MOST IMP. TOPICS FOR DNB

Discussion in 'DNB CET board - DipNB' started by samuel, Aug 22, 2014.

  1. samuel

    samuel New Member

    ANTIGEN PRESENTING CELLS (APCs) :-
    two categories: professional or non-professional.
    1) Professional APCs

    types of APCs which express MHC class II molecules are called professional antigen-presenting cells.
    1)Dendritic cells (DCs)
    2)Macrophages
    3) B-cells
    4)Certain activated epithelial cells

    2) Non-professional APC:-
    A non-professional APC does not constitutively express the Major Histocompatibility Complex class II (MHC class II) proteins required for interaction with naive T cells;
    expressed only upon stimulation of the non-professional APC by certain cytokines such as IFN-γ.
    Non-professional APCs include:
    1)Fibroblasts (skin)
    2)Thymic epithelial cells
    3)Thyroid epithelial cells
    4)Glial cells (brain)
    5)Pancreatic beta cells
    6)Vascular endothelial cells
  2. samuel

    samuel New Member

    Hyperacute rejection takes place within hours of transplantation and is caused by preformed antibodies binding to either ABO blood group or HLA class I antigens on the graft. The recipient may have formed anti-HLA class I antibodies following exposure to allogeneic lymphocytes during pregnancy, blood transfusion, or a previous transplant. Antibody binding triggers a TYPE II HYPERSENSITIVITYreaction, and the graft is destroyed by vascular thrombosis. Hyperacute rejection can be prevented through careful ABO and HLA cross-matching and is now very rare.
  3. samuel

    samuel New Member

    TUBERCULOSIS
    a/k/a KOCH’s disease
    acid fastness – due to MYCOLIC ACID
    Virulence factor --- “CORD factor”

    a) PRIMARY TUBERCULOSIS
    Most commonly seen in children
    a/w unsensitised and unexposed individuals
    source of organism--- exogenous
    most commonly starts as “LATENT DISEASE”
    unilateral hilar lymph enlargement
    GHON’S FOCUS:-
    Subpleural fibrocaseous lesion (CONSOLIDATION) of lung parenchyma (mc---lower part of upper lobe.) microscopically contains epitheloid granulomatous inflammation
    GHON’S COMPLEX:-
    Consists of Subpleural ghon’s focus and involved lymph nodes.
    Ghon's complex found below clavicle.
    RANKE’S COMPLEX :-
    ghon’s focus alongwith FIBROSIS and CALCIFICATION known as RANKE’S COMPLEX.
    SIMON FOCUS
    is a tuberculous (TB) nodule formed in lung apex.
    Due to spread of primary TB infection from elsewhere in the body to lung apex via bloodstream.
    Simon focus nodules are often calcified.

    Fibrosis
    Calcification
    Pleural effusion
    Erythema nodosum
    Phlyctenular conjunctivitis

    b) POST-PRIMARY (=SECONDARY)PULMONARY TUBERCULOSIS

    Seen in previously sensitized host due to reactivation of latent primary lesions
    frequently a/w decreased immune status
    PUHL’S LESION:-
    Lesion in lung apex (upper lobe )(most commonly ---- rt lung>lt lung)
    No lymph node involvement

    ASSMAN FOCUS:-
    infraclavicular lesion of chronic pulmonary T.B.
    Lymph node involvement is RARE.
    secondary TB more likely to cavitate than primary TB.
    Endobronchial spread along nearby airways is relatively common finding, resulting in relatively well-defined 2-4 mm nodules or branching lesions TREE-IN-BUD APPEARANCE on CT
    tuberculoma formation and miliary TB are also recognised patterns of secondary TB.
    c) MILIARY PULMONARY TUBERCULOSIS

    Miliary tuberculosis is uncommon but carries a poor prognosis.
    It represents haematogeneous dissemination of an uncontrolled tuberculous infection.
    seen both in primary and post-primary tuberculosis.
    lungs are usually the easiest location to image.
    Miliary deposits appear as 1-3 mm diameter nodules.
    RICH FOCUS
    is a tuberculous granuloma occurring on brain cortex that ruptures into subarachnoid space, causing tuberculous meningitis.
    WEIGERT’S FOCUS :-
    Subintimal foci in pulmonary vein. ( d/t metastatic caseous TB.)

    SIMOND’S FOCUS:-
    Localized tb foci in liver.

    CONGENITAL TUBERCULOSIS
    Infection with tubercle bacilli either during intrauterine life or before complete passage through birth canal is termed as congenital tuberculosis.
    Three possible modes of infection of fetus:-
    1) Hematogenous infection via umbilical vein
    2) fetal aspiration of infected amniotic fluid
    3) fetal ingestion of infected amniotic fluid
    Most common primary site ----- LIVER ( primary complex in liver is suggestive of congenital TB)
    Most common site --- LUNG
    prognosis is poor
    Revised criteria for diagnosis of congenital tuberculosis ( by Cantwell ) :-
    Proven tuberculosis lesions in the infant plus one of the following:
    i. Lesions occurring in the first week of life,
    ii. A primary hepatic complex
    iii. Maternal genital tract or placental tuberculosis, and
    iv. Exclusion of postnatal transmission by thorough investigation of contacts.
  4. samuel

    samuel New Member

    MILIARY PULMONARY TUBERCULOSIS

    Miliary tuberculosis is uncommon but carries a poor prognosis.
    It represents haematogeneous dissemination of an uncontrolled tuberculous infection.
    seen both in primary and post-primary tuberculosis.
    lungs are usually the easiest location to image.
    Miliary deposits appear as 1-3 mm diameter nodules.
    RICH FOCUS
    is a tuberculous granuloma occurring on brain cortex that ruptures into subarachnoid space, causing tuberculous meningitis.
    WEIGERT’S FOCUS :-
    Subintimal foci in pulmonary vein. ( d/t metastatic caseous TB.)

    SIMOND’S FOCUS:-
    Localized tb foci in liver.
  5. samuel

    samuel New Member

    category A teratogen
    controlled studies show no risk
    acetaminophen, thyroxine, folic acid, magnesium sulfate

    category B teratogen
    no evidence of risk in humans despite risks in animals
    penicillins, cephalosporins, insulin, pepcid, reglan, paxil, prozac, benadryl, dramamine

    category C teratogen
    risk cannot be ruled out, controlled studies are lacking in humans
    codeine, methadone, AT, beta blockers, prilosec, heparin, protamine, robitussin, sudafed

    category D teratogen
    postive evidence of risk but potential benefits may outweight the risks
    aspirin, valium, tetracycline, depakote, lithium

    category X teratogen
    contraindicated in pregnancy
    isotretinoin, danocrine, pravachol, coumadin
  6. samuel

    samuel New Member

    Congenital CMV:

    MC in-utero viral infection: majority are asymptomatic
    Primarily transplacental,
    Clinical:
    bilateral sensorineural hearing loss-MC complication;
    periventricular calcification;
    hepatosplenomegaly;
    chorioretinitis (may lead to blindness)

    Urine culture is gold standard: urine cytology reveals large, basophilic intranuclear inclusions ("owl eyes") in renal tubular cells

    Rx: ganciclovir (begin with this); foscarnet (if the former is not working)
  7. samuel

    samuel New Member

    • Most Common Mediastinal Tumors::
    1. ANTEROSUPERIOR MEDIASTINUM :
    • Most common Tumor/Mass---- Thymoma
    • Most common mediastinal germ cell tumor----Teratoma
    2.Middle Mediastinum:
    • Majority are Cysts ( most common--- bronchogenic cyst)
    3. Posterior Mediastinum:
    • Most common Tumor/Mass----- Neurogenic
    • Overall most common mediastinal mass------ Neurogenic > Thymoma.
  8. samuel

    samuel New Member

    Friedreich’s ataxia

    This is the most common form of inherited ataxia, comprising
    one-half of all hereditary ataxias.

    Extensor plantar responses
    (with normal tone in trunk and extremities), absence of deep tendon
    reflexes, and weakness (greater distally than proximally) are usually
    found.

    Cardiac involvement occurs in 90% of patients

    The cerebral cortex is histologically normal except for
    loss of Betz cells in the precentral gyri..

    The classic form of Friedreich’s ataxia has been mapped
    to 9q13-q21.1, and the mutant gene, frataxin , contains
    expanded GAA triplet repeats in the first intron.

    Frataxin is a mitochondrial protein
    involved in iron homeostasis. Mitochondrial iron accumulation
    due to loss of the iron transporter coded by the mutant frataxin gene
    results.

    Two forms of hereditary ataxia associated with abnormalities in
    the interactions of vitamin E (α-tocopherol) with very low density
    lipoprotein (VLDL) have been delineated. These are abetalipoproteinemia
    (Bassen-Kornzweig syndrome) and ataxia with vitamin E
    deficiency (AVED).
  9. samuel

    samuel New Member

    Fulminant type 1 diabetes:
    • defined as diabetes in which the process of beta-cell destruction and the progression of hyperglycemia and ketoacidosis are extremely rapid.
    • Pathogenesis----- both genetic background—(HLA) human leukocyte antigen genes—and viruses has been suggested.
    • clinical characteristics:
    1) duration of hyperglycemic symptoms is 4 days on average;
    2) high prevalence of preceding common-cold-like and gastrointestinal symptoms;
    3) near-normal level of glycated hemoglobin in spite of very high plasma glucose levels associated with ketoacidosis;
    4) sometimes related to pregnancy;
    5) increased serum pancreatic enzyme levels, absent C-peptide levels, but virtually no detectable autoantibodies against beta cells.
    • presence of the above characteristics strongly indicates the diagnosis of fulminant type 1 diabetes.
    • Once the diagnosis of this disease is suspected, treatment of diabetic ketoacidosis must be started immediately, Otherwise, the death of the patient is likely to occur within 24 h.
  10. samuel

    samuel New Member

    CARDIAC TUMOURS

    1) most common tumor of heart : METASTASES (lung > breast)
    2) MC primary tumor of heart:

    a) MYXOMA in adults

    b) RHABDOMYOMA (not sarcoma) in children
    3) MC primary malignant tumor of heart : ANGIOSARCOMA
    4) most common tumors of the cardiac valves.---- Papillary fibroelastomas
  11. samuel

    samuel New Member

    MASSIVE BLOOD TRANSFUSION
    defined as
    1) adults
    a) replacement of >1 blood volume in 24 hours ,or
    b) >50% of blood volume in 4 hours (adult blood volume is approximately 70 mL/kg).
    2) children,
    • transfusion of >40 mL/kg (blood volume in children over 1 month old is approximately 80 mL/kg).
    electrolyte abnormalities are
    1) hypocalcemia
    2) hypomagnesemia
    3) hypokalemia
    4) hyperkalemia
    5) metabolic alkalosis ( due to excess citrate is converted to bicarbonate in liver)
  12. samuel

    samuel New Member

    CHRONIC NEUTROPHILIC LEUKEMIA____
    1)Philadelphia negative
    2)blasts <1%
    3)immature granulocytes <10%
    4)Peripheral blood leucocytosis >25×109...with neutrophil and band forms >80%
  13. samuel

    samuel New Member

    CHROMOTHRYPSIS---(Means chromosome shattering; a/k/a dramatic chromosome catastrophe)
    1)seen in OSTEOSARCOMAS(other bone cancers too) and GLIOMAS.
    2) dozens to hundreds of chromosomal breaks occurs in single or several chromosomes,then they are repaired haphazardly
    3)this will activate Oncogenes and inactivate Tumor suppressor gene.
    4)its mechanism of carcinogenesis.
  14. samuel

    samuel New Member

    BASOPHILIC STIPPLING
    is ribosomal inclusions in RBCs and stained by ROMANOWSKY STAIN but not stained by PERL'S PRUSSIAN BLUE STAIN (its for iron)
    sideroblastic anemia, lead poisoning, megaloblastic anemia, thalassemia, Arsenic poisoning
    constant finding of thalessemia
  15. samuel

    samuel New Member

    PAPPENHEIMER BODIES
    are iron deposits,
    seen in SIDEROCYTES (siderocytes are intraerythrocytic PERL'S PRUSSIAN BLUE STAIN positive iron granules)
    seen in----- sideroblastic anemia, hemolytic anemia, and sickle cell disease
  16. samuel

    samuel New Member

    1. Tumours of epithelial origin - cytokeratin
    2. Tumours of mesenchymal origin - vimentin
    3. Tumours of smooth muscle origin - smooth muscle actin, desmin
    4. Tumours of skeletal muscle origin - desmin
    5. Glial origin - GFAP
    6. Vascular origin - vWF, CD 31, factor viii, VEGF
    7. Stem cells - CD 34
    8. B cells - CD 19, 20, 21, 22
    9. Pan B cells - CD 19
    10. T cells - CD 1,2,3,5,7
    11. Pan T cells - CD 3
    12. NK cells - CD 16,56
    13. Reed sternberg cell - CD 15, 30
    14. Popcorn RS cell - CD 20, 45
    15. Mantle cell lymphoma - cyclin d1, CD 5
    16. Chronic lymphocytic leukaemia - CD 5, CD 23
    17. Hairy cell leukaemia - annexin a1, CD 25, 103, 11c
    18. Seminoma - PLAP, HCG
    19. Choricarcinoma - HCG
    20. Yolk sac tumour - AFP
    21. Sertoli cell tumour - inhibin
    22. Neuroendocrine tumour - NSE, synaptophysin, chromogranin
    23. Medullary carcinoma thyroid - calcitonin
    24. Ewing's sarcoma - CD 99, mic 2
    25. Malignant melanoma - HMB 45, S 100
    26. GIST - DOG 1, CD 117, CD 34
    27. Apoptotic cells - annexin v
  17. samuel

    samuel New Member

    Paget cells are usually positive for markers of breast epithelium differentiation like:

    Cytokeratin 7
    CAM 5.2
    Low-molecular-weight cytokeratins (negative for high-molecular-weight cytokeratins)
    Vast majority of cases show strong overexpression of the HER2/neu proteinion of the gene
    Positive for mucin
    18-20% of Paget’s cells express S100 protein but contrary to melanoma cells, HMB45 is consistently negative.
  18. samuel

    samuel New Member

    Toker cells are immunophenotypically similar to Paget cells, sharing expression of cytokeratin 7 and CAM 5.2, absence of high-molecular-weight cytokeratin expression, and negative S100- and HMB45-expression. They differ in the negative expression of mucin, HER2/neu, and epithelial membrane antigen. The similarities between Toker and Paget cells have suggested that the former may represent the cell that undergoes malignant transformation in the initial phases of PD. Toker cells can be present in normal patients as well.

    The most accepted explanation for the development of PD is that Paget cells result from the migration of cells from the underlying adenocarcinoma through the epidermis, the so-called epidermotropic theory. This theory is supported by the existence of an underlying carcinoma in about 90% of cases of PD, which usually shares phenotypic similarities with Paget cells.
  19. samuel

    samuel New Member

    Masaoka staging system is a staging system which is commonly adopted for thymomas and is the most important determinant of survival following surgical resection .

    stage I - intact thymic capsule
    stage II - capsular invasion into adjacent mediastinal fat or pleura.
    stage III - macroscopic invasion into adjacent organs, vessels
    stage IV -
    IVa - dissemination in thoracic cavity (i.e pleural or pericardial implants)
    IVb - distant metastases.
  20. samuel

    samuel New Member

    Soft tissue sarcomas occur with greater frequency in patients with the following inherited syndromes:
    Nevoid basal cell carcinoma syndrome (Gorlin syndrome: PTC gene mutation).
    Gardner syndrome (APC mutation).
    Li-Fraumeni syndrome (p53 mutation).
    Tuberous sclerosis (Bourneville disease: TSC1 or TSC2 mutation).
    von Recklinghausen disease (neurofibromatosis type 1: NF1 mutation).
    Werner syndrome (adult progeria: WRN mutation).
  21. samuel

    samuel New Member

    Mesotheliomas are characterized by having long, narrow, branching microvilli with a length to width ratio of around 10-16:1.


    By contrast, adenocarcinomas have short, stubby microvilli with core rootlets.

    Electron microscopy can also be used to confirm the absence of features of adenocarcinoma, such as intracellular mucin and membrane-bound secretory granules. Zymogen vacuoles are not seen in mesothelioma and are useful indicator of adenocarcinoma.
  22. samuel

    samuel New Member

    Diamond-Blackfan syndrome is a rare congenital PRCA that is usually detected at birth, or later during the first 18 months of childhood. Affected individuals usually have a macrocytic anemia. The expression of hemoglobin F and surface “I” antigen in erythrocytes is increased, indicating erythrocyte immaturity.

    About one third of these patients have developmental defects, including cleft palates, macroglossia, craniofacial defects, thumb or upper limb abnormalities, cardiac defects, and urogenital malformations. Growth is often retarded. A modest increased risk for leukemia and neoplasms is noted.

    Diamond-Blackfan syndrome is currently thought to be due to the deletion of genes for ribosomal protein RPS19, which leads to defects in ribosome biogenesis.
  23. samuel

    samuel New Member

    Cystine and brushite are the most ESWL-resistant
    stones followed in descending order by calcium
    oxalate monohydrate (COM), hydroxyapatite,
    struvite, calcium oxalate dihydrate (COD), and uric
    acid....
  24. samuel

    samuel New Member

    Urinary calculi can also be induced by medications when the drugs crystallize and become the primary component of the stones. In this case, urinary supersaturation of the agent may promote formation of the calculi. Drugs that induce calculi via this process include magnesium trisilicate; ciprofloxacin; sulfa medications; triamterene; indinavir; and ephedrine, alone or in combination with guaifenesin.
  25. samuel

    samuel New Member

    COMET TAIL SIGN..helps to distinguish between phelobith and ureter stone.... a tail of soft tissue extending from a calcification, representing the collapsed / scarred / thrombosed parent vein. [it favors phelobith]
  26. samuel

    samuel New Member

    Fatty acid-binding protein, brain a/k/a
    Brain lipid-binding protein (=BLBP)/Brain-type fatty acid-binding protein(=B-FABP)/Fatty acid-binding protein 7/ Mammary-derived growth inhibitor related

    Seen on mature astrocytes...essential for with potential morphogenic activity during CNS development. It is required for the establishment of the radial glial fiber system in developing brain, a system that is necessary for the migration of immature neurons to establish cortical layers
  27. samuel

    samuel New Member

    PAPPILARY CARCINOMA OF THYROID--- nuclear feature is diagnostic ( PSEUDOINCLUSIONS,NUCLEAR GROOVING, OPTICALLY CLEAR NUCLEIAND ORPHAN ANNIE EYE LIKE APPEARENCES)....1)a/w radiation exposure in childhood.
  28. samuel

    samuel New Member

    Frequency of gene mutation in colorectal carcinogenesis
    i) K-RAS – 40 %
    ii) APC- >70%
    iii) Mismatch repair – 15%
    iv) B- catemin →2to 5%
  29. samuel

    samuel New Member

    ROBSON’s classification ( USED FOR RENAL CELL CARCINOMA)
    Stage I- Rcc confined to kidney
    II- extend through renal capsule but confined to Gerota’s fascia
    III- Renal vein / IVC involved
    IV- Tumor spread to local , adjacent organs or distant sites
  30. samuel

    samuel New Member

    Soft tissue sarcomas are malignant tumors that arise in any of the mesodermal tissues of the extremities (50%), trunk and retroperitoneum (40%), or head and neck (10%).

    Garland's triad (also known as the 1-2-3 sign or Pawnbrokers sign) is a lymph node enlargement pattern which has been described in sarcoidosis.

    It comprises of:

    right paratracheal nodes
    right hilar nodes
    left hilar nodes
  31. samuel

    samuel New Member

    S. japonicum
    causes katayama fever... liver fibrosis, liver cirrhosis, liver portal hypertension, splenomegaly, and ascites.

    parasite uses hosts' immune system (granulomas) for transportation of eggs into the gut. The eggs stimulate formation of granuloma around them. The granulomas, consisting of motile cells, carry the eggs to the intestinal lumen.

    Chronic infection can lead to characteristic Symmer's fibrosis (also known as "clay pipe stem" fibroses, these occur due to intrahepatic portal vein calcification which assume the shape of a clay pipe in cross section).

    S. japonicum mainly found in mesenteric or rectal veins.
  32. samuel

    samuel New Member

    Enzymatic markers of different membranes :
    Plasma : Adenyl cyclase, Na+ K+ ATPase
    ER : Glucose-6-phosphatase
    GOLGI APPARATUS : GlcNAc transferase I, Golgi mannosidase II, Galactosyl transferase, Sialyl transferase
    Inner mitochondrial membrane: ATP synthase

    Glucokinase is a cytosolic enzyme
  33. samuel

    samuel New Member

    Codman triangle may be seen in aggressive lesions lik::
    --osteosarcoma
    --metastasis
    --juxtacortical chondrosarcoma
    ---ewings sarcoma
    --osteomyelitis
    ---gaint cell tumor
    -- sumtimes in scurvy due to subperiosteal hemorrhage
    --malignant fibrous histiocytoma
    ---active aneursymal bone cyst
  34. samuel

    samuel New Member

    Sherman's paradox is w.r.t to Fragile X syndrome, which doesnt follow normal XLR inheritance, here males can be carriers (due to premutations they have) these premutations get converted to full blown mutation in oogenesis of next generation daughters, thus chances of disease are more in grand children (40%), than in siblings(9%), this is a paradox because all recessive diseases should reduce with successive generation.
  35. samuel

    samuel New Member

    Important criterias

    1.Halls criteria : Downs syndrome

    2.Dukes criteria:
    Endocarditis/Heart failure

    3.Butchers criteria :mesothelioma

    4.Ann Arbours classifiacation :Hodgki.s lymphoma

    5.Bismuth classification: tumors of hepatic ductal
    system

    6.Nazers Index: Wilsons disz
  36. samuel

    samuel New Member

    7.Pagets Index : Abruptio placentae

    8.Quetlet index: BMI -wt in kg/ht in meter square

    9.Ponderial Index: ht in cm/cube root of body wt
    in kgs 10.Brocas index : Ht in cms-100

    11.Corpulence index : Actual wt/desired wt

    12.Milans crjteria: for liver transplant in HCC

    13.Mayers n cottons grading system: Subglottic
    stenosis

    14.Spaldings criteria: abdominal pregnancy
  37. samuel

    samuel New Member

    15.GCS/Ransons criteria/APACHE score:
    Pancreatitis 16.Ennekings staging : Bone tumors

    17. Mc Donald's criteria: Multiple Sclerosis

    18.Epworths criteria : Sleep apnea

    19.Framminghams criteria/Boston's criteria: CHF

    20.Durie salmon system of staging: Multiple
    myeloma

    21.Lights criteria: pleural effusion
    22.GOLD's
    criteria :COPD
    23.OKUDA staging : HCC 24.Child's
    Turcott pug score/MELD/PELD- Cirrhosis
  38. samuel

    samuel New Member

    Definations related to nephrotic syndrome Remission:Urine albumin nil or trace (or proteinuria of <4 mg/m2/h) for three consecutive early morning specimens.

    Relapse :Urine albumin 3+ or 4+ (or proteinuria >40 mg/m2/h) for three consecutive early morning specimens, having been in remission previously.

    Frequent relapses:Two or more relapses in initial 6 months or more than Three relapses in any 12 months.

    Steroid dependence:Two consecutive relapses while pt. is on alternate day steroids or within 14 days of discontinuation of steroid therapy.

    Steroid resistance:Absence of remission despite therapy with daily prednisolone at a dose of 2 mg/kg per day for 4 weeks.
  39. samuel

    samuel New Member

    Theories of Clubbing::
    1. Neurogenic: Vagal stimulation causes vasodilatation
    and clubbing
    2. Humoural: GH, PTH, oestrogen, PG, bradykinin cause
    vasodilatation and clubbing
    3. Ferritin: Decreased ferritin in systemic circulation
    causes dilatation of A-V anastomosis and hypertrophy
    of the terminal phalanx
    4. Hypoxia: Persistent hypoxia causes opening of deep
    A-V fistulae of the terminal phalanx
    5. Platelet derived growth factor: This factor which is
    released secondary to infection anywhere in the
    body, also causes vasodilatation and this is the latest
    and most acceptable theory for clubbing.
  40. samuel

    samuel New Member

    PHACE syndrome comprises of

    P: posterior fossa malformations
    H: haemangiomas
    A: arterial anomalies
    C: coarctation of the aorta and cardiac anomalies
    E: ocular anomalies
    When sternal clefting is also present it is termed PHACES syndrome.
  41. samuel

    samuel New Member

    Ascending cholangitis
    Given that ascending cholangitis usually occurs in the setting of bile duct obstruction, various forms of medical imaging may be employed to identify the site and nature of this obstruction. The first investigation is usually ultrasound, as this is the most easily available.[1] Ultrasound may show dilation of the bile duct and identifies 38% of bile duct stones; it is relatively poor at identifying stones further down the bile duct. Ultrasound can help distinguish between cholangitis and cholecystitis (inflammation of the gallbladder), which has similar symptoms to cholangitis but appears differently on ultrasound.[7] A better test is magnetic resonance cholangiopancreatography (MRCP), which uses magnetic resonance imaging (MRI); this has a comparable sensitivity to ERCP.[7] Smaller stones, however, can still be missed on MRCP depending on the quality of the hospital's facilities.[1]

    The gold standard (best possible) test for biliary obstruction is still endoscopic retrograde cholangiopancreatography (ERCP). This involves the use of endoscopy (passing a tube through the mouth into the esophagus, stomach and thence to the duodenum) to pass a small cannula into the bile duct. At that point, radiocontrast is injected to opacify the duct, and X-rays are taken to get a visual impression of the biliary system.
  42. samuel

    samuel New Member

    Gama=gama-Aminobutyric acid (GABA) is the chief inhibitory neurotransmitter in the mammalian central nervous system. It plays a role in regulating neuronal excitability throughout the nervous system. In humans, GABA is also directly responsible for the regulation of muscle tone.[1] In insect species GABA acts only on excitatory nerve receptors.

    Although chemically it is an amino acid, GABA is rarely referred to as such in the scientific or medical communities, because the term "amino acid," used without a qualifier, refers to the alpha amino acids, which GABA is not, nor is it incorporated into proteins.

    In spastic diplegia in humans, GABA absorption becomes impaired by nerves damaged from the condition's upper motor neuron lesion, which leads to hypertonia of the muscles signaled by those nerves that can no longer absorb GABA.
  43. samuel

    samuel New Member

    Arthrotomy, Traumatic

    ■ Essentials of Diagnosis
    • Traumatic arthrotomy (opening into a joint) is more serious than
    a simple laceration
    • Because articular cartilage can be irreversibly damaged by bacteria,
    and the joint environment is limited in its ability to fight
    infection, treat all traumatic arthrotomies urgently
    • Usually occurs as an “outside-in” injury but can be “inside-out”
    (ie, from the bone piercing the skin)
    • Needles, knives, bullets, thorns, nails, and bites can be responsible,
    all with bacterial contamination
    • Commonly, the patient has a history of a puncture wound, bite,
    or laceration near a joint; alternatively, an open fracture into or
    adjacent to a joint
    • Compromise of joint sterility may be obvious
  44. samuel

    samuel New Member

    Treatment---Arthrotomy, Traumatic
    • The cornerstone of treatment is to ensure the joint is sterile; secondarily,
    necrotic tissue that may be a nidus for infection must be
    removed
    • Formal arthrotomy is standard treatment; traumatic arthrotomy
    may be used for debridement if it has occurred in a convenient
    place and allows adequate access to the joint
    • Use adequate irrigation to minimize bacterial burden; in more
    subtle arthrotomies, a standard incision or an arthroscopy may be
    used to debride the joint
    • Surfactants and antiseptics that are used in open fractures may not
    be suitable for care of hyaline cartilage contamination
    • If infection is subacute or chronic, include a thorough synovectomy
    in the surgical debridement
    ■ Pearl
    If uncertain whether a joint communicates with a laceration or open
    fracture, inject 50 cc of saline with methylene blue into the joint from
    an uninjured area. If dye appears at the laceration site, the sterility of
    the joint has been compromised.
  45. samuel

    samuel New Member

    Mechanism of action-Tetracycline

    Tetracyclines work by binding the 30S ribosomal subunit and through an interaction with 16S rRNA, they prevent the docking of amino-acylated tRNA. [1]

    Resistance to tetracyclines can arise through drug efflux, ribosomal protection proteins, 16S rRNA mutation, and drug inactivation through the action of a monooxygenase.
  46. samuel

    samuel New Member

    Primary urothelial carcinoma of the upper tract is a rare urological disease and has a propensity for multifocality, local recurrence, and development of metastases. Almost 5% of all urothelial neoplasms occur in the kidney and ureters. The vast majority of upper tract tumors arise in the kidney, comprising 4% to 15% of all primary kidney neoplasms in the United States, whereas ureteral tumors represent only 1%. As a result, urothelial carcinoma of the bladder has been examined to a greater extent than urothelial tumors elsewhere.
  47. samuel

    samuel New Member

    Apolipoprotein
    The protein occurs in the plasma in 2 main isoforms, APOB48 and APOB100. The first is synthesized exclusively by the small intestine, the second by the liver. Both isoforms are coded by APOB and by a single mRNA transcript larger than 16 kb. APOB48 is generated when a stop codon (UAA) at residue 2153 is created by RNA editing. There appears to be a trans-acting tissue-specific splicing gene that determines which isoform is ultimately produced. Alternatively, there is some evidence that a cis-acting element several thousand bp upstream determines which isoform is produced.

    As a result of the RNA editing, APOB48 and APOB100 share a common N-terminal sequence, but APOB48 lacks APOB100's C-terminal LDL receptor binding region. In fact, APOB48 is so called because it constitutes 48% of the sequence for APOB100.

    APOB 48 is a unique protein to chylomicrons from the small intestine. After most of the lipids in the chylomicron have been digested, APOB48 returns to the liver as part of the chylomicron remnant, where it is endocytosed and degraded.
  48. samuel

    samuel New Member

    Central role in ACUTE MYELOID LEUKEMIA------ EPIGENETIC ALTERATIONS ("EPIGENOME")..means DNA methylation and post-translational modifications of histones.

    HAIRY CELL LEUKEMIA---more than 90% of cases have activating point mutations in serine/threonine kinase BRAF.

    NECROPTOSIS: ( hybrid of Necrosis+Apoptosis but considered as NECROSIS)
    • Also known as programmed cell death without caspase activation
    • It is both pathological (ischaemic brain injury, neurodegenerative diseases and viral infections ) and physiological ( formation of mammalian bone growth plate )
    • Under conditions that are insufficient to trigger apoptosis, TNFα activates TNFR1 and in turn induces the recruitment of RIP1and RIP3 kinase and other proteins to form complex (which includes RIP1, RIP3, caspase 8 ).
    • formation of this complex leads to necroptosis (caspase 8 is not activated here in this pathway)
    • Necroptosis differs from Apoptosis by following features (that’s why they are considered as NECROSIS ---- “Caspase independent programmed cell death” )
    1) Shows cell swelling
    2) Cell membrane damage
    3) Presence of inflammation
  49. samuel

    samuel New Member

    CHROMOTHRYPSIS---(Means chromosome shattering; a/k/a dramatic chromosome catastrophe)
    1)seen in OSTEOSARCOMAS(other bone cancers too) and GLIOMAS.
    2) dozens to hundreds of chromosomal breaks occurs in single or several chromosomes,then they are repaired haphazardly
    3)this will activate Oncogenes and inactivate Tumor suppressor gene.
    4)its mechanism of carcinogenesis.

    MASSIVE BLOOD TRANSFUSION
    defined as
    1) adults
    a) replacement of >1 blood volume in 24 hours ,or
    b) >50% of blood volume in 4 hours (adult blood volume is approximately 70 mL/kg).
    2) children,
    • transfusion of >40 mL/kg (blood volume in children over 1 month old is approximately 80 mL/kg).

    Initially TRANSIENT HYPERGLYCEMIA due to glucose in preservatives;
    this leads to insulin release and may cause HYPOGLYCEMIA

    Overall most commonly--- HYPOGLYCEMIA > HYPERGLYCEMIA.

    Most Common cause of death after massive blood transfusion is--- DIC
    (massive RBC transfusion without concomitant repletion of clotting factors may lead to a dilutional coagulopathy.)

    2)TRALI (Transfusion-Related Acute Lung Injury) is the most common cause of major morbidity and death after transfusion. It presents as an acute respiratory distress syndrome (ARDS) either during or within 6 h of transfusion.Most commonly a/w FFP transfusion.
  50. samuel

    samuel New Member

    • MLPA (Multiplex Ligation –dependent Probe Amplification )
    It blends DNA hybridisation, DNA ligation and PCR amplification
    to detect deletions and duplications of any size (it includes size that are too large to be detected by PCR and too small to be amplified by FISH)
    example is CYSTIC FIBROSIS ( it can detect deletion of each of the 27 exons of CFTR gene)

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