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Care of Clients with Problems In Oxygenation,
Fluids and Electrolytes, Metabolism and Endocrine
(NCM103)
Patients With Hepatic, Biliary and Pancreatic Disroders
Accessory OrgansAnatomy and Physiology of theLiver
What are the Functions of the Liver1. 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 thedistal 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. Liverb. Biliary Tractc. Pancreas
2. Assessment of the Liver3. Alterations in the Gall Bladder
a. Cholelithiasisb. Cholecystitisc. Choledocholithiasis
4. Alterations in the Pancreasa. Pancreatitisb. Chronic Pancreatitis
5. Alterations in the Livera. Hepatitisb. Liver Cirrhosis
6. Complications of Liver Cirrhosisa. Portal Hypertensionb. Esophageal Varicesc. Ascitesd. Hepatic Encephalopathy
7. Liver Transplantation
LOOKY
HERE
Hepatic Arteryo Amount of blood receives 300 500 mL/min
of O2 blood from the heart
Hepatic Veino Excretes deoxygenated blood but is FULL of
nutrients (1,000 1500 mL/min)
o Kuppfer Cells Immunity, destroysmicroorganisms
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
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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
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6. Protein Metabolism
7. Storage of Iron and Vitamin
8. Metabolism Detoxification
9. Metabolic Detoxification
BILIARY TRACT1. 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 abdomeno 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 fluido 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 DiseaseAssess
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 downwardAbdominal Assessment:
Murphys Sign
o Painful deep breathing during liver palpationo Client is unable to complete the inspiration; abruptly stops inspiration midwayo 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 lowerquadrant
Specific maneuver for assessing ASCITESo 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 TestBile Formation and Secretion
Test Normal Value1. Direct (Conjugated Bilirubin) 0 0.3 mg/dL2. Indirect (Unconjugated Bilirubin) 0 1 mg/dL3. Total Serum Bilirubin 0.1 1.2 mg/dL
Test Normal Value
1. Total Serum Protein 7.0 7.5 g/dL2. Serum Albumin 3.5 5.5 g/dL3. Serum Globulin 2.5 3.5 g/dL
RESONANT ABOVE
8 cm DULLNESS
RESONANT BELOW
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4. A/G Ratio 1.5:4 to 2.5:1Coagulation Studies
Test Normal Value
1. Prothrombin Time 11.5 14 seconds2. Partial Thromboplastin Time 25 40 seconds
Test Normal Value1. AST (SGPT) 8 20 u/L2. ALT (SGOT) 10 35 u/L3. Alkaline Phosphatase 32 92 u/L4. LDH LDH5. Blood ammonium 150 250 mg/dL
Diagnostic Tests1. Abdominal X-Ray To visualize solid / liquid part2. 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:
CHEAPER7. CT Scan8. 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. Position2. Consent 2. Inhale-exhale THEN HOLD BREATHE
AT THE END OF EXPIRATION!2. NO COUGHING / STRAINING
3. NPO 3. Vital Signs4. Vital SignsLarge 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)
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Types
1. Hemolytic Jaundice (Pre-Hepatic)o Causes:
Blood Transfusions, immune reactions, membrane defectsof 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 Management1. Determine cause of jaundice
a. Health Historyb. Physical Examinationc. Liver Function Testd. Hematologic Test
2. Reduce pruritus and maintenance of skin integritya. Oral cholestyramine-resinb. Antihistamine and phenobarbital
Nursing Management1. Assess:
Assess for any signs of jaundice formation2. Nursing Diagnosis
Impaired skin integrityi. Tepid water / emollient bath
ii. Frequent application of lotioniii. Loose and soft clothingiv. Soft bed linen (e.g. Cotton)v. Keep the room cool
Alteration in body imagei. Encourage verbalization of feelings
ii. Assist in perineal hygiene as needed
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iii. Promote activity as toleratedSURGICAL MANAGEMENT:
- Cholechostomy: Exploration of the CBDAlterations of the Liver
Biliary Tract and Exocrine Pancreas
CHOLETHIASIS1) 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 composition2. Gall Bladder Stasis Bile stasis3. Infection predisposes a person to stone formation4. Genetics and demography
There are Three Types of Gallstones!~
Cholesterol1. Most common type2. Usually smooth and whitish, yellow
Pigment1. Bile contains excess unconjugated bilirubin.2. Blade / earthly calcium bilirubinate
Mixed Combination Minor Constituents1. Calcium Carbonate, bile salts and palmitate
GALLSTONE FORMATION Causes:
1. Too much absorption of water from bile2. Too much absorption of the bile ducts from bile3. Too much cholesterol in bile4. Inflammation of the epithelium Course Followed by Bile:1. During rest2. During Digestion (3 4 hours after meal)
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Unconjugated
bile precipitate
Pathophysiology of Gall Stone Formation
Formation of
pigmentedstones
Malabsorption
disorder
Malabsorption
of bile salts
Bile synthesis
Estrogen
therapyPregnancy
Gallbladder
sludge
Obesity
increase with
age
Hepatic
secretion ofcholesterol
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
CHOLECYSTITISIrritate
gallbladder lining
Ultrasound
Cholecystography
ERCP
Obstruction of the passage for BileAbdominal 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 fullinspiration and
excursion
Bile in the
duodenum
Malabsorption of
Vitamins ADEK
Signs andSymptoms
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, rightshoulderand the rightscapula / the
mid-scapular region
Pain occurs 3 6 hours AFTER HEAVY MEAL / when the client LIES down2. Anorexia & N/V Stimulation of the VAGUS NERVE
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3. Intolerance to FATTY FOODS, sensation of FULLNESS4. Jaundice, bleeding, tenderness and Steatorrhea, clay colored stool
Diagnostic Tests1. Ultrasound
Most sensitive test to detect and visualize stone I: Obstruction, jaundice, allergies to contrast media2. 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 AcidNursing 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 Management1. Medications
Analgesics Antacids, H2 Blockers, Proton Pump Inhibitor (PPI) Antiemetics Antibodies Nitroglycerin
2. Fluid & Electrolyte Balance IV Fluid NPO
ManagementGallstone Dissolution
Cholesterol Dissolving Agents (May have recurrence after 3 5 years)
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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 cholecystitis2. Cholangitis
3. Pancreatitis Position:
Stones in Gall Bladder = PRONE Stones in CBD = SUPINE
SURGICAL MANAGEMENT
PreOp!
1. Consent2. NPO BEFORE MIDNIGHT3. Skin preparation4. Enema5. Antibiotic
Laparoscopic Cholecystectomy I: Symptomatic gallbladder disease, acute cholecystitis Advantage: Minimal trauma to abdomen CI: CholedocholitiasisHow is It DONE?
- Operational port; dissector**- Laparoscope to visualize- Dissecto**- Retractor- USES Pneumoperitoneum to dilate-
USES General Anesthesia!
Laparoscopic VS Open CholecystographyComplications
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 cavityNURSING MANAGEMENT OF SURGICAL PATIENTSPostOp!
1. Monitor respiratory status2. Monitor drainage from biliary tubes and incision site3. Analgesia4. Maintain fluid balance and hydration5. Prevent infection6. 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
1st Day: 300 500 mL of bile Maintenance: 1 2 weeks or 10 days
8th Day RETURN for CHOLANGIOGRAM to know if there ispresence 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 mealand 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 4days
- Client must gradually increase their FATintake
- After the procedure, client MUST void after6 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 purulentdrainage
- NO TENSION ON TUBINGS!
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Acalculous CholecystitisPathophysiology
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 perforationAssessment
- Pain and tenderness in the RUQ radiating to scapula after eating fatty foods and maypersist4 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 Management1. Antibiotics2. Cholecystoctomy = Gall bladder must be decompressed3. Cholecystostomy
a. Surgical drainage of gall bladderb. 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
Assessment- Frequency, mild / severe RUQ pain- Intermittent / progressive jaundice (Clay colored feces, tea colored urine)- Chills and Fever
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 ownenzymes
- Etiology and Risk Factors Alcohol ABUSE! (Men) Biliary Tact Disease (Women) Theres a BACKFLOW Gall bladder Disease (Cholelithiasis) Spasms
- Less Common Cause Trauma (Post-surgical abdomen) Viral infection Penetration duodenal ulcers
NOTES:
If activated in the pancreas, causesdamage
ALCOHOL ACTIVATES PANREATICENZYMES!
Amylase Drug or Lipase for therapy Alcohol Physiochemical Change
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Cysts and abscesses Metabolic disorders (Renal failure, hyperthyroidism, hyperlipidemia) Vascular disease Drugs
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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 isletHyperglycemia
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Assessment1. Pain
a. Abdominal painb. Includes sudden onset of mid Epigastric / LUQ radiating at the backc. Aggravated by a fatty meal, alcohol, or supine position
2. Abdominal tenderness and guarding3. N/V4. Weight loss5. Cullens Signs = Discoloration of abdomen and Periumbilical area6. Turners Sign = Bluish discoloration of the left flank7. Bowel Sounds8. WBC, Glucose, Bilirubin, Alkaline Phosphatase Bone Problems, either CVD
obstruction
9. Serum lipase and amylase, urine amylaseDiagnostic Tests
1. History and Physical Examination2. ERCP3. CT Scan4. Abdominal X-Ray5. 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 Management1. Laparotomy with support drainage2. Debridement with surgical / retroperitoneal drainage3. Subtotal pancreatectomy4. Whipples Surgical procedure (Pancreaticoduodenectomy)
Nursing Management- No Alcohol!
Bed rest Position = Semi fowlers / High fowlers
- NPO and Hydration, NGT suction (To remove gastric contractions), TPN- Supplemental preparations
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- Pain medications, antacids, H2 receptor antagonist, and anticholinergicsChronic Pancreatitis
- Continuous prolonged inflammation and fibrosis process of the pancreas- Fibrin of scar tissueEtiology:
- Alcohol (70 80% of case)- Idiopathic (25%)- Hereditary- Biliary obstruction of pancreatic duct and by stores)
Recurrent and chronic inflammationPathophysiology
Types:
1. Chronic Obstructive Pancreatitis2. Chronic Calcification PancreatitisCalcium Induced Pancreatitis
- Most common form-
Inflammation and sclerosis maintaining at head of pancreas and pancreatic duct
Assessment1. 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 weeks2. Weight loss and malnutrition
3. Hyperglycemia, DM manifestations4. Abdominal distention with flatus and cramps5. Steatorrhea
Diagnostic Tests- ERCP- Imaging Studies: CT, MRCP, Transabdominal ultrasound
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- Secretin Stimulation Test- Lab Study: Serum amylase, lipase bilirubin
Medical Management1. Medications
Pancreatic enzymes rep (Pancreatic Cotazym) Non-opioid to opioid analgesics Antibiotics Antacids H2: Ranitidine (Zantac) PPI CAI: Acetazolamide Antispasmodic Dicyclomine (Bentyl) Antiemetic Antipyretic
2. Diet3. Control DM4. Bile salts
Surgical Management- Whipples- Total pancreatectomy- Chole**- Total Pancreatectomy with S placing- Biliary Stents (Cotton Leung Stent)- Percussing celiac plexus nerve block
Hepatic AlterationsHepatitis
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 Hepatitisa. Male: SHOULD BE LESS THAN 80 mg to be SAFEb. 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
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Diagnostic Tests
Labs: Anemia, Leukocytosis, Bilirubin Biopsy: Fatty hepatic tissue (FATTY LIVER)
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 fatigue2. Maintain nutritional fluid balance: Calorie / CHO, Fat, NO ALCOHOL [2,500 3000 kcal/day]
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3. Bile acid sequestrants (To DILUTE the cholesterol bile containing acid)a. Cholestyramine Questranb. Colestipol Colestid
4. Immunoglobulin prophylaxis (IM Injection)5. Vaccine6. Avoid Hepatotoxic drugs (Acetaminophen [Tylenol], Chlorpromazine [Tranquilizers])
Nursing Management
Assess for history of exposure to risk factors, manifestations, liver function studiesNursing 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: Bed rest / rest periods ADL Personal hygiene No alcohol Vitamin supplements Antiemetics
b. Alteration in nutrition less than body requirements related to anorexia, nausea, impairedabsorption and metabolism of nutrients
Interventions Nutritious meal, NO FATTY FOODS (Low TO MODERATE
PROTEIN)
Small but frequent mealsComplications
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
Clinical Manifestations
Spider angiomasTypes
1. Laennecs Cirrhosis2. Post-Necrotic3. Biliary Cirrhosis4. Cardiac Cirrhosis
LAENNECS CIRRHOSISTypes:
Portal Cirrhosis Alcohol Cirrhosis Micronodular Cirrhosis
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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
damageScarring
Inflammation
Pain
AnorexiaNausea
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
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Hepatitis B
Virus
Enters the vagina,
mucus membranes, skin
Health care workers
Immune system
Liver cell
(Inflammation)
Clinical Cirrhosis
CarrierAcute
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 saltsresulting in nodular regeneration and cirrhosis
SecondaryInflammation: Inflammation, scarring and obstruction of bile ducts outsideof the liver
Pathophysiology
CARDIAC CIRRHOSISPathophysiology
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
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Metabolism of steroid Hormone6
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 Ammonia7
Ammonia Levels
Hepatic Encephalopathy Coma
DeathChanges 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
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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 nutrientsNursing 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:
Vitamin supplements Vit B and FSV (ADE) Vitamin K Injection To improve blood clotting Collaborate with lab technicians, physician, SO
Complications of Liver CirrhosisPortal Hypertension
Abnormally high blood pressure in portal venous system / vena cava that results from obstructionof 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
Pathophysiology
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Clinical Manifestation- Splenomegaly, hemorrhoids, esophageal varices
Diagnostic Evaluation- Splenoportogram: Indirect measurement of portal venous blood flow- Liver Scan
Complications- Hemorrhage
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!CARDINAL SIGN: ESOPHAGEAL BLEEDING (DARK COLORED BLOOD)
Assessment:
- History of alcohol abuse- Hematemesis?- Melena?- Anorexia?- Nausea?- Splenomegaly?- Caput medusae More prominent than
SPIDER ANGIOMA
- Splenic dullness
Clinical Manifestation:- Hematemesis- Anorexia- Nausea- Splenomegaly- Caput medusae- Splenic dullness
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
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1. Gastric Balloon Inflation lumens2. Esophageal Balloon Inflation lumens
Not always inflated for 24 hours During deflation, esophagus balloon will comf 1st before gastric
balloon
3. Gastric aspiration lumen
Complications:1. Esophageal rupture
2. Aspiration3. Pneumonia
Care of Patients with SB Tube!~1. Facilitate placement of tube2. PLACE PATIENT ON A SEMI-FOWLER\S3. 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 rate6. Label each lumen to avoid confusion7. 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 hrs9. Suction gently if cannot expectorate secretions10. Vitamin K therapy or BT11. For severe thirst: Oral hygiene and moist sponges on the lips12. Gastric lavage with cool saline
Surgical Management1. Endoscopic Band Ligation
a. Device with a small rubber band (O ring) at the end of the endoscope Over the varixb. MD places rubber band covered varix which sloughs off after daysc. Important for clients who are taking beta-blocker therapyd. Stops bleeding from varices
2. Portosystemic Shunta. 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 varicesc. Reserved to clients who do not respond to treatmentd. Types:
Portacaval End side/side-side anastomosis of portal vein to IVC Splenorenal From Splenic vein to left vein (artery) hmm 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. Assess2. Tests 2. Nutrition3. Consent 3. IVF
4. Dressing5. Blood and urine
levels
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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
Contributing Factors
- Portal HTN- Plasma colloid osmotic pressure- Flow of hepatic lymph- Hyperaldosteronism- Impaired water excretion
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 girth2. Weight gain3. Shortness of breath4. Striae5. Distended veins in the abdomen6. Umbilical hernias7. Fluid wave8. Bulging flanks when lying supine
Assessment
Dull upon percussion Fluid wave, detect Paracentesis Abdominal x-ray Ultrasound
Medical Management
Transjugular Intrahepatic Portosystemic Shunt (TIPS) Diuretics: Spironolactone (1st 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 toincreased 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
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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-pooralbumin (helps correct the ineffective arterial blood volume that lead to Na
retention)
Nursing Management
Before Procedure1) Explain
2) Consent
3) VS, Abdominal Girth, Weight
4) Empty bladder
5) Position client (Semi fowlers / High fowlers
After ProcedureAssess 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
Surgical Management
LeVeen Shunt (Peritoneal Venous Shunt)Hepatic Encephalopathy (Portal Systemic Encephalopathy)
Accumulation of ammonia (theres already a problem in the conversion of ammonia to urea) andother 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 Shunto Permits reinfusion of ascetic fluid into the venous
system through a silicone catheter with one waypressure-sensitive valve
o One end of the catheter is implanted in to theperitoneal cavity channeled to the SVC where theother end of the catheter is inserted
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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 pharmacologicintervention
Increased risk for injuryMedical Management
1. Assess2. Neomycin
a. Decreases the action of intestinal bacteriab. CI: Renal insufficiency
3. Lactulosea. Promotes excretion of ammonia in stoolb. Ammonia kept in ionized state in colon pH No passage from colon to bloodc. Bowel evacuation Ammonia not absorbed from colond. Fecal flora changed into organisms that do not convert ammonia to urea
4. Antibiotics5. Oral MgSO4 or Enemas after hemorrhage6. IVF and Vitamin: To minimize CHON breakdown
Nursing Management
1. Assess2. Restrict CHON to avoid presence of ammonia from amino acids, provide CHO intake and Vitamin
K supplements
3. Medications4. Protection from injury5. Bed rest
Liver Transplantation For end-stage liver disease 6 18 hours procedure Complications:
1. Cardio and pulmonary problems2. Infection3. Rejection
a. Which occurs on the 4th 6th dayb. CM: TRIF!! Tachycardia, RUQ/flank pain, jaundice, fever (early sign)
4. Hemorrhage5. Atelactasis6. Failure of anastomosis7. Acute renal failure
Nursing Management: Post Operative Monitor signs of rejection Cyclosporine, corticosteroids, Azathioprine (Imuran) > 6 months (Drugs to
prevent rejection)
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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