Fluids and Electrolytes, Metabolism and Endocrine (NCM103) Patients With Hepatic, Biliary and Pancreatic Disroders
Accessory Organs Anatomy and Physiology of the Liver
What are the Functions of the Liver 1. Bile secretion / production (Choleresis Synthesis) 600 1200 mL/day Bile emulsifies the fat!
Enterohepatic Circulation Recycling of bile salts 90% total bile salts o Absorbed at the distal ileum o 18 times recycled
2. Bilirubin Metabolism
4. Vascular and Hematologic Function Store Blood Kuppfer Cells Prothrombin, Fibrinogen, Factors I, II, VII, IX, and X Synthesis Topics Discussed Here Are: 1. Anatomy and Physiology of: a. Liver b. Biliary Tract c. Pancreas 2. Assessment of the Liver 3. Alterations in the Gall Bladder a. Cholelithiasis b. Cholecystitis c. Choledocholithiasis 4. Alterations in the Pancreas a. Pancreatitis b. Chronic Pancreatitis 5. Alterations in the Liver a. Hepatitis b. Liver Cirrhosis 6. Complications of Liver Cirrhosis a. Portal Hypertension b. Esophageal Varices c. Ascites d. Hepatic Encephalopathy 7. Liver Transplantation LOOKY HERE Hepatic Artery o Amount of blood receives 300 500 mL/min of O 2 blood from the heart Hepatic Vein o Excretes deoxygenated blood but is FULL of nutrients (1,000 1500 mL/min) o Kuppfer Cells Immunity, destroys microorganisms Bile Duct Pathway of bile Portal Circulation All blood coming from spleen and intestines and others drain to the liver Hepatic Secretions Intestinal absorption Hepatic resection
jcmendiola_Achievers2013 Vitamin K Absorption Synthesis of Vitamin K Stimulates production of clotting factors Microorganisms make VITAMIN K Vit. K is a FAT SOLUBLE vitamin
5. Fat Metabolism
Protein Metabolism
Function: - Protein Metabolism
NH4 GIVES BRAIN PROBLEMS
Liver Plasma Protein
jcmendiola_Achievers2013 6. Protein Metabolism
7. Storage of Iron and Vitamin
8. Metabolism Detoxification
9. Metabolic Detoxification
BILIARY TRACT 1. Common Bile Duct (CBD) + Composed of cystic and hepatic duct, leads to duodenum + Function: Transports bile to duodenum when food is present in small intestine 2. Cystic Duct + From gallbladder to the Common Bile Duct + Function: Passageway for bile to the gall bladder 3. Gall Bladder + Sac like organ located under the right side of the liver + Function: Storage and concentration of bile + Stimulated to contract by cholecystokinin and motilin
PANCREAS Exocrine: o Gland located behind stomach on left side of abdomen o Pancreatic Enzymes: Amylase Breaks down Carbohydrates (N: 27 131 u/L) Lipase Breaks down Fats (N: 20 180 u/L) Trypsin Breaks down Protein MAJOR PROTEOLYTIC ENZYME Secretin: o Secretin Secretes alkaline fluid o Inhibits action of gastrin Gastric acid secretion and motility
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Cholecystokinin and Acetyl CoA C and A Acinar Cells Enzyme Release Feedback mechanism inhibits secretions of more pancreatic enzymes
Assessment of Liver Disease Assess Hepatotoxic Substances / Infectious Agents Occupational, recreational and travel history History of alcohol and drug use Evaluation of the past medical history Signs and symptoms that suggest liver disease
Technique for palpating the liver Place one hand under the right lower rib cage and press downward
Abdominal Assessment: Murphys Sign o Painful deep breathing during liver palpation o Client is unable to complete the inspiration; abruptly stops inspiration midway o Sharp Pain caused by inflamed liver / gall bladder (Cholecystitis) onto examiners hand
Percussing the Liver Identify upper border (Start at midclavicular line and lower border) Start at right lower quadrant
Specific maneuver for assessing ASCITES o FLUID WAVE TEST
Measuring Abdominal Girth Consistent Landmark Umbilical Area Consistent Position (Standing preferred) Consistent Tape Measure Consistent Time of Day Post void and Before breakfast
Laboratory Test Bile Formation and Secretion Test Normal Value 1. Direct (Conjugated Bilirubin) 0 0.3 mg/dL 2. Indirect (Unconjugated Bilirubin) 0 1 mg/dL 3. Total Serum Bilirubin 0.1 1.2 mg/dL
Test Normal Value 1. Total Serum Protein 7.0 7.5 g/dL 2. Serum Albumin 3.5 5.5 g/dL 3. Serum Globulin 2.5 3.5 g/dL RESONANT ABOVE 8 cm DULLNESS RESONANT BELOW
jcmendiola_Achievers2013 4. A/G Ratio 1.5:4 to 2.5:1 Coagulation Studies Test Normal Value 1. Prothrombin Time 11.5 14 seconds 2. Partial Thromboplastin Time 25 40 seconds
Test Normal Value 1. AST (SGPT) 8 20 u/L 2. ALT (SGOT) 10 35 u/L 3. Alkaline Phosphatase 32 92 u/L 4. LDH LDH 5. Blood ammonium 150 250 mg/dL
Diagnostic Tests 1. Abdominal X-Ray To visualize solid / liquid part 2. Liver Scan To outline the liver, location (tenderness/mass) To detect a tumor Detects possible scarring (Previous inflammation) Put patient on NPO (4 6 hours) Insertion of a dye 3. Splenoportogram To detect pressure on spleen and portal pressure To know if organs / structures compensate through collateral circulation 5. Endoscopic Retrograde Cholangiopancreatography PostOp! Put patient on NPO (2 3 hours) after procedure Assess gag reflex Vital Signs Monitoring! Alterations in BP? Bleeding by irritation, dry mucosal lining Endoscopic Retrograde is used to visualize the hepatobiliary tract 6. MRI REMOVE magnetic objects! Assess claustrophobia Ultrasound: CHEAPER 7. CT Scan 8. Percutaneous Liver Biopsy To collect tissue of liver To know if malignant / benign Right hypochondriac
BEFORE DURING AFTER 1. Test 1. Expose Right Hypochondriac 1. Position 2. Consent 2. Inhale-exhale THEN HOLD BREATHE AT THE END OF EXPIRATION! 2. NO COUGHING / STRAINING 3. NPO 3. Vital Signs 4. Vital Signs Large bore needle 4. No heavy lifting
JAUNDICE Yellow-Greenish Yellow discoloration of sclera, skin and degenerative tissue PreOp! Assess for allergies to iodine Ask consent (Good for 24 hrs)
jcmendiola_Achievers2013 Types 1. Hemolytic Jaundice (Pre-Hepatic) o Causes: Blood Transfusions, immune reactions, membrane defects of erythrocytes, toxic substances in circulation o Problem is in the BLOOD, not the liver! 2. Hepatocellular Jaundice (Intrahepatic)
3. Obstructive Jaundice (Posthepatic)
Clinical Manifestations Yellow Sclera Yellow-orange Skin Clay colored feces Tea-colored urine Pruritus Bile salts in skin Fatigue Anorexia
Medical Management 1. Determine cause of jaundice a. Health History b. Physical Examination c. Liver Function Test d. Hematologic Test 2. Reduce pruritus and maintenance of skin integrity a. Oral cholestyramine-resin b. Antihistamine and phenobarbital
Nursing Management 1. Assess: Assess for any signs of jaundice formation 2. Nursing Diagnosis Impaired skin integrity i. Tepid water / emollient bath ii. Frequent application of lotion iii. Loose and soft clothing iv. Soft bed linen (e.g. Cotton) v. Keep the room cool Alteration in body image i. Encourage verbalization of feelings ii. Assist in perineal hygiene as needed
jcmendiola_Achievers2013 iii. Promote activity as tolerated
SURGICAL MANAGEMENT: - Cholechostomy: Exploration of the CBD
Alterations of the Liver Biliary Tract and Exocrine Pancreas
CHOLETHIASIS 1) Formation of STONES on gallbladder 2) 10 20% of men are affected 3) 20 40% on women
4 Fs Of Gallbladder Disease~ F Female F Fat F Forty F Fertile (Have children)
GALLSTONES Are crystalline structures formed by concentrated (Hardening) or accretion (adherence) of particles, accumulation of normal or abnormal bile constituents
Theories of Gallstone Formation: 1. Bile Change in composition 2. Gall Bladder Stasis Bile stasis 3. Infection predisposes a person to stone formation 4. Genetics and demography
There are Three Types of Gallstones!~ Cholesterol 1. Most common type 2. Usually smooth and whitish, yellow Pigment 1. Bile contains excess unconjugated bilirubin. 2. Blade / earthly calcium bilirubinate Mixed Combination Minor Constituents 1. Calcium Carbonate, bile salts and palmitate
GALLSTONE FORMATION Causes: 1. Too much absorption of water from bile 2. Too much absorption of the bile ducts from bile 3. Too much cholesterol in bile 4. Inflammation of the epithelium Course Followed by Bile: 1. During rest 2. During Digestion (3 4 hours after meal)
jcmendiola_Achievers2013 Unconjugated bile precipitate Pathophysiology of Gall Stone Formation Formation of pigmented stones Malabsorption disorder Malabsorption of bile salts Bile synthesis Estrogen therapy Pregnancy Gallbladder sludge Obesity increase with age Hepatic secretion of cholesterol Supersaturation of Bile with Cholesterol Rapid weight loss Liver excrete extra cholesterol Clofibrate medications Serum cholesterol level Cholesterol excretion into the bile Cholesterol saturate gallstone CHOLECYSTITIS Irritate gallbladder lining Ultrasound Cholecystography ERCP Obstruction of the passage for Bile Abdominal Guarding Facial Grimacing After meal Contraction of the gall bladder RUQ pain, referred to the back shoulders Vagal stimulation N/V Gallbladder distention and inflammation Marked tenderness in the RUQ on deep inspiration Prevents full inspiration and excursion Bile in the duodenum Malabsorption of Vitamins ADEK Signs and Symptoms Bile retention in the gall bladder Bile absorbed in the circulation JAUNDICE! Bile salts in the skin Continuous bile retention in the gall bladder Abscess, necrosis, perforation Seeping into the peritoneal cavity Peritonitis! Pruritus GIT Kidney Clay-colored feces, very dark urine, tea colored
Assessment: 1. Biliary Colic Pain Abrupt In intensity for 30 minutes 1 hour RUQ / Epigastric area, referred to the back, right shoulder and the right scapula / the mid-scapular region Pain occurs 3 6 hours AFTER HEAVY MEAL / when the client LIES down 2. Anorexia & N/V Stimulation of the VAGUS NERVE
jcmendiola_Achievers2013 3. Intolerance to FATTY FOODS, sensation of FULLNESS 4. Jaundice, bleeding, tenderness and Steatorrhea, clay colored stool
Diagnostic Tests 1. Ultrasound Most sensitive test to detect and visualize stone I: Obstruction, jaundice, allergies to contrast media 2. ERCP (Endoscopic Retrograde Cholangiopancreatography) Direct visualization of hepatobiliary system, performed via a flexible endoscope Multiple positions are required during procedures to pass the endoscope 3. MRI To detect neoplasms; diagnose cysts, abscesses and hematomas 4. PTC (Percutaneous Transhepatic Cholangiography) Injection of a dye to the biliary tract Hepatic duct within the liver, CBD (Common Bile Duct), cystic duct and gallbladder are outlined clearly 5. Cholecystography I: Detects gallstones and assess the ability of the gallbladder to fill, concentrate its contents, contract and empty E.g. Contrast agent: Iopanoic Acid
Nursing Diagnoses: - Alteration in comfort: pain related to gallbladder spasms - Alteration in fluid and electrolyte balance related to vomiting
Health Promotion - Fat diet - Ideal Body Weight (IBW) - Limit number of pregnancies - TPN for 1 month (Monitor closely!) - Physical activity
Nursing Management - Pain measures: Verbalization of feelings, Diversional activities - Comfort measures - Diet modifications - Weight loss - Intravenous fluid - ** for signs of dehydration
Medical Management 1. Medications Analgesics Antacids, H 2 Blockers, Proton Pump Inhibitor (PPI) Antiemetics Antibodies Nitroglycerin 2. Fluid & Electrolyte Balance IV Fluid NPO
Management Gallstone Dissolution Cholesterol Dissolving Agents (May have recurrence after 3 5 years)
jcmendiola_Achievers2013 Chenodeoxycholic Acid (CDCA) / Chenodiol 7 mg/kg Ursodeoxycholic Acid (UDCA) / Ursodiol 8 10 mg/kg [6 12 months] Mechanism of Action: Cholesterol synthesis in the bile
NON-SURGICAL MANAGEMENT 1) Through Endoscopy
2) ESWL (Extracorporeal Shockwave Lithotripsy) Symptomatic cholelithiasis with less than 4 stones Stone < 3cm diameter No history of liver / pancreatic disease Or bile duct disease CI: 1. Recent acute cholecystitis 2. Cholangitis 3. Pancreatitis Position: Stones in Gall Bladder = PRONE Stones in CBD = SUPINE
How is It DONE? - Operational port; dissector** - Laparoscope to visualize - Dissecto** - Retractor - USES Pneumoperitoneum to dilate - USES General Anesthesia!
Laparoscopic VS Open Cholecystography Complications Pneumonia / Atelactasis Deep Vein Thrombosis (DVT) Pulmonary Embolism Biliary Tract Injury Hemorrhage PostOp! - DBE - Coughing exercises
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Open Cholecystectomy Consists of excising the gall bladder from the posterior liver wall and ligating the cystic duct, vein and artery Complications Hemorrhage Pneumonia Thrombophlebitis Urinary retention Bile leakage to abdominal cavity
NURSING MANAGEMENT OF SURGICAL PATIENTS PostOp! 1. Monitor respiratory status 2. Monitor drainage from biliary tubes and incision site 3. Analgesia 4. Maintain fluid balance and hydration 5. Prevent infection 6. Maintain NGT (Assess Bowel SOUNDS q4 hours) 7. Assess CVD Status and manifestations of Shock/Hemorrhage
Signs of Bile Leakage - Pain and tenderness (P&T) in the RUQ - Abdominal Girth - Tachycardia - Bile / Blood leaking from wound - BP Drops!
T-Tube - After Cholecystectomy On level with the bed (Bile bag) - ONE HOUR BEFORE and AFTER EATING (CLAMP)! - Normal amount of bile after surgery 1 st Day: 300 500 mL of bile Maintenance: 1 2 weeks or 10 days 8 th Day RETURN for CHOLANGIOGRAM to know if there is presence of obstruction - Nursing Responsibility for Patients with T-Tube _ Semi-fowlers _ Characteristics of drainage _ Report sudden increase in bile output _ Monitor for inflammation and protect skin from irritation As prescribed, clamp tube BEFORE a meal and observe for abdominal discomfort and distention, nausea, chills / fever Unclamp tube if N/V OCCURS! Patient can go back to work after 4 6 weeks Avoid lifting HEAVY OBJECTS
Cholecystitis Inflammation of the gall bladder Types: Acute inflammation = Inflammation without the presence of a stone Chronic Cholecystitis - Instruct that client can go home after 3 4 days - Client must gradually increase their FAT intake - After the procedure, client MUST void after 6 hours! (Assess BLADDER if not voided) - Clay Colored Stool = NO BILE! - Obstruction = Many**Removed - If excess of more than 800 mL, patient can DRINK the BILE with JUICE / NGT - Check for FOUL odor and purulent drainage - NO TENSION ON TUBINGS!
jcmendiola_Achievers2013 Acalculous Cholecystitis
Pathophysiology Acute Calculous Cholecystitis Risk / Predisposing Factors: - 4 Fs of Gall bladder disease - Sedentary Lifestyle! - Ethnic groups (Chinese, Jewish, Italian)
Complications: - Perforation - Pericholecystitis abscess - Fistula Abnormal opening from an organ due to chronic inflammation
Acalculous Cholecystitis Cause / Predisposing Factors: - Multiple Blood transfusions - Gram Negative bacterial sepsis - Tissue damage after burns, trauma / surgery\ - Hyperalimentation - Prolonged fasting - Anesthesia and opioid analgesic - Mechanical Ventilator with PEEP - Patients with DM and systemic arthritis _ Chance of perforation
Assessment - Pain and tenderness in the RUQ radiating to scapula after eating fatty foods and may persist4 6 hours _ Acute: Last several days Pain located in Epigastric, subscapula RUQ region or at times at right scapula Pain starts suddenly, increase steady and peak in about 30 minutes - + Murphys Sign - N/V - Fever - Mild Jaundice - Guarding rigidity and rebound tenderness - Tachycardia - Signs of dehydration _ Chronic Cholecystitis : Temperature is not as high Leukocyte count is LOWER Less severe pain Temperature is not Low Leukocyte count Vague manifestations of indigestion, Epigastric pain, fat intolerance and heart burn Diagnostic Findings: Cholelithiasis, gallbladder wall thickening (3 cm) and delayed visualization / non visualization of gall bladder
Nursing Diagnosis Alteration in comfort: Pain related to disturbance of the gall bladder Alteration in body temperature: Hyperthermia
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Medical Management 1. Antibiotics 2. Cholecystoctomy = Gall bladder must be decompressed 3. Cholecystostomy a. Surgical drainage of gall bladder b. FIRST PROCEDURE BEFORE CHOLECYSTOCTOMY
Nursing Management Diet (Same with Cholelithiasis [ Calories, Protein]) Antibiotics, analgesics, and anti spasmodic as ordered For chronic: Small, low fat meals NPO Status during N/V status Maintenance of Nasogastric decompression Monitor for Complications
Choledocholithiasis Stone formation on CBD Etiology: Same with Cholelithiasis and narrowing of papilla : Stone pass from gall bladder and lodges in the CBD
Surgical Management - Cholecystectomy - PreOp!: ERCP with Endoscopic papillotomy and stone extraction followed by laparoscopic Cholecystectomy - Choledocholithotomy = Drainage of CBD - Cholecystectomy = Drainage for stain
Alterations in the Pancreas Pancreatitis Inflammation of the pancreas Associated with escape of pancreatic enzymes into surgical tissue Classification: Acute Pancreatitis Chronic Pancreatitis
Acute Pancreatitis - Acute inflammatory process of the pancreas resulting in autodigestion of the pancreas by its own enzymes - Etiology and Risk Factors 4 Alcohol ABUSE! (Men) 4 Biliary Tact Disease (Women) Theres a BACKFLOW 4 Gall bladder Disease (Cholelithiasis) Spasms - Less Common Cause 4 Trauma (Post-surgical abdomen) 4 Viral infection 4 Penetration duodenal ulcers NOTES: If activated in the pancreas, causes damage ALCOHOL ACTIVATES PANREATIC ENZYMES! Amylase Drug or Lipase for therapy Alcohol Physiochemical Change
Leakage to peritoneal cavity Board-like abdomen Cullens Sign Turners Sign Decreased Bowel Sounds Exudate with pancreatic enzymes form peritoneal cavity to pleural cavity via transdiaphragmatic lymphatic channels Atelectasis, Pneumonia Hypovolemia Hypertension Cyanosis Cold Clammy Skin! Destruction of pancreatic islet Hyperglycemia
jcmendiola_Achievers2013 Assessment 1. Pain a. Abdominal pain b. Includes sudden onset of mid Epigastric / LUQ radiating at the back c. Aggravated by a fatty meal, alcohol, or supine position 2. Abdominal tenderness and guarding 3. N/V 4. Weight loss 5. Cullens Signs = Discoloration of abdomen and Periumbilical area 6. Turners Sign = Bluish discoloration of the left flank 7. Bowel Sounds 8. WBC, Glucose, Bilirubin, Alkaline Phosphatase Bone Problems, either CVD obstruction 9. Serum lipase and amylase, urine amylase
Diagnostic Tests 1. History and Physical Examination 2. ERCP 3. CT Scan 4. Abdominal X-Ray 5. Lab Work Up: Serum Ca Serum Amylase and Lipase BUN Glucose Bilirubin Alkaline Phosphatase
Nursing Diagnosis - Alteration in comfort: Pain related to inflammation of the pancreas and surrounding tissue - Imbalance nutrition: less than body requirements related to inability to ***
Medical Management - Pain medications - Fluid volume status and electrolyte imbalance - Nutritional status - Exocrine functions - Treat complication
Surgical Management 1. Laparotomy with support drainage 2. Debridement with surgical / retroperitoneal drainage 3. Subtotal pancreatectomy 4. Whipples Surgical procedure (Pancreaticoduodenectomy)
Nursing Management - No Alcohol! 4 Bed rest 4 Position = Semi fowlers / High fowlers - NPO and Hydration, NGT suction (To remove gastric contractions), TPN - Supplemental preparations
jcmendiola_Achievers2013 - Pain medications, antacids, H2 receptor antagonist, and anticholinergics
Chronic Pancreatitis - Continuous prolonged inflammation and fibrosis process of the pancreas - Fibrin of scar tissue
Etiology: - Alcohol (70 80% of case) - Idiopathic (25%) - Hereditary - Biliary obstruction of pancreatic duct and by stores) 4 Recurrent and chronic inflammation
Calcium Induced Pancreatitis - Most common form - Inflammation and sclerosis maintaining at head of pancreas and pancreatic duct
Assessment 1. Abdominal Pancreatitis Continuous intermittent / absent Gnawing feeling / **** cramp like Not relieved with food / antacids Patient experience more pain in supine Attack lasts a few days 2 weeks 2. Weight loss and malnutrition 3. Hyperglycemia, DM manifestations 4. Abdominal distention with flatus and cramps 5. Steatorrhea
Medical Management 1. Medications Pancreatic enzymes rep (Pancreatic Cotazym) Non-opioid to opioid analgesics Antibiotics Antacids H 2 : Ranitidine (Zantac) PPI CAI: Acetazolamide Antispasmodic Dicyclomine (Bentyl) Antiemetic Antipyretic 2. Diet 3. Control DM 4. Bile salts
Surgical Management - Whipples - Total pancreatectomy - Chole** - Total Pancreatectomy with S placing - Biliary Stents (Cotton Leung Stent) - Percussing celiac plexus nerve block
Hepatic Alterations Hepatitis Inflammation of the liver caused by a virus, bacteria or exposure to medications or hepatotoxins Goal of Therapy: Rest the inflamed liver (3 4 months regeneration)
Types 1. Alcoholic Hepatitis a. Male: SHOULD BE LESS THAN 80 mg to be SAFE b. Female: SHOULD BE LESS THAN 40 mg to be SAFE
Clinical Manifestations Anorexia, nausea Abdominal pain Splenomegaly Backing up of blood in the spleen Hepatomegaly Ascites (Accumulation of fluid in the peritoneal cavity) Fever Inflamed liver Encephalopathy Jaundice
Nursing Management - Medications - Assessment - NPO (3 7 days) cystic suction - Physical movement and mental stimulation - Position for comfort - IV fluids replacement of electrolytes
Nursing Management: Vitamins, Carbohydrate diet Administer folic acid ( metabolism), thiamine supplements Steroids SAFEST DRUG OF CHOICE Parenteral fluids Liquid formula to increase caloric intake NO ALCOHOL
2. Viral Hepatitis (P = Preventable, T = Treatable) Hepatitis A Infectious hepatitis (P&T) Hepatitis B Serum hepatitis (P) Hepatitis C Non-A,B hepatitis, post transfusion (P&T) Hepatitis D Delta agent hepatitis Hepatitis E Enterically transmitted or epidemic Non-B hepatitis
Stages: Pre-Icteric / Predominal Stage (No Jaundice Yet!) 2 weeks AFTER EXPOSURE and ENDS WITH APPEARANCE of JAUNDICE Manifestations: Flu-like symptoms, fatigue, malaise, fever Anorexia, N/V Headache, muscle ache Mildpain in the RUQ in bilirubin and enzyme level Icteric Stage (Illness Stage) 1 2 weekds after PRODROMAL PHASE Lasts 2 6 WEEKS ! Manifestations : Pre-icteric signs Jaundice Liver is enlarged Pruritus Light colored stool = If conjugated bilirubin cannot flow on the liver because of an obstruction Brown-colored urine Fever Fatigue Post-Icteric Stage (Recovery Phase) Resolution of jaundice 6 8 weeks prior to exposure Symptoms diminishes, but liver remains to be ENLARGED and TENDER Liver function returns to normal 2 12 weeks prior onset of jaundice Manifestations: Energy levels Pain subsides Minimal to absent GI symptoms Serum bilirubin and enzyme levels return to normal
Medical Management: 1. Reduce fatigue 2. Maintain nutritional fluid balance: Calorie / CHO, Fat, NO ALCOHOL [2,500 3000 kcal/day]
jcmendiola_Achievers2013 3. Bile acid sequestrants (To DILUTE the cholesterol bile containing acid) a. Cholestyramine Questran b. Colestipol Colestid 4. Immunoglobulin prophylaxis (IM Injection) 5. Vaccine 6. Avoid Hepatotoxic drugs (Acetaminophen [Tylenol], Chlorpromazine [Tranquilizers])
Nursing Management Assess for history of exposure to risk factors, manifestations, liver function studies
Nursing Diagnoses: a. Fatigue related to decreased metabolic energy production secondary to liver dysfunction Goal: Client will convey reduced fatigue and heightened energy level as manifested by gradual increase of activity Interventions: 4 Bed rest / rest periods 4 ADL 4 Personal hygiene 4 No alcohol 4 Vitamin supplements 4 Antiemetics b. Alteration in nutrition less than body requirements related to anorexia, nausea, impaired absorption and metabolism of nutrients Interventions 4 Nutritious meal, NO FATTY FOODS (Low TO MODERATE PROTEIN) 4 Small but frequent meals
Complications Chronic Hepatitis Autosomal recessive disease Liver infection for greater 3 6 months Fulminant Hepatitis Severe impairment or necrosis of liver cells and potential liver failure May occur as a complication of HBV, HCV, congenital metabolic disorder Jaundice, coagulation defect, electrolyte disturbance, hypoglycemia, encephalopathy, hepatitis
Liver Cirrhosis A chronic progressive disease of the liver, characterized by Diffuse degeneration, fibrosis (Scarring) and nodule formation
jcmendiola_Achievers2013 Pathophysiology Prolonged alcohol ingestion Enzyme induction and activity of medications Produce end-products ACETYLDEHYDE and FREE RADICALS Toxic effects to the liver NAD (Nicotinic Adenine Dinucleotide) Availability Mitochondrial electrical transport system Protein synthesis Lipid synthesis or ketogenesis Fatty liver! Collagen synthesis Fibrogenesis/ lesions Liver damage Scarring Inflammation Pain Anorexia Nausea Jaundice Ascites Liver, yellow and enlarged Nodules Portal Hypertension Toxic Effects to the LIVER
POST-NECROTIC Occurs after massive liver necrosis Etiology: Post acute viral (Hep B&C) exposure to toxins Scar tissue cause destruction to liver lobules
Pathophysiology
jcmendiola_Achievers2013 Hepatitis B Virus Enters the vagina, mucus membranes, skin Health care workers Immune system Liver cell (Inflammation) Clinical Cirrhosis Carrier Acute Icteric Chronic Hepatitis Convalescent Cirrhosis Progressive liver cell / Hepatodysfunction Fibrosis / Scarring Pressure in the portal circulation Portal HTN!!
BILIARY CIRRHOSIS Characterized by: Prolonged state of bile duct inflammation and jaundice due to retention of bile due to narrowing of ducts Primary Inflammation: Destruction, fibrosis, and destruction of Intrahepatic bile salts resulting in nodular regeneration and cirrhosis Secondary Inflammation: Inflammation, scarring and obstruction of bile ducts outside of the liver Pathophysiology
CARDIAC CIRRHOSIS Pathophysiology
Other Pathophysiology :\...
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1 Glycogenesis and Glycogenolysis and Gluconeogenesis Altered glucose metabolism Energy Weakness, fatigue, malaise 2 FA and TAG Synthesis FA Oxidation and Triglyceride Release Fatty liver Hepatomegaly Energy production Weakness, fatigue, malaise Production of albumin 3 Colloidal osmotic pressure Edema, Ascites 4 Production of clotting factors Altered clotting studies Bleeding tendencies Blood loss Anemia CHON Synthesis (In general) Altered immune function and altered healing Susceptibility to infection 5
jcmendiola_Achievers2013 Metabolism of steroid Hormone 6 Estrogen, Progesterone, Testosterone Male Female Loss of muscular characteristics and development of some feminine characteristics Loss of feminine characteristics and development of some masculine characteristics Aldosterone Na and Water Retention K and H Excretion Edema, Ascites Hypokalemia, Alkalosis Metabolism of Ammonia 7 Ammonia Levels Hepatic Encephalopathy Coma Death Changes in coordination, memory orientation Asterixis Fetor Hepaticus Metabolism of Drugs Drug toxicity 8 Storage of Vitamins and minerals RBC Production Energy Production Anemia 9
Obstruction of bile flow Bile reabsorbed in the blood Fat absorption Vitamin K absorption Clotting factors Bleeding / Anemia Bilirubin in GIT Bilirubin in feces Clay-colored Feces 10 Bile salts in skin Pruritus Jaundice Kidney Dark urine Bilirubin Level
jcmendiola_Achievers2013 Nursing Diagnoses Ineffective tissue perfusion related to bleeding tendencies Imbalanced nutrition: Less than body requirements related to anorexia, impaired liver function and decreased absorption of soluble vitamins secondary to inflammation, obstruction and destruction on the bile duct Activity intolerance related to fatigue and lack of energy due to decreased nutrients
Nursing Interventions - Assess for signs of bleeding (Gums, melena) - Check VS: Signs of shock - Provide sufficient rest and comfort - Monitor / prevent bleeding - Prevent infection - Administer diuretics as ordered (Strict I&O!!) To decrease portal hypertension - Sufficient rest and comfort Relieve pruritus - Promote nutritional intake: TPN, NGT - Health Education: 4 Vitamin supplements Vit B and FSV (ADE) 4 Vitamin K Injection To improve blood clotting 4 Collaborate with lab technicians, physician, SO
Complications of Liver Cirrhosis Portal Hypertension Abnormally high blood pressure in portal venous system / vena cava that results from obstruction of blood flow through the damaged liver pressure at least 12 mmHg Normal venous BP at least 5 10 mmHg Long term portal hypertension cause distended, twisted, collateral veins; transformed to varicosities Collateral channels: Lower esophagus, anterior abdominal wall, parietal peritoneum, rectum- hemorrhoids Pressure; Plasma volume Lymphatic flow
Esophageal Varices Complex tortuous collateral veins (from collateral channels) at the lower end of the esophagus due to prolonged elevation of pressure Life-threatening condition!
Diagnostic Evaluation Barium Swallow NPO After midnight, assess for allergies (Laxatives) Fluids and laxatives AFTER the procedure Stool: White-ish
Medical Management Sclerotherapy
Transjugular Intrahepatic Portosystemic Shunt (TIPS) More than successful 90% Percutaneous placement of a Portosystemic shunt Fluoroscopy, an expandable metal stent is inserted to the hepatic vein through angiogram and then to the liver, a direct portocaval channel Vasopressin Given to stop variceal bleeding MOA: Reduces portal venous blood flow by constricting different afferent arterioles SE: Hypothermia, MI, GI ischemia, Acute renal failure CI: Clients with recent MI (Causes VASOCONSTRICTION) May be given with nitroglycerin (To vasodilate MI patients) Balloon Tamponade Puts pressure of the esophagus and gastric balloon to stop bleeding A.k.a. Sengstaken Blakemore Tube / Minnesota Tube Presence of 4 esophageal opening
jcmendiola_Achievers2013 1. Gastric Balloon Inflation lumens 2. Esophageal Balloon Inflation lumens Not always inflated for 24 hours During deflation, esophagus balloon will comf 1 st before gastric balloon 3. Gastric aspiration lumen Complications: 1. Esophageal rupture 2. Aspiration 3. Pneumonia Care of Patients with SB Tube!~ 1. Facilitate placement of tube 2. PLACE PATIENT ON A SEMI-FOWLER\S 3. Maintain traction by securing tube to a piece of sponge or foam placed on the nose so the balloon wont be displaced 4. Keep scissors at bedside (emergency cut tubes) 5. Monitor respiratory rate 6. Label each lumen to avoid confusion 7. Maintain prescribed amount of pressure as ordered 25 40 mmHg for esophageal balloon 100 120 mmHg for gastric balloon 8. Provide oral/nasal care q 1-2 hrs 9. Suction gently if cannot expectorate secretions 10. Vitamin K therapy or BT 11. For severe thirst: Oral hygiene and moist sponges on the lips 12. Gastric lavage with cool saline
Surgical Management 1. Endoscopic Band Ligation a. Device with a small rubber band (O ring) at the end of the endoscope Over the varix b. MD places rubber band covered varix which sloughs off after days c. Important for clients who are taking beta-blocker therapy d. Stops bleeding from varices 2. Portosystemic Shunt a. Anastomosing = the high pressure portal venous system to low pressure systemic venous system b. MOA: portal venous blood pressure, thus the risk of ruptured esophageal varices c. Reserved to clients who do not respond to treatment d. Types: 4 Portacaval End side/side-side anastomosis of portal vein to IVC 4 Splenorenal From Splenic vein to left vein (artery) hmm 4 Mesocaval End to side or use of graft to anastomose IVC to side of superior mesenteric vein
Nursing Management Assess patent airway Nutrition and Neurologic status Gastric lavage with cool saline Quiet environment Vasopressin Signs and Symptoms of Bleeding and Shock! Early: Tachycardia Late: Bradycardia; BP Health Education Esophageal irritation PeriOp! Nursing Management PreOp! PostOp! 1. Explain 1. Assess 2. Tests 2. Nutrition 3. Consent 3. IVF 4. Dressing 5. Blood and urine levels
jcmendiola_Achievers2013 NO ALCOHOL NO IRRITATING AGENTS No in abdominal / thoracic / portal pressure
Ascites Accumulation of fluid in the peritoneal cavity that results from several pathological changes Due to damaged liver 15 mL/more srum albumin-rich fluid accumulating in the peritoneal cavity = serum osmotic pressure = movement of fluid to peritoneal cavity = ASCITES Inactivation of aldosterone = Na Retention Portal HTN
Pathophysiology Liver damage, cirrhosis Metabolism of aldosterone Na and water retention Hypovolemia Splanchic arterial vasodilation Blood volume Activation of RAAS Albumin synthesis Oncotic pressure, especially in the peritoneal cavity Fibrous tissue and nodules Capillary pressure Obstruction of venous flow
Clinical Manifestations 1. Abdominal girth 2. Weight gain 3. Shortness of breath 4. Striae 5. Distended veins in the abdomen 6. Umbilical hernias 7. Fluid wave 8. Bulging flanks when lying supine
Medical Management Transjugular Intrahepatic Portosystemic Shunt (TIPS) Diuretics: Spironolactone (1 st line of DRUG!) Paracentesis Nursing Diagnoses: - Alteration in fluid volume balance: excess / deficient related to fluid shifts secondary to portal hypertension, hypoalbuminemia and hyperaldosteronism - Ineffective breathing pattern related to increased intra-abdominal pressure on diaphragm Medical Management: - Paracentesis - Albumin IV - Maintain fluid and electrolyte balance (1 L 1.5 L/day) - Dietary modification - Diuretics - Maintain skin integrity - TIPS
jcmendiola_Achievers2013 Transabdominal removal of fluid from the cavity through a puncture of small incisions from the peritoneal cavity Large volume Paracentesis 6 L yields immediate effect in combination with IV infusion of salt-poor albumin (helps correct the ineffective arterial blood volume that lead to Na retention)
Nursing Management Before Procedure 1) Explain 2) Consent 3) VS, Abdominal Girth, Weight 4) Empty bladder 5) Position client (Semi fowlers / High fowlers After Procedure Assess for signs of hypovolemia due to aspiration Assess comfort Dressing Patient education No Na in diet Bed rest Upright position activates RAAS which promotes Na and water retention Promoting skin integrity Weight daily Avoid NSAIDS and Aspirin: Inhibits prostaglandin which leads to Na retention
Hepatic Encephalopathy (Portal Systemic Encephalopathy) Accumulation of ammonia (theres already a problem in the conversion of ammonia to urea) and other toxic metabolites in the blood Ammonia inhibits neurotransmission and synaptic regulators Characterized by altered level of consciousness, neurologic symptoms
Stages of Encephalopathy Prodromal Changes may be subtle Inability to concentrate Forgetfulness, altered sleep habits Agitation, restlessness, memory disturbances, impaired judgment, slurred speech Impending With increasingly obvious impairment, periods of confusion, asterixis Lethargy, disorientation to time, deterioration in handwriting Stuporous Evident severe mental deficits Difficult to arouse Asterixis, incoherence, inability to follow commands, hyperreflexia, muscle twitching Coma FINAL STAGE is DEEP COMA Theres a Babinski reflex (damaged brain), comatose, fetor hepaticus, unresponsive to painful stimuli, possible decorticate / decerebrate
Diagnostic Tests Electroencephalogram: Shows a generalized slowing, increased amplitude of brain waves Surgical Management - LeVeen Shunt o Permits reinfusion of ascetic fluid into the venous system through a silicone catheter with one way pressure-sensitive valve o One end of the catheter is implanted in to the peritoneal cavity channeled to the SVC where the other end of the catheter is inserted
jcmendiola_Achievers2013 Serum ammonia and CSF glutamine levels Electrolyte level Blood gases Hepatic function test results (e.g. bilirubin, prothrombin, albumin and enzymes)
Nursing Diagnosis Ineffective therapeutic regimen related to reduction in protein in the diet in and pharmacologic intervention Increased risk for injury
Medical Management 1. Assess 2. Neomycin a. Decreases the action of intestinal bacteria b. CI: Renal insufficiency 3. Lactulose a. Promotes excretion of ammonia in stool b. Ammonia kept in ionized state in colon pH No passage from colon to blood c. Bowel evacuation Ammonia not absorbed from colon d. Fecal flora changed into organisms that do not convert ammonia to urea 4. Antibiotics 5. Oral MgSO 4 or Enemas after hemorrhage 6. IVF and Vitamin: To minimize CHON breakdown
Nursing Management 1. Assess 2. Restrict CHON to avoid presence of ammonia from amino acids, provide CHO intake and Vitamin K supplements 3. Medications 4. Protection from injury 5. Bed rest
Liver Transplantation For end-stage liver disease 6 18 hours procedure Complications: 1. Cardio and pulmonary problems 2. Infection 3. Rejection a. Which occurs on the 4 th 6 th day b. CM: TRIF!! Tachycardia, RUQ/flank pain, jaundice, fever (early sign) 4. Hemorrhage 5. Atelactasis 6. Failure of anastomosis 7. Acute renal failure Nursing Management: Post Operative Monitor signs of rejection Cyclosporine, corticosteroids, Azathioprine (Imuran) > 6 months (Drugs to prevent rejection)
jcmendiola_Achievers2013 Contraindications: \ Life threatening systemic disease \ Uncontrolled extrahepatic bacterial or fungal infection \ Pre-existing advanced cardiovascular or pulmonary disease \ Multiple, uncorrectable congenital anomalies \ Metastatic making to *** \ Active alcoholism / drug abuse \ Cholangiogram \ HIV Discharge Instruction \ Infection? \ Rejection? \ Medications? \ Potential body changes? \ Follow up care: 2 3 days AFTER
Pathophysiology Pulmonary HTN Liver cell damaged and necrosis Failure to convert ammonia Serum NH3 Glial and nerve cell affectation Altered CNS metabolism and function Form of new compound octopamine False neurotransmitter