Chapter 30 HEPA Flashcards

1
Q

Relate the mechanism of bile formation and elimination to the development of cholestasis and
jaundice

A

-The two basic distinctions are an obstructive type of cholestasis where there is a mechanical blockage in the duct system that can occur from a gallstone or malignancy,

Jaundice occurs by obstruction of outflow of bile causes from structural disorders, cholelithiasis, tumors

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2
Q

Characterize the function of the liver in terms of bilirubin elimination and describe the difference between unconjugated and conjugated hyperbilirubinemia.

A

-as the bilirubin passes through the liver, it converts into conjugated bilirubin.
Unconjugated bilirubin is free biliruin in the blood which is not water soluable

Conjugated hyperbilirubinemia is Diseases that reduce the rate of secretion of conjugated bilirubin into the bile or the flow of bile into the intestine produce a mixed or predominantly conjugated hyperbilirubinemia due to the reflux of conjugates back into the plasma. Elevated conjugated bilirubin levels usually indicate hepatobiliary diseas

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3
Q

List diagnostic tests used to assess liver function and relate them to impaired liver function.

A

-serum levels enzymes are o assess injury to liver cells

ALT: liver specific
AST: not liver specific

Serum protein levels
prothrombin time
Coagulation factors

GGT: measures hepatic excretory functions. Alcohol abuse

Ultrasound - detecting stones
Computerized Tomography -
MIR
BIOPSY

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4
Q

describe hepatitis A, source of infection, incubation period, acute disease manifestations, development of chronic disease, and the carrier state.

A
  • usually benign and self limiting
  • survives in sea, waste water
  • fecal-oral transmission
  • incubation 25-30 days
  • virus excreted in stool 2-3 weeks prior to symptoms

MANIFESTATION
-asymptomatic if !
Vaccine available

>6 years old
Abrupt
Fever, malaise
Nausea, anorexia, abdominal discomfort
Dark urine
Jaundice (not everyone)
Does not cause chronic hepatitis or produce carriers, but can progress to "acute fulmunant"!
Vaccine available
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5
Q

describe hepatitis B, source of infection, incubation period, acute disease manifestations, development of chronic disease, and the carrier state.

A
Transmission
-Infected blood transfusion, perinatal
Oral/sexual contact
Can result in acute, chronic or fulminant
Can produce carrier state
  • long incubation
  • can develop into chronic disease and carrier state
MANIFESTATION
-Jaundice 
Unusually light-colored stool
Fever
Malaise
Gastrointestinal symptoms such as loss of appetite, nausea, and vomiting
Abdominal pain
Frequently there will be no symptoms, and it is only discovered in a blood test
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6
Q

describe hepatitis C, source of infection, incubation period, acute disease manifestations, development of chronic disease, and the carrier state.

A

TRANSMISSION

  • blood transfusion
  • IV
  • SEXUAL INTERCOURSE
  • TATTOO, PIERCING

INCUBATION is 2 to 26 weeks, AV 6 to 12 weeks

MANIFESTATION
-asymptomatic or mild non specific

MOST WILL DEVELOP CHRONIC HEPATITIS
and is a carrier

Chronic Hepatitis
> 6 months
Usually HCV
Fatigue, anorexia, jaundice, elevated serum aminotransferase
Complications: cirrhosis, cancer
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7
Q

pathogenesis and manifestations of acute fulminant hepatitis.

A

PATHO
-Progression from acute hepatitis to encephalopathy in 2-3 weeks with no evidence of chronic liver disease

MANIFESTATION
-GI symptoms
Systemic inflammation
Hemorrhage
Jaundice
Elevated blood ammonia levels
CNS symptoms/Hepatic Encephalopathy
Cerebral edema
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8
Q

Describe the significance and manifestations of hepatic encephalopathy.

A

-Encephalopathy is Accumulation of neurotoxins as liver unable to remove toxins –ammonia!
Usually converted to urea in liver

MANIFESTATION
-Signs of liver failure (slow or rapid)
Asterisis or "flapping tremor"
Personality changes
Speech difficulties
Decreased mental alertness and ability
Coma, convulsions
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9
Q

what is drug-induced liver disease

A
  • unintentional tylenol OD

- age and dose dependant

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10
Q

What is alcohol-induced liver disease and summarize the three patterns of injury

A

genetic and environmental factors
alcohol induced liver disease

1st: Fatty liver disease
Steatosis (liver is yellow), hepatomegaly
Reversible*

2nd: Alcoholic hepatitis
Inflammation & necrosis of liver cells
Rapid onset jaundice/fever/pain/anorexia/ ascites/nausea…. encephalopathy

3rd: Alcoholic cirrhosis
Hepatocyte injury
Nodules compress blood flow

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11
Q

What is nonalcoholic fatty liver disease

A

Fatty liver disease NOT from alcohol
Simple steatosis to inflammation/necrosis (steatohepatitis)

Associated with:
Obesity
DM type 1, hyperlipidemia, insulin resistance
Rapid weight loss
Total parenteral nutrition (TPN)
Manifestations
Usually asymptomatic
RUQ abdominal discomfort
Elevated AST, ALT, INR
Decreased albumin
Normally synthesized in the liver

Potential to result in cirrhosis and end-stage liver disease

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12
Q

Characterize the liver changes that occur with cirrhosis and discuss the manifestations and possible complications

A

-characterized by diffuse fibrosis and nodules with hepatocytes results in scarring and constriction

Causes
Alcohol, viral hepatitis, non-alcoholic liver disease, biliary disease

MANIFESTATION
-Manifestations
Asymptomatic until well-progressed
Weight loss (camouflaged by ascites)
Weakness, anorexia
Diarrhea (usually) or constipation
Hepatomegaly
Jaundice
Pain (epigastric/upper RQ, dull, ache)
Complication
-Portal hypertension
Splenomegaly
Thrombocytopenia
Insulin resistance
Hemorrhoids
Caput medusa
Bleeding
Testosterone/estrogen imbalances
Gynecomastia, testicular atrophy
Spider angiomas/palmar erythema
Encephalopathy
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13
Q

Describe the physiologic basis for portal hypertension and relate it to the development of ascites, esophageal varices, and splenomegly

A

-increased pressure in the portal vein

CAUSES
-Pre-hepatic
Obstructive thrombosis
Portal vein narrowing
Splenomegaly

-Intra-hepatic
Cirrhosis

-Post-hepatic
Right-sided heart failure
Hepatic vein outflow obstruction
Venous thrombosis

ASCITES
-Late stage
Serous fluid
500+ ml
Causes
Portal hypertension
Sodium/water retention by kidneys
Impaired albumin synthesis by liver
Can progress to peritonitis

Splenomegaly/Hypersplenism
Decreases life-span of blood cells
Results in anemia, thrombocytopenia, leukopenia

Increased venous pressure to abdomen, rectum, esophagus
Esophageal Varices
Caput Medusa
Hemorrhoids

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14
Q

Relate the functions of the liver to the manifestations of liver failure.

A

80-90% loss of total liver function
Progressive (d/t alcohol) or rapid (fulminant hepatitis)

MANIFESTATION
GI
Fetor hepaticus: musty, sweet breath

Hematological
Anemia, thrombocytopenia, coagulation defects, leukopenia

Integument
Purpura, bruising, vascular spiders, telangiectasis, spider angiomas, spider nevi, palmar erythema, clubbing, jaundice

Endocrine
Increased androgens/estrogens
Decreased aldosterone

Hepatorenal syndrome
Progressive azotemia, oli (high level of urea, creatinine), guria

Hepatic Encephalopathy

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15
Q

Describe the etiologies and manifestations of hepatocellular cancer

A
CAUSE
-involves liver cells
-Chronic viral hepatitis
Chronic alcoholism
Non-alcoholic fatty liver disease
Environmental exposure (arsenic, food mold by-products)

MANIFESTATION
-Weakness, anorexia, weight loss, fatigue, bloating
Dull abdominal ache
Ascites, jaundice, hepatomegaly

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16
Q

Describe the etiologies and manifestations of cholangiocarcinoma

A

-cancer of the liver bile duct

CAUSE
-Long-standing inflammation
Injury to bile duct epithelium

MANIFESTATION
-Pain, weight loss, anorexia,
Abdominal swelling/mass
Possible jaundice

17
Q

Describe the etiology, risk factors, and manifestations of gallstones

A
CAUSE
-abnormal composition of bile
(starvation, rapid weight loss, pregnancy) - creation of cholesterol crystals
-stasis of bile
-inflammation of gallbladder
-malabsorption disorders

MANIFESTATION
-Asymptomatic unless obstruction occurs
Biliary colic – d/t gallstone lodged in cystic or common bile duct or travelling through ducts resulting in spasm
Abrupt onset, persistent, upper RQ/epigastric pain, referred to back/right shoulder/midscapula
Bilirubinemia
Nausea!

18
Q

Describe acute cholecystitis

A

-inflammation of gallbladder

Acute calculous cholecystitis (85%)
Impacted stoned in cystic duct
Lipases released, bile salts damage epithelium

Acalculous cholecystitis (15%)
d/t ischemia, edema, bile stasis, obstruction
Can progress to gangrene and perforation
Sepsis, trauma, infection, burns, DM, MSOF (multisystem organ failure)

Manifestations
Acute onset, persistent upper RQ/epigastric pain
Mild fever, anorexia, nausea, vomiting
Relief if “calculous”

19
Q

Describe chronic cholecystitis

A

-repeated episodes of acute cholecystitis or irritation of the gallbladder by stones

MANIFESTATION

  • intolerance to fatty food
  • belching
  • discomfort
  • colicky pain
20
Q

Characterize the effects of choledocholithiasis and cholangitis on the bile flow and the potential for hepatic and pancreatic complications

A

Choledocholithiasis is stones int he common duct

Cholangitis is inflammation of the common duct

COMPLICATION
-acute suppuratve cholangitis accompanied by pus

21
Q

Discuss the significance of pancreatic enzymes in the development of pancreatitis

A

-involves autodigestion of pancreatic tissue by inappropriately activated pancreatic enzymes

22
Q

Cite the possible causes and describe the manifestations of acute pancreatitis

A

-Reversible inflammation d/t premature activation of pancreatic enzymes resulting in autodigestion
Activation of trypsin, which activates others!
Tends to occur after age 40

CAUSES
-Gallstones
Alcohol abuse
Less-so; hyperlipidemia, hpercalcemia, viral infections, trauma, medications (thiazide diuretics)

MANIFESTATION
GI
Sudden onset upper LQ/epigastric/periumbilical pain, radiating to back/chest/flank
Abdominal distension/tenderness
Elevated amylase, lipase, bilirubin

CNS
Fever, thirst, agitation, confusion

CVS
Tachycardia, hypotension, massive fluid loss

Respiratory
Tachypnea, dyspnea

Renal
oliguria

COMPLICATION
-Sepsis
ARDS
Acute tubular necrosis
MSOF
23
Q

Describe the manifestations of chronic pancreatitis

A

Progressive/permanent destruction of exocrine pancreas, not reversible
Causes same as acute pancreatitis
-LONG TERM ALCOHOL ABUSE

Manifestations
Similar to acute but less severe, repeated

24
Q

Discuss the risk factors, manifestations, and possible complications of pancreatic cancer

A

RISK FACTOR
-Age, smoking, DM, chronic pancreatitis, genetics

MANIFESTATION
-Dull epigastric pain, radiating to back
Worse in supine position, relief by sitting forward
Worse when eating
-jaundice, weight loss

COMPLICATION

THROMBOPHLEBITIS