Thera 1/3 Hepa Coag Hepatic Coag Laboratory Parameters 3

Question Answer
Hepatitis swelling, inflammation of the liver
Nonalcoholic Steatohepatits (NASH) a common form of chronic liver disease-resembles alcoholic liver disease. Fat deposits cause inflammation and damage to liver cells that can slowly worsen and cause scarring and cirrhosis.
Cirrhosis fibrosis and permanent scarring of the liver, typically from chronic injury (compensated and uncompensated)
Liver failure the failure of the liver to perform biosynthetic functions
Fulmenant hepatic failure liver failure with encephalopathy in patient with previously normal lab values and no history of chronic disease
Infiltrative disease liver is invaded by non-hepatic substances (tumor, amylodosis)
symptoms of liver disease absent/nonspecific: anorexia, fatigue, n/v, mental confusion; late disease: jaundice, dark urine, ascites, peripheral edema
lab tests liver function, but most don't measure liver function at all "labratory pannel" function vs injury (cells die and replaced)
diagnosing lab tests ultrasound, biopsy
lab test panel: Basic Metabolic Panel BMP calcium, CO2, chloride, creatinine, glucose, potassium, sodium, BUN
lab test panel: comprehensive metabolic panel (CMP) routine lab panel: albumin, ALT, AST, total bilirubin, calcium, chloride, CO2, creanitine, glucose, alkaline phosphate, potassium, total protein, sodium, BUN
Why multiple tests at same time? increase sensitivity to catch people with low level inflammation in liver
Amino transferases AST/ALT: <35 units/L. intracellular enzymes that break down amino acids. Convenient and easy to measure (inexpensive).
AST/ALT in liver cells in large amounts, not specific to the liver.
AST (17 hours) aspartate aminotransferase (found in more organs (mitochondria/cytoplasm) liver, muscle, heart, brain, kidney, RBC)
ALT (47 hours) alanine aminotransferase (more liver specific (cytoplasm) more sensitive and specific and a little higher) Liver, mucle, kidney (mainly liver)
Elevated Aminotransferases (5x ULN can turn normal in days) do not reflect degree of liver damage or prognosis (cirrhosis, necrosis, permanent damage). Mild: <2x upper limit of normal. Moderate: 2-5x upper limit of normal. Ingestigate PE, hexpatotoxic meds, and alcohol, more tests, obesity, virus, family +travel
AST/ALT alcoholism ALT typically slightly lower than AST in liver damage. Exception: alcoholic hepatits (chronic). AST to ALT ratio > or equal 2:1 suggests alcoholic liver damage. 1. pyridoxine 5 phosphate-active vitamin B6, 2. alcohol increase release of mitochondrial AST
Lactate dehydrogenase (LED) 60-100 unitsL: elevations reflect tissue injury. less useful to eval patients for liver injury. support diagnosis of heart, liver, RBC, kidney, skel muscle, brain or lungs. more pronounced in ischemic liver injury than ALT; mark hypoxic liver inj
Lab: LDH total vs LDH + enzymes LDH1 (17-27%) myocardium, RBC; LDH2 (27-37%) myocardium RBC brain lung; LDH3 (18-25%) lung, brain, kidney; LDH4 (3-8%) liver skel muscle, kidney; LDH5 (0-5%) liver and skeletal muscle
cholestasis decreased bile flow from either intrahepatic or extrahepatic obstruction. INTRA-scarring, inflammation: biliary cirrhosis, toxins, drugs, metabolites, hormones, alcohol, infection, tumor. EXTRA: gallstone, tumor, stricture, pancreatitis
cholangitis inflammation of bile ducts
cholelithiasis crystallization of bile and its components in gallbladder or bile ducts; gallstones
hyperbilirubinemia elevated biliruben in blood
jaundice/icterus yellowish discoloration of skin/whites of eyes
Alkaline Phosphatase (ALP) 36-92 Units/L: present in liver (biliary tract), bone, intestinal tract, and placenta.
cholesatis: stimulates synthesis and release of ALP (sensitive, easily measured) bile backs up into liver elevating ALP.
Alkaline Phosphatase Elevation extra/intrahepatic: obstructive biliary disease/cirrhosis elevated in children and pregnant women
Isoenzymes ALP seperation is not very reliable, ALP1 Liver disease, ALP2 bone disease. Use GGT to confirm ALP (7 days to resolve after obstruction resolves)
Gamma-Glutamyl Transferase (GGT) 0-30 units/L: present mainly in liver, biliary tract and pancrease (no bone). Most SENSITIVE for hepatobiliary disease. no specific, not route, not stand alone test.
GGT use 1. differentiate source of ALP relevation. 2. evaluate heavy/chronic alcohol use (normal 1/2 life 7-10 days increase to 14/28 days) (50% chance accurate for patients) elevated by enzyme-inducing drugs (alcohol, barbiturates, phenytoin, anti-epileptic)
5'-Nucleotidase (5NT) 0-11 Units/L. present in many tissues. Rise in hepatic obstruction. High sens and speci for hepatobiliary disease. NOT elevated in infancy, childhood, preg, or bone disorder.
5'-Nucleotidase use differentiate source of ALP. more steps to measure and 3x cost of GGT. GGT most commonly used, rises earlier, persists longer.
Bilirubin (0.2-1.0 mg/dL) [0-0.2mg/dL conjugated= bloodstream, blood transfusion/disease make too much. no dark urine] break down of RBC product of hemoglobin catabolism (120 days). Albumin bind. unconjugated: indirect, insolube. Conjugated: direct, soluble.
Total Bilirubin and excretion total=direct+indirect; must be conjugated and excreted in bile. found in urine=water soluble, conjugated: direct, solube
elevated at 2-2.5mg/dL (jaundice, icterus)
Elevated indirect Bilirubin over production(hemolysis) hemolytic anemia, pernicious anemia, sickle cell anemia, blood transfusion LV; decrease liver uptake-sepsis, heart failure; decrease conjugation-severe leiver disease, hepatitis, cirrhosis, gilbert's syndrome, Crigler Najjar sy
Elevated direct Bilirubin impaired hepatic secretions; cholestasis; cholelithiasis; biliary cirrhosis, tumor (m), sotne, stricture; rare disorders (levels of DB rise when liver loses 50% of its excretory function; elevates IDB; reflects hepatobiliary disease (decreased)
Elevated indirect Bilirubin (extras) isolated elevation with little elevation to DB, rarely reflects liver disease, commonly found in hemolytic disease (overproduction)
DB and IDB both can be elevated in hepatits, cirrhosis, post hepatic obstruction, some drug-induced cholestasis.
Jaundice and delta bilirubin jaundice can be slow to resovle in prolonged jaundice there is an increased fraction of delta bilirubin (conjugated0 that is irreversibly bound to albumin
Albumin (3.5-5.0g/dL) protein made by liver, not specific for liver, but good monitoring but long 1/2 life (20 days) makes acute hard to catch. slow rise and fall. 60% total protein(maintains oncotinc pressure, binds d/h) measure of liver (synthetic ability)
Albumin increase/decrease decrease: in liver disease, chronic malnutrition, burns, over hydration, nephrotic syndrome (large volume make albumin look low) increase: anabolic steroids, dehydration (chronic injury, disease/not acute)
Coagulation Factors Most of the coagulation factors are made by the liver (1,2,5,7,9-12, antithrombin, protein C +S, plasminogen.
Factors 2,5,7,10 low when liver disease/injury
liver makes albumin, bile, coagulation factors
coagulation lab tests Prothrombin Time (PT); Activated partial thromboplastin time; measure time it takes for blood to clot
Prothrombin Time profile PT, measures fucntion of extrinsic and common coagulation path (factors 1 (fibrogen), 2,5,7,10)
Activated partial thromboplastim time profile aPTT: measures function of the intrinsic and common pathways of coagulation; factors 1, 2(prothrombin), 5,7,9-12, prekallikren (PK), increased molecular weight kiniogen (HK).
Liver disease PT and aPTT in liver disease, PT prolonged first then aPTT. Factor 7 has shortest half life of 4-6 hours of clotting factors and PT most commonly tested
Prothrombin Time use (11.0-12.5 seconds /lab dep) Liver is soul source of vitamin K dependent clotting factors/sig dimisiehed liver function (>75-80%) may prolong PT. Not sensitive marker for liver damage, but will reflect change in liver function fast (high prognostic value)
INR 1.0 PT is reported as INternational normalied ration=INR. Standardizes result of PT lab to lab no units. elevated=sign+sym+bleeding; therapeutic INR(warfarin): normal for warfarin is not normal fiv 2.0-3.0, Mech HV 2.5-3.5
Liver Fucntion not enough liver cells, can't make albumin (slow changes in liver/long-term) prothrombin (rapid/short/longterm)
Decompensated Liver disease decompensated cirrhosis: jaundice, ascites, portal HTN w/ bleeding esophageal or gastric varices, oligauric hepatic failure, hepatic encephalopathy.
Encephalopahty progressive symptoms cognitive changes, altered sleep, lethargy/apathy, disorientation to time, personality change/inappropriate behavior, osma, unresponsive to painful stimuli
Ammonia (40-80mg/dL) production of amino acid metabolism;metabolized by liver to urea to be excreted by kidneys. Elevated: toxic, hepatic encephalopathy. not Sens or sp, not routine monitoring chronic disease (for improvement or deterioration) acute lever failure
Laboratory Parameters synthetic liver function: albumin, PT/INR; Excretory liver function/cholestasis: bilirubin, alkaline phosphatase, GGT; hepatocellular injury: AST, ALT, LDH;Detoxyfying Liver: ammonia

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