Disorders of Liver, Pancreas, and Gallbladder Flashcards
what is cholelithiasis? cholecystitis etiology? patho? CM?
- Stones form in gallbladder
- Mainly caused by precipitation of cholesterol and bilirubin.
- Often time asymptomatic.
- If blockage of bile ducts occur, may develop into cholecystitis
Etiology:
Obesity, oral contraceptives, family hx, hyperlipidemia
Patho:
Stones form when cholesterol & Ca+ form solid crystals.
* Stone obstructs cystic duct.
* Inflammation of gallbladder causes fibrosis & thickening.
* Pressure against wall of duct causes ischemia & possibly necrosis
CM:
* Pain radiates to subscapular & back: steadily increases for several hrs.
* Jaundice
* Nausea & vomiting
* Heartburn/belching/bloating
* Clay-colored stools
* May cause gangrene & rupture
* Often precipitated by fatty meal
what is pancreatitis? etiology? patho? CM?
- Inflammation of pancreas.
- Digestive enzymes, Lipase & Amylase become active & start auto-digestion
Etiologies: gallstones, hypertriglyceridemia, or ETOH abuse
Patho:
Acute: Inflammation of pancreas; pancreatic enzymes begin autodigestion
Chronic: Inflammatory lesions cause calcification & obstruct flow of pancreatic juices, most often d/t ETOH abuse. Occurs over wks & mos.
CM:
Acute: Steady severe epigastric or LUQ pain radiating to back, nausea, abd. distention, tachycardia, hypotension, fever, decreased BS, jaundice, weakness, pallor.
Chronic: insidious onset of LUQ pain radiating to back, nausea, vomiting, wt loss (poor intake), flatulence, constipation, malabsorption
what is pancreatic cancer? RF? CM? tx?
Difficult to diagnose & tx, poor life expectancy (7%)
Risk factors
– Cigarette smoking
– Obesity
Clinical manifestations
– Pancreatic head tumors: jaundice, malabsorption & wt loss
– Pancreatic tail: abdominal pain & nausea
Treatment
– Surgery
– Chemotherapy
what is jaundice? etiology? patho?
Most characteristic sign of liver dse
Etiology: Increased RBC breakdown or impaired bilirubin metabolism.
Patho:
* RBCs release Heme & globin, Heme releases Fe+
* Bilirubin (unconjugated) released into plasma & transported to liver by albumin
* In liver, bilirubin is conjugated & excreted into bile
* Bilirubin in bile is sent to small intestine, then to colon & broken down to urobilinogen & passed in feces
* Jaundice results from dysfunction anywhere along pathway
how do we evaluate jaundice?
Complete history and physical exam
* ascites, palmar erythema, gynecomastia, testicular atrophy, hair loss (men), central obesity with peripheral muscle wasting
Underlying causes
* Alcoholic liver disease, drug reaction, metastatic or primary malignancy
Diagnostic tests
* Biochemical assays, needle biopsy of liver, ultrasound, CT
what is hepatitis? etiology? patho?
Inflammation of the liver parenchyma.
Etiology:
* many viruses-“Viral hepatitis”
* Hepatitis A, B, C, D, E
* Each virus differs in mode of transmission, incubation period, degree of liver damage, & ability to create carrier state.
Patho:
* Viral infections cause hepatic cell necrosis, scarring, hyperplasia, & infiltration by
phagocytes.
* Distortion of normal structure of liver interferes with flow of blood & bile.
* Obstruction of blood flow causes increased portal pressure & hepatomegaly.
* Jaundice caused by abnormally high accumulation of bile in blood
what are the differences and similarities of Hepatitis A, B, and C?
Hepatitis A
* Onset– abrupt
* Transmission: fecal-oral
* Incubation: 2-7 wks
* Jaundice, RUQ pain, malaise, anorexia, nausea, fever
* Self-limited course
* Tx–supportive
Hepatitis B
* Onset—insidious
* Transmission blood & body fluids
* Incubation-6 wks to 6mos
* Jaundice, rash
Hepatitis C
* Onset-insidious
* Transmission-body fluids & blood
* Incubation 2-12 mos
* 3% world-wide infected-6 types
* Usually asymptomatic
what is cirrhosis of the liver? etiologies?
- Irreversible end stage of many different hepatic injuries
- Fibrotic, nodular, scarred liver which interferes with hepatic blood flow & liver function
- Fibrotic liver
-loss of hepatic function
-obstruction to blood flow from gut
Etiologies
* Chronic ETOH (most common)
* Biliary (obstruction in bile drainage)
* Postnecrotic (viral, toxic hepatitis)
* Cardiac (CHF, liver congestion)
biliary cirrhosis etiology? patho? CM?
End result of ongoing inflammation of bile ducts d/t obstruction results in backup of bile into liver
Pathogenesis- Results in inflammation & scarring of liver with obliteration of bile ducts, diffuse, widespread fibrosis, & nodule formation
CM:
* Weakness, fatigue
* Fever
* Anorexia, wt. loss
* Nausea, vomiting, indigestion
* Change in LOC
* Edema, ascites
* Bruising, spider angiomas, jaundice
* Hepatomegaly
* Hepatic encephalopathy
* Portal hypertension
what is portal hypertension? etiology? patho? CM?
Increase in pressure within the portal vein
Etiology
– Sluggish blood flow results in increased pressure in portal circulation.
– Congested venous drainage of much of the GI tract
– Abnormally high BP in portal venous system.
Pathogenesis: Blood flow through portal system is obstructed, causing blood to back up into portal circulation and increase pressure
Clinical manifestations: Anorexia, varices, ascites
* Major complication is hemorrhage.
what is ascites?
- Accumulation of fluid in peritoneal cavity seen in advanced liver dse.
- Usually complicated by portal HTN & hypoalbuminemia.
- Abd distention results from accumulation of Na+, H20, & protein
what is hepatic encephalopathy? CM?
Damage to brain tissue from cirrhosis of liver d/t too much ammonia in brain tissue.
* Characterized by symptoms ranging from mild confusion and lethargy to stupor and coma.
Clinical Manifestations
* Dementia
* Psychotic symptoms
* Cerebellar/extrapyramidal signs
* Asterixis “liver flap” (classic sign)
* Spastic jerking of hands held in forced extension
* Ammonia level correlates positively with level of encephalopathy
* Mild confusion and lethargy to stupor and coma
what are varices? CM?
Distended, tortuous collateral veins resulting from portal HTN.
* Most commonly located in stomach, esophagus & rectum.
* Increased pressure in portal veins causes collateral vessels to develop between the portal & systemic veins
* 50% mortality in cirrhotic pts.
Clinical manifestations: Bleeding, melena, hematemesis, anemia, shock
