NCM 106: PHARMACOLOGY CHAPTER 22 | LECTURE COLLEGE OF NURSING AND ALLIED MEDICAL SCIENCES 1st SEMESTER A.Y. 2022 – 2023 HEPATOBILIARY SYSTEM LIVER It increases when there is presence of damage in the liver only PT, PTT To determine the clotting time and clotting factors Largest organ Largest gland DIVIDED INTO FOUR LOBES Left Lobe Right Lobe Caudate Lobe Quadrate Lobe CELLS OF THE LIVER Hepatocytes Kupffer AMMONIA When increased, there will be decreased level of consciousness because it is neurotoxic Intervention: Administer lactulose to decrease levels of ammonia HEPATIC DYSFUNCTIONS FUNCTIONS Secretes bile Storage of fat-soluble vitamins Regulates blood glucose level by glycogen, stored in hepatocytes Converts ammonia to urea Ammonia – a byproduct of glucogenic, which converts amino acid to glucose GALLBLADDER Stores bile PANCREAS Releases insulin THREE PANCREATIC JUICES Amylase Lipase Trypsin JAUNDICE Yellow discoloration due to increased serum bilirubin level (< 2mg/dl) MANIFESTATIONS Yellow sclera Yellow-orange skin Clay colored stool Urine: Tea colored Anorexia LABORATORY TESTS Prolonged PT Increased cholesterol Increased bilirubin HEMOLYTIC JAUNDICE Decreased bilirubin Damage in liver cell HEPATITIS Inflammation of the liver DRUG-INDUCED HEPATITS Inflammation or damage of the liver due to drug abuse LIVER PORTAL VEIN Contains 80% of blood rich in nutrients but lacks oxygen HEPATIC ARTERY Blood vessel that contains 20% of oxygenated blood LIVER FUNCTION TESTS AST (SGOT) It increases when there is damage in liver, cardiac muscle, and brain ALT (SGPT) CLINICAL MANIFESTATIONS PRE-ICTERIC STAGE Flu like symptoms Malaise Fatigue Headache Anorexia Agnosia Diarrhea, vomiting, nausea HANNA JEULINE DR. PALAPAL NCM 106: PHARMACOLOGY CHAPTER 22 | LECTURE COLLEGE OF NURSING AND ALLIED MEDICAL SCIENCES 1st SEMESTER A.Y. 2022 – 2023 ICTERIC STAGE (a few days-weeks after preicteric, with infection) Jaundice Dark colored urine Light colored stool Steatorrhea Enlarged liver POST ICTERIC STAGE Convalescence stage With appetite Decreased fatigue MANAGEMENT Administer prescribed medication (immunoglobulin, immunization, antiviral medication) Prevent transmission Encourage proper nutrition HEPATIC CIRRHOSIS/LIVER CIRRHOSIS VIRAL A B C D E MODE OF TRANSMISSION Fecal-Oral route INCUBATION PERIOD 15-50 days Parenterally, perinatal, sex Blood transfusion, sex Same with Hep B Fecal-Oral route 28-160 days 15-160 days 21-140 days OUTCOME Mild with recovery Severe Hepatic cancer Carrier state Affects pregnant women Chronic disease characterized by replacement of normal liver tissue with diffused fibrosis Destruction and fibrotic regeneration of liver cells Fibrotic regeneration – thickening or scarring due to excessive alcohol intake LAENNEC’S CIRRHOSIS “ALCOHOL CIRHHOSIS” Most common Caused by excessive alcohol intake BILIARY CIRRHOSIS Late results of a previous bout of acute viral hepatitis Caused by bile duct disorder Suppressed bile flow Biliary atresia POST HEPATIC CIRRHOSIS Post necrotic cirrhosis Results from chronic biliary obstruction Caused by hepatitis CLINICAL MANIFESTATIONS Liver enlargement Dyspepsia – due to decreased bile production Constipation Gradual weight loss Splenomegaly Spider telangiectasia (Spider angioma in vascular) Caput medusae – abnormal dilation of abdominal blood vessel Portal hypertension – mental deterioration due to increased ammonia CLOTTING FACTORS I – Fibrinogen II – Prothrombin III – Tissue Thromboplastin IV – Calcium ions V – Labile factor VII – Stable factor VIII – Antihemophilic factor IX – Christmas factor X – Stuart-Power factor NORMAL LEVELS FOR TRANSFUSION In case of severe edema and liver problems PACKED RBC – 250 ml WHOLE RBC – 300 ml FRESH FROZEN PLASMA – 200 ml ALBUMIN – 100-180 ml DIAGNOSTIC TESTS SGPT/SGOT – due to increased risk for GI bleeding Serum protein level PT, PTT Liver biopsy NURSING MANAGEMENT Promote adequate nutrition Early phase – high protein diet to promote healing of the liver Late phase (irreversible liver damage) – low protein diet HANNA JEULINE DR. PALAPAL NCM 106: PHARMACOLOGY CHAPTER 22 | LECTURE COLLEGE OF NURSING AND ALLIED MEDICAL SCIENCES 1st SEMESTER A.Y. 2022 – 2023 CLOTTING PROBLEMS MANAGEMENT Give antacid Avoid alcohol intake Avoid visitors due to risk for infection Prevent tissue or skin damage PORTAL HYPERTENSION Elevated pressure in portal veins Increased resistance to blood flow through the portal venous vein CLINICAL MANIFESTATIONS Ascites Rapid weight loss Shortness of breath due to impaired blood flow, decreased oxygenation Caput medusae – seen and radiates to umbilicus area, palpable spleen (hypersplenism) Fluid and electrolyte imbalance – Na & K MANAGEMENT Avoid too much activity Promote bed rest Avoid spicy foods Diet – soft diet only Administer diuretics Measure abdominal girth – early morning before breakfast HEPATIC ENCEPHALOPATHY Neurologic syndrome that develops as complication of liver disease Increased serum ammonia level due to GI bleeding, due to ruptured varices caused by portal hypertension CLINICAL MANIFESTATIONS Changes in mental status Motor disturbances Mood alterations Asterixis – involuntary flapping of the hands “flapping tremors” Fetor hepaticus – sweet, slightly fecal order to the breath Increased bilirubin level MANAGEMENT Administer prescribed medications Lactulose – to evaluate bowel movement waste products stocked in colon Antibiotics (neomycin) – to halt bacteria that increases ammonia Decrease protein in diet Monitor vital signs FOR DETERIORATION (MENTAL) Monitor serum ammonia Administer lactulose Perform gastric lavage: silicone Paracentesis – do not aspirate fluid <1500 ml ESOPHAGEAL VARICES Upper bleeding Hemorrhagic process Dilation of tortuous vein GALLBLADDER DISORDERS MANAGEMENT Asses for epistaxis and gum bleeding Use soft-bristle toothbrush Monitor level of consciousness Administer vasopressin Balloon tamponade – to control the bleeding using NGT Variceal band ligation RISK FACTORS Obesity Gender (women because of increased dose of estrogen) CHOLELITHIASIS Formation of calculi (stones) in the gallbladder HANNA JEULINE DR. PALAPAL NCM 106: PHARMACOLOGY CHAPTER 22 | LECTURE COLLEGE OF NURSING AND ALLIED MEDICAL SCIENCES 1st SEMESTER A.Y. 2022 – 2023 Changes in the bile components due to cirrhosis and infection CLINICAL MANIFESTATIONS Pain at RUQ Nausea and vomiting Fat intolerance Leukocytosis Jaundice Epigastric pain Increased lipase and amylase Cholecystitis Hemorrhage CLINICAL MANIFESTATIONS Turner’s sign – bluish discoloration of skin, specifically in the trunk Cullen’s sign – purple discoloration around the umbilicus Abdominal tenderness and distention Decreased blood pressure Hypovolemia which can lead to hypovolemic shock due to internal bleeding (as manifested by turner’s and cullen’s sign) CHOLECYSTITS Inflammation of the gallbladder Can be acute or chronic Obstruction of cystic duct – there is no bile flow Due to septicemia (blood infection); and overuse of analgesics, opioids: tramadol DIAGNOSTIC TESTS CBC with APC (increased WBC) Lipid profile (increased amylase and lipase) Electrolytes (decreased calcium) IV Fluid: D5NM, D5NR CLINICAL MANIFESTATIONS With tenderness at RUQ Murphy’s sign with pain Heartburn MANAGEMENT Opioids Histamine – to decrease pancreatic acid Drug of choice for pain – Morphine NPO Maintain fluid and electrolyte valance through IV fluids DIAGNOSTIC TESTS Whole abdominal ultrasound (NPO at Post Midnight) Abdominal Xray Abdominal CT scan ERCP – Endoscopic Retrograde Cholangiopancreatography PHARMACOLOGICAL MANAGEMENT Ursodeoxycholic (urso) – dissolves gallstones, administer morphine Low fat diet High protein diet SURGICAL APPROACH Lap Chole Cholecystectomy Choledochotomy – surgical incision of the common bile duct ACUTE PANCREATITIS Inflammation of the pancreas CAUSES Self-digestion of enzymes – trypsin HANNA JEULINE DR. PALAPAL
