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Pathophysiology > Module 7: Gastrointestinal System > Flashcards

Module 7: Gastrointestinal System Flashcards

1
Q

Liver inflammation

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

A

Hepatitis

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2
Q

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

A

HEPATITIS A VIRUS (Acute)

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3
Q

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)

A

HEPATITS E VIRUS (Acute)

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4
Q
  • 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
A

HEPATITIS B VIRUS (HBV) Acute and Chronic

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5
Q

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

A

HEPATITIS C VIRUS (HCV) Chronic

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6
Q

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

A

HEPATITIS D (HDV) Acute and Chronic

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7
Q

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

A

HEPATITIS E VIRUS (HEV) Acute

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8
Q

Name the 5 Drug induced liver disease / Drug induced hepatitis

Clue: ACE, CHL,INH,METH,AMI

A

Acetaminophen
Chlorpromazine
Isoniazid
Methotrexate
Amiodarone

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9
Q

Can cause same histology and clinical outcome as alcoholic hepatitis

A

Amiodarone

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10
Q

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

A

Methotrexate

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11
Q

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

Susceptibility to injury increases with age

A

INH (Isoniazid)

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12
Q

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

A

Chlorpromazine

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13
Q

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

A

Acetaminophen

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14
Q

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)

A

Cholesterol

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15
Q

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

A

Pigment stones

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16
Q

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

A

smooth green/black to brown

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17
Q

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

A

black pigment stones

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18
Q

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

A

Calcium bilirubinate stones

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19
Q

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

A

Cholelithiasis

20
Q

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

A

Cholecystitis

21
Q

Inflammation of the stomach lining

A

Gastritis

22
Q

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

A

Acute Gastritis

23
Q

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

A

Chronic Gastritis

24
Q

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

A

Atrophic Gastritis

25
Q

increased attack (Hyperacidity, Zollinger Ellison
Syndrome), or

decreased defense (H.Pylori, Stress, Drugs [NSAIDs & Corticosteroids], Smoking)

A

PEPTIC ULCER DISEASE

26
Q
  • 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

A

PEPTIC ULCER DISEASE

27
Q

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

A

ACUTE PANCREATITIS

28
Q

Inflammation of the Intestines

A

GASTROENTERITIS

29
Q

Etiology:
* Staph aureus (poor food handling)
* Bacillus cereus (fried rice at cereal) (mostly found in cereal)

Symptoms:
* Onset within 4hrs
* Vomiting, *stomach cramps, diarrhea

A

TOXIGENIC DIARRHEA (Food Poisoning)

30
Q

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

A

ESCHERICHIA COLI (“Traveler’s Diarrhea”)

31
Q

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

A

ETEC: (Enterotoxigenic E. coli)

32
Q

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

A

EIEC: (Enteroinvasive E. coli)

33
Q

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

A

EPEC: (Enteropathogenic E. coli)

34
Q

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

A

EHEC: (Entero-Hemorrhagic E. coli)

35
Q

Etiology:
* Salmonella typhi
* typhoid fever, improperly cooked meal

Management:
* Ceftriaxone +/- Ciprofloxacin

A

SALMONELLA; TYPHOID

36
Q

Risk to pregnant women & immunocompromised

Etiology:
* Listeria monocytogenes – (G-Pos)
* Soft cheeses & cold deli meats

A

LISTERIOSIS (LISTERIA)

37
Q

Etiology:
* Vibrio cholerae

Symptoms:
* profuse rice-water stools

Management:
* fluid replacement

Prognosis:
* self-limiting

NB: dysenteric organisms
* Salmonella, Shigella, Entamoeba histolytica

A

CHOLERA

38
Q

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)

A

Viral Gastroenteritis

39
Q

What type of Gastroenteritis are the following?

TOXIGENIC DIARRHEA (Food Poisoning)
ESCHERICHIA COLI (“Traveler’s Diarrhea”)
SALMONELLA; TYPHOID
LISTERIOSIS (LISTERIA)
CHOLER

A

Bacterial Gastroenteritis

40
Q
  • 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

A

Constipation

41
Q

Protozoa and Helminths

Transmission:
* Fecal-oral - (ingestion of dormant cysts in contaminated
food/water)

Diagnosis:
* Stool samples (looking for cysts) under microscopy

A

PARASITIC GUT INFECTIONS

42
Q

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

A

GIARDIA

43
Q

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

Treatment:
* nitazoxanide

A

CRYPTOSPORIDIUM

44
Q

The Amoebic Dysentery
Pathogenesis:
* Intestinal Invasions > Ulcerations > Dysentery (Bloody Diarrhea)

Diagnosis:
* Cysts in Stools

Management:
* Metronidazole

A

ENTAMOEBA HISTOLYTICA

45
Q

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

A

HELMINTHIC INFECTIONS

Pathophysiology (7 decks)

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