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Pathophysiology Exam 3 > Lecture 27 > Flashcards

Lecture 27 Flashcards

1
Q

Viral Hepatitis

A

Common infection of the liver -> results in hepatic cell destruction, necrosis, and autolysis -> edema and swelling of interstitium -> collapse of capillaries and decreased blood flow, tissue hypoxia and scarring and fibrosis

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2
Q

How do the five major forms of viral hepatitis differ?

A

Variation in signs, symptoms, and epidemiologic progression -> often clinically impossible to differentiate without serological tests

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3
Q

Hepatitis Type A

A

Infectious or short-incubation hepatitis; contaminated food and water via fecal-oral route

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4
Q

Hepatitis Type B

A

Serum or long-incubation hepatitis; transfusion and needles

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5
Q

Hepatitis Type C

A

Most transfusion cases (~20% of all hepatitis); risk of hepatocellular carcinoma

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6
Q

Hepatitis Type D

A

Delta; requires presence of Type B; blood products and personal contact

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7
Q

Hepatitis Type E

A

Most common in developing countries; contaminated water

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8
Q

What forms of prevention and treatment are recommended for viral hepatitis?

A
  • Vaccination against hepatitis A and B to provide immunity to these viruses before transmission
  • Rest to minimize energy demands
  • Avoiding alcohol to prevent further hepatic damage
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9
Q

What type of virus is hepatitis?

A

HBV: DNA Virus
Other four: RNA Virus

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10
Q

What is different about HAV and HEV?

A

Do not cause chronic hepatitis and cirrhosis does not develop

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11
Q

How is viral hepatitis transmitted?

A

HAV and HEV are enteral and the other three are parenteral

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12
Q

Non-viral Hepatitis

A

Inflammation of the liver that usually results from exposure to certain chemicals and drugs (ex: industrial chemicals, acetaminophen, paracetamol, Tylenol)

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13
Q

What is the leading cause of acute liver failure?

A

Acetaminophen

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14
Q

What is the result of non-viral hepatitis?

A

Hepatic cellular necrosis, scarring, Kupffer cell hyperplasia, and infiltration by mononuclear phagocytes occur with varying severity

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15
Q

What worsens the effects of non-viral hepatitis?

A

Alcohol, anoxia, and pre-existing liver disease

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16
Q

What are the direct effects of alcohol?

A

Increasing fluidity of biological membranes (disrupts cell function)

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17
Q

What are the indirect effects of alcohol?

A

In part a consequence of its metabolism

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18
Q

Alcoholic fatty liver (Alcoholic steatohepatitis)

A
  • Alcohol invariably produces fatty changes in a dose- dependent manner because of:
    1. Increased fatty acid synthesis (from glucose available after reaching ~100g threshold for storage as glycogen or from breakdown of stored glycogen)
    2. Decreased fatty acid oxidation (use of fat as energy source)
    3. Decreased export of fats in the form of lipoproteins
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19
Q

What are the mechanisms of hepatotoxic injury by ethanol?

A
  1. Disorganizes the lipid portion of cell membranes (leads to adaptive changes in their composition)
  2. Alters the capacity of liver cells to cope with environmental toxins
  3. Oxidation of ethanol produces acetaldehyde (toxic and reactive intermediate)
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20
Q

Compare and contrast the three enzymes used to convert alcohol to acetaldehyde.

A

All three work by stripping two H+ atoms from ethanol molecule but each handles the H+ differently

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21
Q

What is the result of excess H+ and acetaldehyde produced in the ADH pathway?

A

Damages mitochondria, disrupts microtubules, and alters proteins that can induce autoimmune responses -> hepatocyte injury

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22
Q

Explain the steps that occur in the ADH (alcohol dehydrogenase) pathway.

A
  1. Ethanol enters the cytosol <-> acetaldehyde (NAD+ -> NADH)
  2. Acetaldehyde ->Mitochondria
  3. Excess H+
  4. Mitochondria -> acetaldehyde dehydrogenase -> acetate -> circulation
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23
Q

Explain the process of the MEOS (microsome-ethanol oxidizing system) pathway.

A
  1. Detoxification: drugs, steroids, vitamins A and D, fatty acids, carcinogens
  2. Ethanol enters the smooth ER -> cytochrome P-450 (NADP ->NADPH)
  3. Release acetaldehyde and excess of oxygen radicals
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24
Q

What is the result of the MEOS pathway producing oxygen radicals and acetaldehyde?

A

Lipid peroxidation -> membrane damage

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25
Q

What is the result of up-regulating the MEOS pathway?

A

Affects detoxification activity of hepatocytes -> accumulation of potential toxicants

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26
Q

What is the result of alcohol metabolism?

A

Produces excess amounts of NADH -> Increased NADH -> induces fatty acid synthesis -> signals liver cells to compound it to glycerol -> triglycerides -> triglycerides accumulate -> fatty liver

Excess of NADH can also lead to hypoglycemia from lack of glucose synthesis

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27
Q

How does tumor necrosis factor alpha correlate with chronic liver disease?

A

Causes a slowdown and arrest of the flow of bile in bile ducts (cholestasis)

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28
Q

How does interleukin-6 correlate with chronic liver disease?

A

Interleukin-6 released by Kupffer cells stimulates the synthesis of acute-phase proteins by hepatocytes

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29
Q

How does Transforming growth factor beta correlate with chronic liver disease?

A

Secreted by Kupffer cells and hepatocytes; stimulates the synthesis of type I collagen by hepatic stellate cells (fibrosis compromises the portal venous blood flow)

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30
Q

Steatosis

A

Fat accumulation in hepatocytes; reversible if alcohol consumption stops

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31
Q

How does a viral infection, alcohol, or bacterial toxins cause injury to the liver?

A

Injures hepatocytes by a mechanism involving the production of proinflammatory cytokines (TNF-alpha, TGF-beta, IL-6) produced by Kupffer cells

32
Q

Compare the cells of the liver under normal conditions vs. cirrhosis.

A
  1. Normal: hepatic perisinusoidal cells store fat-soluble vitamin A in the cytoplasm and produce collagen fibers and extracellular matrix components deposited in the perisinusoidal space of Disse and around the central vein of the hepatic lobule
  2. Cirrhosis: progressive fibrosis; perisinusoidal cells transform into myofibroblasts and become the main collagen-producing cells of the cirrhotic liver
33
Q

Explain the effects of cirrhosis in the liver.

A
  • The lumen of the sinusoids constricts -> increases vascular resistance (to flow of portal venous blood in hepatic sinusoids) -> portal hypertension
  • Cytokines (hepatocytes, Kupffer cells, infiltrating lymphocytes in space of Disse) stimulate production of type I collagen by perisinusoidal cells
  • Deposit of type I collagen in the space of Disse -> fibrosis -> alters the flow of portal venous blood into the hepatic sinusoids
34
Q

Explain the pathophysiology of portal hypertension.

A
  1. Increased portal vascular resistance
  2. Increased portal pressure (portal hypertension)
  3. Reduced portal inflow to liver
  4. Development of collateral circulation (varices)
  5. Increased circulating vasodilators
  6. Reduced vasoconstrictor sensitivity (glucagon, adenosine)
  7. Peripheral vasodilation or splanchnic vasodilation
  8. Hyperdynamic circulation/ maintenance of portal hypertension
35
Q

What are the treatment options for ascites?

A
  1. Diuretic and sodium restriction therapy
  2. Removal of large volumes of peritoneal fluid (paracentesis)
  3. Patients with refractory ascites: shunting procedures that connect peritoneal space with venous system usually at jugular vein (ex: LeVeen shunt)

Drainage of fluid does not have any beneficial effect on primary condition

36
Q

Primary Sclerosing Cholangitis

A

Scarring of bile ducts caused by inflammation

37
Q

What causes Primary Sclerosing Cholangitis (PSC)?

A
  • Unknown
  • Immune system reaction to infection or toxin may trigger the disease (genetically predisposed)
38
Q

What other disease is associated with PSC?

A

Inflammatory bowel disease: ulcerative colitis and Crohn’s disease

39
Q

What are the treatment options for PSC?

A

Liver transplant

40
Q

What is the result of chronic inflammation of the bile ducts in the liver?

A
  • PSC
  • Tissue scarring (cirrhosis)
  • Narrowing and hardening of ducts
  • Result in liver cell death and loss of liver function
41
Q

What is the result of scarring of the bile ducts stopping or slowing the flow of bile out of the liver?

A

Frequent infections may occur in bile ducts (risk is increased following surgical procedure to expand badly scarred bile duct or remove a stone blocking a bile duct)

42
Q

What are the complications associated with Primary Sclerosing Cholangitis (PSC)?

A
  1. Portal hypertension
  2. Bile duct cancer (increased risk of cancer in the bile ducts of gallbladder)
  3. Colon cancer (PSC associated with IBD)
43
Q

How does alcohol impact the liver?

A
  1. Fatty liver
  2. Alcoholic hepatitis
  3. Scarring
44
Q

How do viral infections impact the liver?

A
  1. Liver cell necrosis
  2. Inflammation
  3. Fibrosis
45
Q

Cirrhosis

A

Chronic liver disease characterized by loss of normal structure and function (scarring of the liver due to attempted repair)

46
Q

What are the clinical features of cirrhosis?

A
  • Collateral veins
  • Ascites
  • Splenomegaly
  • Jaundice
  • Muscle wasting
  • Hepatic Renal Syndrome (Oliguria-Anuria, edema)
  • Hepatic Encephalopathy (ammonia/urea, failure of detoxification of putative NT, coma)
47
Q

Hepatorenal syndrome

A

Onset of renal failure in individuals with severe chronic liver disease in whom there are no intrinsic morphologic or functional causes for the renal failure (8% incidence)

48
Q

What is the prognosis of hepatorenal syndrome?

A

Poor:
1. Rapid-onset form: 2 weeks
2. Insidious-onset form: 6 months

20% of people with hepatic failure die of hepatorenal syndrome

49
Q

What are the treatment options for hepatorenal syndrome?

A
  • Resistant to treatment
  • Liver transplant
50
Q

Explain the impacts of the development of hepatorenal syndrome.

A
  1. Biliary cirrhosis or portal cirrhosis (increased portal pressure -> portal hypertension -> increased hydrostatic pressure in mesenteric capillaries)
  2. Peritoneal transudation: Ascites
  3. Decreased plasma circulating volume
  4. Angiotensin II and decreased renal perfusion
  5. Aldosterone
  6. Sodium retention
  7. Decreased water excretion
  8. Cirrhotic liver: decreased albumin production and decreased oncotic pressure in mesenteric capillaries
51
Q

Hepatic Encepthalopathy

A
  • Manifested by a spectrum of disturbances in consciousness, ranging from subtle behavioral abnormalities to marked confusion and stupor, to deep coma and death
  • Regarded as a disorder of neurotransmission in the CNS and neuromuscular system
  • Associated with elevated levels of false NTs and ammonia in the blood and CNS -> impair neuronal function and promote generalized brain edema
  • Increase in aromatic amino acids (ex: phenylalanine, tyrosine, tryptophan)
  • Increase in serum ammonia
52
Q

Explain the increase in aromatic amino acids seen with Hepatic Encephalopathy.

A
  • converted into false NTs (ex: y-aminobutyric acid)
  • Cirrhotic liver cannot detoxify putative NTs/neurotoxins
53
Q

Explain the increase in serum ammonia seen with Hepatic Encephalopathy.

A

Due to defective urea cycle that cannot metabolize ammonia

54
Q

How is ammonia seen in a normally functioning system?

A
  • Ammonia (NH3) derives from amino acid metabolism and urease-producing bacteria in the bowel
  • Diffusible and is reabsorbed into the portal vein for delivery to the urea cycle in the liver -> metabolized into urea and excreted by kidneys
55
Q

Ammonium (NH4+)

A

Not reabsorbed in the bowel and is excreted in the stool

56
Q

What factors correlate with encephalopathy?

A
  1. Increased protein: dietary or blood in GI tract (increases bacterial conversion of urea into ammonia)
  2. Alkalosis: keeps ammonia in NH3 state (diuretics produce metabolic alkalosis)
  3. Portosystemic shunts: consequent to portal cirrhosis (shunt ammonia away from the liver -> normally metabolizes ammonia in the urea cycle)
57
Q

Cholesterol Gallstone

A
  • Crystals ranging from 100% pure (rare) down to 50%
  • pale yellow, round to ovoid, and have finely granular, hard external surface
  • Arise exclusively in the gallbladder and are composed of cholesterol
58
Q

Cholelithiasis

A

Gallstones

59
Q

Black Pigment Gallstones

A
  • Oxidized polymers of the calcium salts of unconjugated bilirubin
  • Associated with hemolysis and cirrhosis
  • Found in sterile gallbladder bile
60
Q

Brown Pigment Gallstones

A
  • Pure calcium salts of unconjugated bilirubin
  • Associated with parasitosis and bacterial infections
  • Found in infected intrahepatic or extrahepatic ducts
61
Q

How does the gallbladder function during normal fasting conditions?

A

Sphincter of Oddi contracts and bile flows into gallbladder where it is concentrated and stored

62
Q

How does the gallbladder function during normal conditions after a meal?

A

Hormonally (ex: CCK) and neurally mediated contraction of the gallbladder releases concentrated bile into small intestines

63
Q

Explain how gallstones are formed.

A
  • Excessive cholesterol or bile pigments together with hypomotility of gallbladder leads to nucleation of crystals and hyper-secreted mucus traps the crystals and aggregates them into stones
  • Hypomotility of gallbladder further contributes to crystal growth
64
Q

Biliary Dyskinesia

A

Motility disorder that affects the gallbladder and sphincter of Oddi (specifically the gallbladder = gallbladder dyskinesia)

65
Q

What are the three phases of gallstone formation?

A
  1. Supersaturation
  2. Nucleation
  3. Stone Growth
66
Q

What factors contribute to the formation of gallstones?

A
  • Hypersecretion of biliary cholesterol
  • Crystallization promoting and inhibiting factors
  • Gallbladder hypomotility
  • Arachidonyl lecithin
  • Prostaglandins
  • Mucin and calcium
67
Q

What factors play a role in the formation of pigment stones?

A
  • Decreased secretion of biliary acids
  • Increased secretion of unconjugated bilirubin into the bile
  • Infection of the biliary tract
68
Q

Biliary Colic

A
  • Pain in the abdomen due to obstruction usually be stones in the cystic duct or common bile duct of the biliary tree
  • Typically occurs after eating a large, fatty meal that causes contraction of the gallbladder
69
Q

Acalculous Cholecystitis

A
  • Tends to occur following major surgery, trauma, or critical illness
  • Total parenteral nutrition is a cofactor
  • More serious implication than stone-associated cholecystitis
  • Gangrene and perforation of the wall and empyema develop more rapidly than in calculous cholecystitis
69
Q

Cholecystitis

A
  • May or may not be associated with cholelithiasis
  • Chronic or acute
  • Secondary infection of ulcer, gallstone, decubitus ulcer, carcinoma (adenocarcinoma), cholecystoenteric fistula, pancreatic obstruction
70
Q

Squamous Cell Carcinoma in Gallbladder

A
  • Mutations of tumor suppressor genes p53 and FHT, proto oncogenes KRAS, cell cycle control gene CDKN2A are common
  • Inflammation is leading cause
  • Overexpression of COX2 linked to invasiveness and may be exacerbated in chronic cholecystitis
71
Q

Hepatobiliary Cancers

A

Liver can give rise to tumors, but it is even more often involved by tumor metastases (primary tumors of GI tract, lungs, breasts)

72
Q

Malignant Hepatobiliary Carcinomas

A
  • Hepatocellular
  • Cholangiocellular (liver)
  • Gallbladder
  • Extrahepatic bile duct
73
Q

Malignant Hepatobiliary Sarcomas

A

Kupffer cells

74
Q

Benign Hepatobiliary Adenomas

A

Hepatocellular and biliary tract

Pathophysiology Exam 3 (10 decks)

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