most newborns, this mild jaundice is due to the immaturity of the baby's liver, which leads to a slow processing of bilirubin. It generally appears at 2 to 4 days of age and disappears by 1 to 2 weeks of age.

    Jaundice of prematurity:
    occurs frequently in premature babies since they are even less ready to excrete bilirubin effectively. Jaundice in premature babies needs to be treated at a lower bilirubin level than in full term babies in order to avoid complications.

    Breastfeeding jaundice:
    jaundice can occur when a breastfeeding baby is not getting enough breast milk because of difficulty with breastfeeding or because the mother's milk isn’t in yet. This is not caused by a problem with the breast milk itself, but by the baby not getting enough to drink.

    Breast milk jaundice:
    Iin 1% to 2% of breastfed babies, jaundice may be caused by substances produced in their mother's breast milk that can cause the bilirubin level to rise. These can prevent the excretion of bilirubin through the intestines. It starts after the first 3 to 5 days and slowly improves over 3 to 12 weeks.

    Blood group incompatibility (Rh or ABO problems):
    if a baby has a different blood type than the mother, the mother might produce antibodies that destroy the infant's red blood cells. This creates a sudden buildup of bilirubin in the baby's blood. Incompatibility jaundice can begin as early as the first day of life. Rh problems once caused the most severe form of jaundice, but now can be prevented with an injection of Rh immune globulin to the mother within 72 hours after delivery, which prevents her from forming antibodies that might endanger any subsequent babies.

    Symptoms and Diagnosis:

    Jaundice usually appears around the second or third day of life. It begins at the head and progresses downward. A jaundiced baby's skin will usually appear yellow first on the face, followed by the chest and stomach, and finally, the legs. It can also cause the whites of an infant's eyes to appear yellow.

    Since many babies are now released from the hospital at 1 or 2 days of life, it is best for the baby to be seen by a doctor within 1 to 2 days of leaving the hospital to check for jaundice. Parents should also keep an eye on their infants to detect jaundice.

    If you notice your baby’s skin or eyes looking yellow you should contact your child's doctor to see if significant jaundice is present.

    At the doctor's office, a small sample of your infant's blood can be tested to measure the bilirubin level. Some offices use a light meter to get an approximate measurement, and then if it is high, check a blood sample. The seriousness of the jaundice will vary based on how many hours old your child is and the presence of other medical conditions.

    When to Call the Doctor
    Your doctor should be called immediately if:

    •jaundice is noted during the first 24 hours of life
    •the jaundice is spreading or getting more intense
    •your baby develops a fever over 100° Fahrenheit (37.8° Celsius) rectally
    •if your child starts to look or act sick
    Also call the doctor right away if the color deepens, your baby is not feeding well, or if you feel your baby is sleepier than usual. It is difficult to tell how significant jaundice is just by looking at a baby, so any baby who has yellow eyes or skin should be checked by the doctor.

    Treatments

    In mild or moderate levels of jaundice, by 1 to 2 weeks of age the baby will take care of the excess bilirubin on its own. For high levels of jaundice, phototherapy — treatment with a special light that helps rid the body of the bilirubin by altering it or making it easier for your baby's liver to get rid of it — may be used.


    More frequent feedings of breast milk or supplementing with formula to help infants pass the bilirubin in their stools may also be recommended. In rare cases, a blood exchange may be required to give a baby fresh blood and remove the bilirubin.

    If your baby develops jaundice that seems to be from breast milk, your doctor may ask you to temporarily stop breastfeeding. During this time, you can pump your breasts so you can keep producing breast milk and you can start nursing again once the condition has cleared.

    If the amount of bilirubin is high, your baby may be readmitted to the hospital for treatment. Once the bilirubin level drops and the treatment is stopped, it is unlikely that treatment for jaundice will need to be restarted.
  40. harsha.

    harsha. Guest

    51) Transmitted by faeco-orally, Except ?
    Mode of Transmission

    HAV and HEV are transmitted by faeco-oral route through contamination of water and food.

    Important mechanisms of transmission of HBV are mother to infant in perinatal period, parenteral (through infected needles and syringes, blood transfusion), and sexual routes. Intimate physical contact especially in infants and children has also been postulated to cause transmission of HBV infection. HCV is usually transmitted by parenteral route; the risk of transmission by household contact and sexual activity appears to be very low. HDV which needs the presence of HBV for its multiplication is transmitted like HBV. Only limited information is available for HGV; this virus can certainly be transmitted by parenteral route.

    MODE OF TRANSMISSION

    Hepatitis A & E -- Faecal-oral

    Hepatitis B ---contaminated blood and blood products contaminated (unsterile) syringes and needles

    Unsafe sex .-- perinatal, intimate physical contact between children or mother & child

    Hepatitis C, D & G -- contaminated blood and blood products contaminated (unsterile) syringes and needles
  41. Suman.

    Suman. Guest

    52) Beta-Thalassemia inherited as ……..?


    Beta-thalassemia is a common autosomal recessive disorder resulting from over 200 different mutations of β-globin gene. It results mainly from mutations either decreasing (Beta) or eliminating (Beta°) the expression of Beta-globin gene (1). Furthermore β-thalassemia is the most common inherited blood disorder

    Beta-thalassemia is the most common inherited single gene disorder worldwide, and glucose-6-phosphate dehydrogenase (G6PD) deficiency is the most common human enzyme deficiency.
  42. Suman.

    Suman. Guest

    53) Foreign body inhaled usually lodges in which lung?

    ANS: Right Lung


    Foreign body inhalation is a common and life-threatening emergency, and is most prevalent in young children. The traditional view is that tracheobronchial Anatomy determines that an inhaled foreign body is more likely to enter the right main bronchus.

    This view has been challenged in young children, in whom the distribution of inhaled objects is more evenly distributed between the bronchi.

    We, therefore, investigated tracheobronchial Anatomy relevant to foreign body inhalation in children.

    Materials and methods: One hundred and fifty-six normal pediatric chest radiographs were selected from a large electronic database. Eight groups of radiographs were identified: supine (n=76) and erect; males (n=84) and females; aged <3 years (median age 12 [0.5–29] months) and ≥3 years (median age 126 [48–180] months). Tracheobronchial widths and angles were determined using a standardized technique with good reproducibility.

    Results Overall, children had a proximal right main bronchus that was consistently steeper and slightly wider than the left (P<0.001), becoming more vertical in the erect position (P=0.0001). In most children, the carina was positioned to the left of the mid-trachea, but in 34% of cases (40% of infants), it was to the right of the mid-trachea. The effects of age and gender were otherwise minimal.


    Conclusion On the basis of tracheobronchial Anatomy , an inhaled foreign body is more likely to enter the right bronchial tree than the left in children of all ages. However, the variability in the position of the carina with respect to the mid-trachea may explain why this right-sided preference is less marked in children compared to adults.
  43. Suman.

    Suman. Guest

    54) Change in blood viscosity causes ………?



    Viscosity is a property of fluid related to the internal friction of adjacent fluid layers sliding past one another (see laminar flow) as well as the friction generated between the fluid and the wall of the vessel. This internal friction contributes to the resistance to flow. The viscosity of plasma is about 1.8-times the viscosity of water (termed relative viscosity) at 37°C and is related to the protein composition of the plasma. Whole blood has a relative viscosity of 3-4 depending upon hematocrit, temperature, and flow rate.

    The viscosity of whole blood is strongly influenced by three factors:

    1. hematocrit, 2. temperature 3. flow

    1. Hematocrit is an important determinant of the viscosity of blood. As hematocrit increases, there is a disproportionate increase in viscosity (see figure to right). For example, at a hematocrit of 40%, the relative viscosity is 4. At a hematocrit of 60%, the relative viscosity is about 8. Therefore, a 50% increase in hematocrit from a normal value increases blood viscosity by about 100%. Such changes in hematocrit and blood viscosity occur in a patients with polycythemia.

    2. Temperature also has a significant effect on viscosity. As temperature decreases, viscosity increases. Viscosity increases approximate 2% for each °C decrease in temperature. This effect has several implications. For example, when a person's hand is cooled by exposure to a cold environment, the increase in blood viscosity contributes to the decrease in blood flow (along with neural-mediated thermoregulatory mechanisms that constrict the vessels). The use of whole body hypothermia during certain surgical procedures also increases blood viscosity and therefore increases resistance to blood flow.

    3. The flow rate of blood also affects viscosity. At very low flow states in the microcirculation, as occurs during circulatory shock, the blood viscosity can increase quite significantly. This occurs because at low flow states there are increased cell-to-cell and protein-to-cell adhesive interactions that can cause erythrocytes to adhere to one another and increase the blood viscosity.
  44. Suman.

    Suman. Guest

    56) Food poisoning 4-6 hrs organism responsible ……..?

    Organism responsible: ----> Staphylococcus aureus

    Description : -----> Produces a heat-stable toxin

    Habitat: ----> Nose and throat of 30 to 50 percent of healthy population; also skin and superficial wounds.

    Types of Foods: -----> Meat and seafood salads, sandwich spreads and high salt foods.

    Symptoms : -----> Nausea, vomiting and diarrhea within 4 to 6 hours. No fever.

    Cause : -----> Poor personal hygiene and subsequent temperature abuse.

    Temperture Sensitivity: -----> No growth below 40o F. Bacteria are destroyed by normal cooking but toxin is heat-stable.
  45. Suman.

    Suman. Guest

    57) Dreaming is common in which type of sleep?


    A dream is mental activity (thoughts, images, emotions) occurring during sleep.


    Most dreams occur in conjunction with rapid eye movements; hence, they are said to occur during REM-sleep, a period typically taking up 20-25% of sleep time.


    Infants are believed to dream during about 50% of their sleep time. Dreams occurring during non-REM periods are said to occur during NREM-sleep.


    Sleep researchers divide up sleep time into stages, mainly defined by the electrical activity of cortical neurons represented as brain waves by an electroencephalograph (EEG). The EEG records electrical activity in the brain by connecting surface electrodes to the scalp. The stages of sleep occur in sequence and then go backward to stage 1 and REM-sleep about 90 minutes later. This cycle recurs throughout the night with the REM period typically getting longer at each recurrence.


    Typically, a person will have four or five REM periods a night, ranging from 5 to 45 minutes each in duration. There is some evidence, however, that REM-sleep evolved before dreaming and that the two are independent of one another.

    The REM-dream state is a neurologically and physiologically active state. When a person is in deep sleep there is no dreaming and the waves (called delta waves) come at a high amplitude about 3 per second. In REMsleep, the waves come at a rate of about 60-70 per second and the brain generates about five times as much electricity as when awake. Blood pressure, heart rate, breathing rate, etc. can change dramatically during REM-sleep.

    Since there is generally no external physical cause of these states, the stimuli must be internal, i.e., in the brain, or external and non-physical. The latter explanation--that dreams are a gateway to a paranormal or supernatural realm--seems to be largely without merit, although it is very ancient.


    Each of the following may have contributed to this misconception: dreams of dead persons, dreams of being in distant places or of raveling back or forth in time, dreams that seem prophetic, and dreams that are so strange, curious or bizarre that they call out for a paranormal nterpretation. The fact that the part of the brain that controls REM is the pons, a primitive section of the brain stem that controls reflexes like breathing, would support the notion that the stimuli for the physiological changes
  46. Suman.

    Suman. Guest

    58) Second heart sound is due to ……..?

    Heart sounds

    The heart sounds are the noises (sound) generated by the beating heart and the resultant flow of blood through it. This is also called a heartbeat.

    The first heart sound (S1) : ---->produced by the turbulent flow against the closed AV valves.

    S1
    The first heart tone, or S1, forms the "lubb" of "lubb-dub" and is composed of components M1 and T1. It is caused by the sudden block of reverse blood flow due to closure of the atrioventricular valves, i.e. mitral and tricuspid, at the beginning of ventricular contraction, or systole.


    When the pressure in the ventricles rises above the pressure in the atria, venous blood flow entering the ventricles is pushed back toward the atria, catching the valve leaflets, closing the inlet valves and preventing regurgitation of blood from the ventricles back into the atria. The S1 sound results from reverberation within the blood associated with the sudden block of flow reversal by the valves.


    second heart sound (S2): ------>produced by the turbulent flow against the closed semilunar valves .

    S2
    The second heart tone, or S2, forms the "dub" of "lubb-dub" and is composed of components A2 and P2. It is caused by the sudden block of reversing blood flow due to closure of the aortic valve and pulmonary valve at the end of ventricular systole, i.e beginning of ventricular diastole.

    As the left ventricle empties, its pressure falls below the pressure in the aorta, aortic blood flow quickly reverses back toward the left ventricle, catching the aortic valve leaflets and is stopped by aortic (outlet) valve closure. Similarly, as the pressure in the right ventricle falls below the pressure in the pulmonary artery, the pulmonary (outlet) valve closes. The S2 sound results from reverberation within the blood associated with the sudden block of flow reversal.


    -------------


    S3
    Main article: Third heart sound
    Rarely, there may be a third heart sound also called a protodiastolic gallop, ventricular gallop, or informally the "Kentucky" gallop as an onomatopoeic reference to the rhythm and stress of S1, S2, and S3 together (S1=ken; S2=tuc; S3=ky).

    It occurs at the beginning of diastole after S2 and is lower in pitch than S1 or S2 as it is not of valvular origin. The third heart sound is benign in youth and some trained athletes, but if it re-emerges later in life it may signal cardiac problems like a failing left ventricle as in dilated congestive heart failure (CHF.)

    S3 is thought to be caused by the oscillation of blood back and forth between the walls of the ventricles initiated by inrushing blood from the atria. The reason the third heart sound does not occur until the middle third of diastole is probably because during the early part of diastole, the ventricles are not filled sufficiently to create enough tension for reverberation. It may also be a result of tensing of the chordae tendineae during rapid filling and expansion of the ventricle..


    S4
    Main article: Fourth heart sound
    The rare fourth heart sound is sometimes audible in healthy children and again in trained athletes, but when audible in an adult is called a presystolic gallop or atrial gallop. This gallop is produced by the sound of blood being forced into a stiff/hypertrophic ventricle.

    It is a sign of a pathologic state, usually a failing left ventricle. The sound occurs just after atrial contraction ("atrial kick") at the end of diastole and immediately before S1, producing a rhythm sometimes referred to as the "Tennessee" gallop where S4 represents the "tenn-" syllable. The combined presence of S3 and S4 is a quadruple gallop. At rapid heart rates, S3 and S4 may merge to produce a summation gallop.
  47. Suman.

    Suman. Guest

    63) Spleenectomy is helpful in ……..?

    Splenectomy sometimes necessary


    Hodgkin's disease, a serious form of cancer that causes lymph nodes to enlarge. Splenectomy is often performed in order to find out how far the disease has progressed.


    Thrombotic thrombocytopenic purpura (TTP). TTP is a rare disorder marked by fever, kidney failure, and an abnormal decrease in the number of platelets. Splenectomy is one part of treatment for TTP.


    Autoimmune hemolytic disorders. These disorders may appear in patients of any age but are most common in patients over 50. The red blood cells are destroyed by antibodies produced by the patient's own body (autoantibodies).


    Myelofibrosis. Myelofibrosis is a disorder in which bone marrow is replaced by fibrous tissue. It produces severe and painful splenomegaly. Splenectomy does not cure myelofibrosis but may be performed to relieve pain caused by the swollen spleen.


    Thalassemia. Thalassemia is a hereditary form of anemia that is most common in people of Mediterranean origin. Splenectomy is sometimes performed if the patient's spleen has become painfully enlarged.
  48. Suman.

    Suman. Guest

    64) Incineration done for which of the following?


    Incineration is a waste treatment technology that involves the combustion of organic materials and/or substances.[1] Incineration and other high temperature waste treatment systems are described as "thermal treatment". Incineration of waste materials converts the waste into incinerator bottom ash, flue gases, particulates, and heat, which can in turn be used to generate electric power. The flue gases are cleaned of pollutants before they are dispersed in the atmosphere.

    Incineration with energy recovery is one of several waste-to-energy (WtE) technologies such as gasification, Plasma arc gasification, pyrolysis and anaerobic digestion. Incineration may also be implemented without energy and materials recovery.
  49. Suman.

    Suman. Guest

    65) Anti-gliadin antibodies are seen in?

    Anti-gliadin antibodies are produced in response to gliadin, a prolamin found in the wheat. In bread wheat it is encoded by three different genomes, AA, BB, and DD. These genomes can produce slight different gliadins, which can cause the body to produce different antibodies. Some of these antibodies can detect proteins in specific grass taxa such as Triticeae (Triticeae glutens), while others react sporadically across with certain species in those taxa, or over many taxonomically defined grass tribes.

    Anti-gliadin IgA: -->
    This antibody is found in ~80% of patients with coeliac disease.[1][2] It is directed against the alpha/beta and gamma (α,β,γ) gliadins.[3] It is also found in a number of patients who are not enteropathic. Some of these patients may have neuropathies that respond favorably to gluten elimination diet. This is referred to as gluten-sensitive idiopathic neuropathy.[4] Clinically these antibodies and IgG antibodies to gliadin are abbreviated as AGA.

    Anti-gliadin IgG: ----->
    IgG antibodies is similar to AGA IgA, but is found at higher levels in patients with the IgA-less phenotype. It is also associated with coeliac disease and idiopathic gluten sensitivity.[5][6][7] and IgA-less is associated with Coeliac disease. Anti-gliadin antibodies are frequently found with anti-transglutaminase antibodies.

    Anti-gliadin IgE:-->
    The IgE antibodies are more typically found in allergy-related conditions such as urticaria, asthma, and wheat-dependent exercise-induced anaphylaxis. The target of the most allergenic antibodies are ω-5 gliadin,[8] that is encoded by the Gli-1B gene found on the B haplome (Aegilops speltoides derived) of wheat.
  50. Suman.

    Suman. Guest

    66. The following are example of Apootosis Except- a) Graft versus host disease
    b) Menstrual cycle
    c) Pathological atrophy following duct obstruction d) Tumour necrosis

    Ans: b)



    Menstruation refers to the monthly shedding of the lining of the uterus (the womb), released through the vagina. The menstrual cycle begins the first day a woman bleeds – in other words, the first day of a period.

    --------------

    Apoptosis:

    Programmed cell death is called apoptosis.

    Programmed cell death is needed to destroy cells that represent a threat to the integrity of the organism.

    Examples:

    Cells infected with viruses:

    One of the methods by which cytotoxic T lymphocytes (CTLs) kill virus-infected cells is by inducing apoptosis.

    --
    Cells of the immune system:

    As cell-mediated immune responses wane, the effector cells must be removed to prevent them from attacking body constituents. CTLs induce apoptosis in each other and even in themselves. Defects in the apoptotic machinery is associated with autoimmune diseases such as lupus erythematosus and rheumatoid arthritis.


    Cells with DNA damage:

    Damage to its genome can cause a cell
    •to disrupt proper embryonic development leading to birth defects
    •to become cancerous.
    Cells respond to DNA damage by increasing their production of p53. p53 is a potent inducer of apoptosis.


    Cancer cells:
    Radiation and chemicals used in cancer therapy induce apoptosis in some types of cancer cells.

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