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Do you want a great review source for the Absite 2014? Would you like this source tobe modeled after the original Absite Killer? If you do, then this book is for you. Itcovers high yield Absite topics in over 300 pages

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  • ABSITE KILLER 2014

    Do you want a great review source for the Absite 2014? Would you like this source tobe modeled after the original Absite Killer? If you do, then this book is for you. Itcovers high yield Absite topics in over 300 pages. All of the topics are hyperlinkedfrom the table of contents to make reviewing specific topics easier.

    New updates will be uploaded monthly and will be available for free after a purchaseby sending an email to [email protected].

    Last updated: 12/31/13

    TABLE OF CONTENTS (WITH LINKS)

    ABDOMINAL COMPARTMENT SYNDROME:

    ACALCULOUS CHOLECYSTITIS:

    ACHALASIA:

    ACTIVATED PROTEIN C: XIGRIS:

    ACUTE PHASE RESPONSE:

    ACUTE RENAL FAILURE:

    ADRENAL MASS:

    AIR EMBOLISM:

    AMASTIA:

    AMINOCAPROIC ACID: AMICAR:

    ANAL CANCER:

    ANAL SPHINCTER DYSFUNCTION:

    ANEMIA:

    ANOVA:

    ANTIBODIES:

    APPENDICEAL MUCOCELE:

    BANKED BLOOD:

    BARRETTS ESOPHAGUS:

    BASE DEFICIT:

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  • BILIARY ATRESIA:

    BIOTECHNOLOGY:

    BLEOMYCIN:

    BLOOD PRESSURE CUFF:

    BREAST DEVELOPMENT:

    BUDD CHIARI SYNDROME:

    BURNS:

    CARBON MONOXIDE POISONING:

    CARDIAC MYXOMAS:

    CARDIAC OUTPUT: CARDIAC INDEX: CO: CI:

    CHOLECYSTOKININ: CCK:

    CHOLEDOCHAL CYSTS:

    CHOLESTEROL:

    CLOSTRIDIUM DIFFICILE: C. DIFFICILE:

    COARCTATION OF THE AORTA:

    COHORT STUDY:

    COLLAGEN:

    COLON CANCER:

    COMPARTMENT SYNDROME:

    CONDYLOMA ACCUMINATA:

    CO2 EMBOLISM:

    COX INHIBITORS:

    CRYOPRECIPITATE:

    DDAVP: DESMOPRESSIN:

    DESMOID TUMORS:

    DIABETES INSIPIDUS:

    DIAPHRAGMATIC INJURIES:

    DIFFUSE ESOPHAGEAL SPASMS:

    DISSEMINATED INTRAVASCULAR COAGULOPATHY: (DIC:)

    DIVERTICULITIS:

    DNA:

    DUODENAL ATRESIA:

    ECMO:

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  • ENDOPLASMIC RETICULUM:

    ERRORS: TYPE I ERRORS: TYPE II ERRORS: TYPE III ERRORS:

    ERYTHROMYCIN:

    ESOPHAGEAL PERFORATION: ESOPHAGEAL RUPTURE:

    EXTRINSIC PATHWAY:

    FACTORS:

    FACTOR V LEIDEN:

    FACTOR VIII:

    FAMILIAL ADENOMATOUS POLYPOSIS: FAP:

    FATTY ACIDS:

    FIBRIN:

    FLAIL CHEST:

    FLUIDS: NORMAL SALINE: LACTATED RINGERS:

    FLUIDS: MAINTENANCE FLUIDS:

    FOCAL NODULAR HYPERPLASIA: FNH:

    FORMIC ACID BURNS:

    FUNCTIONAL GENOMICS:

    GALLSTONE ILEUS:

    GASTRIC CANCER: GASTRIC ADENOCARCINOMA:

    GASTRIC LYMPHOMA:

    GAStRIC VARICES:

    GASTRIN:

    GASTROESOPHAGEAL REFLUX DISEASE: (GERD:)

    GASTROINTESTINAL BLEEDING:

    GASTROINTESTINAL STROMAL TUMORS: GIST:

    GASTROSCHISIS:

    GLASGOW COMA SCALE: GCS:

    GLEEVEC:

    GLYCOLYSIS:

    GLUCONEOGENESIS:

    GYNECOMASTIA:

    HEMOGLOBIN OXYGEN BINDING CURVE:

    HEMOPHILIA:

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  • HEMORRHAGE:

    HEMORRHOIDS:

    HEMOSTASIS:

    HEPARIN:

    HEPARIN INDUCED THROMBOCYTOPENIA: HIT:

    HEPATIC ADENOMA:

    HERNIAS:

    HIATAL HERNIA:

    HISTAMINE:

    HYPERCOAGULABLE STATES:

    HYPERHOMOCYSTEINEMIA:

    HYPERKALEMIA:

    HYPERPARATHYROIDISM:

    HYPOCALCEMIA:

    HYPOKALEMIA:

    INCIDENCE:

    INHALED ANESTHETICS:

    INR:

    INTESTINAL ATRESIA:

    INTRA-AORTIC BALLOON PUMP: IABP:

    INTRINSIC PATHWAY:

    INTUSSUSCEPTION:

    LACTIFEROUS DUCTS:

    LAPAROSCOPY:

    LIVER ABSCESS: PYOGENIC:

    LIVER CANCER: HEPATOCELLULAR CARCINOMA:

    LUNG ABSCESS:

    LUNG CANCER:

    LUPUS ANTICOAGULANT:

    MAINTENANCE FLUIDS:

    MALIGNANT HYPERTHERMIA:

    MAMMOGRAPHY:

    MASTITIS:

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  • MEAN ARTERIAL PRESSURE: MAP:

    MECONIUM ILEUS:

    MELANOMA:

    META-ANALYSIS:

    MITOCHONDRIA:

    MOTILIN:

    MUCOSA ASSOCIATED LYMPHOID TISSUE: MALT:

    NECROTIZING FASCIITIS:

    NECROTIZING PANCREATITIS:

    NEUROBLASTOMA:

    NITRIC OXIDE: NO:

    NITROUS OXIDE PNEUMOPERITONEUM: N2O PNEUMOPERITONEUM:

    NUCLEOLUS:

    NUCLEUS:

    OMEPRAZOLE:

    OMPHALOCELE:

    OXALATE STONES:

    PALLIATIVE CARE:

    PARADOXICAL ACIDURIA:

    PARAESOPHAGEAL HERNIA:

    PARALYTICS:

    PARATHYROID GLANDS:

    PARATHYROID HORMONES: PTH:

    PARATHYROIDECTOMY:

    PHEOCHROMOCYTOMA:

    PLASMA MEMBRANE:

    PLASMIN:

    PORT WINE STAIN: CAPILLARY HEMANGIOMA:

    POSTSPLENECTOMY SEPSIS:

    POSTTRANSPLANT LYMPHOPROLIFERATIVE DISORDER: PTLD:

    PREGNANCY:

    PREVALENCE:

    PROSTACYCLIN:

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  • PROTAMINE:

    PROTEIN C:

    PROTEIN S:

    PRUNE BELLY SYNDROME:

    PSEUDOMYXOMA PERITONEI OF APPENDICEAL ORIGIN:

    PT:

    PTT:

    PULMONARY EMBOLISM:

    PULMONARY LYMPH NODES:

    PYLORIC STENOSIS:

    RADIATION THERAPY:

    RECOMBINANT FACTOR VIIa: NOVOSEVEN:

    RECTUS SHEATH HEMATOMA:

    REFEEDING SYNDROME:

    REJECTION:

    RENIN:

    RESPIRATORY QUOTIENT: RQ:

    RHABDOMYOLYSIS:

    RNA:

    SARCOMAS:

    SECRETIN:

    SENSITIVITY:

    SHORT GUT SYNDROME: SHORT BOWEL SYNDROME:

    SILVADENE:

    SILVER NITRATE:

    SKIN GRAFTS:

    SOMATOSTATIN:

    SPECIFICITY:

    SULFAMYLON:

    SUPERIOR VENA CAVA SYNDROME: SVC SYNDROME:

    SURGICAL SITE INFECTIONS: SSI: SSIs:

    SYSTEMIC VASCULAR RESISTANCE: SVR:

    TENSION PNEUMOTHORAX:

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  • TESTICULAR CANCER:

    TETRALOGY OF FALLOT:

    THROMBIN:

    THROMBOXANE:

    THYROGLOSSAL CYSTS:

    THYROID STORM:

    TRACHEA:

    TRACHEOESOPHAGEAL FISTULAS: TE FISTULAS:

    TRACHEOSTOMY:

    TRANSFUSION REACTIONS:

    TRANSLATION:

    ULCERATIVE COLITIS:

    UMBILICAL HERNIAS:

    UREMIA:

    URINARY TRACT INFECTIONS: UTI: UTIs:

    VASODILATION:

    VENTRICULAR SEPTAL DEFECTS: VSDs:

    VITAMIN D:

    VITAMIN K:

    VON WILLEBRAND DISEASE: VON WILLEBRANDS DISEASE: VWD:

    VON WILLEBRAND FACTOR: VWF:

    WARFARIN: COUMADIN:

    WOUND HEALING:

    ZENKERS DIVERTICULUM:

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  • TABLE OF CONTENTS (LIST, NO LINK)

    - Abdominal compartment syndrome

    - Acalculous cholecystitis

    - Achalasia

    - Activated protein C (Xigris)

    - Acute phase response

    - Acute renal failure

    - Adrenal mass

    - Air embolism

    - Amastia

    - Aminocaproic acid (Amicar)

    - Anal cancer

    - Anal sphincter dysfunction

    - Anemia

    - ANOVA

    - Antibodies

    - Appendiceal mucocele

    - Banked blood

    - Barretts esophagus

    - Base deficit

    - Biliary atresia

    - Biotechnology

    - Bleomycin

    - Blood pressure cuff

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  • - Breast development

    - Budd Chiari syndrome

    - Burns

    - Carbon monoxide poisoning

    - Cardiac myxomas

    - Cardiac output, cardiac index

    - Cholecystokinin (CCK)

    - Choledochal cysts

    - Cholesterol

    - Clostridium difficile (C. difficile)

    - Coarctation of the aorta

    - Cohort study

    - Collagen

    - Colon cancer

    - Compartment syndrome

    - Condyloma accuminata

    - CO2 embolism

    - Coumadin (see Warfarin)

    - COX inhibitors

    - Cryoprecipitate

    - DDAVP (Desmopressin)

    - Desmoid tumors

    - Diabetes insipidus

    - Diaphragmatic injuries

    - Diffuse esophageal spasms

    - Disseminated intravascular coagulopathy (DIC)

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  • - Diverticulitis

    - DNA

    - Duodenal atresia

    - ECMO

    - Endoplasmic reticulum

    - Errors (Type I, Type II, and Type III errors)

    - Erythromycin

    - Esophageal perforation / Esophageal rupture

    - Extrinsic pathway

    - Factors

    - Factor V Leiden

    - Factor VIII

    - Familial adenomatous polyposis (FAP)

    - Fatty acids

    - Fibrin

    - Flail chest

    - Fluids: Normal saline, lactated ringers

    - Fluids: Maintenance fluids

    - Focal nodular hyperplasia (FNH)

    - Formic acid burns

    - Functional genomics

    - Gallstone ileus

    - Gastric cancer (Gastric adenocarcinoma)

    - Gastric lymphoma

    - Gastric varices

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  • - Gastrin

    - Gastroesophageal reflux disease (GERD)

    - Gastrointestinal bleeding

    - Gastrointestinal stromal tumors (GIST)

    - Gastroschisis

    - Glasgow coma scale (GCS)

    - Gleevec

    - Glycolysis

    - Gluconeogenesis

    - Gynecomastia

    - Hemoglobin oxygen binding curve

    - Hemophilia

    - Hemorrhage

    - Hemorrhoids

    - Hemostasis

    - Heparin

    - Heparin induced thrombocytopenia (HIT)

    - Hepatic adenoma

    - Hernias

    - Hiatal hernia

    - Histamine

    - Hypercoagulable states

    - Hyperhomocysteinemia

    - Hyperkalemia

    - Hyperparathyroidism

    - Hypocalcemia

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  • - Hypokalemia

    - Incidence

    - Inhaled anesthetics

    - INR

    - Intestinal atresia

    - Intra-aortic balloon pump (IABP)

    - Intrinsic pathway

    - Intussusception

    - Lactiferous ducts

    - Laparoscopy

    - Liver abscess: pyogenic

    - Liver cancer (hepatocellular carcinoma)

    - Lung abscess

    - Lung cancer

    - Lupus anticoagulant

    - Maintenance fluids

    - Malignant hyperthermia

    - Malrotation and midgut volvulus

    - Mammography

    - Mastitis

    - Mean arterial pressure (MAP)

    - Meconium ileus

    - Melanoma

    - Meta-analysis

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  • - Mitochondria

    - Motilin

    - Mucosa associated lymphoid tissue (MALT)

    - Necrotizing fasciitis

    - Necrotizing pancreatitis

    - Neuroblastoma

    - Nitric oxide (NO)

    - Nitrous oxide pneumoperitoneum (N2O pneumoperitoneum)

    - Nucleolus

    - Nucleus

    - Omeprazole

    - Omphalocele

    - Oxalate stones

    - Palliative care

    - Paradoxical aciduria

    - Paraesophageal hernia

    - Paralytics

    - Parathyroid glands

    - Parathyroid hormones (PTH)

    - Parathyroidectomy

    - Pheochromocytoma

    - Plasma membrane

    - Plasmin

    - Port wine stain (capillary hemangioma)

    - Postsplenectomy sepsis

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  • - Posttransplant lymphoproliferative disorder (PTLD)

    - Pregnancy

    - Prevalence

    - Prostacyclin

    - Protamine

    - Protein C

    - Protein S

    - Prune belly syndrome

    - Pseudomyxoma peritonei of appendiceal origin- PT

    - PTT

    - Pulmonary embolism

    - Pulmonary lymph nodes

    - Pyloric stenosis

    - Radiation therapy

    - Recombinant factor VIIa (Novoseven)

    - Rectus sheath hematoma

    - Refeeding syndrome

    - Rejection

    - Renin

    - Respiratory quotient (RQ)

    - Rhabdomyolysis

    - RNA

    - Sarcomas

    - Secretin

    - Sensitivity

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  • - Short gut syndrome / Short bowel syndrome

    - Silvadene

    - Silver nitrate

    - Skin grafts

    - Somatostatin

    - Specificity

    - Sulfamylon

    - Superior vena cava syndrome (SVC syndrome)

    - Surgical site infections (SSIs)

    - Systemic vascular resistance (SVR)

    - Tension pneumothorax

    - Testicular cancer

    - Tetralogy of Fallot

    - Thrombin

    - Thromboxane

    - Thyroglossal cysts

    - Thyroid storm

    - Trachea

    - Tracheoesophageal fistulas (TE fistulas)

    - Tracheostomy

    - Transfusion reactions

    - Translation

    - Ulcerative colitis

    - Umbilical hernias

    - Uremia

    - Urinary tract infections (UTIs)

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  • - Vasodilation

    - Ventricular septal defects (VSDs)

    - Vitamin D

    - Vitamin K

    - von Willebrand Disease (vWD)

    - von Willebrand Factor (vWF)

    - Warfarin

    - Wound healing

    - Xigris (see Activated protein C)

    - Zenkers diverticulum

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  • ABDOMINAL COMPARTMENT SYNDROME:

    QUESTION: A 27 year old man is in the ICU 6 hours after splenectomy following amotor vehicle accident. The patient had a prolonged transport time and received 20units of blood prior to arrival. Currently, his peak airway pressures are 65 (plateaus50), his abdomen is distended, he is not making any urine, and his bladder pressure is40. His CVP is 18.

    What is the diagnosis and what is the treatment for the diagnosis?

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    ANSWER:

    - This patient has classic signs of abdominal compartment syndrome.

    - Objectively, a bladder pressure >25-30 suggests abdominal compartment syndrome.

    - Decreased urine output (from compression of the IVC resulting in decreased cardiacoutput) and elevated ventilation pressures are part of the syndrome.

    - Treatment of abdominal compartment syndrome is decompressive laparotomy.

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  • QUESTION: What is the following bladder pressures is an absolute indication for adecompressive laparotomy?

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    ANSWER:

    - Generally, no specific bladder pressure prompts therapeutic intervention, except whenthe pressure is >35 mmHg.

    - Rather, emergent decompression is carried out when intra-abdominal hypertensionreaches a level at which end-organ dysfunction occurs.

    - Mortality is directly affected by decompression, with 60% mortality in patientsundergoing presumptive decompression, 70% mortality in patients with a delay indecompression, and nearly uniform mortality in those not undergoing decompression.

    - Abdominal hypertension is classified by grade, with Grade I (mild) being >10 mmHg(13mmH20).

    - Grade IV hypertension or >35 mmHg ( 48cmH2) is an absolute indication fordecompressive laparotomy..

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  • ACALCULOUS CHOLECYSTITIS:

    QUESTION: A 45-year-old man has a 50% total body surface area third-degree burn.On hospital day 7, fever, marked leukocytosis, and right upper quadrant pain develop.His blood pressure is 130/80 mmHg and his heart rate is 110 beats per minute.Ultrasonography shows a distended gallbladder but is negative for gallstones.Antibiotics are initiated. What is the next step in management?

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    ANSWER: Hepatoiminodiacetic acid (HIDA) scan

    - The presentation is most consistent with acalculous cholecystitis (see response toquestion 13). The initial study of choice is US, which can be performed at the bedside.

    - If the US findings are negative and the patient is not critically ill, the next study wouldbe an HIDA scan with morphine.

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    QUESTION: What ultrasound findings support a diagnosis of acalculous cholecystitis?

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  • ANSWER:

    - Findings that would confirm the diagnosis would include thickening of the gallbladderwall, sludge, and pericholecystic fluid.

    - If the US findings are negative and the patient is not critically ill, the next study wouldbe an HIDA scan with morphine.

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    QUESTION: What is a positive finding of acalculous cholecystitis on HIDA scan?.

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    ANSWER:

    - A positive study finding would demonstrate nonfilling of the gallbladder withvisualization of the tracer in the liver and small bowel.

    - Morphine decreases the rate of false-positive HIDA scan results because it leads tosphincter of Oddi contraction and thus increases the likelihood of filling of thegallbladder in the absence of cholecystitis.

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    QUESTION: True or false: The incidence of perforation with acalculous cholecystitisis higher than with calculous cholecystitis.

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  • .ANSWER: True

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  • QUESTION: Acalculous cholecystitis is seen in association with severe burns.

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    ANSWER: True

    - Acalculous cholecystitis typically occurs in critically ill, highly stressed patients, suchas those who have experienced severe trauma, sepsis, burns, or multisystem organfailure.

    - The etiology is unclear but is likely related to a combination of ischemia to thegallbladder from a low flow state and marked gallbladder distention, as well as bilestasis due to a lack of gallbladder contraction (many patients are on total parenteralnutrition).

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    QUESTION: True or false: The US findings in acalculous cholecystitis may be normal.

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    ANSWER: True

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  • QUESTION: True or false: In severely ill patients, emergency laparoscopiccholecystectomy is the treatment of choice.

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    ANSWER: False.

    - Acalculous cholecystitis requires urgent intervention, preferably cholecystectomy.

    - However, if the patient is too ill for surgery, percutaneous US or computedtomography guided cholecystostomy is the treatment option of choice.

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    QUESTION: True or false: Acalculous cholecystitis may be caused by cystic arterythrombosis.

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    ANSWER: True

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  • QUESTION: How do you diagnose acalculous cholecystitis?

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    ANSWER:

    - The diagnosis can be very difficult to make because (1) patients are often intubatedand sedated, thus not allowing a thorough physical examination; (2) US findings are notpathognomonic; and (3) HIDA scanning can have false-positive results due to the factthat the patients are fasting.

    - Thus, the diagnosis of acalculous cholecystitis requires a high index of suspicion andmay need to be a diagnosis of exclusion.

    - The classic findings are fever, leukocytosis, right upper quadrant pain and tenderness,elevation of liver function test results (bilirubin and alkaline phosphatase), a thickenedgallbladder wall on US without stones, and nonvisualization of the gallbladder onHIDA scanning.

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    MuradResaltado

  • QUESTION: What is the initial diagnostic study of choice for acalculous cholecystitis?

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    ANSWER: Ultrasound

    - US is the initial diagnostic study of choice and can be performed at the bedside in theintensive care unit.

    - In a recent prospective study, US findings were considered positive if three majorcriteria were present: wall thickness greater than 4 mm, hydrops, and sludge.

    - The sensitivity was only 50% and the specificity 94%.

    - In stable patients in whom the diagnosis is unclear after US, an HIDA scan can beperformed with morphine (67% sensitivity and 100% specificity).

    - Failure to visualize the gallbladder is the most sensitive and specific finding.

    - Leakage into the pericholecystic space suggests perforation.

    - An HIDA scan is not recommended in critically ill patients in whom a delay in therapycan be potentially fatal.

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    MuradResaltado

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  • ACHALASIA:

    QUESTION: Is achalasia due to increased or decreased ganglion cells?...ANSWER: Achalasia is due to decreased ganglion cells....QUESTION: Achalasia results from a problem with ganglion cells in ________'splexus...ANSWER: Achalasia results from decreased ganglion cells in Auerbachs plexus...QUESTION: Does achalasia result in absence of peristalsis or increased peristalsis?...ANSWER: Achalasia results in the absence of peristalsis...QUESTION: Does achalasia result in esophageal constriction or dilation?...ANSWER: Achalasia results in esophageal dilation...QUESTION: What image does achalasia look like on Barium swallow?.

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  • ..ANSWER: Achalasia looks like a bird's beak on Barium swallow...QUESTION: In terms of peristalsis, what do you expect to see on manometry ofsomeone with achalasia?...ANSWER: In achalasia, manometry shows no peristalsis...QUESTION: Are the LES pressures high or low in achalasia?...ANSWER: In achalasia, there are high LES pressures...QUESTION: Is there too much LES relaxation or does the LES fail to relax inachalasia?.

    .

    .ANSWER: Achalasia is failure of the LES to relax...QUESTION: What is the treatment for achalasia?.

    ANSWER: The treatment for achalasia is laparoscopic or thoracoscopic Hellermyotomy

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  • ACTIVATED PROTEIN C: XIGRIS:

    QUESTION: What is the mechanism of Xigris (activated protein C)?

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    ANSWER:- The mechanism of action of Xigris (activated protein C) is fibrinolysis.

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    QUESTION: What is an important side effect of Xigris?

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    ANSWER:- The side effects of Xigris is bleeding. (QUESTION)

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  • ACUTE PHASE RESPONSE:

    QUESTION: What factors are increased during the acute phase response?

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    ANSWER:- The factors that increase during the acute phase response are:

    INCREASED:

    - C-reactive protein (an opsonin, activates complement)

    - amyloid A and P

    - Fibrinogen

    - Haptoglobin

    - Ceruloplasmin

    - Alpha-1 antitrypsin

    - Alpha-1 antichymotrypsin

    - C3 (complement)

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    .

    QUESTION: What factors are decreased during the acute phase response?

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    .

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  • ..

    ANSWER:- The factors that decrease during the acute phase response are:

    DECREASED

    - Albumin

    - Transferrin

    - Fibronectin

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  • ACUTE RENAL FAILURE:

    QUESTION: An FeNA of less than what % suggests a low volume, pre-renal picture?...ANSWER: A FeNA 30 is indicative of a low volume, pre-renal picture..

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    MuradResaltado

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  • ADRENAL MASS:

    QUESTION: What finding on an adrenal mass on CT scan is the most suggestive ofadrenal cancer?

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    ANSWER: Size > 6cm.

    - The size of the adrenal mass on imaging studies is the single most important criterionto help diagnose malignancy.

    - In the series reported by Copeland, 92% of adrenal cancers were >6 cm in diameter.

    - Other CT imaging characteristics suggesting malignancy include tumor heterogeneity,irregular margins, and the presence of hemorrhage and adjacent lymphadenopathy orliver metastases.

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    MuradResaltado

    MuradResaltado

    MuradResaltado

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  • AIR EMBOLISM:

    QUESTION: How do you treat an air embolism?

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    ANSWER:

    - Although estimated to occur in only 0.2 to 1% of patients, an air embolism can bedramatic and fatal.

    - Treatment may prove futile if the air embolus is larger than 50ml.

    - If an embolus is suspected, the patient should immediately be placed into a left lateraldecubitus Trendelenburg position, so the entrapped air can be stabilized within the rightventricle.

    - Aspiration via a central venous line accessing the heart may decrease the volume ofgas in the right side of the heart, and minimize the amount traversing into the pulmonarycirculation.

    - Subsequent recovery of intracardiac and intrapulmonary air may require open surgicalor angiographic techniques.

    - Prevention requires careful attention to technique.

    .

    .

    .

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    MuradResaltado

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    MuradResaltado

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  • AMASTIA:

    QUESTION: Absence of the breast (amastia) is associated with which geneticdisorder?

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    ANSWER: Poland syndrome.

    POLAND SYNDROME

    - Absence of the breast (amastia) is rare and results from an arrest in mammary ridgedevelopment that occurs during the sixth fetal week.

    - Poland's syndrome consists of hypoplasia or complete absence of the breast, costalcartilage and rib defects, hypoplasia of the subcutaneous tissues of the chest wall, andbrachysyndactyly.

    TURNER'S SYNDROME

    - Turner's syndrome (ovarian agenesis and dysgenesis) may have polymastia as acomponent.

    FLEISCHER'S SYNDROME

    - Fleischer's syndrome (displacement of the nipples and bilateral renal hypoplasia) mayalso have polymastia as a component.

    KLINEFELTER'S SYNDROME

    - Klinefelter's syndrome (XXY) is manifested by gynecomastia, hypergonadotropichypogonadism, and azoospermia.

    - There is an increased risk of breast cancer in men with Klinefelter's syndrome.

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    MuradResaltado

    MuradResaltado

    MuradResaltado

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  • AMINOCAPROIC ACID: AMICAR:

    QUESTION: What is the mechanism of action of Amicar?

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    ANSWER:- The mechanism of action of aminocaproic acid (Amicar) is inhibition of plasmin.

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  • ANAL CANCER:

    QUESTION: What is the treatment for squamous cell carcinoma of the anal canal?...ANSWER: The treatment for squamous cell carcinoma of the anal canal is the Nigroprotocol...QUESTION: True or false: The treatment of squamous cell carcinoma of the anal canalis NOT surgery...ANSWER: True. The treatment of squamous cell carcinoma of the anal canal is NOTsurgery. The treatment is the Nigro protocol...QUESTION: The Nigro protocol is made up of which treatment modalities?...ANSWER: The Nigro protocol consists of chemotherapy and radiation therapy..

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  • ANAL SPHINCTER DYSFUNCTION:

    QUESTION: Is a resting pressure of 20 mmHg indicative of normal internal sphincterfunction or dysfunction of the internal sphincter?

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    ANSWER: A resting pressure of 20 mmHg indicates internal sphincter dysfunction.

    - The resting pressure in the anal canal reflects the function of the internal analsphincter (normal: 40 to 80 mmHg)

    - The squeeze pressure, defined as the maximum voluntary contraction pressure minusthe resting pressure, reflects function of the external anal sphincter (normal: 40 to 80mmHg above resting pressure)

    - The high-pressure zone estimates the length of the anal canal (normal: 2.0 to 4.0 cm)

    - The rectoanal inhibitory reflex can be detected by inflating a balloon in the distalrectum.

    -

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  • ANEMIA:

    QUESTION: What are the laboratory findings in iron deficiency anemia?

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    ANSWER:- The laboratory findings in iron deficiency anemia are low MCV, low ferritin, high transferrin and high TIBC.

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    .

    QUESTION: What are the laboratory findings in anemia of chronic disease?

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    ANSWER:- The laboratory findings in anemia of chronic disease are low to normal MCV, normal or high ferritin, and lowTIBC. (TOPIC)

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  • ANOVA:

    QUESTION: True or false: ANOVA compares means for more than 2 groups....ANSWER: True...QUESTION: Does ANOVA use quantitative or qualitative data when comparing themeans of more than 2 groups?...ANSWER: ANOVA uses quantitative data when comparing the means of more than 2groups...

    QUESTION: True or false: ANOVA is a t-test for more than 2 groups...ANSWER: True

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  • ANTIBODIES:

    QUESTION: Which antibodies can act as opsonins?...ANSWER: IgG and IgM are opsonins...QUESTION: Which antibodies are able to fix complement?...ANSWER: IgG and IgM are able to fix complement. 2 IgGs or 1 IgM is needed to dothis. ...QUESTION: Which antibody level decreases after splenectomy?...ANSWER: After a splenectomy, you will have decreased levels of IgM...QUESTION: Which antibody is made first during an immune reaction?...ANSWER: IgM is made first during an immune reaction...

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  • QUESTION: Which antibody is found in secretions?...

    ANSWER: IgA is found in secretions...QUESTION: True or false: IgD is found on the surface of B cells and its function isunclear...ANSWER: True...QUESTION: What antibody is the most abundant antibody in serum?...ANSWER: IgG...QUESTION: Which antibody cross the placenta?...ANSWER: IgG...

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  • QUESTION: Which antibody is involved in allergic reactions?...ANSWER: IgE is involved in allergic reactionsQUESTION: Which antibody is involved in type I hypersensitivity reactions?...ANSWER: IgE is involved in type I hypersensitivity reactions...QUESTION: Which antibody causes histamine release from mast cells and basophils?...ANSWER: IgE causes histamine release from mast cells and basophils...QUESTION: Which antibodies is secreted during a parasitic infection?...ANSWER: IgE is secreted in response to parasitic infections...

    QUESTION: Which portion of an antibody is responsible for antigen recognition? Thevariable region or the constant region?...

    ANSWER: The variable region of antibody is responsible for antigen recognition.

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  • APPENDICEAL MUCOCELE:

    QUESTION: At the time of laparoscopic surgery for presumed appendicitis, the patientis noted to have a mucous-filled, distended appendix measuring 3 cm in diameter. Thereis no acute inflammation or signs of perforation. What is the best next step inmanagement?

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    ANSWER: Conversion to open appendectomy with pathologic confirmation of anegative margin at the base of the appendix

    - An intact mucocele presents no future risk for the patient.

    - However, the opposite is true if the mucocele has rupture and epithelial cells haveescaped into the peritoneal cavity.

    - As a result, when a mucocele is visualized at the time of laparoscopic examination,conversion to open laparotomy is recommended.

    - Conversion from a laparoscopic approach to a laparotomy ensures that a benignprocess will not be converted to a malignant one through mucocele rupture.

    - In addition, laparotomy allows for thorough abdominal exploration to rule out thepresence of mucoid fluid accumulations.

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  • QUESTION: True or false: The presence of a mucocele of the appendix does notmandate performance of a right hemicolectomy.

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    ANSWER: True.

    - The principles of surgery include resection of the appendix, wide resection of themesoappendix to include all the appendiceal lymph nodes, collection and cytologicexamination of all intraperitoneal mucus, and careful inspection of the base of theappendix.

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  • QUESTION: For appendiceal mucocele, when is a right hemicolectomy indicated?

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    ANSWER: Positive margin at base of appendix or positive lymph nodes

    - Right hemicolectomy, or preferably cecectomy, is reserved for patients with a positivemargin at the base of the appendix or positive periappendiceal lymph nodes.

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  • BANKED BLOOD:

    QUESTION: Which factors are low in banked blood?

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    ANSWER:- Factors that are low in banked blood are 2,3-DPG, and factors V and VIII (labile factors)

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    QUESTION: Banked blood results in a shift in the oxygen dissociation curve in whichdirection?

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    ANSWER:- Shift in the O2 dissociation curve in banked blood is a left shift. (higher affinity of Hgb to O2).

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    QUESTION: What is the effect of 2,3 DPG on the oxygen dissociation curve?

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  • ..

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    ANSWER:- The effect of 2,3 DPG on the oxygen dissociation curve is that it causes a RIGHT shift by decreasing Hgbaffinity to O2.

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  • BARRETTS ESOPHAGUS:

    QUESTION: .Barrett's esophagus refers to what type of mucosal change?

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    ANSWER: Barrett's refers to the change in esophageal epithelium from squamous tocolumnar.

    .

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  • BASE DEFICIT:QUESTION: What is the probability of death for a patient with a base deficit of -6?

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    ANSWER: 25%.

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  • BILIARY ATRESIA:

    QUESTION: What is the most important surgical cause of jaundice in the newborn?

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    ANSWER: Biliary atresia

    - The most important surgical cause of jaundice in the newborn is biliary atresia, whichis an obliterative process of the extrahepatic bile ducts and is associated with hepaticfibrosis.

    - The infant produces acholic stools and demonstrates a failure to thrive.

    - Left untreated, it will progress to liver failure and portal hypertension.

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    .

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    .

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    QUESTION: How is biliary atresia diagnosed?

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    .

    ..

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    ANSEWR: Nuclear scanning.

    - Nuclear scanning after pretreatment with phenobarbital is a useful study.

    - One is specifically looking to see whether the radionuclide appears in the intestine,

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  • which would confirm that the extrahepatic bile ducts are patent.

    - This finding excludes biliary atresia.

    - If the radionuclide is normally concentrated in the liver but not excreted and themetabolic screen results are normal, this is highly suggestive of biliary atresia.

    - The presence of a gallbladder does not exclude the diagnosis of biliary atresia.

    .

    .

    QUESTION: What is the treatment for biliary atresia?

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    ANSWER: Kasai procedure (hepatoportoenterostomy)

    - The most effective treatment of biliary atresia is portoenterostomy, as described byKasai.

    - The procedure involves anastomosing an isolated limb of jejunum to the transectedducts at the liver plate.

    - The likelihood of surgical success is increased if the procedure is performed beforethe infant reaches the age of 8 weeks.

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    QUESTION: What is the indication for liver transplantation in biliary atresia?

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    .

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  • ..

    .

    ANSWER: Sympatomatic after Kasai procedure

    - If the patient remains symptomatic after the Kasai operation, he or she will requireliver transplantation.

    - Independent risk factors that predict failure of the procedure include bridging liverfibrosis at the time of surgery and postoperative cholangitis episodes.

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  • QUESTION: Optimal management for an 8-month-old girl with biliary atresia in whoma Kasai operation (hepatoportoenterostomy) failed would be what?

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    ANSWER: liver transplantation.

    - The Kasai operation, in which an isolated limb of the jejunum is anastomosed to thetransected ducts at the liver plate, is the operation of choice for biliary atresia.

    - However, in a subset of patients, the Kasai operation is unsuccessful, and theyeventually require liver transplantation for progressive liver failure and recurrent boutsof cholangitis.

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  • BIOTECHNOLOGY:Q: What is the difference between southern blotting, northern blotting, and westernblotting? .

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    A:

    - Southern blotting refers to the technique of transferring DNA fragments from anelectrophoresis gel to a membrane support, and the subsequent analysis of the fragmentsby hybridization with a radioactively labeled probe.

    - Southern blotting is named after E. M. Southern, who in 1975 first described thetechnique of DNA analysis.

    - It enables reliable and efficient analysis of size-fractionated DNA fragments in animmobilized membrane support.

    - Northern blotting refers to the technique of size fractionation of RNA in a gel and thetransferring of an RNA sample to a solid support (membrane) in such a manner that therelative positions of the RNA molecules are maintained.

    - The resulting membrane then is hybridized with a labeled probe complementary to themRNA of interest.

    - Signals generated from detection of the membrane can be used to determine the sizeand abundance of the target RNA.

    - In principle, Northern blot hybridization is similar to Southern blot hybridization (andhence its name), with the exception that RNA, not DNA is on the membrane.

    - Analyses of proteins are primarily carried out by antibody-directed immunologictechniques.

    - For example, Western blotting, also called immunoblotting, is performed to detectprotein levels in a population of cells or tissues, whereas immunoprecipitation is usedto concentrate proteins from a larger pool.

    - There is no technique known as Eastern blotting.

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  • BLEOMYCIN:

    QUESTION: What is the main side effect of Bleomycin?...ANSWER: The main side effect of Bleomycin is pulmonary fibrosis

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  • BLOOD PRESSURE CUFF:

    QUESTION: The width of a blood pressure cuff should be what percentage of thecircumference of the patient's arm?

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    ANSWER: 40%.

    - If the cuff is too narrow (relative to the extremity), the measured pressure will beartificially elevated.

    - Therefore, the width of the cuff should be approximately 40% of its circumference.

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  • BREAST DEVELOPMENT:

    QUESTION: Which of the hormone is primarily responsible for differentiation of thebreast ductal epithelium?

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    ANSWER: Progesterone

    - Estrogen initiates ductal development, whereas progesterone is responsible fordifferentiation of epithelium and for lobular development.

    - Prolactin is the primary hormonal stimulus for lactogenesis in late pregnancy and thepostpartum period.

    - It upregulates hormone receptors and stimulates epithelial development.

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  • BUDD CHIARI SYNDROME:

    QUESTION: 25 year old woman develops jaundice and ascites 2 weeks afterchildbirth. This is most likely related to what type of venous thrombosis?

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    ANSWER:

    - Postpartum hepatic vein thrombosis (Post-partum Budd Chiari Syndrome) is rare andrelated to the relative hypercoagulable state that occurs following pregnancy.

    - Patients with hypercoagulable syndromes seem more susceptible to the problem.

    - The best test for post partum hepatic vein thrombosis is a mesenteric angiogram withvenous phase contrast.

    - MRI would also be a useful test but is not as sensitive as an angiogram.

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  • BURNS:

    QUESTION: What is the most common infection in patients with large (>35%) severeburns ?

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    ANSWER: Although urinary tract infection is the most common infection in surgerypatients, pneumonia is the leading cause of infection in patients with severe burninjuries.

    - Inhalation injury, decreased immunity, fluid resuscitation causing pulmonary edema,and requirement for mechanical ventilation all lead to increased risk for pneumonia.

    - In some series, 60-70% of all patients with large severe burns get pneumonia.

    .

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  • CARBON MONOXIDE POISONING:

    QUESTION: Shock following severe carbon monoxide poisoning is most commonlywhat type of shock?

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    ANSWER: Vasodilatory shock. Causes of vasodilatory shock include hypoxic lacticacidosis, carbon monoxide poisoning, decompensated and irreversible hemorrhagicshock, terminal cardiogenic shock, and postcardiotomy shock.

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    .

    .

    .

    QUESTION: Treatment for carbon monoxide poisoning is primarily what?

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    ANSWER:

    - The treatment of choice for carbon monoxide poisoning is oxygen.

    - For severe poisoning, hyperbaric oxygen therapy can be used.

    .

    .

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  • .

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  • QUESTION: The affinity of carbon monoxide for hemoglobin is how many times greaterthan oxygen?

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    ANSWER:

    - Another important contributor to early mortality in burns is carbon monoxide (CO)poisoning resulting from smoke inhalation.

    - The affinity of CO for hemoglobin is approximately 200-250 times more than that ofoxygen, which decreases the levels of normal oxygenated hemoglobin and can quicklylead to anoxia and death.

    - Unexpected neurologic symptoms should raise the level of suspicion, and an arterialcarboxyhemoglobin level must be obtained because pulse oximetry is falsely elevated.

    .

    .

    .

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  • CARDIAC MYXOMAS:

    QUESTION: What is the most common location for cardiac myxomas ?

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    ANSWER: Left atrium..

    - Myxomas are the most common primary tumor of the heart.

    - The majority (60%75%) arise in the left atrium, with most of the remaining in theright atrium.

    - Very few are found in the right or left ventricle.

    - Myxomas are gelatinous tumors with a propensity for embolization.

    - They can also obstruct or damage the mitral valve, leading to symptoms of heartfailure.

    - Diagnosis is made by transthoracic or transesophageal echocardiography.

    - Treatment is surgical excision.

    - They are benign but have a tendency to recur.

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  • CARDIAC OUTPUT: CARDIAC INDEX: CO: CI:

    QUESTION: What is the difference between cardiac output and cardiac index? (writedown equations).

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    .

    ANSWER:- The equation for the cardiac output is CO = SV X SR.

    - The equation for the cardiac index is CI = CO / BSA

    - [Cl = CO/BSA; CO=SV X HR; therefore, CI = (SV X HR)/BSA]

    - The cardiac index is computed by dividing the cardiac output by the body surface area.

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  • CHOLECYSTOKININ: CCK:

    QUESTION: Where is cholecystokinin produced?...ANSWER: Cholecystokinin (CCK) is released by I-cells of the small intestines...QUESTION: What is the effect of cholecystokinin on the gallbladder?...ANSWER: Cholecystokinin stimulates contraction of the gallbladder...QUESTION: What is the effect of cholecystokinin on the sphincter of Oddi?...ANSWER: Cholecystokinin relaxes the Sphincter of Oddi...QUESTION: What is the effect of cholecystokinin on pancreatic enzyme secretion?...ANSWER: Cholecystokinin increases pancreatic enzyme secretion...

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  • CHOLEDOCHAL CYSTS:

    QUESTION: What is the most common type of choledocha cyst?

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    ANSWER: Type I

    - Choledochal cysts have been classified into five types.

    - The most common is type I, which is fusiform dilatation of the bile duct.

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    QUESTION: Multiple diffuse dilatations of the intrahepatic ducts are known associatedwith which type choledochal cysts?

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    ANSWER: Type IV choledochal cysts = Carolis disease

    - Caroli disease is a type V choledochal cyst that causes multiple bile duct dilatationsthat are limited to the intrahepatic bile ducts.

    - The cysts lead to recurrent bouts of cholangitis and have a risk of malignancy.

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  • - If the Caroli disease is limited to one lobe, partial hepatectomy is potentially curative.In patients with diffuse Caroli disease, liver transplantation can provide satisfying long-term results.

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  • CHOLESTEROL:

    QUESTION: What molecule serves as the plasma carrier of cholesterol?

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    ANSWER:- The plasma carrier of cholesterol is VLDL.

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    QUESTION: In which organ is cholesterol formed?

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    ANSWER:- The organ where cholesterol is formed is the liver.

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    QUESTION: What enzyme is the rate limiting step in cholesterol formation?

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    ANSWER:

    - The rate limiting step in cholesterol formation is HMG CoA reductase.

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  • CLOSTRIDIUM DIFFICILE: C. DIFFICILE:

    QUESTION: Treatment of severe C. difficile proctosigmoiditis which is unresponsiveto intravenous antibiotics may include what type of enema?

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    - Management of C. difficile colitis should include immediate cessation of the offendingantimicrobial agent.

    - Patients with mild disease (diarrhea but no fever or abdominal pain) may be treated asoutpatients with a 10-day course of oral metronidazole.

    - Oral vancomycin is a second-line agent used in patients allergic to metronidazole or inpatients with recurrent disease.

    - More severe diarrhea associated with dehydration and/or fever and abdominal pain isbest treated with bowel rest, IV hydration, and oral metronidazole or vancomycin.

    - Proctosigmoiditis may respond to vancomycin enemas.

    - Recurrent colitis occurs in up to 20% of patients and may be treated with a longercourse of oral metronidazole or vancomycin (up to 1 month).

    - Reintroduction of normal flora by ingestion of probiotics has been suggested as apossible treatment for recurrent or refractory disease.

    - Fulminant colitis, characterized by septicemia and/or evidence of perforation, requiresemergent laparotomy.

    - A total abdominal colectomy with end ileostomy may be lifesaving.

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  • COARCTATION OF THE AORTA:

    QUESTION: Coarctation of the aorta most commonly occurs in what anatomic location?

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    ANSWER: Thoracic aorta just distal to the left subclavian artery.

    - Aortic coarctation is a congenital narrowing of the thoracic aorta, usually occurringdistal to the left subclavian artery, at the point of insertion of the ductus arteriosus.

    - Coarctation may go undetected until adolescence or young adulthood.

    - Patients may present with severe upper extremity hypertension in association withweak or absent lower extremity pulses.

    - Conventional treatment has been with open thoracic aortic surgery.

    - However, it more recently has been treated successfully with endovascular techniques.

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  • COHORT STUDY:

    QUESTION: Is cohort study a prospective study or a retrospective study?...ANSWER: A cohort study is a prospective study...QUESTION Is a cohort study randomized or nonrandomized?...ANSWER: A cohort study is nonrandomized...QUESTION: True or false: A prospective cohort study is a non-random assignment to atreatment group...ANSWER: True...

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  • COLLAGEN:

    QUESTION: True or false. Tensile strength is never equal to prewound strength. It isonly 80% of what it used to be....ANSWER: True. The tensile strength is never equal to the pre-wound strength.

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    QUESTION: Which type collage is the most abundant?...ANSWER Collagen Type I is the most abundant throughout...QUESTION: Which type collagen is the principal collagen in scar?...ANSWER: Type I collagen is the principal collagen in scar...QUESTION: Which type collagen is the most abundant in a healing wound?...ANSWER: Type III collagen is the principal collagen in healing wound..

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  • COLON CANCER:

    QUESTION: What gene mutations are associated with colon cancer?

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    ANSWER: The genetic defects and molecular abnormalities associated with thedevelopment and progression of colorectal adenomas and carcinoma are as follows:

    - Mutations may cause activation of oncogenes (K-ras) and/or inactivation of tumor-suppressor genes [APC, DCC (deleted in colorectal carcinoma), p53].

    - Colorectal carcinoma is thought to develop from adenomatous polyps by accumulationof these mutations.

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    .

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  • COMPARTMENT SYNDROME:

    QUESTION: When performing a four-compartment fasciotomy for compartmentsyndrome, medial and lateral incisions are created. Which compartments is openedthrough the medial incision? Through the lateral incision?

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    ANSWER:

    - Compartment pressures are relieved in the leg by medial and lateral incisions.

    - Through the medial incision, long openings are then made in the fascia of thesuperficial and deep posterior compartments.

    - Through the lateral incision, the anterior and peroneal compartments are opened.

    .

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  • CONDYLOMA ACCUMINATA:

    QUESTION: How is the treatment for extensive perianal condyloma accuminata (analwarts)?.

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    ANSWER:

    - Treatment of anal condyloma depends on the location and extent of disease.

    - Small warts on the perianal skin and distal anal canal may be treated in the office withtopical application of bichloracetic acid or podophyllin.

    - Although 60 to 80% of patients will respond to these agents, recurrence andreinfection are common.

    - Imiquimod (Aldara) is an immunomodulator that recently was introduced for topicaltreatment of several viral infections, including anogenital condyloma.

    - Initial reports suggest that this agent is highly effective in treating condyloma locatedon the perianal skin and distal anal canal.

    - Larger and/or more numerous warts require excision and/or fulguration in theoperating room.

    - Excised warts should be sent for pathologic examination to rule out dysplasia ormalignancy.

    - It is important to note that prior use of podophyllin may induce histological changesthat mimic dysplasia.

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  • CO2 EMBOLISM:

    QUESTION: A 35 year old woman undergoing routine laparoscopic bilateral tuballigation develops severe hypotension, tachycardia, and drop in her end tidal CO2. Theanesthesiologist states the patient still has bilateral breath sounds. What is the mostlikely diagnosis?

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    ANSWER:

    - The most likely diagnosis in this patient is CO2 embolism.

    - End tidal CO2 specifically reflects the exchange of CO2 from blood to the alveolus.

    - A gradual rise in ETCO2 usually reflects impaired exchange from lung collapse oratelectasis.

    - A sudden drop in ETCO2 can be from something simple like disconnection from theventilator or something more serious such as an embolus.

    - The abrupt drop in ETCO2 following an embolus is from the interruption of CO2exchange at the alveolar level.

    - Because of the hypotension associated with a drop in ETCO2 in the above patient, themost likely diagnosis is CO2 embolism.

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  • COX INHIBITORS:

    QUESTION: Which drugs irreversibly inhibits platelet COX (cyclooxygenase)? What isthe mechanism of action of ibuprofen, celebrex, clopidogrel, and aspirin.

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    ANSWER:

    - Arachidonic acid released from the platelet membranes is converted by COX toprostaglandin G2 (PGG2) and then to prostaglandin H2 (PGH2), which, in turn, isconverted to TXA2.

    - TXA2 has potent vasoconstriction and platelet aggregation effects.

    - Arachidonic acid may also be shuttled to adjacent endothelial cells and converted toprostacyclin (PGI2), which is a vasodilator and acts to inhibit platelet aggregation.

    - Platelet COX is irreversibly inhibited by aspirin and reversibly blocked by NSAIDsbut is not affected by COX-2 inhibitors.

    - Ibuprofen is a nonsteroidal anti-inflammatory drug (NSAID) and reversibly affectsplatelet COX.

    - Both aspirin and clopidogrel irreversibly inhibit platelet function, clopidogrel throughselective irreversible inhibition of ADP-induced platelet aggregation and aspirinthrough irreversible acetylation of platelet prostaglandin synthase.

    - Celebrex is a COX-2 inhibitor and therefore does not affect platelet COX.

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  • CRYOPRECIPITATE:

    QUESTION:When should cryoprecipitate be given to a patient needing a massivetransfusion of packed RBCs?

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    TABLE: COMPONENT THERAPY ADMINISTRATION DURING MASSIVETRANSFUSION

    FRESH FROZEN PLASMA (FFP)

    - As soon as the need for massive transfusion is recognized.

    - For every 6 units of red blood cells (RBCs), give 6 units of FFP (1:1 ratio)

    PLATELETS

    - For every 6 units of RBCs and plasma, give one 6-pack of platelets.

    - Six random-donor platelet packs = 1 apheresis platelet unit

    - Keep platelet counts >100,000 ul/ during active hemorrhage control

    - After first 6 units of RBCs, check fibrinogen level.

    - If 100 mg/dL, give 20 units of cryoprecipitate (2g fibrinogen)

    - Repeat as needed, depending on fibrinogen level.

    QUESTION: True or false: cryoprecipitate contains vWF-VIII.

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  • ..ANSWER: True. Cryoprecipitate contains fibrinogen and vWF-VIII...

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  • QUESTION: Cryoprecipitate is used in patients with what disease?...ANSWER: Cryoprecipitate is used in von Willebrand's disease and hemophilia A(factor VIII deficiency). It is also used in DIC if fibrinogen is low.

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  • DDAVP: DESMOPRESSIN:

    QUESTION: What is the mechanism of action of DDAVP?

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    ANSWER:- The mechanism of action DDAVP is that it causes release of vWF.

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    QUESTION: What conditions are usually treated with DDAVP?

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    ANSWER:- Conditions treated with DDAVP include uremia, von Willebrand disease, and Aspirin.

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  • DESMOID TUMORS:

    QUESTION: What gene is associated with desmoid tumors of the chest wall?

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    ANSWER: Adenomatous polyposis coli (APC)

    - Desmoid tumors have recently been shown to possess alterations in the adenomatouspolyposis coli / Beta-catenin pathway, and cyclin D1 dysregulation is thought to play asignificant role in their pathogenesis.

    - Associations with other diseases and conditions are well documented, especiallythose with similar alterations in the adenomatous polyposis coli pathway, such asfamilial adenomatous polyposis (Gardner's syndrome).

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  • DIABETES INSIPIDUS:

    QUESTION: Is diabetes insipidus due to elevated ADH or low ADH?...ANSWER: Diabetes insipidus is due to low ADH...QUESTION Do patients with diabetes insipidus have high urine output or low urineoutput?...ANSWER: Patients with diabetes insipidus have high urine output...QUESTION: Do patients with diabetes insipidus have a low urine specific gravity or ahigh urine specific gravity?...ANSWER: Patients with diabetes insipidus have a low urine specific gravity...QUESTION: Do patients diabetes insipidus have high serum osmolarity or low serumosmolarity?...ANSWER: Patients with diabetes insipidus have a high serum osmolarity...

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  • QUESTION: Do patients with diabetes insipidus have high serum Na or low serumNa?...ANSWER: Patients with diabetes insipidus have a high serum sodium concentration...QUESTION. Do patients with diabetes insipidus have a high urine sodium or a lowurine sodium?...ANSWER: Patients with diabetes insipidus have a low urine sodium

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  • DIAPHRAGMATIC INJURIES:

    QUESTION: Diaphragm injuries involve which side of the chest more commonly, rightor left? Are diaphragmatic injuries easy are hard to detect on CT scan?

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    ANSWER:

    - Diaphragm injuries are more common with blunt trauma and are more common on theleft (liver projects the right side)

    - Diaphragm injuries are hard to find on CT scan unless there is gross herniation

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  • DIFFUSE ESOPHAGEAL SPASMS:

    QUESTION: What is the medical treatment of diffuse esophageal spasm?

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    ANSWER: The medical treatment of diffuse esophageal spasm includes calciumchannel blockers, nitrates, and antispasmodics

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  • DISSEMINATED INTRAVASCULAR COAGULOPATHY:(DIC:)QUESTION: What hematologic factors do you take into account when diagnosingsomeone with DIC?

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    ANSWER: Platelets, INR, PTT, fibrinogen, and fibrin split products.

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    QUESTION: Are platelets high or low in DIC?

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    ANSWER: Platelets are low in DIC.

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    QUESTION: Is the INR normal or prolonged in DIC?

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    ANSWER: The INR is prolonged in DIC.

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    QUESTION: Is the PTT normal or prolonged in DIC?

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    ANSWER: The PTT is prolonged in DIC.

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  • QUESTION: Is the fibrinogen level high or low in DIC?

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    ANSWER: The fibrinogen level is low in DIC.

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    QUESTION: Is the fibrin split products high or low in DIC?

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    ANSWER: Fibrin split products are elevated in DIC.

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  • DIVERTICULITIS:

    QUESTION: Approximately 5% of patients with complicated diverticulitis develop afistula to an adjacent organ. The most commonly involved organ is what?

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    ANSWER: The most commonly involved organ is the bladder.

    - Approximately 5% of patients with complicated diverticulitis develop fistulasbetween the colon and an adjacent organ.

    - Colovesical fistulas are most common, followed by colovaginal and colo-entericfistulas.

    - Colocutaneous fistulas are a rare complication of diverticulitis.

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  • DNA:Q: Approximately how many genes are present in the human genome?

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    A:

    - The human genome has an estimated 25,000 to 30,000 genes, and overall it is 99.9%identical in all people.

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  • DUODENAL ATRESIA:

    QUESTION: A newborn has bilious vomiting. Plain films reveal a distended gastric airbubble and a markedly dilated proximal duodenum. What is the most likely diagnosis?

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    ANSWER: Duodenal atresia

    - The history and radiograph findings are consistent with duodenal atresia.

    - Duodenal atresia occurs because of failure of vacuolization of the duodenum from itssolid core state.

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    QUESTION: What conditions are associated with duodenal atresia?

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    ANSWER: Down syndrome, biliary atresia

    - It is associated with prematurity, Down syndrome, maternal polyhydramnios,malrotation, annular pancreas, and biliary atresia.

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  • QUESTION: What is the typical presentation of an infant with duodenal atresia?

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    ANSWER:

    - In most cases, the duodenal obstruction is distal to the ampulla of Vater, and infantspresent with bilious emesis in the neonatal period.

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    QUESTION: What is the classic radiographic finding suggesting duodenal atresia?

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    ANSWER: double-bubble sign

    - The classic radiographic finding is the "double-bubble sign" (an air-filled stomach, afunctioning pylorus, and a distended proximal duodenal bulb).

    - If there is no distal bowel gas, complete atresia is confirmed and no further studies are

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  • necessary.

    - Conversely, if distal air is present, an upper gastrointestinal contrast study should bedone because other diagnoses are possible.

    - This is important to exclude midgut volvulus.

    - The finding of distal air in association with a double bubble could also indicate aduodenal stenosis or web or an annular pancreas that does not cause a completeobstruction.

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  • QUESTION: What is the treatment for duodenal atresia?

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    ANSWER:

    - The treatment of duodenal atresia is surgical bypass of the obstruction as either a side-to-side or proximal transverse-to-distal longitudinal duodenoduodenostomy or aduodenojejunostomy.

    - When the proximal duodenum is markedly dilated, a tapering duodenoplasty may beperformed.

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  • ECMO:

    QUESTION: What are the indications for ECMO in neonates?

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    ANSWER:

    - In neonates with respiratory distress syndrome, management includes high-frequencyventilation surfactant and inhaled nitric oxide.

    - When those interventions fail, ECLS is used.

    - ECLS can be performed by either venovenous or venoarterial cannulation.

    - The major indications for ECLS include meconium aspiration, respiratory distresssyndrome, persistent pulmonary hypertension, sepsis, and CDH.

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  • ENDOPLASMIC RETICULUM:

    QUESTION: Which type of ER makes cytoplasmic proteins? Which type of ER makesproteins for export?

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    ANSWER:- The endoplasmic reticulum that makes cytoplasmic proteins is the smooth endoplasmic reticulum.

    - The endoplasmic reticulum that makes proteins for export is the rough endoplasmic reticulum.

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  • ERRORS: TYPE I ERRORS: TYPE II ERRORS: TYPE IIIERRORS:

    QUESTION: In terms of the null hypothesis, what kind of an error is a Type I error?...ANSWER: A Type I error rejects the null hypothesis incorrectly. It falsely assumesthere was a difference when no difference exists....QUESTION: In terms of the null hypothesis, what kind of error is a Type II error?...ANSWER: A Type II error accepts the null hypothesis incorrectly. This can be due to small sample size. For example, the treatments are interpreted as equal when there isactually a difference...QUESTION: What is a Type III error?...ANSWER: A Type III error is made when the conclusion is not supported by the datafrom the study

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  • ERYTHROMYCIN:

    QUESTION: Erythromycin increases gastrointestinal motility by which mechanism?...ANSWER: Erythromycin binds the motilin receptor, and activates it to increasegastrointestinal motility

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  • ESOPHAGEAL PERFORATION: ESOPHAGEALRUPTURE:

    QUESTION: What is the key to survival in esophageal rupture?...ANSWER: In esophageal rupture, the key to survival is early diagnosis....QUESTION: What percentage of patients with esophageal rupture die if the diagnosis ismade after 36 hours?...ANSWER: 85% of patients who are diagnosed with esophageal perforation more than36 hours after the incident die.....

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  • EXTRINSIC PATHWAY:

    QUESTION: Which two factors are involved in the initiation of the extrinsic pathway(PT)?...

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    .ANSWER: In the extrinsic pathway, tissue factor reacts with factor VII to initiate thecoagulation process leading up to fibrin production...

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    QUESTION: Summarize the extrinsic pathway: include the lab test associated with it,the factors involved, and the final product...

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    .ANSWER: Extrinsic path tested with PT. Tissue factor + VII --> activated X --> fibrin

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  • FACTORS:

    QUESTION: Which factors are present at low levels in banked blood?

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    ANSWER:- The factors that are at low levels in banked blood are factor V and factor VIII.

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    QUESTION: Which factor is not made by the liver?

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    ANSWER:- The only factor that is not made in the liver (but instead is made by the reticuloendothelial cells) is Factor VIII.

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  • QUESTION: Which factor is activated during cardiopulmonary bypass?

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    ANSWER:- The factor that is activated during cardiopulmonary bypass is Factor XII (Hageman factor) necessitating a needfor Heparin.

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  • FACTOR V LEIDEN:

    QUESTION: True or false: The most common risk factor for spontaneous venous thromboembolism is factorV leiden.

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    ANSWER: TRUE.

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    QUESTION: What exactly is the problem in Factor V Leiden?

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    ANSWER:- The problem in Factor V Leiden is a defect on factor V, which leads to resistance to activated protein C.

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  • QUESTION: Patients with factor V Leiden are predisposed to thrombosis because theyhave a genetic mutation in factor V which is what effect made on factor V?

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    ANSWER:

    - A third major mechanism of inhibition of thrombin formation is the protein C system.

    - On its formation, thrombin binds to thrombomodulin and activates protein C toactivated protein C (APC), which then forms a complex with its cofactor, protein S, ona phospholipid surface.

    - The APC-protein S complex cleaves factors Va and VIIIa so they are no longer able toparticipate in the formation of tissue factor-VIIa or prothrombinase complexes.

    - Of interest is an inherited form of factor V that carries a genetic mutation, called factor V Leiden, that is resistant to cleavage by APC and thus remains active(procoagulant).

    - Patients with factor V Leiden are predisposed to venous thromboembolic events.

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  • FACTOR VIII:

    QUESTION: Factor VIII is the only factor not made in the liver. Where is it made?...

    ANSWER: Factor VIII is the only factor not made in the liver. It is made byreticuloendothelial system.

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  • FAMILIAL ADENOMATOUS POLYPOSIS: FAP:

    QUESTION: In patients who have undergone total proctocolectomy for FAP, what is themost common cause of death?

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    ANSWER:

    - The most common cause of death in these patients is duodenal cancer.

    - Patients