Lecture 1 (GI)- Exam 1 Flashcards

Question

Lower Mucosal Esophageal Ring (Schatzki ring or B ring) * What are they? * Often referred to as what?

Answer 1

* Mucosal projection that involves the most distal esophagus. * Often referred to as "steakhouse syndrome" and may present with non-progressive dysphagia for solids (especially steaks).

Answer 2

* **Upper esophageal web** * Iron-deficiency anemia * Hypothyroidism * Glossitis &/or cheilitis * Gastritis * Dysphagia (even without presence of a web)

Answer 3

* **90% are women** * Predominantly in northern hemisphere/ Scandinavian/Northern descent * Tx: Iron replacement alone may reverse some of the pathologic web changes; dilation of web * **Increased incidence of esophageal SCCA**

Answer 4

* High amplitude, repetitive, non-peristaltic nonfunctioning esophageal contractions * Often presents as chest pain/MI symptoms in a high stress patients (does not have to be with food but can worsen with food) * “Corkscrew/rosary bead/or Nutcracker” esophagus on barium swallow (study of choice)

Answer 5

* **Normal function of the LES** * Intermittent presence of normal peristaltic sequences (allows food mvt * Tx with NTG and CCB (to relax) + Psychotherapy (ppl with this do not like to eat so they need therapy) * Peppermint known to reduce spasms (NOT for ppl with poor LES)

Answer 6

* Submucosal non-malignant mass * Won’t know this until biopsy * Arise from circular or longitudinal smooth muscle * Round filling defect * Splitting of barium around tumor * Esophagus appears widened on AP view

Answer 7

* Herniation of part of the stomach through the esophageal hiatus in the diaphragm and into the chest, and may be sliding or paraesophageal. * The presence of hiatus hernia will not itself lead to reflux

Answer 8

Dx: Bowel sounds in chest Management * Typically medical (addressing GERD) * Surgical - fundoplication

Answer 9

Pyrosis or Heartburn * “Burning” pain that radiates from the epigastrium * Usually seen with GERD Regurgitation * Sudden, effortless return of small volumes of gastric or esophageal contents into the pharynx

Answer 10

* Transient or sustained inappropriate relaxation of lower esophageal sphincter (LES), not associated with swallowing * Acid-rich stomach contents reflux into esophagus, resulting in esophageal damage

Answer 11

* Associated with hiatal hernia, obesity (increase abdominal weight so increase thoraic pressure) , neurological problems, medications. * Identify red flags : dysphagia (difficult), odynophagia (pain), weight loss (cancer) or bleeding.

Answer 12

1. Impaired LES-low pressures or frequent transient LES relaxation 2. Hypersecretion of acid 3. Decreased acid clearance resulting from impaired peristalsis or abnormal saliva production 4. Delayed gastric emptying or duodenogastric reflux of bile salts & pancreatic enzymes.

Answer 13

* Fatty foods * Chocolate * Ethanol * Peppermint * Caffeine * Nicotine * Calcium channel blockers * Nitrates

Answer 14

* Pregnancy * Obesity * Bending * Lifting * Straining * Tight-fitting clothes

Answer 15

* Heartburn (pyrosis) – hallmark symptom * Dx: Clinical via history

Answer 16

* Burning, substernal, radiating upward, * Worse 30 to 60 minutes after meals & lying supine (at night) * Relieved with sitting up & antacids * 10% of patients present with atypical “anginal” type CP * **Always R/O MI or other cardiac causes.**

Answer 17

* Severity of symptoms does not correlate well with degree of esophageal mucosal damage * Physical Exam findings nonspecific * Diagnosis of GERD best made by History

Answer 18

* Prolonged monitoring of esophageal pH for 12 to 24 hours is the most reliable means of diagnosing acid reflux. * Stop PPI for 10 days prior to the test * A pH electrode is passed through the nose or mouth to 5 cm above the manometrically determined LES. * Acid reflux is defined when there is a decrease of esophageal pH to less than 4 (>4% of time over 24 hours).

Answer 19

Lifestyle Modifications H2 Blockers * Ranitidine (Zantac) * Famotidine (Pepcid)

Answer 20

Moderate/Severe or frequent symptoms (2+ episodes/week) or erosive esophagitis * Proton Pump Inhibitors – 8 week therapy heals 86% of esophagitis * Omeprazole (Prilosec) * Lansoprazole (Prevacid) * Pantoprazole (Protonix) * Esomeprazole (Nexium)

Answer 21

* Symptoms similar to reflux * History of recurrent food obstructions at younger than expected age * History of atopy * Clinically: see “Trachealization” of esophagus

Answer 22

* Histology: Needs more than 15 eosinophils in biopsy * Treatment: PPI’ s, trigger food avoidance, topical (inhaled) steroids * If with a stricture there is high incidence of complications while doing dilation

Answer 23

* Replacement of the squamous epithelium of esophagus by columnar epithelium often due to severe esophageal reflux * Diagnosed by endoscopy with biopsy * Change in tissue has potential for esophageal carcinoma (adenocarcinoma)

Answer 24

* Distal esophagus is replaced by Barrett mucosa, producing a darker, slightly erythematous gross appearance. * Large ulcerating adenocarcinoma in distal esophagus that extends into upper stomach.

Answer 25

Adenocarcinoma * Majority develop as a complication of Barrett’s metaplasia due to chronic GERD * Most arise in the distal 1/3 of the esophagus Squamous Cell * Chronic ETOH and smoking are associated with increased risk (unrelated to acid)

Answer 26

* Dysphagia (most common) * Solids->Liquids * Weight loss * Regurgitation, Aspiration w/ Pneumonia may occur with complete obstruction

Answer 27

* Chest pain (mediastinum) * Hiccups (diaphragm)-> Vagus Never * Hoarseness (recurrent laryngeal nerve)

Answer 28

Esophageal cancer-> Apple core lesion ## Footnote Usually find after weight loss and dysphagia.

Answer 29

* Surgical resection – if there is no widespread metastasis * XRT (squamous cell is more radiosensitive than adenocarcinoma) - excellent palliative treatment for obstructive symptoms. * Chemotherapy

Answer 30

* AST, ALT (found in muscle also – so MI will show higher LFT’s) * Chronic hepatitis – elevated LFT’s for >6months ## Footnote ALT is slightly more specific for liver damage. (L for liver)

Answer 31

**Alkaline Phosphatase**, GGT and/or bilirubin ## Footnote * Alk Phos (also found in bones and placenta) – located near ducts of the liver – elevation shows obstructive type pattern. Can be due to pancreatic CA, gallstones in common bile duct. * GGT – helpful if only have elevated Alk Phos level and AST/ALT are normal. Can see if it’s a bone problem (Paget’s). If GGT is elevated along with Alk Phos = liver problem. If GGT is normal and Alk Phos is elevated – bone etiology.

Answer 32

Tests for Liver synthetic Function * Albumin, PT/INR Tests for Biliary excretion * Bilirubin ## Footnote * Total – direct bili = indirect bili * CMP gives you all but GGT and direct bili. Can order those separately. * Albumin – liver makes it – low albumin in cirrhosis. * All clotting factors except factor 8 are made by liver. PT checks factor 7 – most sensitive. * Elevated indirect bili – not really a liver problem – could be hemolysis.

Answer 33

1. Aspartate Aminotransferase (AST) also known as serum glutamic oxaloacetic transaminase (SGOT) 1. Alanine Aminotransferase (ALT) also known as serum glutamic pyruvic transaminase (SGPT) 1. Elevation of the aminotransferases indicates inflammation and/or injury to hepatocytes.

Answer 34

Alcoholic Hepatitis and Alcoholic Cirrhosis * Mild to moderate elevations of ALT and AST (usually to <500 IU) with * AST greater than ALT (ratio >2:1) Extrahepatic obstruction (def look for GGT and Alk Phos) * Moderate elevations of ALT and AST to <500 IU

Answer 35

Viral, toxic, or ischemic hepatitis * Extreme elevations of ALT and AST >500 IU AST and ALT may be normal in some patients despite significant disease (i.e. hemochromatosis)

Answer 36

## Footnote big jumps in acute infections and toxicity

Answer 37

* Present in liver, bone, placenta, and intestine * Measure serum γ-glutamyltranspeptidase (GGTP) {also known as gamma-glutamyl transferase (GGT)} to determine if the elevated alkaline phosphatase is from a hepatic origin * **Elevation of GGTP/GGT indicates a hepatobiliary source**

Answer 38

Significant elevations of hepatic alkaline phosphatase occur in HEPATIC OBSTRUCTION * Strictures * Neoplasm * Pancreatitis * Primary Biliary Cirrhosis/Cholangitis (PBS) * Primary Sclerosing Cholangitis (PSC) – R/O Crohn’s or UC

Answer 39

* Statins, ACE, antibiotics specially Augmentin, acetaminophen( only if an overdose), Imuran, Isoniazid, anti seizures medications, etc. * Cholestatic (Alk phos/GGT)

Answer 40

* Elevated in chronic alcoholic liver disease * Elevated in cholestatic disease (Primary Biliary Cirrhosis/Cholangitis, Primary Sclerosing Cholangitis)

Answer 41

* Significantly elevated in metastatic disease to the liver * Slight elevations may be seen in hepatitis, cirrhosis, extrahepatic obstruction, and congestive hepatomegaly

Answer 42

1) PROTHROMBIN TIME (PT, INR) * Elevated in severe liver damage and indicates a poor prognosis( Because PT/INR reflects hepatic synthesis of factors I, II, V, VII, X) 2) SERUM ALBUMIN * Low in Significant liver disease ## Footnote To R/O cause of elevated PT INR give them Vit K. If Vit K deficient – it will improve their PT/INR. If liver cause, Vit K wont do anything.

Answer 43

Acute insult with elevated transaminases does not immediately affect synthetic function

Answer 44

What else will cause hypoalbuminemia? * Nephrosis, malabsorption (sprue or bacterial overgrowth, Cancer). What else will cause an elevated PT/INR? * Coumadin, malabsorption of Vit K (Fat soluble), High amounts of ABX.

Answer 45

Total Bilirubin Unconjugated Bilirubin = Indirect Bilirubin * Bound to albumin and gets conjugated in liver Conjugated Bilirubin = Direct Bilirubin * Stored in liver, excreted to colon (which converts to urobilinogen-> causes the brown color of stool) or bile

Answer 46

* bili in urine (tightly bound to albumin) but elevated urobilinogen in urine (liver cant keep up with too much and its not bound to albumin or there is not enough albumin secondary to liver disease). * Unconjugated hyperbilirubinemia usually results from dysregulation in the bilirubin metabolism that includes increased production, impaired hepatic uptake, and decreased conjugation of bilirubin. * Elevated direct bili (liver problem) – spills out into blood – will have elevated bili and urobilinogen in urine.

Answer 47

Present only with elevated direct bilirubin (not bound to albumin – gets excreted) * Hepatitis * Hepatocellular jaundice * Biliary Obstruction

Answer 48

You need to ask what they eat * Carrots contain beta carotene which can discolor the skin

Answer 49

Unconjugated Bilirubin = Indirect Bilirubin (usually not given, so you have to calculate) * I=T-D Conjugated Bilirubin = Direct Bilirubin

Answer 50

suspect nicking or accidental removal of common bile duct due to bad visibility.

Answer 51

Portal HTN * Palmar erythema * Caput Medusae (round ligament revasclularized)

Answer 52

* Encephalopathy (increased ammonia NH3) * Asterixis (asynchronous flapping – liver flap/ also ESRD) * Fetor hepaticus (halitosis) * Bruising (clotting factors low and platelets can be trapped in liver) and Spider Nevi * Ascites (low albumin) ## Footnote Spider nevi – blanch – higher pressure in BV

Answer 53

* Splenomegaly * Lower extremity edema * Muscle wasting (Temporalis muscle, interosseous muscles) * Gynecomastia (high estrogen state) * Testicular Atrophy (estrogen high)

Answer 54

Fever, RUQ pain, with the jaundice (Charcot’s Triad)

Answer 55

* Bronzed skin of Hereditary Hemochromatosis * Track marks (IV drug use) * Kayser-Fleischer ring of Wilson’s Disease->Copper metabolism problem

Answer 56

"Pre-hepatic jaundice” - occurs when there is a fault somewhere upstream of conjugation. * Hemolysis * Gilbert’s Disease * Neonatal Jaundice * Crigler-Najjar Syndrome

Answer 57

* Common cause of elevated unconjugated bilirubin * Known as hemolytic jaundice * RBC cell lysis leads to overload of unconjugated bilirubin that is not excreted/CONJUGATED through liver fast enough

Answer 58

Differentials: * Sickle cell anemia, hereditary spherocytosis, TTP, autoimmune hemolytic anemia, thalassemia minor Treatment * Geared towards cause * Phototherapy or exchange transfusions may help

Answer 59

Due to: * Excess fetal destruction of red cells * Immature uptake and conjugation pathways in the neonatal liver * Absence of gut flora to metabolize bile pigments. Prematurity, dehydration, and breast feeding may increase neonatal jaundice

Answer 60

* Jaundice peaks between the second and fifth day of life, and should subside within two weeks * Main concern is kernicterus

Answer 61

* Completely benign cause of jaundice with elevated total and unconjugated bilirubin * A congenital defect in the liver's uptake and conjugation pathways causing elevation of unconjugated bilirubin, but normal LFT’s

Answer 62

* Occurs in about 4-16% of the population, usually in adolescence; M>F. * Usually identified following illness, starvation/dehydration, or surgery. * Not a liver problem and work-up is rarely required unless other causes of hyperbilirubinemia are being worked up.

Answer 63

* There is no bilirubin in the urine, which remains its usual color * There is more than the usual trace of urobilinogen in the urine * The bilirubin in the blood is unconjugated (preliver problem – hemolysis or Gilbert’s)

Answer 64

Inherited disorders resulting in conjugated hyperbilirubinemia and normal LFTs (typically asymptomatic) * Dubin-Johnson Syndrome * Rotor Syndrome * biliary atresia in newborns

Answer 65

* **Dubin-Johnson Syndrome: Mutation in the transporter gene** that moves the bilirubin from the hepatocyte to the bile canaliculus -> Asymptomatic elevations in conjugated bilirubin * **Rotor Syndrome**: Defect in the ability of the hepatocyte to store bilirubin -> Asymptomatic elevations in conjugated bilirubin * Consider biliary atresia in newborns who develop clay colored stools (no bili in stool) and have elevated direct bili ## Footnote For Dubin and rotor, you need to do genetic testing

Answer 66

* Also known as Primary Biliary Cholangitis * Seen more commonly in women ages 30-65 y/o * Progressive, immune mediated destruction of the interlobular bile ducts only

Answer 67

* SXS: fatigue and pruritis-> Jaundice, xanthomas, skin hyperpigmentation, steatorrhea (floating stool), bone pain from osteoporosis complications (i.e. compression fractures) * Labs: cholestatic picture – elevated alkaline phosphatase and GGT.

Answer 68

* Diagnosis – **Elevated Antimitochondrial antibody (AMA); Elevated serum IgM levels** * **Liver Biopsy – destructive lesions of the bile ducts** * Treatment – **Ursodeoxycholic acid** (replaces toxic bile acids) improves pruritis, slows progression of disease, and delays the need for liver transplant. ## Footnote Do AMA test and do liver Bx.

Answer 69

* Inflammation of the Extrahepatic ducts OR Intrahepatic ducts leading to fibrosis * 70% of pts with PSC have IBD ->Cholestatic picture: elevated alk phos and GGT * May lead to cirrhosis * TX - liver transplant if severe

Answer 70

ERCP image shows mural irregularity of the cystic duct (arrows) due to primary sclerosing cholangitis

Answer 71

* Primary Sclerosing Cholangitis * Gallstones * Pancreatic Cancer (causing extrahepatic compression of bile ducts) * Cholangiocarcinoma (causing bile duct obstruction)

Answer 72

* Primarily spread fecal -> oral route * Direct contact with HAV infected person * Ingestion of HAV contaminated water or food

Answer 73

Acute Infection * Hepatitis A Antibody IgM (HAV-Ab IgM) * Total HAV Ab is positive (includes IgM too) Past infection = Immunity (vaccine) * Total Hepatitis Antibody (+Total HAV Ab) w/ a **negative** HAV Ab IgM – patient is vaccinated

Answer 74

* Hep A doesn’t have a chronic stage. * IgM is positive in acute – MAC +M and Acute * IgM is negative in immune or if no disease is present. But there is no chronic stage in Hep A so it’s a vaccine. * Can measure IgG (immune) IgM (acute) or total Ab’s.

Answer 75

## Footnote * Acute, Immune/vaccinated or at risk (no disease) * Total is really never tested unless you’re looking for vaccination.

Answer 76

* Incubation period: Average 30 days * Onset:Acute with Malaise, nausea, vomiting, jaundice, dark urine, diarrhea, etc * Treatment: Supportive (hydration and anti-nausea meds) * Course: Usually self-limiting (recovery within 6-12 months). No associated carrier state or chronic hepatitis.

Answer 77

**Pre-exposure (vaccine and/or IG) travelers to intermediate and high HAV-endemic regions Individual risk se**tting

Answer 78

Post-exposure: vaccine or IG (within 14 days) Routine * household and other intimate contacts Selected situations * institutions (e.g., day care centers) * common source exposure (e.g., food prepared by infected food handler)

Answer 79

* Parenteral exposure to HBV infected blood * Sexually/Salivary transmitted (except breast milk) * Perinatal ## Footnote In horizontal transmission, viruses are transmitted among individuals of the same generation, while vertical transmission occurs from mothers to their offspring

Answer 80

* Incubation period 1-3 months * Acute vs chronic. 90% will get through symptoms and will recover. 10% will become chronic. Most likely in patients with vertical transmission. * Chronic patients may develop HCC without going through cirrhosis

Answer 81

## Footnote Most will spontaneously recover but some will go to chronic stage.

Answer 82

* HBsAg (+) = chronic carrier or active disease * HBsAb/Anti-HBs (+) = immunity (vaccinated) or previous disease (recovered) * HBcAb(IgM) = acute disease exposure or active infection * HBcAb/Anti-HBc(IgG) = previous disease exposure ## Footnote * HBsAg is used to make vaccines * Test core – Anti-HBc – to see if its acute or chronic Hep B. If Anti-HBs is positive, test Anti-HBc for acute (+ IgM) or chronic (IgM negative; IgG positive). * Core antibody does not provide any protection from the disease.

Answer 83

* HBeAg (+) = active viral replication * HBeAb (+) = strong viral suppression (i.e. seroconversion) * HBV-DNA < 105 = chronic carrier or well suppressed * HBV-DNA > 105 = active chronic infection (Higher HBV DNA levels = higher risk of Cirrhosis or hepatocellular carcinoma) ## Footnote * Hbe – for envelope – measures the amount of infectivity. HBe Ag positive – high infectivity. Anti HBeAg negative – low infectivity * HBV-DNA unreliable and tests a viral load

Answer 84

Antigens – acute infection Antibodies * Surface (Ag or Ab) – Immunity via vaccine or recovery from infection with immunity * Envelope (Ag or Ab) – Measures degree of infectivity * Core (IgM or IgG) – Discriminates Acute vs Chronic infection

Answer 85

HBe to see infectivity

Answer 86

Don’t treat Acute HepB and wait until chronic stage because they have a chance to recover. Don’t start them on toxic interferon meds yet.

Answer 87

Treatment options for Chronic Hepatitis B who are serum HBsAg+, HBeAg/HBV-DNA-positive pts with symptoms, elevated AST, ALT levels & Liver biopsy evidence of chronic hepatitis * Pegylated Interferon * Lamivudine * Adefovir * Entecavir * Telbivudine * Tenofovir

Answer 88

Results in anti HBe seroconversion with clinical, biochemical, & histologic improvement in 40% of cases

Answer 89

* Vaccinate against Hepatitis A (don’t want to damage the liver anymore than already have) * Avoid hepatotoxic medications & Alcohol * Screen for Hepatocellular Carcinoma: AFP + RUQ US (Q6-12 months) * If Portal HTN is present, manage complications. ## Footnote They arent more susceptible to Hep A but they will probably die if they do get it.

Answer 90

* Universal vaccination of all children and adults is recommended in US * Check anti-HBs titers 1-2 months after completion of the vaccine (not all respond to vaccine)

Answer 91

Vaccine targeted to high-risk groups * Health care workers * Men who have sex with men * Persons who use IV drugs * Hemodialysis pts * Patients with hemophylias * Household & sexual contacts of HBsAg carriers * Neonates in endemic areas or high-risk neonates in lower-risk areas

Answer 92

Repeat the 3 vaccine doses & repeat anti-HBs 1-2 months after completion Persons who do not have a protective concentration of anti-HBs after revaccination should be tested for HBsAg. ## Footnote You want it >10. Less than 10 – did not develop protection so repeat the vaccine.

Answer 93

* If the HBsAg test result is positive, the person should receive appropriate management, and any household, sex, or needle-sharing contacts should be identified and vaccinated * Persons who test negative for HBsAg should be considered susceptible to HBV infection and should be counseled about precautions to prevent HBV infection and the need to obtain HBIG postexposure prophylaxis for any known or likely parenteral exposure to HBsAg-positive blood

Answer 94

* It requires the hepatitis B virus to survive and replicate * Coinfection with Hepatitis B * No specific treatment or vaccine available for Hepatitis D. Vaccinate patients for Hepatitis B

Answer 95

* Most common cause of liver transplant and chronic hepatitis in the US * Viral Properties: Caused by flavi-like virus with RNA genome of > 9,000 nucleotides(similar to yellow fever virus, dengue virus)

Answer 96

Incubation Period * 2-8 weeks * 85-90% will develop chronic hepatitis CDC recommendation to screen all baby boomers, because that is the highest risk group, and 75 % does not know they have it.

Answer 97

* More common than Hep B (resolves more quickly). * Their LFT will be border line elevated with HCAg is positive. * IV drug abuse is really most common cause.

Answer 98

* **Percutaneous transmission accounts for > 90% of transfusion associated hepatitis cases** * **IV drug use accounts > 50% of reported cases** * Little evidence for frequent sexual (horizontal) or perinatal (vertical) transmission * Often asymptomatic and presents frequently in the chronic phase with borderline consistent elevated LFTs

Answer 99

* New onset Hepatitis C is usually asymptomatic * Patients usually present in the chronic stage with mild persistent elevation of LFTs or sequella of liver disease

Answer 100

* Individuals at an increased risk for HCV (i.e. patients with a history of injection drug use, homelessness) * Individuals born in the United States between 1945 and 1965 (*New recommendation)

Answer 101

Measure Ab because RNA is not reliable ## Footnote * Test to order Anti-HCV or HCV Ab * RNA test isnt very reliable. If negative – cant say patient doesn’t have Hep C.

Answer 102

Hep C acute is less severe than Acute Hep B.

Answer 103

* Viral Genotyping (some types are worse than others) * Liver biopsy to see severity and prognose treatment

Answer 104

* Diabetes mellitus occurs three times more frequently in HCV-infected persons * Glomerulonephritis * Essential mixed cryoglobulinemia, a condition involving the presence of abnormal proteins in the blood * Porphyria cutanea tarda, an abnormality in heme production that causes skin fragility and blistering * Non-Hodgkins lymphoma may occur more frequently

Answer 105

Options for Hepatitis C for Genotype 1 (most difficult to treat) are protease inhibitors * Ledipasvir/sofosbuvir (Harvoni) – once daily * Boceprevir (Victrelis) – PO three times a day * Telaprevir (Incivek) – PO every 8 hours * Most common side effects: Anemia (that may respond to Epogen) and Skin Rash (may be life threatening in telaprevir) ## Footnote * 65-75% cure rate (double to triple that of standard therapy) * Most patients only need 8-24 weeks rather than the usual 48 weeks

Answer 106

* Pegylated interferon in combination with ribavirin SQ x 24-48 weeks * Contraindications to therapy: LOTS OF THEM (see below) * Common adverse events: influenza-like symptoms. Psychiatric side effects (depression, irritability, insomnia) ## Footnote Major uncontrolled depressive illness, organ transplant, autoimmune hepatitis or other autoimmune condition known to be exacerbated by peg - interferon and ribavirin, untreated thyroid disease , pregnant or unwilling to comply with adequate contraception , severe concurrent medical disease (severe hypertension, heart failure, significant coronary heart disease, poorly controlled diabetes, chronic obstructive pulmonary disease), Age less than 2 years, known hypersensitivity to drugs used to treat HCV.

Answer 107

* Vaccinate against Hepatitis A & B * Avoid hepatotoxic medications & Alcohol * Screen for Hepatocellular Carcinoma: AFP + RUQ US (Q6-12 months) * If Portal HTN is present, manage complications.

Answer 108

* Similar to hepatitis A in its mode of transmission (fecal-oral) and in the involvement of contaminated water. * Highly contagious * Differs from hepatitis A : a high incidence of mortality, particularly in pregnant women * Increased incidence of fetal demise ## Footnote Similar to HepA and more severe in pregnants. Seen in 3rd world Countries.

Answer 109

Clinicians who may encounter pediatric patients with hepatitis of unknown etiology to consider adenovirus testing. * Adenovirus 41 type was noted in 5 children in Alabama with acute live failure Nucleic acid amplification testing (NAAT, e.g. PCR) is preferred for adenovirus detection and may be performed on respiratory specimens, stool or rectal swabs, or blood.

Lecture 1 (GI)- Exam 1 Flashcards

(148 cards)