University:
Camosun College
Course:
NURS132 | Promoting Health and Wellbeing
Academic year:

2023
Views:

133

Pages:

3
Author:

Aysha A

ALCOHOLIC LIVER DISEASE espectim of disease /disorder." fath chonge HEPATIC Revenues fibrosis STEATOSIS (FATTY LIVER ALCOHOLIC HEPATITIS ALCOHOLK CIRRHOSIS • Necrosis of Hepatocytes •Inflamination Nalling Bockers Fatty change •Diffinse loss of architecture fibrosis METABOLISM OF ETHANOL • Regenerating nachules. Formation of Acetaldehyde Ethanol- → Aretaldehyda 1) Alkohol dehydrogenaz 2) cytochrome P450 2E1 3) Catalase Alkohol dehydrogenask Fresent in the cytoplasm of liver and is the main enzyme system CYTOCHROME P450 201 When blood alkohol levels are high, the microsomal ethanol oxidizing systen -genetrate ROS (MEOS) porticipate. ③ CATALASE Presat in Peloxisomes and is of minor importance ETOLOGY OF ALCOHOLIC LIVER DISEASE not NADP MICROSOMES NADPH CYIREI APH EROS MITO CHONDRIA + NAD Ethanol NAD NADH Aretaldehyde NAPH ALDH CYTOLASM OF HEPATOCYTE CATALASE PERO XISOMES Acetic acid ETIOLOGY RISK FACTORS! ) Gender: Fonale are more susceptible to ALD than modes. Estrogen increases (gut permeabilit to endotoxins) (gut-deived) and increased prmenbility / produces of pro-inf. Eytokines & Chemokines resulting in injury to liver calls. Ethinint 141 3) Gonetha Frictions. 4) Ass. conditions: Iron overload & crank inf. with HCV & HBV. PATHOGENESIS Mechanism of Liver injury by ETHANOL OXIDATIVE STRESS/ROS Netabolism. f Alcohol Liver by CYP2E1in microsomes prodicos (ROS Couse. LIPID PEROXIDATION of cell membrane Injury to HEPATOCYTE 2 IMMUNER INF. MECHANISMS BY FORMING CHEMICAL ADDUCTS Acetaldy frooms chemical Cadicts with wellde protems in and forms (necantiyenswtich mitiate immune response Couse call injung similar to Antoimmune-like disease hepatocytes 3 Increased REDOX (NADHINAD + Ratio) I NAD occur in both cytoplasm hepatocytes. as well aus mitochondria of Ethanol Decreased. NAP in cytoplasm NAD NAPH II NADI, inhibits oxidation of Fatty Avels Accumulation of (FAT) in Liver. (Mitochondria) Aretalde de Acetic Acid Transpre Antioxidant alutathione from NADH NAD Ratio↑ istoplasm mitochondrica ROS nenkalize oxidant. Transport is impaired Comater Ros MITOCHONDRIAL DYSFUNCTION" 4) Increased PRODUCTEN OF FRO-INFOCYTOKINES •In Inkestral flora, alcohol causes the release LPOPOLYSACCHARIDE-LPS) of endotoxin) Grom(-) Bacteria PORTAL CIRCULATION production of TNF-2 & other CYTOKINES (IL-6, TGF-2) from macrophages & Kuppfer cells?. → INJURY TO LIVER CELLS. Impaired PROTEA SOME FUNCTION Remove irrege & tanaged Botein. in AC) Function impaired houfficient degradation of (UBIQUITIN acc. of UBIQUITIN. in the FORM OF MALLORY BODIES . ↳ death of hepathocytes & Release (cytokines) (IL-)8. sustain Meatrophils Inflammatis damagi DIRECT TOXICITY BY FORMING PROTEIN APDUCT Acetal do ny de + Aducts TOXIC He pataye HYPOXIC PAMACIE Contribules Arer of Hepatic loble Lowest oxygen tension & High susceptibilit & hypoch induced damage. REINCED LEVELS OF ADH & ALDH ISOENZYME Efficiens of Alcohol metaldism Expressin of (ADH) R ALDH iso enzyme. Ab Metabdism of ME THIONINE Methionine Bereased jung bvels of Glutathione e sensitices the liver to exidine 9) Malnutrition & def of Vitamins ✓ Thiamine. x imp digestive function 16) Induction of Enzymes P-450 enzymes in Liver on and increases catabolism. Induced by Alcohol Competes with oόταν επέζησε Toxic metabolites