Final_Hepatic Flashcards
Hepatic blood flow is provided by
hepatic artery + portal vein (dual afferent blood supply)
Hepatic arterial blood flow is controlled by
arterial smooth muscle and autonomic regulation
Reduction in portal vein flow is compensated by
hepatic arterial buffer response
Acute liver failure - signs and symptoms
● Fatigue ● Lethargy ● Anorexia ● Nausea/ vomiting ● Jaundice ● RUQ tenderness ● Change in liver span ● Ascites ● Encephalopathy ● Cerebral Edema (↑ICP)
Hepatic drug metabolism
Hepatic biotransformation
○ Phase I: + oxygen or - hydrogen carried out by mixed function oxidase (Oxidation, Reduction, Hydrolysis (involves breaking of ester bonds))
○ Phase II: Involves conjugation of active metabolites with glutathione, sulfate, glycine or glucuronic acid into inactive substrates (Conjugation)
- Hepatic Microsomal Enzymes – CYP450
- inducers: ETOH, phenobarb, st johns wort
- inhibitors: Cimetidine, ritonivir, grapefruit juice, CCBs, erythromycin, itraconazole, nefazodone
normal hepatic blood flow is
25% of CO
portal vein flow is
not regulated
-vulnerable to: systemic HOTN, dec CO
reduction in portal vein flow is compensated by
hepatic arterial buffer response
hepatic arterial buffer response
○ ↓ portal vein flow leads to ↑ hepatic arterial flow
○ Stimulated by ↓ pH + O2 levels, ↑ CO2
portal vein
- Supplies 3x blood flow as hepatic artery (75% of blood flow)
- Venous blood - but still supplies 45-50% O2 to liver
portal triad
- hepatic artery
- hepatic portal vein
- bile duct
Hepatitis etiology
Chronic Liver disease - one cause = Chronic viral hepatitis
- Persistent hepatic inflammation > 6 m
- result of infxn with hepatitis B or C
Chronic Liver disease - categories
- Cirrhosis of the liver
a. Functioning liver tissue replaced by scar tissue
b. Progressive decrease in hepatic blood flow - Fibrosis of the liver
a. Overgrowth of scar tissue d/t infxn, inflammation, injury, or healing
b. Can inhibit the organs proper functioning
chronic liver disease - s/s
-Non-specific symptoms (Anorexia, weight loss, weakness, fatigue)
- Jaundice
○ Portal HTN → diverts blood away from liver, lower albumin levels → lead to a buildup of bilirubin → causes jaundice
○ Normally: RBCs broken down in spleen into indirect bilirubin (very lipid soluble, hard for kidneys to remove) → indirect bilirubin goes to liver for conjugation → turns into direct bilirubin
○ Direct bilirubin: water soluble, easy for kidneys to remove
○ Albumin = plasma protein that binds to direct bili, keep in circulation
○ ↓albumin levels + ↑bilirubin → leaking bilirubin→ jaundice
- Spider angioma
- Palmar erythema
- Hepatomegaly
- Splenomegaly
gastroesophageal varices
-Can lead to massive bleeding r/t portal hypertension
-Varice - large vein that became distended d/t collapsed valves
-Major cause of morbidity and mortality
Can Precipitate Encephalopathy From Blood In GI tract
(Risk of GI bleed → upper GI bleed → digesting too much protein (blood) → hepatic encephalopathy)
-Management: Balloon tamponade, vasopressin, somatostatin (octreotide), propranolol
-Sclerotherapy, variceal banding/hemoclip, electrocoagulation
complications of liver disease
- hyperdynamic circulation
- gastroesophageal varices
- hepatic encephalopathy
- pulm: hepatopulmonary syndrome, portopulmonary HTN
- ascites
- hematologic: anemia, thrombocytopenia leukopenia, coag factor deficiencies
- renal: hepatorenal syndrome, hyponatremia/hypokalemia
- hypoalbuminemia