Module 7: Gastrointestinal System Flashcards by LENNIE BELLE PORTENTO

Liver inflammation

Etiology
* viral infection
* toxins
* drugs
* other (immune mediated

Hepatitis

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Etiology
* Hepatitis A Virus (most common viral hepatitis worldwide)

Pathogenesis
* fecal-oral transmission, virus is directly cytopathic to the liver but does not lead to
cirrhosis

Signs
* jaundice (after 1-2 weeks) (due to intrahepatic cholestasis)
o inc. conjugated bilirubin
* > pale stools
* > dark urine
* +/- hepatomegaly
* +/- splenomegaly
* +/- tender lymphadenopathy
* rarely - hepatic encephalopathy & death

HEPATITIS A VIRUS (Acute)

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Very similar to Hep A but high mortality in pregnancy (20% > DIC in 3rd Trimester)

Etiology
* Hepatitis E virus (a herpes virus)

Pathogenesis
* Virus is directly cytopathic to the liver
Clinical Features
* fecal-oral transmission (incl. vectors: dogs/pigs/rodents

Prognosis
* 1-2% mortality (from fulminant hepatic failure)
* 20% mortality in pregnancy (from DIC in 3rd trimester)

HEPATITS E VIRUS (Acute)

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transmission via parenteral route or equivalent
vertical transmission
occurs during 3rd trimester or early post-partum

*HBsAg +ve, HBeAg +ve mothers ––> 90% of infants infected
*HBsAg +ve, anti-HBe +ve mothers ––> 10-15% infected
* give HBIG and full HBV vaccination to newborns of HBsAg +ve mothers (90% effective)

incubation period: 6 weeks to 6 months
infectivity: during HBsAg positivity

HEPATITIS B VIRUS (HBV) Acute and Chronic

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Transmission is chiefly parenteral

*Transfusions (HCV is the most common cause of post-transfusion hepatitis)
*IV drugs use
*Sexual transmission occurs but risk is less than with HBV
*40% of cases have no risk factors

Clinical incubation period: 5-10 weeks
AST and ALT levels fluctuate (unlike Hep A or B)
More than half progress to chronic liver disease

Treatment:
*no accepted vaccine

HEPATITIS C VIRUS (HCV) Chronic

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Infectious only in the presence of HBV because HBV surface antigens are required for replication.

Transmission: Close personal contact or Transmission of blood

Types of Infection: Coinfection and Superinfection

Prevention: HBV vaccine

HEPATITIS D (HDV) Acute and Chronic

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Fecal-oral transmission occurring in epidemics in Asia, Africa, Central America
* most have mild disease, but in 3rd trimester of pregnancy 10-
20% have fulminant liver failure
* serology: anti-HEV

Prevention
* no vaccine available

HEPATITIS E VIRUS (HEV) Acute

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Name the 5 Drug induced liver disease / Drug induced hepatitis

Clue: ACE, CHL,INH,METH,AMI

Acetaminophen
Chlorpromazine
Isoniazid
Methotrexate
Amiodarone

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Can cause same histology and clinical outcome as alcoholic hepatitis

Amiodarone

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May rarely cause cirrhosis, especially in the presence of obesity, diabetes, alcoholism

Scarring develops without symptoms or changes in liver enzymes, therefore biopsy may be needed in long-term treatment

Methotrexate

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20% develop elevated transaminases but < 1% develop clinically
significant disease

Susceptibility to injury increases with age

INH (Isoniazid)

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Cholestasis in 1% after 4 weeks; often with fever, rash, jaundice, pruritus and eosinophilia

Chlorpromazine

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Metabolized by hepatic cytochrome P450 system
* can cause fulminant hepatic failure
* hepatic necrosis resulting in increased
aminotransferases, jaundice, possibly hepatic encephalopathy, acute renal failure, death

Acetaminophen

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Type of Stone?
(80%) = mixed (> 70% cholesterol by weight),
radiolucent

Risk factors:
* Female, fat, fertile, forties
* North American First Nations peoples have
highest incidence
* diabetes mellitus (DM), pancreatitis
* malabsorption, terminal ileal resection or disease
(e.g. inflammatory bowel diseases)

Cholesterol

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(20%), may be radio-opaque (Seen in xray)

Pigment stones

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What Pigment stones are composed of unconjugated bilirubin, calcium, bile
acids?

smooth green/black to brown

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What Pigment stones are associated with cirrhosis, chronic hemolytic states?

black pigment stones

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What Pigment stones are associated with bile stasis, (biliary strictures, dilatation and biliary infection (Clonorchis sinensis)?

Calcium bilirubinate stones

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Presence of stones in gallbladder

Pathogenesis:
* Imbalance of cholesterol and its solubilizing agents, bile salts and lecithin concentrations
* If hepatic cholesterol secretion is excessive then bile salts and lecithin are “overloaded”, supersaturated cholesterol precipitates and can form gallstones

Cholelithiasis

Inflammation of gallbladder resulting from sustained obstruction of cystic duct by gallstone (80%)
* No cholelithiasis in 20% (acalculous)
* Murphy’s sign

Cholecystitis

Inflammation of the stomach lining

Gastritis

Type of Gastritis?
o 15% Alcohol
o NSAIDs > Inhibits COX > dec Prosƚaglandin >
Hyperacidity > Inflammation
o Severe Burns > dec Plasma Volume > Sloughing of
Stomach Mucosa

Acute Gastritis

Type of Gastritis?
80% Bacterial - Helicobacter Pylori (Most Common)

Chronic Gastritis

Type of Gastritis?
Autoimmune “Pernicious Anemia” (Antibodies against Parietal Cell & IF > B12 Deficient

Atrophic Gastritis

increased attack (Hyperacidity, Zollinger Ellison Syndrome), or decreased defense (H.Pylori, Stress, Drugs [NSAIDs & Corticosteroids], Smoking)

PEPTIC ULCER DISEASE

* Small, single, round, punched out ulcer * 90% in duodenum or lesser-curve of stomach. * Healing peptic ulcers have radiating mucosal folds due to scar contraction Clinical Features: * Burning epigastric pain; (most severe when hungry, relieved by food) * Nausea & vomiting * Anorexia & weight loss * Hematemesis/melena * Perforation > acute peritonitis

PEPTIC ULCER DISEASE

Is the sudden inflammation of the pancreas, causing abdominal pain, digestive enzyme release, and potential organ damage. Etiology: * 50% - gallstones (cholelithiasis) > ampulla/common bile duct obstruction * 40% - alcohol abuse * 10% infections/metabolic (inc. Ca in hyperparathyroidism) DKA, uremia pregnancy / trauma / ischemia / duodenal ulcer /scorpion venom / drugs / unidentified Grey Turner’s and Cullen Sign

ACUTE PANCREATITIS

Inflammation of the Intestines

GASTROENTERITIS

Etiology: * Staph aureus (poor food handling) * Bacillus cereus (fried rice at cereal) (mostly found in cereal) Symptoms: * Onset within 4hrs * Vomiting, *stomach cramps, diarrhea

TOXIGENIC DIARRHEA (Food Poisoning)

Is a type of bacteria commonly found in the intestines of humans and animals, some strains of which can cause foodborne illness and infections.

ESCHERICHIA COLI (“Traveler’s Diarrhea”)

Type of E.coli? * Produces Toxins * Traveler’s Diarrhea

ETEC: (Enterotoxigenic E. coli)

Type of E.coli? * Active Intestinal Invasion/Destruction * Traveler’s Dysentery

EIEC: (Enteroinvasive E. coli)

Type of E.coli? * Sporadic disease in babies and children

EPEC: (Enteropathogenic E. coli)

Type of E.coli? * Most important * The Serious One: * produce verotoxin > destroys platelets & RBCs > hemolytic-uremic syndrome (HUS) > kidney failure + bleeding + dysentery

EHEC: (Entero-Hemorrhagic E. coli)

Etiology: * Salmonella typhi * typhoid fever, improperly cooked meal Management: * Ceftriaxone +/- Ciprofloxacin

SALMONELLA; TYPHOID

Risk to pregnant women & immunocompromised Etiology: * Listeria monocytogenes – (G-Pos) * Soft cheeses & cold deli meats

LISTERIOSIS (LISTERIA)

Etiology: * Vibrio cholerae Symptoms: * profuse rice-water stools Management: * fluid replacement Prognosis: * self-limiting NB: dysenteric organisms * Salmonella, Shigella, Entamoeba histolytica

CHOLERA

Etiology: * 80% norovirus (adult diarrhea) * Rotavirus (kid diarrhea <3 y/o); usually from day care centers * Fecal-oral transmission Symptoms: * Vomiting (projectile) * Diarrhea * + Flu-like illness - (fever, irritability, poor feeding, myalgia)

Viral Gastroenteritis

What type of Gastroenteritis are the following? TOXIGENIC DIARRHEA (Food Poisoning) ESCHERICHIA COLI (“Traveler’s Diarrhea”) SALMONELLA; TYPHOID LISTERIOSIS (LISTERIA) CHOLER

Bacterial Gastroenteritis

* Lack of fiber in diet * The passage of infrequent or hard stools with straining (<50 ml per day) Treatment: (in increasing order of potency) * Surface acting (soften and lubricate) * Docusate salts and mineral oils * Bulk forming * Bran, psyllium seeds * Osmotic agents * Lactulose, sorbitol, magnesium citrate, magnesium sulfate, magnesium hydroxide, sodium phosphate * Cathartics

Constipation

Protozoa and Helminths Transmission: * Fecal-oral - (ingestion of dormant cysts in contaminated food/water) Diagnosis: * Stool samples (looking for cysts) under microscopy

PARASITIC GUT INFECTIONS

is a microscopic parasite that infects the small intestine, leading to a diarrheal illness known as giardiasis Pathogenesis: * not toxigenic; rather, it covers the brush border > malabsorption Diagnosis: * cysts in stools Complications: * Chronic infection * Malabsorption * Malnutrition * Fatty stools Treatment * Metronidazole

GIARDIA

Transmission: * ingestion of oocysts (contaminated drinking water/public pools) * can survive chlorination Treatment: * nitazoxanide

CRYPTOSPORIDIUM

The Amoebic Dysentery Pathogenesis: * Intestinal Invasions > Ulcerations > Dysentery (Bloody Diarrhea) Diagnosis: * Cysts in Stools Management: * Metronidazole

ENTAMOEBA HISTOLYTICA

Clinically significant helminths are “soil transmitted” 1. Infection via swallowing infected eggs a) Ascaris lumbricoides (roundworm) b) Trichuris trichiura (whipworm) 2. Infection via Active skin penetration a) Strongyloides stercoralis (threadworm) b) Ancylostoma duodenale (hookworm) - Management: * Albendazole

HELMINTHIC INFECTIONS