| Term 
 
        | hepatocellular or cytotoxic: 
 metabolic mediated
 immune mediated
 steatosis mechanisms
 |  | Definition 
 
        | most common mechanisms of hepatocellular/cytotoxic injury |  | 
        |  | 
        
        | Term 
 | Definition 
 
        | potential mechanism of drug induced liver disease: 
 hepatocellular or cytotoxic
 
 drugcovalently binds to intracellular proteins or DNA disrupting cell function
 
 this can lead to production of chemicals toxic to cells and/or sensitization to cytokines that can impact cell function
 
 most common type of DI liver injury
 
 examples:  APAP, furosemide
 diclofenac
 
 may cause apoptosis and necrosis
 |  | 
        |  | 
        
        | Term 
 | Definition 
 
        | potential mechanism of drug induced liver disease: 
 hepatocellular or cytotoxic
 
 medication processing forms haptens which stimulate an immune response
 
 these haptens can induce humoral responses (formation of antibodies) or cellular immune responses (T-helper cell mediated)
 
 examples:  sulfamethoxazole, nitrofurantoin, cabamazepine, nivirapine, phenytoin, trazodone
 
 may cause apoptosis and necrosis
 |  | 
        |  | 
        
        | Term 
 | Definition 
 
        | potential mechanism of drug induced liver disease: 
 hepatocellular or cytotoxic
 
 due to accumulation of fatty acids in mitochondria (aka mitochondrial injury)
 
 medications can impair either major pathway involved in hepatocyte fatty acid elimination
 primary pathways of fatty acid elimination include microsomal triglyceride transfer protein (MTP) and mitochondrial oxidation
 
 microvesicular steatosis - due to acute injury and accumulation of tiny fat droplets.  hepatocyte fat accumulation does not displace the cell's nucleus
 
 macrovesicular steatosis - due to chronic injury and accumulation of large fat droplets.  hepatocyte fat accumulation will displace the cell's nucleus.
 
 examples:  aspirin, valproic acid, tetracyclines, alcohol
 |  | 
        |  | 
        
        | Term 
 | Definition 
 
        | potential mechanism of drug induced liver disease: 
 injury is due to blockage or interference of the bile canaliculus or direct bile duct injury (ex. pure cholestasis)
 
 additional mechanisms include disruption of ATP dependent transportation of proteins or pumps
 
 examples:  chlorpromazine, erythromycin, amoxicillin/clavulanic acid, carbamazepine, TPN, sulfonamides, sulfonylureas, ACE inhibitors, phenothiazines
 |  | 
        |  | 
        
        | Term 
 | Definition 
 
        | potential mechanism of drug induced liver disease: 
 injury is due to veno-occlusion or hepatic vein thrombosis of efferent hepatic blood flow
 
 this causes congestion and blood filled cavities (peliosis) within the liver
 
 examples:  andorgens, estrogens, azathiopurine, tamoxifen
 |  | 
        |  | 
        
        | Term 
 | Definition 
 
        | injury is due to alterations of DNA that causes benign or malignant neoplasms 
 examples:  hormone agents
 |  | 
        |  | 
        
        | Term 
 
        | nausea/vomiting abdominal pain
 fatigue
 anorexia
 pruritus
 weight loss/gain
 |  | Definition 
 
        | common signs and symptoms of DI hepatocholestatic disease are very non-specific and include: |  | 
        |  | 
        
        | Term 
 
        | jaundice coagulopathy
 hypo/hyperglycemia
 ascites
 spontaneous bacterial peritonitis (SBP)
 electrolyte abnormalitites
 encephalopathy with increased intracranial pressue (ICP)
 variceal hemorrhage
 hepatorenal syndrome (HRS)
 malabsorption of fat soluble vitamins (DEAK)
 |  | Definition 
 
        | mpt and complications of severe hepatocholestatic disease include: |  | 
        |  | 
        
        | Term 
 
        | aspartate aminotransferase (AST) alanine aminotransferase (ALT)
 alkaline phosphatase (Alk Phos)
 lactate dehydrogenase (LDH)
 gamma-glutamyltransferase (GGT)
 5'-nucleotidase (5NC)
 albumin (Alb)
 transferrin saturation (TSAT)
 bilirubin, conjugated/direct
 prothrombin time (PT/INR)
 
 liver biopsy is NOT recommended for routine use in the diagnosis of DI hepatocholestatic disease
 |  | Definition 
 
        | common lab measures used in assessing DI liver diseases |  | 
        |  | 
        
        | Term 
 
        | single increased dose cumulative dose
 pharmacokinetic interactions
 pharmacodynamic interactions
 |  | Definition 
 
        | drug related risk factors for patients receiving medications that are potentially hepatotoxic |  | 
        |  | 
        
        | Term 
 
        | obesity diabetes mellitus
 hyperlipidemia
 hyperthyroidism
 renal dysfunction
 chronic hepatitis B or C
 acquired immunodeficiency syndrome
 juvenile rheumatoid arthritis
 systemic lupus erythematosus
 |  | Definition 
 
        | health condition related risk factors for a patient receiving medications that are potentially hepatotoxic |  | 
        |  | 
        
        | Term 
 
        | other and younger age female sex
 malnutrition
 alcohol consumption
 illicit drug use
 household or occupational exposures
 genetic predisposition (CYP2C19 deficiency, N-acetyltransferase deficiency, glutathione synthetase or transferase deficiency)
 |  | Definition 
 
        | patient related risk factors for patients receiving medicatiosn that are potentially hepatotoxic |  | 
        |  | 
        
        | Term 
 
        | a.	Seek medical attention (ex. primary care provider, pharmacist) if experiencing nausea, vomiting, unexplained weight loss, or abdominal pain for several days with no other identified causes 
 b.	Go to hospital/ER immediately if experiencing increased abdominal girth, altered mental status, peripheral edema, bleeding episodes, prolonged pruritus, jaundice, or reduced urine output
 
 c.	Do not take any new medications, OTC products, and/or herbal/health products without consulting a health care professional
 
 d.	Inform health care professionals (ex. primary care provider, pharmacist) of all medications and health related products (herbals, vitamins, supplements) being taken for health and/or wellness
 
 e.	Avoid excessive alcohol use, illicit drug use, and environmental exposures known to cause hepatotoxic reactions
 
 f.	Follow up with primary care/prescribing provider regularly and at appropriate time intervals after initiation and/or medication dose changes.  Inform patient if routine liver function monitoring is needed and when follow up is needed for recommended lab monitoring.
 |  | Definition 
 
        | patient education for medications that are potentially hepatotoxic |  | 
        |  | 
        
        | Term 
 
        | 1 = alcohol 2 = acetaminophen
 |  | Definition 
 
        | what are the #1 and #2 causes of DI liver dysfunction? |  | 
        |  |