patho- hepatic and biliary system

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Last updated 11:54 PM on 9/30/22
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cholelithiasis
pigment stones and cholesterol stones in bladder
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pigment stones
unconjugated pigments in bile precipitate to form stones
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pigment stones must be __________ _______
surgically removed (cant be dissolved)
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cholesterol stones
normal constituent of bile
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cholesterol stones are _________ in water
insoluble
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cholelithiasis patho
-dec bile acid synthesis
-inc cholesterol synthesis in liver
-bile supersaturated with cholesterol
-precipitate out of bile to form stones
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cholelithiasis clinical manifestations
-no pain and mild symptoms
-epigastric distress (fullness)
-abdominal distress
-vague RUQ pain
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cholelithiasis: epigastric distress may follow a
meal rich in fried/fatty food
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cholelithiasis stool characteristics
gray/clay-colored
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cholelithiasis risk factors
-cystic fibrosis
-diabetes
-changes in weight
-illeal resection/disease
-estrogen
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cholecystitis
inflammation of gallbladder (acute/chronic)
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cholecystitis clinical manifestations
-pain
-tenderness
-rigidity of RUQ (can radiate to right shoulder)
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cholecystitis patho
-gallstones = obstructs bile outflow
-blood vessels become compressed
-vascular supply compromised
-gangrene with risk of perforation
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liver function tests
-serum aminotransferase
-alanine aminotransferase (ALT)
-aspartate aminotransferase (AST)
-gamma-glutamyl transferase (GGT)
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serum aminotransferase
indicators of injury to liver cells
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serum aminotransferase detects _______
hepatitis
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alanine aminotransferase (ALT)
-levels inc in liver disorders and alcohol
-monitors course of hepatitis, cirrhosis, effects of treatments may be toxic to liver
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ALT is very _______ _______
liver specific
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aspartate aminotransferase (AST)
-not specific to liver diseases
-inc levels in cirrhosis, hepatitis, and liver cancer
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gamma-glutamyl transferase (GGT)
levels associated with cholestasis
-alcohol liver disease
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hepatic dysfunction
-acute/chronic cirrhosis of liver
-alcohol liver failure
-infection
-fatty liver disease
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2 types of fatty liver disease
-non alc fatty liver disease (NAFLD)
-non alc steatohepatitis (NASH)- most common
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metabolic function of liver
-glucose metabolism
-ammonia conversion
-protein metabolism
-fat metabolism
-vitamin and iron storage
- bile formation
-bilirubin excretion
-drug metabolism
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symptoms related to hepatic dysfunction
-jaundice
-portal hypertension
-ascites and varices
-hepatic encephalopathy or coma
-nutritional deficiencies
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jaundice
yellow/greenish-yellow sclera and skin caused by inc serum bilirubin levels
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jaundice bilirubin levels
> 2 mg/dL
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types of jaundice
-hemolytic
-hepatocellular
-obstructive
-hereditary hyperbilirubinemia
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hemolytic jaundice
inc destruction of RBC; plasma rapidly flooded with bilirubin so liver cant excrete bilirubin as quickly as its formed
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hepatocellular jaundice
inability of damaged liver cells to clear normal amounts of bilirubin from blood
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obstructive jaundice
extrahepatic obstruction may be caused by occlusion of bile from a gallstone, inflammatory process, tumor, pressure from enlarged organ
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hereditary hyperbilirubinemia
inc serum bilirubin levels, resulting from several inherited disorders
(can produce jaundice)
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which jaundices are most associated with liver disease
hepatocellular and obstructive
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hepatocellular clinical manifestations
-mild/severely ill
-lack of appetite
-nausea/vomiting
-weight loss
-malaise
-fatigue
-weakness
-headache, chills, fever, infection
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obstructive clinical manifestations
-dark orange-brown urine
-clay-colored stool
-dyspepsia
-intolerance of fats
-impaired digestion
-pruritus
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portal hypertension
obstructed flow through the liver results in inc pressure throughout portal venous system
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portal hypertension symtpoms
-ascites
-esophageal varices
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ascites
fluid peritoneal cavity
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ascites causes
-portal hypertension
-vasodilation of splanchnic circulation
-changes in ability to metabolize aldosterone
-dec synthesis of albumin
-movement of albumin into peritoneal cavity
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hepatic encephalopathy
2 major alterations underlie its development in cute and chronic liver disease
-hepatic insufficiency
-portosystemic shunting
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hepatic insufficiency
inability of liver to detoxify toxic by-products of metabolism
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portosystemic shunting
collateral vessels develop allowing elements of portal blood to enter systemic circulation
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early signs of hepatic encephalopathy
-mental changes
-motor disturbances
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esophageal varices clinical manifestations
-hematemesis
-malena
-general deterioration
-shock
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viral hepatitis
systematic viral infection causes necrosis and inflammation of liver cells
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hepatitis pairings
-A + E
-B + C
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A + E route
fecal-oral route
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B + C route
bloodborne
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hepatitis D only occurs in
pt w hepatitis b
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nonviral hepatitis
toxic and drug induced
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hepatitis A incubation
2-6 weeks
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hepatitis A lasts for
4-8 weeks
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hepatitis A clinical manifestations
-mild flue-like symptoms
-low-grade fever
-anorexia
-jaundice and dark urine (late)
-indigestion/epigastric distress
-enlargement of liver and spleen
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hepatitis B transmitted by
blood, saliva, semen, and vaginal secretions
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hepatitis B cause
cirrhosis and liver cancer
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hepatitis B incubation
1-6 months
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hepatitis B manifestations
-variable
-similar to HAV
-loss of appetite
-dyspepsia
-abdominal pain
-generalized aching
-malaise
-weakness
-jaundice ( maybe)
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hepatitis C transmitted through
needle sticks and sharing of needles
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hepatitis C is _____ ________ bloodborne infection
most common
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hepatitis C causes _____ cases of liver cancer
1/3
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hepatitis C= most common reason of _______ _________
liver transplant
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hepatitis c incubation
15-160 days (variable)
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hepatitis c symptom's are
mild
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hepatitis E transmitted through
contaminated water
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hepatitis E incubation
15-65 days
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hepatitis E resembles A by
-self limiting
-abrupt onset
-not chronic
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hepatitis D transmitted
blood and sexual contact
-IV/injection drugs
-hemodialysis
-multiple blood transfusions
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hepatitis D incubation
30-150 days
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hepatitis D drug treatment
interferon alfa
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hepatitis D likely to develop
fulfillment liver failure/chronic active hepatitis and cirrhosis
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types of hepatic cirrhosis
-alcoholic
-post necrotic
-biliary
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alcoholic cirrhosis
scar tissue surrounds portal area
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post necrotic cirrhosis
broad bands of scar tissue
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biliary cirrhosis
scarring occurs in liver around bile ducks
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cirrhosis manifestations
-liver enlargement
-portal obstruction
-ascites
-infection and peritonitis
-varices
-GI varices
-edema
-vitamin deficiency
-anemia
-mental deterioration
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cirrhosis: men ____ more affected
twice
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cirrhosis: women _____ risk for ETOH liver disease
greater
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ETOH cirrhosis
episodes of necrosis of liver cells
more scar tissue than healthy tissue
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primary liver tumors
-hepatis B and C
-hepatocellular carcinoma
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liver metastasis
-few cancers originate in liver
-frequent site of metastatic cancer
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liver cancer clinial manifestations
-dull persistent pain in RUQ, back or epigastrium
-weight loss
-anemia
-anorexia
-weakness
-jaundice
-bile ducts occluded
-ascites
-obstructed portal veins
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acute pancreatitis
pancreatic duct becomes obstructed and enzymes back up
causing autodigestion and inflammation of pancreas
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chronic pancreatitis
progressive inflammatory disorder with destruction of pancreas
-cells replaced by fibrous tissue
-pressure with in pancreas inc
-obstructs pancreas and common bile ducts
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pancreatitis patho
-self digestion of pancreas (trypsin) causes acute pancreatitis
-gallstones enter common bile duct and obstruct flow of bile into pancreatic duct
-activated enzymes leading to vasodilation, necrosis, erosion, and hemorrhage
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pancreatitis causes
-bacterial/ viral infections
-blunt abdominal trauma
-PUD
-meds (corticosteroids, oral contraceptives)
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pancreatic cysts
local necrosis occurs bc of acute pancreatitis
-collections of fluid wailed off by fibrous tissue
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pancreatic cancer: sites of lesions
head, body, tail of pancreas
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pancreatic cancer clinical manifestations
-pain
-jaundice
-weight loss (rapid)
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pancreatic cancer risk factors
-age
-smoking
-environment/occupational chemicals
-diet inc fat and meat
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pancreatic cancer treatment
-palliative
-chemo
-radiation (limited)
-surgery
90
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vitamin K deficiency
-synthesis of coagulation factors depend on vitamin K
-common in malnourished pt

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