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PAT202 WINTER > w10 liver > Flashcards

w10 liver Flashcards

1
Q

what is portal hypertension?

A
  • abnormally high blood pressure in the portal venous system caused by resistance to portal blood flow
  • caused by disorders that obstruct or impeded blood flow through any component of the hepatic portal system
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2
Q

what are causes of portal hypertension

A

-Vascular remodeling with intrahepatic shunts, thrombosis, inflammation, fibrosis (liver cirrhosis, hepatitis)

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3
Q

what happens if long-term portal hypertension persists?

A

varices, splenomegaly, hepatopulmonary syndrome, ascites, and hepatic encephalopathy

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4
Q

what is the normal liver under pressure?

A

12mmhG

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5
Q

problems r/t portal HTN-Varices: Distended, tortuous, collateral veins

A

Prolonged elevation of pressure in the hepatic portal vein causes collateral veins to open between the portal vein and systemic veins and their transformation into varices

  • they are called caput medusae, hemorrhoidal varices
  • rupture of varices can cause life-threatening hemorrhage
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6
Q

problems r/t portal HTN-splenomegaly

A
  • Portal hypertension contributes to congestive splenomegaly caused by increased pressure in the splenic vein
  • Thrombocytopenia from platelet sequestration is the most common symptom of congestive splenomegaly –> increased bleeding tendency
  • also predictive of severity of esophageal varices
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7
Q

portal HTN and–> Hepatopulmonary syndrome (HPS)

A

-Respiratory complications of advanced liver disease and portal hypertension
HPS: Pulmonary vasodilation, increase pulmonary venous congestion, R-to-L shunting leading to hypoxemia
there is NO treatment for this

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8
Q

portal HTN and portopulmonary hypertension (PPH)

A

-Associated with vascular remodeling and pulmonary artery vasoconstriction. No specific clinical manifestations but may see dyspnea, cyanosis, digital clubbing
treatment–> target the pulmonary arterial vasculature to decrease pulmonary HTN W/ various medication options, and liver transplant

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9
Q

what is ascites?

A

accumulation of fluid in the peritoneal cavity

-traps body fluid in the peritoneal cavity -which decreases fluid available for normal physiologic functions

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10
Q

what causes ascites?

A

Cirrhosis, right heart failure, abdominal malignancies, nephrotic syndrome, and malnutrition

other contributing factors–> : Portal hypertension, decrease in albumin synthesis by liver, splanchnic arterial vasodilation, renal sodium and water retention

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11
Q

what is the overflow theory of ascites?

A

Capillary hydrostatic pressure–> capillary osmotic pressure =water to peritoneal cavity

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12
Q

what is the underfill theory of ascites?

A

increase in hepatic sinusoidal hydrostatic pressure and decrease in plasma oncotic pressure w/ weeping of lymph fluid from the surface of the liver and decreases plasma volume activity which activates ADH and RAAS volume overload

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13
Q

what is the forward theory r/t ascites?

A

Both. Circulating nitric oxide and carbon monoxide –> splanchnic vasodilation. decreases systemic vascular resistance overcomes compensatory cardiac output. Stimulation of baroreceptors activates renal sodium retention. Combined portal hypertension and splanchnic vasodilation –> fluid transudation and lymph formation –> ascites

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14
Q

clinical manifestations of ascites?

A
  • Abdominal distention, increased abdominal girth, weight gain
  • dyspnea
  • increased RR, –> should assume a semi-flower’s position
  • peripheral edema
  • Dilutional hyponatremia
  • Bacterial peritonitis –> fever, chills, abdominal pain, decreased bowel sounds, cloudy ascitic fluid
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15
Q

what is our treatment for ascites?

A
  • dietary salt salt restriction and potassium-sparing diuretics, vasopressin receptor-2 antagonists are effective for dilutional hyponatremia
  • Albumin may be given
  • Monitor for hyponatremia and hypokalemia
  • Paracentesis (but need to consider other risks)
  • Treat bacterial peritonitis
  • Peritoneovenous shunt and transjugular intrahepatic portosystemic shunt (TIPS) maybe offered
  • Liver transplant
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16
Q

what is hepatic encephalopathy?

A
  • Complex neurologic syndrome characterized by impaired behavioral, cognitive, and motor function
  • May develop rapidly during acute fulminant hepatitis (type A); after portosystemic bypass or shunting (type B); or slowly during the course of cirrhosis, chronic liver disease, or portosystemic bypass (type C)
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17
Q

what are risk factors of hepatic encephalopathy?

A

-advanced liver disease, gastrointestinal bleeding, increased dietary protein, electrolyte imbalance, and hypoxia

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18
Q

what is the pathophysiology of hepatic encephalopathy?

A
  • Results from a combination of biochemical alterations that affect neurotransmission
  • Liver dysfunction and collateral vessels that shunt blood around the liver to the systemic circulation permit neurotoxins and other harmful substances absorbed from the gastrointestinal tract to accumulate and circulate freely to the brain
  • Ammonia cannot be converted to urea by the diseased liver –> Reaches the brain –> Metabolized to glutamine, with osmotic disturbances and alterations in cerebral blood flow that interfere with neurotransmitters and cause astrocyte edema (cytotoxic edema) and oxidation
  • increase BBB permeability (vasogenic edema)–> astrocytes swelling, brain edema, and intracranial hypertension
  • excessive amount of gamma-miobutryic acid (GABA) and a decrease LOC
  • Infection, hemorrhage, inflammation, electrolyte imbalance, sedatives, and analgesics also can precipitate stupor and coma in the presence of liver disease
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19
Q

manifestations, evaluation and treatment of hepatic encephalopathy

A
  • Initial: Subtle changes in personality, memory loss, irritability, lethargy, and sleep disturbances
  • In acute liver failure, symptom onset can be rapid: Confusion, disorientation to time and space, asterixis, slow speech, bradykinesia, stupor, convulsions, and coma
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20
Q

how do we diagnosis hepatic encephalopathy?

A

History of liver disease, clinical manifestations and psychometric testing; EEG, blood chemistry, liver function tests

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21
Q

how do we treat hepatic encephalopathy?

A

-Correction of fluid and electrolyte imbalances; manage cerebral edema with hypertonic saline, mannitol or hypothermia; dietary proteins; prevent ammonia absorption in the colon; reduce gut ammonia

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22
Q

what is jaundice? “icterus”

A

Yellow or greenish pigmentation of the skin caused by hyperbilirubinemia (total plasma bilirubin concentrations >2.5–3 mg/dL)

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23
Q

what causes jaundice?

A

-Extrahepatic obstruction to bile flow (gallstones)
-Intrahepatic obstruction (hepatocellular disease such as cirrhosis or hepatitis)
-Prehepatic obstruction: Excessive production of bilirubin (excessive hemolysis of red blood cells)
normal in newborns ONLY

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24
Q

what are the clinical manifestations of jaundice?

A
  • Dark urine
  • Clay-colored stools
  • Yellow discoloration possibly occurring first in the sclera of the eye and then progressing to the skin
  • Skin xanthomas (cholesterol deposits) and pruritus
  • Anorexia, malaise, fatigue
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25
Q

what is the treatment of jaundice?

A

-Correct the cause: Jaundice is only a sign of an underlying disorder.

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26
Q

what is Hepatorenal syndrome (HRS)

A

Renal failure results from arterial vasodilation of the splanchnic vasculature, decreasing effective blood volume and renal vasoconstriction
-decrease in blood volume and decrease in BP–> causes renal perfusion and a decrease in GFR and oliguria (type 1)
intrarenal vasoconstriction as a key characteristic

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27
Q

what is the diagnosis of Hepatorenal syndrome (HRS)

A

: Exclude other causes; Blood work (potassium, creatinine), urine osmolality and specific gravity; investigate secondary problems

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28
Q

treatment of Hepatorenal syndrome (HRS)

A

-Systemic vasoconstrictors (α-adrenergic agonists and octreotide) and albumin, TIPS (as a bridge to liver transplant), liver and kidney transplantation

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29
Q

what is viral hepatitis

A

it is a common systemic disease affecting primary the liver

-various viral strains produce various forms of hepatitis

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30
Q

what are the characteristics of viral hepatitis?

A
  • Size of virus
  • Incubation phase
  • Route of transmission
  • Onset
  • Carrier state
  • Severity
  • Chronic hepatitis
  • Age-group affected
  • Prophylaxis
31
Q

what is hepatitis A?

A

can be feral-oral, parenteral, or sexual route but usually transmitted by fecal-oral route
-can be found in feces, bile, and sera of infected individuals

32
Q

what are risk factors of hepatitis A?

A
  • Crowded, unsanitary conditions

- Food and water contamination

33
Q

how do we prevent hepatitis A?

A
  • Handwashing and use of gloves
  • Administration of immunoglobulin before exposure or early in the incubation period
  • Administration of vaccines
34
Q

what is hepatitis B?

A
  • usually transmitted parenterally and sexually transmitted

- maternal-infant transmission occurs if the mother is infected during the third trimester

35
Q

what are the risk factors of hepatitis b?

A
  • Immunosuppressed people or on immunosuppressive drugs
  • Hemodialysis, multiple blood transfusions
  • Multiple sex partners
  • Share needles, syringes or other drug equipment
36
Q

what are the preventions for hepatitis b?

A
  • Hepatitis B vaccine prevents the transmission and development of hepatitis B
  • Hepatitis B immunoglobulin provides post-exposure prophylaxis against hepatitis B
37
Q

what is hepatitis C?

A

-usually transmitted parenterally
-is responsible for most cases of posttransfusion hepatitis
-is also implicated in infections r/t to IV drugs use and human immunodeficiency viral (HIV) infection
coinfection w/ hepatitis B is common
-approx 80% of those w/ hepatitis c develops chronic liver disease

38
Q

what are risk factors of hepatitis c?

A

HBV infection

39
Q

what are the prevention for hepatitis C?

A

no vaccines is available

-administer antiviral medications

40
Q

what is the pathophysiology of hepatitis?

A

-Hepatic cell necrosis, scarring, Kupffer cell hyperplasia, and infiltration by mononuclear phagocytes occur
Inflammatory processes can damage and obstruct bile canaliculi –> cholestasis and obstructive jaundice
Cell-mediated immune mechanisms (e.g., cytotoxic T cells, T regulatory cells, and natural killer cells)
-damage is most severe in Hep B and Hep C
-viruses cause liver cell apoptosis
-Hep associated w/ acute liver failure

41
Q

what are the clinical manifestations of hepatitis?

A

The clinical signs of viral hepatitis are similar, including nausea, malaise, stomach pain, and jaundice
-The symptoms range from no symptoms to fulminating hepatitis, with rapid onset of liver failure and coma
-Acute viral hepatitis causes abnormal liver function test results
increase serum aminotransferase values, increase aspartate transaminase (AST) and increase alanine transaminase (ALT)
-Elevation may not be consistent with extent of cellular damage

42
Q

incubation phase of hepatitis?

A
  • Virus replicating and manifestations vary depending on the virus
  • Many be no symptoms but there can be serologic and serum enzyme markers
43
Q

Prodromal (preicteric) - begins about 2 weeks after exposure

-of hepatitis

A
  • Ends with appearance of jaundice
  • Fatigue, anorexia, malaise, nausea, vomiting, headache, hyperalgia, cough, low-grade fever
  • RUQ abdominal pain common and weight loss 2-4 kg
  • Infection highly transmissible during this phase
44
Q 
Icteric phase (jaundice) - begins 1-2 weeks after prodromal phase 
w/ hepatits
A
  • Hepatocellular destruction and intrahepatic bile stasis causes Jaundice (icterus)
  • Urine may be dark and stools clay coloured from conjugated hyperbilirubinemia
  • Liver enlarged, smooth and tender
  • Mild and transient itching
  • Serum bilirubin levels range from 5 to 10 mg/dL, with conjugated bilirubin fraction increasing
45
Q

recovery phase of hepatitis

A

begins with resolution of jaundice about 6-8 weeks after exposure

  • Liver may be still enlarged and tender but symptoms diminish
  • Chronic active hepatitis may begin at this phase (associated with HBV, HCV, and HDV infection)
46
Q

evaluation and treatment of hepatitis

A
  • Physical activity may be restricted
  • A low-fat, high-carbohydrate diet is beneficial if bile flow is obstructed
  • No direct contact with blood or body fluids of individuals with Hep B or Hep C
  • A combined vaccine for HAC and HBV available
  • Hepatitis B immunoglobulin provides passive prophylactic immunity against HBV
47
Q

what is the is first-line therapy for treatment-naïve HBV patients?

A
  • TAF (tenofovir alafenamide), TDF (tenofovir disoproxil fumarate), or ETV (entecavir)
  • due to its potency and low rates of antiviral resistance
48
Q

what are the clinical guidelines of hepatitis b?

A
  • Objective of treatment is to prevent the development of cirrhosis and its consequences
  • Antiviral treatment is determined based on 2 main factors: HBV DNA and ALT levels
  • Patients with significant inflammation or fibrosis should be considered for treatment
  • All patients with cirrhosis and detectable HBV DNA should be treated
49
Q

what are the clinical guidelines for hepatitis C?

A
  • Objective of treatment is a sustained virologic response which is an absence of viremia 12 weeks after completion of antiviral therapy
  • Certain patient subgroups, particularly those with severe liver fibrosis or cirrhosis, should get therapy as soon as possible
  • Suggested workup prior to beginning HCV therapy: CBC, liver enzymes and function, creatinine, serology to exclude other infections and liver diseases, live disease staging, HCV RNA
50
Q

what is cirrhosis?

A
  • Is an irreversible inflammatory fibrotic disease that disrupts liver function and even liver structure
  • Most common causes are alcohol abuse and HCV
  • Cirrhosis develops slowly over a period of years
  • Its severity and rate of progression depend on the cause
51
Q

what are the complications of cirrhosis?

A

-Jaundice, portal hypertension, ascites, hepatic encephalopathy, varices with gastrointestinal bleeding, hepatorenal syndrome, hepatopulmonary syndrome, and portopulmonary syndrome

52
Q

cirrhosis cont

A

Structural changes result from:
-Injury (alcoholism, viruses, steatosis, chemicals)
Fibrosis
–Kupffer cell activation with release of inflammatory mediators, ROS, growth factors, and activation of fibrogenic hepatic stellate cells
–Biliary channels and blood flow become obstructed → cause jaundice and portal hypertension
–Because of the hypertension, blood is shunted away from the liver, and hypoxic necrosis develops

53
Q

what are the causes of cirrhosis?

A
  • Hepatitis virus—B and C (common)
  • Excessive alcohol intake (common)
  • Idiopathic (common)
  • Nonalcoholic fatty liver disease (NAFLD), also known as nonalcoholic steatohepatitis (NASH)
  • Autoimmune disorders
  • Hereditary metabolic disorder
  • Prolonged exposure to chemicals (e.g., carbon tetrachloride, cleaning and industrial solvents, copper salts)
  • Hepatic venous outflow obstruction
54
Q

what is acute (fulminant) live failure?

A

From severe impairment or necrosis of liver cells without preexisting liver disease or cirrhosis. Causes: Acetaminophen overdose, concurrent liver disease (acute on chronic liver failure), complications of viral hepatitis

55
Q

what is the patho of acute (fulminant) liver failure?

A

Edematous hepatocytes and patchy areas of necrosis and inflammatory cell infiltrates disrupt the parenchyma. The death of hepatocytes may be caused by viral or toxic injury or immunologic and inflammatory damage with necrosis or apoptosis

56
Q

what are the manifestations of acute (fulminant) liver failure

A

-Anorexia, vomiting, abdominal pain, progressive jaundice (initial signs), ascites and gastrointestinal bleeding; Coma, renal failure

57
Q

how do we diagnosis acute (fulminant) liver failure?

A

LFTs (liver function tests) (bilirubin, transaminases, ammonia), PT/INR

58
Q

what are the treatments of acute (fulminant) liver failure

A

Critical care, addressing the cause, artificial liver support, liver transplantation

59
Q

what is alcoholic liver disease?

A
  • Abuse of any alcoholic beverage can result in alcoholic liver disease
  • The severity of the illness is proportional to the amount and length of alcohol drank, and formation of acetaldehyde
  • The spectrum of alcoholic liver disease includes steatosis, alcoholic hepatitis, and alcoholic cirrhosis (fibrosis)
  • Oxidation of alcohol, causing damage to hepatocytes
  • malnutrition can can be a risk factor for cirrhosis -many alcohols are malnourished
60
Q

what is the patho behind alcoholic fatty liver (steatosis)

A

May be asymptomatic
Mildest form and reversible if drinking stopped
It can be caused by chronic ingestion of relatively small amounts of alcohol
-women more than 1 alcohol drink/day (14kg)
-men 2 alcoholic drinks/day (28kg)
-increase lipogenesis and decrease fat acid oxidation and decrease in fat metabolism by hepatocytes are primary causes of fat accumulation (triglyceride deposition) inside the liver
-fat accumulation may be aided by lipids mobilized from adipose tissue or dietary fat consumption

61
Q

what is Alcoholic hepatitis (steatohepatitis)

A

characterized by:

  • inflammation
  • Degeneration and necrosis of hepatocytes
  • Infiltration of neutrophils, macrophages, and lymphocytes
  • Immunologic alterations
  • Oxidative stress leading to lipid peroxidation
62
Q

what is the mechanism of Alcoholic hepatitis (steatohepatitis)

A

-Mechanism of hepatocyte injury not clearly understood
-Inflammatory mediators, acetaldehyde, reactive oxygen and nitrogen species and genetic factors involved
-Alcohol increases gut permeability contributing to inflammation, oxidative stress and severity of alcoholic liver disease
Inflammation and necrosis stimulate fibrosis

63
Q

what causes alcoholic cirrhosis?

A

Caused by:

  • The toxic effects of alcohol metabolism on the liver
  • Immunologic alterations
  • Oxidative stress from lipid peroxidation
  • Malnutrition
  • Alcohol is transformed to acetaldehyde
  • Acetaldehyde
64
Q

alcoholic cirrhosis

A
  • Alters metabolism of vitamins and minerals
  • Disrupt cytoskeletal and membrane function
  • Altered enzyme and protein synthesis
  • Diminished hormone and ammonia degradation
  • Stimulate formation of autoantibodies specific to hepatic cells
  • Increased gut permeability
  • Cellular damage stimulates inflammatory response
65
Q

alcoholic cirrhosis cont

A

-Inflammation and necrosis result in excessive collagen formation
-Fibrosis
-Transforming growth factor-beta (TGF-β) contributes to fibrosis and is produced in part by activated Kupffer cells
TGF- β activates hepatic stellate cells and transforms them to myofibroblasts –> produce excess collagen
-Fibrosis and scarring alter the liver structure and obstruct biliary and vascular channels
-Hepatocytes lose regenerative ability

66
Q

clinical manifestations -Steatosis

A
  • causes no specific symptoms or abnormal liver function test results
  • The clinical features of alcoholic cirrhosis depend on the duration of the disease and the severity of liver damage
  • Can be mild or severe
  • Non-specific symptoms
  • Fatigue, weight loss, and anorexia
  • Manifestations of acute illness
  • Nausea, anorexia, fever, abdominal pain, and jaundice
67
Q

alcoholic cirrhosis clinical manifestations

A
  • Multiple-system disease
  • Causes hepatomegaly, splenomegaly, ascites, gastrointestinal hemorrhage, portal hypertension, hepatic encephalopathy, and esophageal varices
  • Anemia
  • Risk of infection greater
68
Q

evaluation of alcoholic cirrhosis

A
  • Diagnosis based on individual history and manifestations
  • Results of liver function abnormal
  • Serologic studies
  • increase liver enzymes: ALT, AST, γ-glutamyltransferase
  • increase bilirubin
  • decrease serum albumin levels
  • Malnutrition often present
69
Q

treatment of cirrhosis

A
  • Cessation of alcohol
  • Rest, a nutritious diet
  • Corticosteroids, antioxidants, drugs that slow fibrosis
  • Management of complications: Ascites, gastrointestinal bleeding, infection, and encephalopathy
70
Q

what is Nonalcoholic fatty Liver disease and nonalcoholic steatohepatitis

A

Is the infiltration of hepatocytes with fat, primarily triglycerides; occurs in absence of alcohol intake

71
Q

what are the risk factors of Nonalcoholic fatty Liver disease and nonalcoholic steatohepatitis

A
  • Polygenic susceptibility, obesity (including obese children), high levels of cholesterol and triglycerides, metabolic syndrome, type 2 diabetes mellitus, and alterations in the gut microbiome
  • Usually asymptomatic and may remain undetected for years
72
Q

Nonalcoholic fatty Liver disease and nonalcoholic steatohepatitis

A

treatment

73
Q
A
  • Lifestyle modification with diet and exercise

- Pharmacotherapy with insulin sensitizers, vitamin E (antioxidant), and lipid-lowering drugs may be considered.

74
Q

pharmacotherapy of hepatitis

A

-The best treatment for viral hepatitis is prevention through immunization (HAV and HBV available)
-HAV vaccine
-Communities and countries with high infection rates
-The immunoglobulins induce passive protection and provide prophylaxis for about 3 months
-HBV vaccine
-Recommended for all children
-Post-exposure treatment: hep-B immunoglobulins and antiviral agents such as interferon alfa-2a, lamivudine, or adefovir
HCV drug therapy
-Rebetron (interferon alfa-2b and ribavirin) → after 24 weeks, 30-50% will respond with ↑liver function
–>If response not attained, can be continued as long as 12-18 months
-Peginterferon alfa-21 and peginterferon alfa-2b recently approved
–>Attaches polyethylene glycol to interferon to extend activity

PAT202 WINTER (16 decks)

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