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jcmendiola_Achievers2013

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


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


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

ncm103 26th acce i

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