ALL INDIA PRE PG ENTRANCE EXAM 13 JAN 2008-POST RECALLS HERE

Discussion in 'NEET 2013 All india Exam' started by Dr.Sachin1984, Jan 11, 2008.

  1. FASFUR.

    FASFUR. Guest

    All are true about diploic veins except

    1. Lined by single layer endothelium supported by elastic tissue
    2. Present in cranial bones
    3. Valveless/thin walled
    4. Develop by 8th week of IUL


    Ans. 4. Seen at 8 weeks.
    Explanation: Primordia of skull (centre of ossification) start apeearing at 6-8th week(4) of intrauterine life.
    The skull is unilamellar at birth without any diploe.The diploic veins start to develop at around 2 years with the diploe.
    -At around 4th year the diploe appears and gets maximally differentiated by 35th year when the diploic veins are quite prominent radiologically.
    *Diploic veins are very thin(3) lined by endothelium, which is supported by some elastic tissue(1).
    -The are valveless(3) veins of the cranial bones(2), as are the other intracranial veins.
    -They anastomose with the dural venous sinuses, epicranial veins & meningeal veins.
    -Thrombosis of superior sagittal sinus may be caused by spread from diploe by diploic veins.
    References:
    Pg. 1580; Grays Anatomy (38th Ed.)
    Pg. 484; Grays Anatomy (39th Ed.)
    Pg. 96; BD Chaurasia-Vol-3 (4th Ed.)
  2. FASFUR.

    FASFUR. Guest

    Which is NOT a digastric muscle
    1. Omohyoid
    2. Sternocleidomastoid
    3. Occipitofrontalis
    4. Muscular fibres in the ligament of Trietz

    Ans. 2. Sternocleidomastoid
    Explanation: Sternocleidomastoid(2) has 2 heads and one belly, like biceps brachii muscle.
    -Muscles like omohyoid(1) and occipitofrontalis(3), have 2 bellies like superior & inferior belly of OH & occipital & frontal belly of OF.
    *Ligament of trietz is a fold of mesentery at the duodeno-jejunal junction.
    -This ligament contain a belly of skeletal muscle arising from the left crus of diaphragm and another belly of smooth muscle arising from the muscle coat of duodeno-jejunal flexure.
    Note:Gastrocnemius is a muscle with 2 heads & 2 bellies-it is also a digastric muscle !

    References:
    Pg. 113-14,500,536,538,1165;Grays Anatomy (39th Ed.)
    Pg. 369,262;Last clinical Anatomy (11th Ed.)
    Pg. 32;K L moore (5th Ed.)
  3. Dermatology answers

    Hi all

    I am an asst prof of dermatology at MAMC Delhi
    Just to clear the mess
    here are the answers to the q related to skin

    contact allergy associated with

    a. anaphylactoid reactions
    b. IgE mediated reactions
    c. CMI
    d. Type II rtn
    c

    . 57male with patchy loss of scalp hair, eyebrows & beard with grey hair...

    a. alopecia areata
    b. anagen effluvium
    c. telogen effluvium
    d. androgenic alopecia

    a
    58. DOC for pregnant woman in 2nd trimister with pustular psoriasis

    a. prednisolone
    b. dapsone
    c. acitretin
    d. methotrexate

    a
    59. female with painful long standing persistent oral lesions.

    a. pemphigus vulgaris
    b.aphthosis
    c. EM
    d. Bullous pemphigoid

    a
    60 DOC for tertiary syphilis

    a. procaine penicillin
    b. benzathine penicilline
    c. crystalline penicilin
    d. Doxycycline

    b
    61 Dharmendra index & jopling's classification is for...

    a.Tb
    b. leprosy
    C .Syphilis
    d Leishmaniasis

    b
    62 DOC for lepra II rections..

    a. thalidomide
    b. corticosteroids
    c. clofazimine
    d.dapsone

    a
    63. NF-1 asso with

    a. choroidal hemangioma
    b. glaucoma
    c.
    d.

    b
    64. male from West Bengal with hyperkeratosis of palm and soles with, transverse nail lines

    a. chronic arsenic poisoning
    b. Pb poisoning
    c. Au poisonong
    d. Thallium poisoning

    a
    65. immunomodulator for genital warts is..

    a. imiquimod
    b. Zn
    c. Calcium
    d. Podophyllin

    a
    66. not an antifungal...

    a. caspofungin
    b. undecyclinic acid
    c. ciclopirox
    d. clofazamine

    d
    67 yaws all true except
    Is an STD

    68 All are zoonosis except

    1. HIV
    2. Plague
    3.JE
    4.TB
    1
  4. Dr Kapil.

    Dr Kapil. Guest

    thanx Dr. Kabir for the dermatology Q/A
  5. james.

    james. Guest

    Anaeroid manometer,

    Anaeroid manometer, once caliberated carefully can give blood pressure measurement similar to that of mercury manometer, the gold standard"

    Friends kindly give your opinoin regarding this statement given as option for one of our questions and a option that has been almost overlooked.
    Lets not forget that many hospitals and health care facilities in Europe are voluntarily removing mercury manometers and replacing them with aneroid or automated measuring because of risk of mercury toxicity....
  6. askrags

    askrags Guest

    nf1

    hi guys nf1 causes congenital glaucoma. ref yanoff. it has been given that it is know to cause congenital glaucoma.
  7. askrags

    askrags Guest

    regarding rx of cns syphilis, the table in Harrison says penicillin g or procaine penicillin. so wats the definite answer for that??? cos i think both options were there in the question. atleast benzathine penicillin is not used.
  8. james.

    james. Guest

    Following drugs are contraindicated in G6PD deficiency EXCEPT :
    a.Primaquine
    b.Quinine
    c.Pyrimethamin
    d.Chloroquine

    Most text books say Quinine, Primethamine and Chloroquine to be safe drugs in G6PD deficiency..
    Nelson also include Chloroquine in their list of antimlarials causing hemolysis in G6PD deficiency, but this is not included in the table in harrison..

    Is this ques wrongly framed or Should it have been the other way following drugs are safe in G6PD deficiency EXCEPT ????????
    Only the AIIMS people know the answer...

    Here is the list of drugs which are safe in G6PD deficiency ( Wintrobe) -
    Drugs that can be safely given in therapeutic dosage in patients of G6PD deficiency with nonspherocytic hemolytic anemia8

    1. Acetaminophen

    2. Acetophenetidine (Phenacetin)

    3. Aminopyrine

    4. Actazoline

    5. Antipyrine

    6. Ascorbic acid (vitamin C)

    7. Benzhexol

    8. Chloramphenicol

    9. Chlorguanidine (Proguanil)

    10. Colchicin

    11. Diphenylhydramine

    12. Isoniazide

    13. Levo dopa

    14. Menapathine

    15. P-Aminobenzoic acid

    16. Phenylbutazone

    17. Phenytoin

    18. Probenacid

    19. Procainamide

    20. Pyrimethamine

    21. Quinine, Qunidine, Chloroquine, Mefloquine

    22. Proguanil

    23. Halofantrine

    24. Streptomycin

    25. Sulfacytine

    26. Sulfadiazine, Sulfamerazine, Sulfisoxazole

    27. Trimethoprim
  9. kavish.

    kavish. Guest

    Least imp. in case of non -communicablele diseses?
    a)temporal asso.
    b)strenth of ass.
    c)specificity of asso.

    REF:park/19th/85
    most non communicable diseses are d/t multiple factors,so one to one relationshoip is not possible
  10. shacks.

    shacks. Guest

    SMITH urology on Ureteric colic...

    Tanagho SMITH'S UROLOGY, 16e > Chapter 16. Urinary Stone Disease

    "Renal colic and noncolicky renal pain are the 2 types of pain originating from the kidney. Renal colic usually is caused by stretching of the collecting system or ureter, while noncolicky renal pain is caused by distention of the renal capsule. These symptoms may overlap, making a clinical differentiation difficult or impossible. Urinary obstruction is the main mechanism responsible for renal colic. This may be mimicked by the pain a patient experiences when a retrograde ureteropyelogram is performed under local anesthesia, with excessive pressure resulting in overdistention of the collecting system. This pain is due to a direct increase in intraluminal pressure, stretching nerve endings.

    Renal colic does not always wax and wane or come in waves like intestinal or biliary colic but may be relatively constant. Renal colic implies an intraluminal origin. Patients with renal calculi have pain primarily due to urinary obstruction.

    Local mechanisms such as inflammation, edema, hyperperistalsis, and mucosal irritation may contribute to the perception of pain in patients with renal calculi. In the ureter, however, local pain is referred to the distribution of the ilioinguinal nerve and the genital branch of the genitofemoral nerve, whereas pain from obstruction is referred to the same areas as for collecting system calculi (flank and costovertebral angle), thereby allowing discrimination.

    The vast majority of urinary stones present with the acute onset of pain due to acute obstruction and distention of the upper urinary tract. The severity and location of the pain can vary from patient to patient due to stone size, stone location, degree of obstruction, acuity of obstruction, and variation in individual Anatomy (intrarenal versus extrarenal pelvis, for example). The stone burden does not correlate with the severity of the symptoms. Small ureteral stones frequently present with severe pain, while large staghorn calculi may present with a dull ache or flank discomfort.

    The pain frequently is abrupt in onset and severe and may awaken a patient from sleep. The severity of the pain is worsened by the unexpected nature of its onset. Patients frequently move constantly into unusual positions in an attempt to relieve the pain. This movement is in contrast to the lack of movement of someone with peritoneal signs; such a patient lies in a stationary position.

    The symptoms of acute renal colic depend on the location of the calculus; several regions may be involved: renal calyx, renal pelvis, upper and mid ureter, and distal ureter. An orderly progression of symptoms as a stone moves down the urinary tract is the exception"
  11. melosqueak

    melosqueak Guest

    Hyperlipidaemia – a risk factor for femoral head osteonecrosis (Legg-Calvè-Perthes-Like disease) in children with AIDS: case report Although treatment of children infected with HIV with protease inhibitors has improved the survival of these patients, various adverse side effects have been reported, including metabolic abnormalities, such as hyperlipidaemia. We describe a case of hip osteonecrosis in an adolescent with AIDS who was being treated with protease inhibitors. There is a possible relation with hyperlipidemia. F.M.G., white, 11 years old, AIDS A2, started to receive AZT and DDI when he was 7 years old. In April 1999, the patient had a significant increase in viral load and so the antiretroviral therapy was switched to d4T, 3TC and Ritonavir. Triglyceride plasma levels reached 460mg/dl after this switch and were always above the reference value. In December 1999, the patient complained of pain in the right hip. On physical examination, he had limited movement of this joint. Magnetic resonance imaging of the right hip showed flattening, deformity and fragmentation of the femoral head, compatible with osteonecrosis. Few cases of femoral head osteonecrosis have been associated with HIV infection, in the absence of the classic risk factors for osteonecrosis. Metabolic risk factors include hypertriglyceridaemia. The immunological disorders that occur in the HIV infection may predispose the patient to avascular osteonecrosis and metabolic disorders, particularly hypertriglyceridemia, while the use of protease inhibitors, may be considered an additional risk factor for osteonecrosis. Given the importance of premature diagnosis and to avoid complications of osteonecrosis, we recommend evaluation of musculoskeletal symptoms in children

    source-Brazilian Journal of Infectious Diseases Braz J Infect Dis vol.6 no.3 Salvador June 2002
  12. kavish

    kavish Guest

    Q.Pt. on antiretroviral T/t with limited abduction and internal rotation at hip Jt.d/t?
    a)T.B.
    b)Avascular necrosis??


    i Avascular necrosis (AVN) of the femoral head is an emerging complication in HIV infected patients. It has been reported that the incidence of AVN in HIV patients is 0.45%, which is 45 times greater than in the normal population
    In recent reports AVN has been associated with the use of protease inhibitor-containing (PI) regimens, since antiretroviral therapy may cause hyperlipidemia and osteoporosis [1,3]. On the other hand, in some patients, AVN may develop before PI therapy begins [1]. It has been suggested that the HIV condition itself, or some other factors, such as hypercholesterolemia, hypertriglyceridemia, corticosteroid use and alcohol abuse may increase the risk of AVN development in these patients



    REF2:http://www.sciencedirect.com/scienc...serid=10&md5=4feb8f5321cedb81a056d630141d88de
    The wide use of protease inhibitors (PI) as part of a highly active antiretroviral (HAART) regimen is associated with the development of several side effects. Among these, the development of avascular necrosis (AVN) of the bone is being reported more frequently and it has been related both to the use of PI and to HIV-1 infection itself. We report here a case of AVN of the bone in a patient taking the new PI lopinavir (LPV)/ritonavir (RTV) as part of a HAART regimen.


    REF3:http://www.springerlink.com/content/rxcexpr5kab3x9k6/Avascular Necrosis of the Femoral Head: A Side Effect of Highly Active Antiretroviral Therapy (HAART) in HIV Patients?
    Journal Infection
    Publisher Urban & Vogel


    AVN of the hip produces groin pain that intermittently radiates down the anteromedial thigh. Some patients note increased pain and a distinct clicking with motion, particularly when rising from sitting. They have limited motion (particularly flexion, abduction, and internal rotation) and adopt an antalgic gait. A click may be elicited by externally rotating the flexed abducted hip
  13. saurabh.

    saurabh. Guest

    ALL TESTS R USD TO DIFF BW UNCOMPLICATED UTI N ACUTE PYELONEFRITIS XCPT...


    1. BACT COUNT MORE DAN 10 RAISD TO 8
    2. ANTIBODY TO TOM HARSFALL PROTEIN
    3. LOSS OF CONCENTRING CAPACITY


    ANSWER 2. TOM HORSFALL protein is a common constt of normal kidney
    an antibody wud b +nt in all cases of suspected renal damage so hw wud it diff bw uncomplctd uti n pyelonephritis
    d ref is basd on various text abt tom horsfall protein....

    All of the folowin inhibit THROMBIN xcpt
    1. natural Antithronbin 3 in blood
    2. chymotrypsin
    3. alfa antitrypsin
    4. alfa microglobulin(nt sure bt dis option)
    ANSWER ?

    Delayd prolongd leakage due to
    1. endothelial retraction
    2. leaky new blood vessels
    3. endothelial necrosis
    ANSWER most prob 1. ref Robbins7/50-52
    its a bit confusin n dibolical....pls help urslf


    Regardin Antigen presentin cells false is
    (rembrd d answer) B cells dont prolifrte after initial xposure....
  14. saurabh.

    saurabh. Guest

    Antibody to Tammhorsfall protein can defferentiate between Acute pyelonephritis and Uncomplicated UTI..See Schriver's text book of nephrology which says
    "The usefulness of measuring serum antibodies to Tamm-Horsfall protein (THP) for diagnosing the level of acute urinary tract infections in adult women was evaluated. There was a significant (p less than 0.001) elevation of IgG and IgA anti-THP in pregnant and non-pregnant women with acute pyelonephritis compared to women with acute cystitis. The changes in anti-THP antibody titre among patients with acute pyelonephritis varied considerably, limiting the value of determining such antibodies for diagnostic purposes. Patients with febrile infections of non-renal origin demonstrated an antibody response comparable to the pyelonephritis patients. One explanation for these results could be that fever is associated with transient rental tubular damage, thus exposing THP to the immune system. Polyclonal antibody activation seems less likely since neither an IgM antibody response to THP, nor an increase in antibody titre to poliovirus could be demonstrated.
    An increase in antibody levels against O antigen and Tamm-Horsfall protein was noted only in patients with acute pyelonephritis indicating that antibody determinations can be useful in differentiating between upper and lower urinary tract infection caused by Proteus in similarity to those caused by E. coli. In contrast no difference in adhesive ability was noted comparing Proteus strains causing acute pyelonephritis or cystitis. In sera from ten girls with acute pyelonephritis, antibodies of the IgG-class to Tamm-Horsfall protein were found in significantly increased titres; in contrast, titres in sera from six girls with acute cystitis did not differ from those of healthy controls. The results suggest that determination of Tamm-Horsfall antibodies may prove useful for differentiating between upper and lower urinary-tract infection"
  15. saurabh.

    saurabh. Guest

    Ques on Diffuse esophageal spasm -
    Which of the folowing is diagnostic of DES?
    a.Esophageal manometry
    b. Barium swallow

    I'm giving references from various sites and text books..

    emedicine -
    "Barium swallow is the best imaging study to aid in the diagnosis of esophageal spasm"
    "Manometry is the best modality to help diagnose DES. The classic definition is more than 2 uncoordinated contractions during 10 consecutive wet swallows (≥20% simultaneous esophageal contractions during standardized stationary motility testing). At least one peristaltic contraction must be present. Artificial neural networks may be useful in the recognition and objective classification of primary esophageal motor disorders investigated with stationary esophageal manometry recordings"

    Learning Surgery: The Surgery Clerkship Manual - by Stephen F. Lowry, Rocco G. Ciocca, Candice Rettie - 2005 - 791 page
    "Esophageal manometry is diagnostic, but the classic pattern of diffuse spasm is uncommon in patients presenting with chest pain"
  16. saurabh.

    saurabh. Guest

    mutation of the gene causes nephrotic syndrome
    1.nephrin
    2.podocin
    3.actn4
    4.wt1


    nephrin and podocin are structural proteins


    perhaps there is a new hypothesis called protein mutation ,coming up courtesy AIIMS
    i m annoyed as this nasty bite took away my 3 costly minutes in hall
  17. saurabh.

    saurabh. Guest

    Barlett RH, Andrews AF, Toomasien JM, et al : Extracorporesl membrane oxygenation(ECMO) for newborn respiratory failure: 45 cases. Surgery 92:425-433.

    Specific indications for ECMO
    1. MAS
    2. PPHN
    3. RDS
    4.GBSPneumonia
    5. CDH
    6. Barotrauma?Air leak syndrome
    7. Postop cardiac failure (After repair of congenital heart defect)

    In a 1995 report from Extracorporeal life support organization, an 81% survival rate was reported in nearly 10,000 patients. The results for various diagnosis are as follows.
    MAS - 94%
    PPHN - 84%
    RDS - 84%
    Pneumonia/Sepsis - 76%
    Air leak syndrome - 73%
    CDH - 58%
  18. Fasfur.

    Fasfur. Guest

    Which is not a composite muscle
    1. Rectus femoris*
    2. Adductor magnus
    3. Pectineus
    4. Biceps femoris

    Ans.1 Rectus femoris
    Explanation:
    *Muscles like adductor magnus, pectineus, biceps femoris etc. are called as composite muscles as they are doubly innervated.
    Reference:
    1.Pg. 64; BDC-Vol 2 (4th Ed.)
    Bronchial artery supplies upto
    1. Tertiary bronchioles
    2. Respiratory bronchioles
    3. Alveolar sac
    4. ?

    Ans. 2. Respiratory bronchioles
    Explanation:
    *Bronchial arteries supply the bronchial wall as far as the respiratory bronchiole.
    -Bronchial arteries are derived from the descending thoracic aorta as direct or indirect branches.
    -Right bronchial artery is single and a branch of 3rd posterior intercostal artery.
    -Left lung has 2 bronchial arteries (and are direct branches from aorta)
    -There are pre-capillary anastomoses between bronchial & pulmonary arteries.
    -Lungs survive even if the bronchial arteries were shut off,due to dual vascularity (pulmonary & bronchial circulation)

    References:
    Pg 1078;Grays Anatomy (39th Ed.)
    Pg. 227;BDC-vol 1 (4th Ed.)

    Q.Lymph flow from the foot is
    1. Increased when an individual rises from the supine to standing position
    2. Increased by massaging the foot
    3. Increased When capillary permeability is decreased
    4. Decreased when the valves of the leg veins are incompetent

    Ans. 2. Increased by massaging the foot

    Reference:
    Pg 793; Ganong(21st Ed.)

    Artery to vas deferens is a branch of
    1. Inferior epigastric
    2. Superior vesical
    3. Cremasteric
    4. Middle rectal

    Ans. 2. Superior vesical
    Explanation: Vas deferens is supplied by a separate artery, which is a branch of superior vesical artery(2).
    -This artery of vas deferens anastomoses with the testicular artery.
    *Testis is mainly supplied by the testicular artery, an anterior branch of aorta.
    -Testis receives additional blood from the artery of ductus deferens and also from cremasteric(3) branch of inferior epigastric artery(1).
    Note: In varicocele treatment, we ligate both the testicular artery and vein quite high up.
    -The artery being ligated to include the venae commitantes running along with it.
    (Remember, venae commitantes anastomose with the internal spermatic veins and if left open can lead to reccurence of varicoceles!)
    -In this operation, testis survives, despite ligating the testicular artery, because of its additional arterial supply from cremasteric branch & artery of ductus deferens.
    * Venous drainage of ductus deferens is to pelvic venous plexus and lymphatics reach the External & internal iliac lymph nodes.

    References:
    Pg 1131,1306;Grays Anatomy (39th Ed.)

    Nerve supplying the Skin lying above great saphenous vein
    1.Femoral /Saphenous
    2.Superficial peroneal
    3.Sural
    4.Tibial


    Ans. 1. Femoral /Saphenous
    Explanation: Great saphenous vein lies in the medial side of the leg and thigh.
    It is accompanied by Saphenous nerve all along, the nerve which supplies the medial aspect of leg and dorsum of foot till the ball of great toe.
    *Saphenous nerve itself is a branch of femoral nerve and can get damaged while venesection of great saphenous vein is carried out.
    *The skin over the medial thigh is mainly supplied by the medial cutaneous branch of femoral nerve.

    References:
    Pg. no. 47,48;BD Chaurasia-vol. 2 (4th Ed.)
    Pg. no. 584; Keith L Moore (5th Ed.)


    All are true about diploic veins except

    1. Lined by single layer endothelium supported by elastic tissue
    2. Present in cranial bones
    3. Valveless/thin walled
    4. Develop by 8th week of IUL


    Ans. 4. Seen at 8 weeks.
    Explanation: Primordia of skull (centre of ossification) start apeearing at 6-8th week(4) of intrauterine life.
    The skull is unilamellar at birth without any diploe.The diploic veins start to develop at around 2 years with the diploe.
    -At around 4th year the diploe appears and gets maximally differentiated by 35th year when the diploic veins are quite prominent radiologically.
    *Diploic veins are very thin(3) lined by endothelium, which is supported by some elastic tissue(1).
    -The are valveless(3) veins of the cranial bones(2), as are the other intracranial veins.
    -They anastomose with the dural venous sinuses, epicranial veins & meningeal veins.
    -Thrombosis of superior sagittal sinus may be caused by spread from diploe by diploic veins.
    References:
    Pg. 1580; Grays Anatomy (38th Ed.)
    Pg. 484; Grays Anatomy (39th Ed.)
    Pg. 96; BD Chaurasia-Vol-3 (4th Ed.)

    Which is NOT a digastric muscle
    1. Omohyoid
    2. Sternocleidomastoid
    3. Occipitofrontalis
    4. Muscular fibres in the ligament of Trietz

    Ans. 2. Sternocleidomastoid
    Explanation: Sternocleidomastoid(2) has 2 heads and one belly, like biceps brachii muscle.
    -Muscles like omohyoid(1) and occipitofrontalis(3), have 2 bellies like superior & inferior belly of OH & occipital & frontal belly of OF.
    *Ligament of trietz is a fold of mesentery at the duodeno-jejunal junction.
    -This ligament contain a belly of skeletal muscle arising from the left crus of diaphragm and another belly of smooth muscle arising from the muscle coat of duodeno-jejunal flexure.
    Note:Gastrocnemius is a muscle with 2 heads & 2 bellies-it is also a digastric muscle !

    References:
    Pg. 113-14,500,536,538,1165;Grays Anatomy (39th Ed.)
    Pg. 369,262;Last clinical Anatomy (11th Ed.)
    Pg. 32;K L moore (5th Ed.)


    All are tributaries/connections of cavernous sinus except
    1.Superficial middle cerebral vein
    2.Deep middle cerebral vein
    3.Superior petrosal sinus
    4.Inferior petrosal sinus


    Ans. 2.Deep middle cerebral vein.
    Explanation: Deep middle cerebral vein(2) runs in the lateral sulcus of cerebrum and joins the anterior cerebral vein & Striate veins.
    The resultant vein is called basal vein which is going to drain into the great cerebral vein of Galen.
    *Superficial middle cerebral vein(1) also runs in the lateral sulcus of cerebrum and drains into the cavernous sinus.
    It gets connected to deep middle cerebral vein and also to superior sagittal sinus & transverse sinus by anastomosing veins.
    *Superior & inferior petrosal sinuses (3 & 4) are considered to drain the blood of cavernous sinus towards the internal jugular vein.
    Note 1: It is customary to consider venous blood entering cavernous sinus from the anterior end and leaving it towards postero-inferior direction, ultimately into the internal jugular vein.
    Neverthless, blood can flow in either direction since, the venous sinuses are valveless channels.
    Note 2: Superficial middle cerebral vein can carry an emboli from cavernous sinus thrombosis towards the cerebrum.

    References:
    Pg. no. 387;BD Chaurasia-vol. 3 (4th Ed.)
    Pg. no. 464, 492 ;Last clinical Anatomy (11th Ed.)
    Pg. no. 914; Keith L Moore (5th Ed.)

    All of the following cells are found in lung except
    1.Clara cells
    2.Kulchitsky cell
    3.Langerhans cells
    4.Brush cells


    Ans.3.langerhans cell
    Explanation: Langerhans cell(3) the immature dendritic cells present in the skin,reaching lungs only in abnormal conditions like Histiocytosis.
    *Langerhans cells are abundant in the lymph nodes and are also evident in the gastro-intestinal epithelium.
    *Brush cells(4):lung bronchioles are lined by brush cells,having microvilli and are in association with the nerve terminals.
    *Kulchitsky cells(2) are the neuro-endocrine cells found in the lungs,secreting amines (APUD).
    *Clara cells(1) are the non-ciliated cuboidal (or columnar) cells in the lining of terminal & respiratory bronchioles, and secrete surfactant lipoproteins.
    References:
    Pg. no. 82,1057; Grays Anatomy ; 39th Ed.


    The final common pathway for horizontal gaze is nucleus
    1.Abducent
    2.Occulomotor
    3.Trochlear/Hypoglossal
    4.Vestibular


    Ans. 1.Abducent
    Explanation: Subcortical centre for lateral/horizontal conjugate gaze lies in the abducent nucleus (pons), though some authors take it to be PPRF (para-median pontine reticular formation) and others nucleus prepositus hypoglossi.
    -This centre receives input from the contralateral frontal eyefield and moves ipsilateral lateral lateral rectus and contralateral medial rectus muscle via projections of MLF (medial longitudinal fasciculus).
    *PPRF lesion leads to inactivity of saccadic movements by lateral rectus & contralateral medial rectus.
    -There is loss of horizontal saccades directed towards the side of the lesion but pursuit & vergence movements are preserved.
    *One and a half syndrome: Unilateral abducent & bilateral MLF lesion. On attemted lateral gaze, the only muscle functional is the intact lateral rectus .
    *MLF connects the nuclei controlling eyeball muscles - (LR6 SO4)3 and mediates nystagmus & lateral conjugate gaze.
    -Its fibres originate in vestibular(4) nucleus & terminate in abducent, trochlear(3) and occulomotor(2) nuclei.
    -It coordinates eyeball movements with the head.
    References:
    Pg no. 131;the human nervous system by Barr (8th Ed.)
    Pg. no. 285,205;BRS neuroanatomy; 3rd edition
  19. aayush.

    aayush. Guest

    murray and nadel's text book of resiratory medicineys about bronchial circulations



    separate systemic circulation supplies blood flow to the airways from the carina to the terminal bronchioles. In addition, bronchial arteries provide nutritive flow to the lower trachea, airway nerves, and lymph nodes.[17][18] Blood flow in the bronchial circulation is normally less than 3% of the cardiac output. The drainage of bronchial vessels into the pulmonary circulation and the large veins has a complex arrangement ( Fig. 6.2 ). Interconnections have been demonstrated between bronchial vessels and precapillary, capillary, and postcapillary vessels of the pulmonary circulation.[19] Despite the fact that the normal adult lung remains viable without the bronchial circulation (and without innervation as well), as in the case of the transplanted lung, bronchial blood flow is critical in the development of the lungs in the fetus and contributes to gas exchange in many varieties of congenital cardiac anomalies. It is now recognized that a striking increase in the size and number of bronchial arteries (due to angiogenesis) occurs in certain lung diseases such as pulmonary fibrosis, lung carcinomas, and disorders characterized by pulmonary vascular occlusion.[20][21][22] Neovascularization of the systemic circulation into the lung after pulmonary artery obstruction has been confirmed and studied in the human, sheep, pig, rat, and mouse.

    There is considerable variation in the number and origin of the bronchial arteries in the human adult. In a study of 150 cadavers by Cauldwell and colleagues,[23] the majority of bronchial arteries arose directly from the aorta; in just over 40% of their series, there were two arteries to the left lung and one artery to the right lung. The right bronchial artery originated from the first right intercostal artery in some cases. Variable numbers of smaller minor branches emerged from vessels in and near the mediastinum and crossed into each lung. As soon as bronchial arteries entered the lung, they became invested in the layer of connective tissue surrounding the bronchi and began branching. Ordinarily, two or three bronchial arterial branches, which anastomose with each other to form a peribronchial plexus with an elongated and irregular mesh, accompany each subdivision of the conducting airways.

    The amount of blood flow to the lung through the bronchial arterial circulation is low and therefore has never been measured accurately in humans. The results of studies in dogs indicate that bronchial blood flow to the left lung is about 1% of the cardiac output, with about 50% of this flow directed to the lung parenchyma and the remainder to the trachea and bronchi.[22] There is no reason to believe that bronchial blood flow in humans differs substantially from that in dogs; therefore, estimates of total bronchial blood flow to both lungs of about 1% to 2% of the cardiac output seem reasonably accurate.

    Venous blood from capillaries supplied by bronchial arteries returns to the heart by two different pathways (see Fig. 6.2 ). True bronchial veins are found only at the hilum; they are formed from tributaries that originate around the lobar and segmental bronchi and from branches from the pleura in the neighborhood of the hilus. Bronchial venous blood empties into the azygos, hemiazygos, or intercostal veins and then flows into the right atrium. Veins that originate from bronchial capillaries within the lungs unite to form venous tributaries that join the pulmonary veins; these communicating vessels are called bronchopulmonary veins. Blood leaving the capillary bed around terminal bronchioles flows through anastomoses with alveolar capillaries, and then the mixture of blood returns to the left atrium through pulmonary veins.

    The distribution of bronchial arterial inflow between the two available venous outflow pathways has never been determined in humans, and only tentative conclusions can be drawn from the technically difficult studies in experimental animals. These studies indicate that about 25% to 33% of the bronchial arterial supply returns ultimately to the right atrium via bronchial veins, and 67% to 75% flows into the left atrium via pulmonary veins.[22]

    Controversy still exists concerning the presence and significance of bronchopulmonary arterial anastomoses, which are direct vascular connections between pulmonary arteries and bronchial arteries. The available evidence suggests that bronchopulmonary arterial anastomoses do exist.[22] They occur sporadically and infrequently in normal lungs, are more easily demonstrable in the lungs of infants than in the lungs of adults, and may increase considerably in number in certain pathologic disorders.

    so i think my vote goes in favour of terminal bronchiole.you may pick your veiw
  20. shacks.

    shacks. Guest

    1. Pulmonary Vascular Diseases - by Kenneth M. Moser - The severity of pulmonary venous hypertension can be graded radiologically more accurately than precapillary pulmonary hypertension.
    Mild venous hypertension, on the order of 12-18mmHg, is manifested as constriction of lower zone vessels and dilatation of upper.
    Moderate venous hypertension levels, on the order of 18-25mmHg, produces more marked caliber changes between the upper and lower zones and usually, early signs of interstitial edema.
    Severe venopus hypertension at levels of above 25mmHg, generally produces alveolar edema. The resultant pulmonary densities tend to clear more rapidly in the peripheral lung fields, thereby producing the well known “butturfly” or “batwing” distribution of pulmonary edema.

    2. Cold agglutinin disease (CAD) is associated with IgM antibodies usually directed at the red cell I antigen. It occurs in adult patients, and may be primary or secondary to another disease process. Paroxysmal cold hemoglobinuria (PCH) is caused by the so-called Donath-Landsteiner antibody, an IgG hemolysin. With the decline in syphilis, PCH is uncommon and seen rarely outside the pediatric population.
    Nearly all cold agglutinins are IgM. A few reports of IgG or IgA agglutinins are recorded, and a mixed IgM-IgG has been seen in infectious mononucleosis and angioimmunoblastic lymphadenopathy . Those with non-IgM antibodies are more likely to be secondary to another disease and less likely to display specificity for the I antigen .

    3. Yaws - Park,19th ed, Page 283 - Yaws is a chronic contagious NON VENEREAL disease cause by T.pertenue.

    4. Water/soil-borne diseases of public health importance
    Protozoa: Naegleria, acanthamoeba, cyclospora, cryptosporidia
    Bacteria: Tetanus, melioidosis, leptospirosis
    Fungi: Histoplasmosis, coccidioidomycosis, N.A. blastomycosis, S. A. blastomycosis, chromoblastomycosis, sporotrichosis
    Roundworms: Hookworm, CLM, VLM, strongyloidiasis, baylisascariasis
    Flukes: Schistosomiasis
    http://www.epidemiology.vcu.edu/MPH_Program/Course_Outlines/EPID621.htm

    5. BP measured by Spyghmomanometer is greater than Intra arterial measurements - Aashish gupta notes

    9. Park, page 103 - Isolation has distinctive value in control of Pneumonic plague.

    10. Most common predisposing factor for pl. accreta is PREVIOUS CS

    12. Secondary tumors in Retinoblastoma are radiation induced. No role for chemo. P53 mutation is also associated with Osteosarcoma. We have discussed this in the same forum...

    14. Role of ECMO in NEC is much debated. Have got no reference for it.
    But surgery for NEC is resection of necrotic bowel with proximal enterostomy and distal mucous fistula placement. But at some centers end to end anastomosis done - depends on percentage of necrotic intestine.. Reference from Greenfield - The operative indications in NEC invariably are associated with the presence of intestinal necrosis with or without frank perforation. Conventional operative intervention is aimed at treating the complications of NEC (i.e., intestinal necrosis) rather than preventing or stopping the factors that cause the disease. In general, resection of intestine involved with NEC does not prevent further extension of disease in other involved areas of the bowel. For isolated segmental disease, the traditional surgical treatment of NEC is resection of necrotic bowel with proximal enterostomy and distal mucous fistula placement. In infants with diffuse NEC, multiple resections with several enterostomies may be required. The primary operative goal is an expedient operation with preservation of as much intestinal length as possible, including the ileocecal valve. Because the risk of developing short-gut syndrome is substantial in infants with diffuse disease, it is rational to preserve marginal areas with a planned second-look operation to reevaluate viability. Accurate measurement of the remaining bowel length is important from a diagnostic and prognostic standpoint, with the length of bowel resected determined by the extent of necrosis. Resection with primary anastomosis in selected infants with NEC has been reported (77), with a recent study observing recurrent NEC in 22% and strictures in 17% of 18 treated infants following primary anastomosis (78). Complete intestinal necrosis of the small intestine and colon is uncommon in infants with NEC (Fig. 97.22). Faced with the dilemma of certain immediate death or the sequelae of short gut syndrome, some surgeons have reported intestinal reconstruction and survival following proximal jejunal diversion without enterectomy. The mortality rate in this desperate circumstance remains high.

    17. Antibodies sganist Tammhorsfall protein can distinguish between Upper UTI and lower UTI.. Ans will be either Option A - Concentrating ability or Option C - Bacterial colony count >108
    Reference from Schriver text book of Nephrology -
    The usefulness of measuring serum antibodies to Tamm-Horsfall protein (THP) for diagnosing the level of acute urinary tract infections in adult women was evaluated. There was a significant (p less than 0.001) elevation of IgG and IgA anti-THP in pregnant and non-pregnant women with acute pyelonephritis compared to women with acute cystitis. The changes in anti-THP antibody titre among patients with acute pyelonephritis varied considerably, limiting the value of determining such antibodies for diagnostic purposes. Patients with febrile infections of non-renal origin demonstrated an antibody response comparable to the pyelonephritis patients. One explanation for these results could be that fever is associated with transient rental tubular damage, thus exposing THP to the immune system. Polyclonal antibody activation seems less likely since neither an IgM antibody response to THP, nor an increase in antibody titre to poliovirus could be demonstrated.
    An increase in antibody levels against O antigen and Tamm-Horsfall protein was noted only in patients with acute pyelonephritis indicating that antibody determinations can be useful in differentiating between upper and lower urinary tract infection caused by Proteus in similarity to those caused by E. coli. In contrast no difference in adhesive ability was noted comparing Proteus strains causing acute pyelonephritis or cystitis. In sera from ten girls with acute pyelonephritis, antibodies of the IgG-class to Tamm-Horsfall protein were found in significantly increased titres; in contrast, titres in sera from six girls with acute cystitis did not differ from those of healthy controls. The results suggest that determination of Tamm-Horsfall antibodies may prove useful for differentiating between upper and lower urinary-tract infection.
  21. Abrar.

    Abrar. Guest

    Rh factor is?
    a)mucopolysaccharide
    b)fatty acid
    c)antibod
    d)collagen(not sure abt this but was surely not protein)
  22. aayush.

    aayush. Guest

    The treatment of choice for severe type 2 reactions (ENL) is thalidomide, except in pregnant or potentially pregnant women. Thalidomide requires that patients and the prescribing physician be enrolled in the System for Thalidomide Education and Prescribing Safety (STEPS) program to avoid the drug's teratogenic effects. The mechanism of action of thalidomide is incompletely understood but is likely to include inhibition of TNF. The dose of thalidomide for ENL varies, depending on the severity of the reaction. In patients with ENL and high fever, frank arthritis, and large subcutaneous plaques, up to 100 mg four times daily may be required to achieve a clinical response. Once a clinical response is achieved, the dose of thalidomide may be tapered to a maintenance dose of 50 to 100 mg given once daily at night (because thalidomide is sedating). For milder cases of ENL, 50 to 100 mg per night may be sufficient to achieve and maintain control. ENL in women of childbearing age and thalidomide-unresponsive cases may respond to corticosteroids. Antileprosy chemotherapy, including rifampin, should be continued in patients with ENL.


    cecil text book of medicine 23rd edition 2007 chapter 347
  23. aayush.

    aayush. Guest

    In APS, the homeostatic regulation of blood coagulation is altered; however, the mechanisms of thrombosis are not yet defined. One hypothesis postulates a defect in cellular apoptosis, which exposes membrane phospholipids to the binding of various plasma proteins, such as beta-2 glycoprotein I. Once bound, a phospholipid-protein complex is formed and a neoepitope is uncovered, which subsequently becomes the target of autoantibodies. Recent evidence suggests that oxidized beta-2 glycoprotein I is able to bind to and activate dendritic cells in a manner similar to activation triggered by Toll-like receptor 4 (TLR-4), which could amplify the production of autoantibodies.1

    Other proposed mechanisms for the hypercoagulable effect of aPL antibodies, which may or may not depend on beta-2 glycoprotein I, include the following:

    Production of antibodies against coagulation factors, including prothrombin, protein C, protein S, and annexins
    Activation of platelets to enhance endothelial adherence
    Activation of vascular endothelium, which, in turn, facilitates the binding of platelets and monocytes
    Reaction of antibodies to oxidized low-density lipoprotein, thus predisposing to atherosclerosis and myocardial infarction (MI)
    Complement activation has been increasingly recognized as a possible significant role in the pathogenesis of APS. Emerging evidence from murine models suggests that APL-mediated complement activation may be a primary event in pregnancy loss.2

    Clinically, the series of events that leads to hypercoagulability and recurrent thrombosis can affect virtually any organ system, including the following:



    Peripheral venous system (deep venous thrombosis [DVT])
    Central nervous system (cerebrovascular accident [CVA], sinus thrombosis)
    Hematologic (thrombocytopenia, hemolytic anemia)
    Obstetric (pregnancy loss, eclampsia)
    Pulmonary (pulmonary embolism [PE], pulmonary hypertension
    Dermatologic (livedo reticularis, purpura, infarcts/ulceration)
    Cardiac (Libman-Sacks valvulopathy, MI)
    Ocular (amaurosis, retinal thrombosis)
    Adrenal (infarction/hemorrhage)
    Musculoskeletal (avascular necrosis of bone
  24. aayush.

    aayush. Guest

    QUESTIONS from Campbell-Walsh Urology Review Manual, 2nd Edition -

    NOV AIIMS 07
    The left renal vein crosses the abdominal aorta:
    a. anteriorly, just above the superior mesenteric artery.
    b. anteriorly, just below the superior mesenteric artery.
    c. posteriorly, at the level of the superior mesenteric artery.
    d. anteriorly, just below the inferior mesenteric artery.
    e. anteriorly, just above the inferior mesenteric artery.
    Ans- b. anteriorly, just below the superior mesenteric artery.
    The left renal vein crosses the aorta anteriorly below the takeoff of the superior mesenteric artery. [p 8]

    Persistent fetal lobation identified in the kidney of an adult patient:
    a. indicates the presence of a congenital renal disorder.
    b. indicates childhood renal injury due to infection.
    c. is observed only with long–standing obstructive uropathy.
    d. is a normal variant.
    e. is never seen.
    Ans - d. is a normal variant.
    It is neither unusual nor abnormal to see persistence of some degree of fetal lobation throughout adult life (see Fig. 1–20). [p 20]

    Ureteral peristalsis requires:
    a. intact sympathetic input.
    b. intact parasympathetic input.
    c. both sympathetic and parasympathetic input.
    d. intact spinal cord.
    e. intrinsic smooth muscle pacemakers in the renal collecting system.
    Ans - e. intrinsic smooth muscle pacemakers in the renal collecting system.
    Normal ureteral peristalsis does not require outside autonomic input but rather originates and is propagated from intrinsic smooth muscle pacemaker sites located in the minor calyces of the renal collecting system. [p 40]

    After fracture of the penis (disruption of the tunica albuginea), if Buck's fascia remains intact, the hematoma will be visible in:
    a. the perineum in a butterfly pattern.
    b. the penis and scrotum only.
    c. the penis, scrotum, and perineum, and tracking up the anterior abdominal wall.
    d. the shaft of the penis only.
    e. the shaft and glans of the penis.
    Ans - d. the shaft of the penis only.
    Bleeding from a tear in the corporal bodies (e.g., penile fracture) is usually contained within Buck's fascia, and ecchymosis is limited to the penile shaft. [p 72]

    Which of the following is NOT a characteristic feature of SIADH?
    a. Hyponatremia with excretion of urine that is not maximally dilute (greater than 100 mOsm/kg).
    b. Maintained Na+ balance, so that urine Na+ concentration reflects intake and is usually high.
    c. Hypouricemia with plasma uric acid concentration less than 4 mg/dl, indicative of increased urate clearance.
    d. Associated with malignancies, pulmonary diseases, and central nervous system disorders.
    e. Low blood pressure because of volume depletion.
    Ans - e. Low blood pressure because of volume depletion.
    SIADH occurs most commonly with bronchogenic tumors and is found in 8% of patients with small cell carcinoma of the oat cell type. It is associated with volume expansion. [p 206]

    The main site of renal HCO3– reabsorption is the:
    a. proximal convoluted tubule.
    b. medullary TAL of Henle.
    c. distal convoluted tubule.
    d. cortical collecting duct.
    e. medullary collecting duct.
    Ans - a. proximal convoluted tubule.
    The bulk of the filtered HCO3– is reclaimed in the proximal nephron, with approximately 80% of the filtered HCO3– reabsorbed within the proximal convoluted tubule. [p 211]

    AIPGE 08
    In their course from the seminiferous tubule to the epididymis, sperm pass through, in order:
    a. straight tubules, efferent ductules, rete testis.
    b. rete testis, straight tubules, efferent ductules.
    c. efferent ductules, rete testis, straight tubules.
    d. straight tubules, rete testis, efferent ductules.
    e. rete testis, efferent ductules, straight tubules.
    Ans - d. straight tubules, rete testis, efferent ductules.
    Septa form 200 to 300 cone–shaped lobules, each containing one or more convoluted seminiferous tubules. Each tubule is U–shaped and has a stretched length of nearly 1 m. Interstitial (Leydig) cells lie in the loose tissue surrounding the tubules and are responsible for testosterone production. Toward the apices of the lobules, the seminiferous tubules become straight (tubuli recti) and enter the mediastinum testis to form an anastomosing network of tubules lined by flattened epithelium. This network, known as the rete testis, forms 12 to 20 efferent ductules and passes into the largest portion of epididymis, the caput. [p 76]

    What causes the pain associated with a stone in the ureter?
    a. Obstruction of urine flow with distention of the renal capsule
    b. Irritation of the ureteral mucosa by the stone
    c. Excessive ureteral peristalsis in response to the obstructing stone
    d. Irritation of the intramural ureter
    e. Urinary extravasation from a ruptured calyceal fornix
    Ans - a. Obstruction of urine flow with distention of the renal capsule.
    Pain is usually caused by acute distention of the renal capsule, usually from inflammation or obstruction. [p 84]

    Contrast agent–induced reactions including urticaria, edema, and hypotension are thought to be:
    a. immunoglobulin G mediated.
    b. anaphylactoid.
    c. delayed–type hypersensitivity.
    d. immunoglobulin E mediated.
    e. a type 1 allergic reaction.
    Ans - b. anaphylactoid.
    The mechanism of these reactions to contrast material most likely differs from that of type 1 allergic reactions and is therefore termed anaphylactoid. [p 125]
  25. Fasfur.

    Fasfur. Guest

    Which is not a feature of conus medullaris syndrome
    1.Begins at the level of lower 3 sacral and coccygeal spinal segment
    2.Absent knee and ankle jerks
    3.Plantar flexor Reflex
    4.Saddle anesthesia

    Ans. Absent knee and ankle jerks

    Explanation:
    Basic antomy:
    *LMN lesions make all the muscles go into flaccid paralysis.
    -All the reflexes are lost (deep tendon like knee & ankle reflexes,as well as superficial reflexes like plantar reflex will be lost)
    Note: Root value of Knee jerk is L-2,3 & 4 and ankle jerk is S-1.

    *Babinski reflex is a superficial reflex with afferents from the outer margin of foot and the sole, including the ball of great toe.
    -Sensory nerves involved are :sural L5,S1,2;lateral plantar nerve S2,3 & medial plantar nerve S1,2.
    -Efferent component is deep peroneal (L-5) which contracts extensor hallucis longus resulting in upgoing toe.
    *Babinski reflex is present in UMN type of lesions.

    *Conus medullaris syndrome(CMS) and Cauda equina syndrome(CES) both are LMN lesions.

    * CMS is going to damage all the spinal cord segments from the level of S-3, till Co(1).
    -It is usually secondary to an intramedullary tumour (like ependymoma) and the onset is sudden & bilateral.
    -Sensory loss is in saddle shaped area(4) around the anal aperture (dermatome S-3 onwards are affected)
    -Bladder & bowel disturbances will be crippling (controlled by root value-S-2,3 & 4) and so will be the sexual performance.
    -Knee & ankle jerks are present(2) in the conus medullaris syndrome.
    -As is evident their spinal segment level is higher than the lesion and are thus unaffected.
    *Plantar reflex will be flexor(3) and is normal.
    -Its because the plantar reflex arc is higher than the level of the lesion in CMS and remains unaffected.

    *Cauda equina syndrome(CES):
    1.Spinal segments affected are L-3 to Co
    2.Usually result from a nerve root tumour (unilateral presentation);
    3.Unilateral saddle shaped Anaesthesia is observed.
    4.Unilateral knee & ankle reflexes are lost.
    5.Incontinence & sexual functions are not damaged severly (since the lesion is unilateral)
    6.Plantar reflex will be lost on the affected side (superficial reflexes are lost in LMN lesions!)

    References:
    1.Pg. 1416,787; Gray's Anatomy (39th Ed.)
    2.Pg. 166;Snell's neuroanatomy (6th Ed.)
    3.Pg. 72;High yield neuroanatomy (3rd Ed.)


    Vessel in paraduodenal fossa is
    1. Inferior mesenteric vein
    2. Middle colic artery(?)
    3. Left colic artery(?)
    4. Splenic vein

    Ans.1. Inferior mesenteric vein
    Explanation:
    *Paraduodenal fossae are the clinically important peritoneal recesses,because they are the potential sites of internal hernia & their strangulation.
    *Inferior mesenteric vein(1) lies in the paraduodenal recess in 20 % of population.
    -An incarcerated hernia in the paraduodenal fossa may thrombose the inferior mesenteric vein.
    -There is a danger of cutting the vein ,while cutting peritoneum to release the hernia.
    *Middle colic artery (2) runs in the transverse mesocolon , whereas, left colic(3) passes behind the peritoneum .
    -These are the feeder vessels for the marginal artery of Drummond.
    *Splenic vessels (4)runs in the splenorenal ligament along with the tail of pancreas.
    Note: All the above vessels are in the double fold of peritoneum except the left colic artery.

    References:
    Pg 235;BDC-vol.2(4th Ed.)


    child with meconuria & absent anus

    a. anoplasty
    b. transverse colostomy
    c. sigmoid colostomy
    d. perineal exploration

    here is what i found on emedicine com

    Staging
    Imperforate anus was historically classified based on the position of the distal-most aspect of the colon in relation to the levator ani muscles. Malformations at or above the levator muscle complex were defined as high anomalies. Infralevator lesions were termed low and were considered simpler and were associated with better prognosis. This system was based on the now obsolete Wingspread classification.

    Information obtained from the posterior sagittal approach has led to an anatomic classification that lists malformations based on their specific Anatomy . The following is a list of the most common malformations:


    Perineal fistula

    This malformation is associated with good prognosis, occurs in either sex, and involves a closed anus with a small connection opening on the perineal body.


    Some babies with this malformation have a small loop of skin at the anal opening that resembles a bucket-handle. This is pathognomonic for perineal fistula.


    Some boys may have no visible perineal opening but may accumulate mucous or meconium in the fistula, which can extend up the median raphe of the scrotum and resembles a black cord (meconium) or a string of pearls (mucous).


    This malformation is amenable to primary neonatal pull-through.


    Healthy girls who have normal-sized anal openings and small-appearing perineal bodies do not have perineal fistula. This is easily determined by measuring the size of the anus using Hegar dilators. The anus of an average-term newborn should be approximately 12 mm but varies with the size of the child. The "correct" size of the perineum is largely a matter of experience.


    Vestibular fistula

    This malformation is associated with good prognosis and is easily diagnosed upon physical examination based on the appearance of a small opening at the posterior aspect of the vestibule. The opening is external to the hymen and is, therefore, not vaginal.


    The term vaginal fistula was commonly and incorrectly used to describe vestibular fistula. True solitary congenital rectovaginal fistula is exceedingly rare.


    Vestibular fistula is safely treated with diverting colostomy, although some pediatric colorectal surgeons repair this malformation primarily in the newborn period without using colostomy.


    Cloaca

    Persistent cloaca is a malformation in females that encompasses a spectrum of defects, including the presence of a common channel that incorporates the urethra, vagina, and rectum.


    The length of the common channel correlates with complexity and prognosis. Shorter channels (<3 cm) have fewer associated malformations and carry a better prognosis. Longer channels have more complex malformations and poorer prognosis.


    One half of all girls with this malformation have 2 hemivaginas and many have hydrocolpos.


    This malformation is easily diagnosed upon physical examination based on the presence of a solitary perineal orifice. Females with this malformation often have very small-appearing labia.


    All children with cloacae should undergo colostomy shortly after birth.


    Bulbar urethral fistula


    This malformation observed in boys is relatively common.


    No fistula is observed upon physical examination, and urinalysis often shows meconium.


    Colostomy is essential to relieve obstruction, prevent urinary soiling, and to allow for distal colostography, which clarifies the malformation for definitive surgical repair.


    Prostatic urethral fistula

    This malformation observed in boys is rarer than bulbar fistula and carries a poorer prognosis.


    The diagnosis and treatment algorithm are identical to those of bulbar fistula, although the surgical procedures used differ.


    Bladder-neck fistula

    This rare malformation observed in males (10% of all malformations in males) carries a very poor prognosis.


    Most patients with bladder-neck fistula require bowel-management regimens.


    The diagnosis and treatment algorithm are identical to those of bulbar and prostatic fistulas, although the surgical procedures used differ.


    This fistula is best approached abdominally.


    Absent fistula

    This malformation can occur in either sex, is somewhat rare, and is associated with a good prognosis. It is commonly associated with trisomy 21.


    Diagnosis is primarily by exclusion.


    Lateral pelvic radiography is performed in babies who have no external evidence of fistula, who pass no meconium after 24 hours, and who have no meconium in the urine.


    If the pelvic rectal pouch is within 1 cm of the anal dimple, a primary pull-through may be performed. In these instances, a fistula is unlikely but should be definitely excluded using the proper surgical technique.


    If the surgeon opts for colostomy, the absence of a fistula is confirmed using distal colostography.


    Cloacal exstrophy

    This extremely rare malformation can occur in either sex but is most common in boys. It encompasses a spectrum that includes variant forms of covered exstrophy. The classic form is devastatingly complex.


    Affected children have an omphalocele and a large extrophied cloacal plate on their lower abdominal wall. They have 2 hemibladders separated by an intestinal plate, often with prolapsed terminal ileum that proceeds distally to include an extrophied urethral plate flanked by 2 hemiphallic or hemiclitoral structures.


    All children with cloacal exstrophy have some degree of pubic symphysis diastasis and may have a spinal malformation, most commonly myelocystocele.


    Thankfully, this complex malformation is rare but it has devastating implications on quality of life.



    TREATMENTSection 5 of 10 Authors and Editors Introduction Clinical Workup Treatment Medication Follow-up Miscellaneous Multimedia References


    Medical Care
    Newborns with imperforate anus should not be fed and should receive intravenous hydration. Life-threatening comorbidities take precedence and must be treated first.

    If a urinary fistula is suspected, broad-spectrum antibiotics can be administered, although anaerobic coverage is unnecessary within the first 48 hours of life. Any cardiac murmurs identified upon physical examination should be evaluated using echocardiography prior to surgical intervention. The remainder of treatment includes diagnostics and surgical evaluation and management.

    Surgical Care
    The decision-making process aims to determine which children should undergo primary repair in the neonatal period and which children require colostomy and definitive repair in a staged fashion. Children with anorectal malformations may undergo one or several of the following surgical procedures based on the child's presentation, physical examination findings, and imaging study findings.

    Neonatal colostomy

    A colostomy is performed in children who are not amenable to primary pull-through either because of malformation complexity (any urinary fistula in boys, vestibular fistula and cloaca in girls, no fistula in either sex >1 cm from perineal skin) or associated comorbidity.


    The colostomy is usually fashioned through a left lower quadrant incision. The colon is divided at the point where the descending colon meets the sigmoid colon, and both ends are brought to the abdominal wall. By fashioning the colostomy at this location, the entire sigmoid colon is kept in place; thus, when the pull-through is eventually performed, a large portion of the colon is available for the surgeon to bring down to the perineal skin.


    The mucous fistula (the downstream segment) should be very small, flush with the skin, and far enough from the proximal end to be outside the colostomy appliance (or under the flange) to avoid continued urinary soiling with feces.


    During this operation, the distal segment of the colon must be exhaustively irrigated to clean out the impacted meconium, which is always significant. This prevents postdiversion urinary sepsis and allows for effective distal colostography.


    Primary neonatal pull-through without colostomy

    Many pediatric surgeons opt for primary pull-through in children with perineal fistulas (or no fistulas) and close (<1 cm) rectal pouches on 24-hour lateral pelvic radiography. Some pediatric surgeons who specialize in colorectal problems often offer the same procedure for girls with vestibular fistulas.


    Cystoscopy is usually performed to rule out associated malformation. This is performed immediately prior to the pull-through operation. A Foley catheter is inserted following the cystoscopy.


    The preferred surgical approach is the posterior sagittal approach developed by Peña et al.

    The child is placed in the prone position with generous padding under the face and chest and a large bolster under the hips to elevate the area of interest.


    A muscle stimulator is used to show the precise position of the rectal muscle complex to enable exact division at the midline. The midline for this operation is defined by the line that precisely divides the muscle complex in half.


    Dissection proceeds until the rectal pouch is identified. The pouch is then mobilized until adequate length is obtained and the rectum is fully separated from its attachment to the genitourinary tract. Even if the structures do not communicate, they remain intimately associated until fully mobilized. This step ensures that the surgeon does not miss a fistula that was missed on urinalysis findings.


    Once the rectum has been mobilized, the muscle stimulator is used to mark the anterior and posterior limits of the muscle complex. The perineal body is then reconstructed, and the rectum is tacked down in the middle of the muscle complex. The posterior wound is closed and anoplasty is performed.


    Posterior sagittal pull-through with colostomy

    This approach is used in boys with rectourinary fistula (bulbar, prostatic, or bladder-neck fistula), in girls with cloaca or vestibular fistula, and in patients of either sex who do not have a fistula when the rectal pouch is further than 1 cm on 24-hour lateral prone abdominal radiography.


    The approach is also used in children who may have malformations that were amenable to primary neonatal pull-through but were unable to undergo such a procedure because of extreme prematurity or other comorbidity.


    Colostomy is performed after 24 hours (or immediately if one of the above diagnoses is made based on either physical examination findings or meconium in the urine).


    Several weeks following colostomy, distal colostography is performed, and the specifics of the malformation are clarified.


    Cystoscopy is usually performed to clarify Anatomy and to rule out associated malformation. This is performed immediately prior to the pull-through operation. A Foley catheter is inserted following the cystoscopy, except in girls with cloaca.


    The reconstructive procedure varies based on the malformation, but the essential concepts include identifying and separating the rectum from other structures, dividing and ligating any fistulas, and fully reconstructing the pelvic Anatomy with placement of the rectum within the confines of the muscle complex. Procedures for specific malformations are as follows:

    Vestibular fistulas are directly visible but have the longest common wall between the rectum and vagina and require significant delicate mobilization to avoid holes in either structure.


    The posterior sagittal approach is used in boys with bulbar or prostatic urethral fistulas. The rectum is isolated and opened, and the fistula is identified through progressive distal opening. Once the fistula is identified, the rectum proximal to it may be mobilized, and the fistula is then ligated. Reconstruction then proceeds with primary pull-through, as described above.


    Abdominal (open or laparoscopic) and posterior sagittal approaches are best in boys with bladder-neck fistulas because the fistula is best identified in the abdomen.


    Cloaca procedures are complex. A short–common-channel cloaca can be repaired using total urogenital mobilization. The posterior sagittal wound is opened into the cloaca, which is then further proximally opened until the urethral orifice is identified and catheterized. The rectum is then sought. In girls with 2 hemivaginas (50%), the rectum opens in the vaginal septum, although significant asymetry may be present. After identification, the rectum is separated from the urogenital tract and completely mobilized. The urogenital tract is then mobilized as a solitary structure until the urethral orifice reaches the perineum. This is then reconstructed, and the muscle is marked to enable creation of an adequate vaginal opening and perineal body without impinging on rectal space.


    A long–common-channel cloaca repair often necessitates formal separation of the bladder and vagina, which requires laparotomy and ureteral catheterization. Vaginal replacement is sometimes necessary if the vaginal length is insufficient for reconstruction.


    Colostomy closure: Once the wound has completely healed and postoperative dilations have achieved their goal (ie, the neoanus is at the desired size), the colostomy may be closed in traditional surgical fashion.


    Facial colliculus located at
    1. Pons
    2. Medulla
    3. Mid brain
    4. Interpeduncular fossa

    Ans. 1. Pons
    Explanation:
    *Facial colliculus is an elevation seen in the floor of 4th ventricle ,at the posterior aspect of lower pons.
    -The colliculus is raised by the fibres of facial nerve, looping around the abducent nucleus.
    -This bend in the fibres of facial nerve is called internal genu.
    -External genu is found in petrous temporal bone, where facial nerve takes another sharp bend.
    -Facial nerve shows a geniculate ganglion here at the bend(genu).
    *superior & inferior colliculi are present at the dorsum of midbrain (tectum).

    References:
    1. Pg 342;BDC(4th Ed.)
    2. Pg 291;Gray's Anatomy (39th Ed.)




    Which of the following is the type of joints between ear ossicles
    1. Primary cartilaginous
    2. Secondary cartilaginous
    3. Synovial
    4. Fibrous

    Ans. 3. Synovial
    Explanation:
    *Ear ossicles have multiaxial synovial(3) joints between them.
    -Maleus & incus form saddle variety of synovial joint, whereas, Incudo-stapedial joint is ball & socket.
    *All the three ossicles develop in cartilage and are cartilagenous bones.
    -Malleus & incus develop in the cartilage of 1st pharyngeal arch, whereas, Stapes develops in second arch with the styloid process & upper hyoid.
    -Since the joints are between cartilagenous bones, the articular cartilage will be of hyaline variety.
    Note: Synovial joints formed by the Membranous bones are atypical and are lined by fibro-cartilage (as articular cartilage).
    -E.g.,Temporomandibular joint (condylar synovial) & sternoclavicular joint (saddle synovial),their articular cartilage is not hyaline but fibro-cartilage.
    *Fibrous(4) joints are present in the skull as sutures & gomphosis.
    -Syndesmosis is also a fibrous joint as observed between radis & ulna and the posterior part of sacro-iliac joint.
    *Secondary cartilagenous(2) joints (symphysis) are usually in the midline,e.g., Manubrio-sternal & xiphisternal joints along with the pubis symphysis.
    *Primary cartilagenous(1) joints (synchondrosis) is seen between the sphenoid & occipital bone (at clivus) and also in the growing bone (epiphysio-diaphyseal joint).
    -First rib has got 2 anterior Synchondrosis as compared to the other true ribs (They have got only one)

    References:
    1.Pg 262; BDC:Vol-3(4th Ed.)
    2.Pg 658,103; Gray's Anatomy (39th Ed.)



    In their course from the seminiferous tubule to the epididymis, sperm pass through, in order:
    1. Straight tubules, efferent ductules, rete testis
    2. Rete testis, straight tubules, efferent ductules
    3. Efferent ductules, rete testis, straight tubules
    4. Straight tubules, rete testis, efferent ductules

    Ans 4. Straight tubules, rete testis, efferent ductules
    Explanation:
    *The sperms form in the seminiferous tubules(spermatogenesis) and pass on to the straight tubules.
    -Sperms further enter a network of tubules (rete testis), where they are exposed to high concentration of estrogen.
    -The sperms get concentrated in rete testis, and if they don't,infertility can result (due to diluted semen).
    -Now, the sperms reach efferent ductules(lined by ciliated columnar epithelium).
    And finally, the sperms are in the epididymis (lined by pseudo-stratified columnar epithelium with stereo-cilia)
    *stereo-cilia are also seen in the internal ear hair cells are believed to absorb the fluids (Cilia ia a misnomer)
    -The sperms will be stored in the epididymis before their ejaculation.

    References:
    1. Pg. 430; Ganong (21st edition)
    2. Pg. 1309; Gray's Anatomy (39th Ed.)


    All are the absent in Mullerian agenesis except
    1. Uterus
    2. Vagina
    3. Ovary
    4. Uterine tube

    Ans. 3. Ovary
    Explanation:
    *Mullerian duct is a mesodermal derivative and gives rise to uterus & uterine tubes.
    -It also forms mesodermal part of the vagina, when it meets with the sino-vaginal bulbs(which forms endodermal part of vagina)
    *Now if mullerian ducts are absent, there will be no uterus(1) & uterine tubes(4).
    -Vagina(2) will also not form because it is the mullerian duct which induces the formation of vagina.
    *Ovaries are present, since they arise from a separate source-the genital ridges
    Note:1.This patient will have amenorrhoa, which cannot be corrected.
    2.This lady can be a surrogate mother by contributing oocyte for in vitro fertilization.


    Earliest sign of puberty in girls is
    1. Breast budding
    2. Growth Spurt
    3. Menarche
    4. Apearance of pubic and axillary hair

    Ans. 1. Breast budding
    Explanation:
    *Puberty is the period when reproductive capabilities are reached and conception is possible.
    -The first sign of puberty onset is thelarche (Development of breast-breast budding (1)).
    *Pubarche (4) will occur next and will be followed by Menarche(3).
    -Pubarche: axillary & pubic hair appearance (4); Menarche: first menstrual period.

    References:
    Pg.423;Ganong (21st Ed.)



    Chorionic villus biopsy is done in all except
    1.Neural tube defects
    2.Thalaessemia
    3.Myotonic dystrophy
    4.Down syndrome

    Ans. 1.Neural tube defects

    Explanation:
    *CVS can be done after 10th week (earlier than amniocentesis)
    -Earlier results reduce maternal stress by going for a possible therapeutic abortion(if indicated) at an early stage.
    -A trans abdominal route is taken if the pregnancy exceeds 12th week.
    Indications:
    1. Karyotyping-the most common indication. E.g., Down syndrome(4)
    2. Haemoglobinopathies-E.g., Thalassemia(2), sickle cell disease etc.
    3. Biochemical studies-E.g., Gaucher's disease, Niemann-Pick disease,Tay-Sach's disease etc.
    4. Single gene defects-E.g., Myotonic dystrophy(3),cystic fibrosis, Huntington's disease,phenylketonuria etc.
    *Neural tube defects(1) are diagnosed by ultrasound and estimation of alpha-fetoprotein in maternal serum or amniotic fluid.

    References:
    1.Pg 120,294;Langman (10th Ed.)
    2.Pg 422;Ganong (21st Ed.)




    Which is not a composite muscle
    1. Rectus femoris*
    2. Adductor magnus
    3. Pectineus
    4. Biceps femoris

    Ans.1 Rectus femoris
    Explanation:
    *Muscles like adductor magnus, pectineus, biceps femoris etc. are called as composite muscles as they are doubly innervated.
    Reference:
    1.Pg. 64; BDC-Vol 2 (4th Ed.)
    2.Pg.1467;Grays Anatomy (39th Ed.)



    Low radial nerve injury causes all except
    1. Loss of extension of fingers
    2. Sensory loss to dorsum of hand
    3. Paralysis of brachioradialis
    4. Extensor carpi radialis brevis paralysis

    Ans. 3.Paralysis of brachioradialis
    Explanation:
    *Radial nerve course: It emerges out from the radial groove and enter the anterior compartment of arm.
    -Here it gives muscular branches to brachioradialis and extensor carpi radialis longus.
    _Then it reaches the anterior aspect of lateral epicondyle and divides into 2 terminal branches:
    1.PIN (posterior interosseous nerve) & 2. Superficial cutaneous branch to postero-lateral hand.
    -PIN supplies extensor carpi radialis brevis(ECRB) as well as all the extensors of fingers including thumb.
    *Now, in a lesion of radial nerve below radial groove, there should be paralysis of ECRB(4) & finger extensors(1).
    -There should also be cutaneous loss on the postero-lateral hand(2).
    *Only option that appears to be the answer is paralysis of brachioradialis(3)...and this will happen only if the nerve was damaged...
    ...Below the radial groove & above its terminal branches...
    E.g., Supra-condylar fracture of humerus (Low radial nerve palsy).
    -Here brachioradialis might escape the injury and will not be paralysed.

    References:
    Pg No. 814,858, 887;Grays Anatomy (39th Ed.)



    What causes the pain associated with a stone in the ureter
    1. Obstruction of urine flow with distention of the renal capsule
    2. Irritation of the ureteral mucosa by the stone
    3. Excessive ureteral peristalsis in response to the obstructing stone
    4. Irritation of the intramural ureter

    Ans 1. Obstruction of urine flow with distention of the renal capsule.
    Explanation:
    *Since, the question is a direct pick from Campbell-Walsh Urology Review Manual, we are left with no logical discussion on the question and accept the provided answer.
    *The problem with the question is that it is not mentioning whether the pain is constant or colicky...!
    *Colicky pain due to ureteric stone occurs because of hyperperistalsis in the proximal part of the ureter above the obstruction.
    -Afferents from the ureter travel in the segments T-11,12 & L-1,2.
    -Depending upon the level of obstruction the pain may be referred to the loin(lumbar) region and shifts antero-inferiorly to groin(inguinal region) as the stone advances in the ureter.
    -This referred pain may also be felt in the anterior thigh or external genitalia along the distribution of genitofemoral nerve (L1 &2).

    References:
    1.Pg. 84;Campbell-Walsh Urology Review Manual, 2nd edition,Volume 1,Chapter 5. Urinary Tract Imaging-Basic Principles,Ques 1.
    2.Pg. no. 304;BD Chaurasia-Vol 2 (4th Ed.)
    3.Pg. no. 394; Keith L Moore; 5th Ed.


    .Lymph flow from the foot is
    1. Increased when an individual rises from the supine to standing position
    2. Increased by massaging the foot
    3. Increased When capillary permeability is decreased
    4. Decreased when the valves of the leg veins are incompetent

    Ans. 2. Increased by massaging the foot

    Reference:
    Pg 793; Ganong(21st Ed.)

    Bronchial artery supplies upto
    1. Tertiary bronchioles
    2. Respiratory bronchioles
    3. Alveolar sac
    4. ?

    Ans. 2. Respiratory bronchioles
    Explanation:
    *Bronchial arteries supply the bronchial wall as far as the respiratory bronchiole.
    -Bronchial arteries are derived from the descending thoracic aorta as direct or indirect branches.
    -Right bronchial artery is single and a branch of 3rd posterior intercostal artery.
    -Left lung has 2 bronchial arteries (and are direct branches from aorta)
    -There are pre-capillary anastomoses between bronchial & pulmonary arteries.
    -Lungs survive even if the bronchial arteries were shut off,due to dual vascularity (pulmonary & bronchial circulation)

    References:
    Pg 1078;Grays Anatomy (39th Ed.)



    Artery to vas deferens is a branch of
    1. Inferior epigastric
    2. Superior vesical
    3. Cremasteric
    4. Middle rectal

    Ans. 2. Superior vesical
    Explanation: Vas deferens is supplied by a separate artery, which is a branch of superior vesical artery(2).
    -This artery of vas deferens anastomoses with the testicular artery.
    *Testis is mainly supplied by the testicular artery, an anterior branch of aorta.
    -Testis receives additional blood from the artery of ductus deferens and also from cremasteric(3) branch of inferior epigastric artery(1).
    Note: In varicocele treatment, we ligate both the testicular artery and vein quite high up.
    -The artery being ligated to include the venae commitantes running along with it.
    (Remember, venae commitantes anastomose with the internal spermatic veins and if left open can lead to reccurence of varicoceles!)
    -In this operation, testis survives, despite ligating the testicular artery, because of its additional arterial supply from cremasteric branch & artery of ductus deferens.
    * Venous drainage of ductus deferens is to pelvic venous plexus and lymphatics reach the External & internal iliac lymph nodes.

    References:
    Pg 1131,1306;Grays Anatomy (39th Ed.)
  26. DK.

    DK. Guest

    Manual strangulation injuries of the larynx


    Laryngeal injuries secondary to manual strangulation are seen more often by the Forensic pathologist than by the otolaryngologist. Forces sufficient to cause thyroid and cricoid cartilage fractures are usually sufficient to cause acute asphyxia and death. However, due to the static nature of the compressive forces applied in strangulation, fractures of the cartilaginous framework may occur without obvious mucosal disruption or submucosal hematoma formation. If the victim survives the initial assault and the injuries go unrecognized and untreated, delayed life-threatening airway obstruction of long-term vocal dysfunction may result. Computed tomography seems to be an excellent noninvasive technique to evaluate and verify cartilaginous laryngeal fractures and soft-tissue injury. Recognition of the potential for such injuries is the key to management and treatment


    R. B. Stanley Jr and D. G. Hanson
  27. DK.

    DK. Guest

    Colostomy versus anoplasty

    The decision to perform an anoplasty during the newborn period or to delay the repair and perform a colostomy is based on physical examination findings in the newborn, the appearance of the perineum, and changes that occur during the first 24 hours of life.

    Operating earlier and in a single stage is potentially beneficial to the patient, but this should be decided carefully, based on the specific circumstances of the newborn and the experience of the surgeon. A more conservative approach is warranted in neonates with low birth weight and associated cardiac or respiratory conditions. The indications for colostomy compared with anoplasty based on sex are as follows:

    Newborn boys

    Anoplasty - Rectoperineal fistula
    Colostomy - Rectobulbar urethral fistula, rectoprostatic urethral fistula, rectovesical fistula, imperforate anus without fistula, rectal atresia
    Newborn girls
    Anoplasty - Rectoperineal fistula
    Colostomy - Rectovestibular fistula, imperforate anus without fistula, persistent cloaca, rectal atresia, rectovaginal fistula
    Decision-making in newborn boys with anorectal anomalies

    In 80-90% of newborn boys, clinical evaluation and urinalysis provide enough information for the surgeon to decide whether a colostomy is required.

    After birth, an intravenous line is placed for fluids and antibiotics. A nasogastric tube is inserted to keep the stomach decompressed to avoid the risk of vomiting and aspiration.

    Meconium is not usually observed at the perineum in a newborn with rectoperineal fistula until at least 16-24 hours of life. Abdominal distension does not develop during the first few hours of life but is required to force meconium through a rectoperineal fistula, as well as through a urinary fistula. This is because the most distal part of the rectum in these children is surrounded by a funnel-like voluntary muscle structure that keeps part of the rectum collapsed and empty. The intra-abdominal pressure must be high enough to overcome the tone of the muscles that surround the rectum to force meconium through the fistula. Therefore, the decision to perform a colostomy or an anoplasty must be delayed for 16-24 hours while the surgeon evaluates for clinical evidence of the newborn’s anorectal anomaly.

    Clinical inspection of the buttocks is important. A flat bottom or flat perineum, as evidenced by the lack of a midline gluteal fold and the absence of an anal dimple, indicates that the patient has poor muscles in the perineum. These findings are associated with a high malformation; therefore, a colostomy should be performed.

    Perineal signs found in patients with low malformations include the presence of meconium at the perineum, a bucket-handle malformation (ie, a prominent skin tag located at the anal dimple, below which an instrument can be passed), and an anal membrane (through which meconium is visible).

    Newborn boys with rectoperineal fistula do not require a colostomy. They can undergo a posterior sagittal anoplasty.

    Newborn boys with evidence of a rectourinary tract communication should undergo fecal diversion with a colostomy.If none of the clinical signs to reveal the location of the anorectal anomaly are evident by 24 hours, obtaining radiographs can help. This situation is necessary in only approximately 10% of patients. Obtain cross-table lateral radiographs with the newborn prone, with the pelvis elevated, and with a radiopaque marker placed on the perineum (see Image 3). Rarely, radiography reveals the column of air in the distal rectum to be within 1 cm of the perineum; in these instances, treatment is similar to that for rectoperineal fistula, and a newborn perineal operation may be performed. If the air column is more than 1 cm from the perineum, a colostomy is indicated.

    Some authors have performed definitive repair in the newborn period. Advantages to this approach include avoiding colostomy and repairing the malformation earlier; however, because the surgeon does not know the precise anorectal defect, the urinary tract is at considerable risk. To definitively determine the patient's anorectal defect, perform distal colostography, which requires the presence of a colostomy. Without this information, an operation in the newborn period is, essentially, a blind perineal exploration. The surgeon may not be able to locate the rectum and may find and damage other unexpected structures (eg, posterior urethra, seminal vesicles, vas deferens, ectopic ureters) during the search for the rectum. Finally, without fecal diversion, the risk of dehiscence and infection exists. These complications may compromise the chance of achieving bowel function.

    The rare exception occurs when the cross-table lateral radiograph obtained at 16-24 hours reveals that the rectum is located just below the coccyx. In this case, the rectum may be reached from the posterior sagittal approach.

    Obtain urinalysis and place gauze over the penis to reveal the presence of fecal matter in the urine, which is considered evidence of a rectourinary fistula.

    Abdominal ultrasonography must be performed to evaluate for the presence of an obstructive uropathy. At the same time, spinal ultrasonography may be performed to evaluate for spinal anomalies, including the presence of a tethered cord.

    Methods to reveal the location of the distal rectum before 16 hours of life are flawed because of the contracted state of the funnel-like sphincter mechanism. Typically, the funnel-shaped muscle structure is contracted unless overcome with a distending force. Tests such as MRI, ultrasonography, CT scanning, or injection of contrast through the perineum falsely locate the distal rectum as high in the pelvis.

    Distal colostography (typically obtained 1 mo after colostomy opening) must have adequate pressure to demonstrate a fistula from the rectum to the urinary tract. If pressure is inadequate, this method also falsely locates the distal rectum as high in the pelvis.

    Once the patient recovers from colostomy and demonstrates good growth and development, the definitive operation can be planned 4-8 weeks later.

    Surgical therapy
    As discussed above, the surgeon must decide in the newborn period whether the child requires fecal diversion with a colostomy or if a primary procedure is possible.

    Colostomy

    A descending colostomy with separated stomas is recommended. The advantages of this type of colostomy include the following:Only a small portion of distal colon is defunctionalized.
    In patients with large rectourinary fistulae who pass urine into the bowel, the urine comes out easily through the mucous fistula, avoiding the problems of hyperchloremic acidosis caused by urine absorption. Urinary tract infections are also avoided.
    Washing and cleaning the portion of the colon distal to the colostomy is relatively easy.
    Distal colostography is easy to perform.
    The sigmoid loop is kept distal to the colostomy, which provides enough length to reach the perineum during the definitive pull-through procedure.
    The separated stomas prevent spillage of stool from proximal to distal bowel, which avoids impacted distal stool and urinary tract infections.
    Prolapse with this technique is uncommon. Proximal stoma prolapse in a normally rotated colon should not occur with this technique because the colon is well fixed to the retroperitoneum just before the colostomy rises to skin level. Because the distal stoma is in a mobile portion of the colon, it may prolapse. The distal stoma must intentionally be made small, both to avoid prolapse and because it is used only for irrigations and radiologic studies.
    When performing a colostomy in the newborn, the distal bowel should be irrigated to remove all the meconium. This prevents formation of a megasigmoid, which may cause constipation.
    Colostomy errors include the following:

    Too-distal sigmoidostomy: In this most common error, the colostomy is placed too distal and interferes with the pull-through procedure.
    Right upper sigmoidostomy: Instances of inadvertent sigmoid colostomy placed in the right upper quadrant during attempts to perform a transverse colostomy have been reported. Anchoring of the sigmoid in the right upper quadrant interferes with the pull-through procedure.
    Incomplete diverting of stool: An error occurs when a loop colostomy does not divert the stool completely and allows for distal stool impaction and urinary tract infections.
    Megarectum: Transverse colostomies may produce megarectum.
    Definitive repair

    Repair of an anorectal malformation requires a meticulous, delicate technique and a surgeon with experience in treating these defects.
    The posterior sagittal approach is ideal for defining and repairing anorectal anomalies.
    Anorectal abnormalities in 90% of newborn boys may be repaired solely with a posterior sagittal approach, whereas 10% require an additional abdominal component (with laparotomy or laparoscopy) to mobilize a very high rectum.
    All anorectal malformations in newborn girls may be repaired with the posterior sagittal approach, with the exception of approximately 30% of instances of persistent cloaca. In this 30%, the rectum or vagina is high enough to also require an abdominal approach.
    A Foley catheter is placed first; then, patients are placed in the prone position with the pelvis elevated.
    The posterior sagittal incision length varies depending on the anorectal defect. Perineal fistulas are repaired with a minimal posterior sagittal incision that is large enough to divide the external sphincter and to mobilize the anus back to the center of the external sphincter. The sphincter mechanism is always located posterior to the fistula site. This operation may be performed in the neonatal period without a protective colostomy.
    The posterior sagittal approach is based on the fact that nerves do not cross the midline. Remaining exactly in the midline, the surgeon preserves the innervation of all the important pelvic structures.
    An electrical stimulator helps reveal the location of the sphincteric mechanism. The parasagittal fibers, the muscle complex, and the levators are identified during the dissection. The external sphincter is represented by muscle fibers that run parallel to the midline in a parasagittal fashion. A muscle structure termed the levator mechanism lies medial to these fibers and represents the lower end of the funnel-like voluntary muscle.
    The levator mechanism extends in continuum down to the skin, but this was not known prior to the use of the posterior sagittal approach. Electrically stimulated, the parasagittal fibers elicit a contraction that results in shortening of the same fibers. The rectum pushes forward toward the pubic bone when the upper portion of the levators are stimulated. Stimulating the lower part of the funnel-like muscle structure elevates the anal dimple. This group of muscle fibers, termed the muscle complex, extends from the levator mechanism down to the skin and is located immediately medial to the parasagittal fibers.
    The surgeon opens the posterior sagittally. The skin and subcutaneous tissue are divided, and the parasagittal fibers below are divided in the midline, as is the muscle complex.
    The levator muscle is then opened, and the rectum is found, except in patients with a true supralevator malformation (10% of cases), in whom the surgeon finds a genitourinary structure.
    When the rectum is located, its posterior wall is opened in the midline to demonstrate the presence of a fistula. This posterior incision in the rectum is carried down to the fistula site.
    The rectum and urethra share a common wall. Meticulous dissection is required to separate the distal rectum from the urethra. A submucosal dissection must be performed in the first 5 mm above the fistula site.
    The rectum is separated from the urinary tract. This dissection is facilitated through placing multiple 6-0 silk sutures in the rectal mucosa to exert uniform traction.
    The opening in the urethra is then closed with absorbable suture.
    Once the rectum is separated, it is then mobilized down to reach the perineum by circumferentially dividing the bands and vessels that hold the rectum up in the pelvis. The intramural blood supply of the rectum is excellent; therefore, the rectum remains viable. Because the newborn depends on this intramural blood supply, preventing damage to the rectal wall is vital.
    Once the rectum is fully mobilized, the size of the rectum and the available space must be assessed. The rectum occasionally requires tapering to fit the limits of the sphincteric mechanism. The tapering should take place on the posterior wall so that the suture lines of the tapered rectum and the closed urethral fistula do not lie next to each other.
    The rectum is placed in the limits of the sphincter mechanism, which is reconstructed in the midline. The rectum is sutured to the perineal skin (anoplasty).
    In 10% of newborn boys with this defect, the rectum enters the urinary tract at the bladder neck level. The repair of this malformation involves a posterior sagittal incision and an abdominal component. All the muscle structures are divided in the midline, leaving the urinary tract untouched. The pathway just under the coccyx and sacrum is identified, and the abdomen is entered in this area of the pelvic retroperitoneum. The rectum is pulled through this space, and the sphincter mechanism is reconstructed around it.
    To mobilize the rectum off of the bladder neck, an abdominal component is required via laparoscopy or laparotomy. The fistula is ligated with great care to avoid injuring the ureters and vas deferens: the plane of dissection must be made close to the bowel wall of the rectosigmoid, 2-3 cm above the peritoneal reflection. The rectum is then mobilized for adequate length to reach the perineum without tension.
    The fistula is divided and sutured with absorbable material. The rectum is passed through to the posterior sagittal incision and an anoplasty is performed.
    In patients with imperforate anus without fistula, the same meticulous dissection is required to separate the distal rectum from the urinary tract as in patients with rectourinary fistulae, because the rectum and urethra still share a common wall.
    In patients with rectovestibular fistula, the posterior sagittal incision may be shorter than in newborn boys with rectourethral fistulae. Often, the entire levator mechanism does not need to be divided; only the external sphincter, muscle complex, and part of the lower portion of the levator mechanism require division. The rectum and posterior vagina share a common wall; this separation is the most difficult part of the operation. Once the rectum is completely mobilized, a perineal body is constructed, and the rectum is placed within the limits of the sphincter mechanism.
    A rare malformation, rectal atresia, occurs in 1% of patients. The anal canal is normal, and, externally, the anus appears typical. However, a blockage exists 1-2 cm from the anal skin and is usually found when the nurse tries to pass a thermometer. These babies should undergo colostomy at birth; definitive repair involves a posterior sagittal approach and an end-to-end anastomosis between the upper rectal pouch and the anal canal.
  28. Sarrah.

    Sarrah. Guest

    all are true abt superantigens excpet..
    a.thye activate the t lymphocytes biding to tlr 4. or so(not exactly rem thsi option..
    b. they bind both to TH CELS and APCS(cd4)
    c.they cross link mhc 2 and cd4 ...
    d. THEY BIND TO ANTIGEN BINDING CLEFT..

    ans is D. THEY BIND TOANTIGEN BINDING CLEFT SITE..

    ref is from kaplan notes for USMLE immunlogy..
    page no 350..
    SUPERANTIGENS ae viral or bacterial proteins tat cross link the variable beta domain of a T cell receptor to an alpha chain of a class 2 MHC . this cross linkage provides an avtivating signal that induces T CELL ACTIVATION AND PROLIFERATIOn in absence of antigen SPECIFIC RECOGNITION of peptides i MHC clas 2 groove.. because superantigens BIND OUTSIDE OF ANTIGEN BINDIG CLEFT , they activate any c lones of T cells ex[ressing a particular variable beta sequence and thus cause polyclonal activation of Tcells, resulting in the overproduction of IFN gamma. this in turn activates macrophages, resulting in overexpression of proinflammatory cytokines (IL 1 IL 6 and TNF ALPHA). excess amts of these cytokines induce systemic toxicity . molecules produced during infectious processes and kown to act as superantigens include staphyloccocal enterotoxins.toxic shock syndorome toxin 1(TSST 1) and streptococcal pyrogenic pyrogenic exotoxins
  29. Sorabh

    Sorabh Guest

    regarding the question on pneumocystis carinii/ jiroveci .. the answer should be commonly associated with cmv and not only seen in immunocompromised
    reference .. harrison pg 1050
    CMV may itself contribute to further
    T lymphocyte hyporesponsiveness, which often precedes superinfection
    with other opportunistic pathogens, such as Pneumocystis. CMV
    and Pneumocystis are frequently found together in immunosuppressed
    patients with severe interstitial pneumonia
  30. Guest

    Guest Guest

    A haemangioma was found on the left of the falciform ligament of the liver. Surgeon dissecting Couinaud’s segments of liver to the left of attachment of falciform ligament resects which lobes
    1. 2,3
    2. 1,4b
    3. 2,4a
    4. 1,4a

    Ans. 1. 2,3
    Explanation:
    *Segment II & III lie to the left of the falciform ligament and will be resected in this patient.
    *Couinaud divided liver into various segments based upon the distribution of portal & hepatic veins.

    *Resection of liver is either non-anatomical or anatomical.
    -Non-anatomocal resection are minor and doesn't follow Couinaud's segmentation.
    -Major removals follow the Couinaud classification for putting the lines of resection.
    *The intersegmental hepatic veins serve as a surgical landmark (as do the pulmonary veins in the lungs-they are also intersegmental in distribution).
    -These hepatic veins provide surgical planes to dissect the liver, but also are a major source of bleeding, which the surgeon has to bear with.

    -Caudate (comma shaped) lobe is the beginning of the segmental nomenclature and is taken as segment - I (posterior segment).
    -Quadrate lobe is considered under left medial segment and is numbered segment -IV.
    NOTE: Segments are numbered in anti-clockwise direction when LIVER is visualised in posterior view.
    -Except for the caudate lobe (segment I), the liver is divided into right & left livers based on the primary (1 degree) division of the portal triad into right and left branches.
    -The plane between the right and left livers being the main portal fissure in which the middle hepatic vein lies.

    *Healy & Schroy segmentation is also followed widely,where arterial & biliary tree is the reference.

    References:
    1.Pg 1217; Gray's Anatomy (5th Ed.)
    2.Pg 294; KL Moore(5th Ed.)


    Not a somatic efferent nerve
    1. III rd
    2. IV th
    3. VII th
    4. XII th

    Ans. 3. VII th
    Explanation:
    *All the skeletal muscles are under GSE (or simply SE) except the muscles of branchial arch.
    -GSE : General somatic efferent.
    E.g., Biceps brachii is supplied by musculocutaneous nerve, which comes under GSE column.

    *Branchial arch muscles are the skeletal muscles under SVE (special visceral efferent) column.
    E.g., Facial nerve(3) supplies the facial expression muscles, which are derivatives of 2nd branchial arch (SVE).

    *Eye ball muscles are supplied by 3 nerves: (LR6 SO4)3.
    -Occulomotor(1) & Trochlear(2) nerves supply the muscles which are not a derivative of branchial arch, hence are under GSE.
    *Tongue muscles, supplied by hypoglossal(4), develop from the occipital myotomes and not branchial arches, hence they are also under GSE.
  31. anjum

    anjum Guest

    aipge

    not composite muscle
    1 pectineus
    2diagastric
    3rectus femoris
    4adductor magnus
    ans is rectus femoris

    synovial carcinoma
    x,18(this is the answer)

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