Chronic Stable Angina and Unstable Angina: Diagnosis, Medications, and Management, Exams of Nursing

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Chronic Exam II

Module 5: Cardiac Conditions Part I

Atherosclerosis: Hardening of the arteries. Begins as soft deposits of fat that harden with age. Coronary Artery Disease: Narrowing of the coronary arteries on the heart caused in major part by atherosclerosis. Characterized by focal deposit of cholesterol and lipid, primarily within the intimal wall of the artery. Endothelial lining altered as a result of inflammation and injury. When is CAD a Chronic Issue? Chronic Stable Angina: Intermittent chest pain that occurs over a long period with the same pattern of onset, duration, and intensity of symptoms

• Primary reason for insufficient blood flow is narrowing of coronary arteries by atherosclerosis
• Referred pain in left shoulder and arm is from transmission of the pain message to the cardiac nerve roots Unstable Angina : Acute Coronary Syndrome or MI > BOTH emergencies! [Frequently unrelieved with nitro] Prinzmetal’s (Variant) Angina: Occurs at rest usually in response to spasm of major coronary artery , may occur in the absence of CAD
• Seen in patient with hx of migraine headaches and Raynaud’s phenomenon
• Clinical manifestation o Chest pain o Marked, transient ST-segment elevation
• May occur during REM sleep
• May be relieved by moderate exercise or may disappear spontaneously CVD Risk Factors Non-Modifiable: Increased age Male sex at birth Race/ethnicity (AA, Mexican, native Hawaiian, Asian) Family Hx Genetic Predisposition Congenital abnormality Modifiable: Cigarette smoking Hyperlipidemia HTN Hyperglycemia Obesity Inactivity Stress Excess ETOH Use Clinical Manifestations Angina (Reversible myocardial ischemia d/t O2 demand>supply) Numbness, tingling SOB Lab Changes EKG Changes Early Risk factors addressed Medicine/Lifestyle treatment Chronic Active monitoring of labs Risk factor reducing medications (anti-HTN, anti-HLD, etc.) Lifestyle modification emphasized Acute ACS or MI Stents or Coronary Artery Bypass Graft Surgery Emphasis on reducing long-term effects of acute illness Chronic Increased medication and monitoring vigilance Consideration for functional limitations and tailored recommendations based on acute illness sequelae Palliative/ Chronic Surgical intervention no longer an option Focus on managing symptoms and maintaining functional capacity

Coronary Artery Disease Diagnostics and Procedures Diagnostics Clinical Sx: understand the pain, numbness, SOB Labs: CMP; glucose, Ca, Na, K 3.5-5. Lipid Panel; Cholesterol< 200, LDL< 160, HDL> 40-60, Triglycerides< 150 Inflammatory Markers; C-reactive protein Coagulation Studies; PT/INR, platelets, fibrinogen Cardiac Markers; CK-MB and CK total, Troponin HbA1C < 6.5%; Pre= 5.7-6.4% Radiographical Testing: Exercise Stress Test, Cardiac Cath Exercise Stress Test ; using treadmill/bike with EKG Dobutamine Stress Test ; use an ionotrope to increase HR Goals; Determine if there is decreased blood flow/oxygenation to the heart with activity, and what parts are affected. Cardiac Catheterization ; Gold standard for assessing coronary arteries. Fluoroscopy and angioplasty Opportunity to place stents and open flow 3-vessel disease is not usually amenable to stents Cardiac Cath Pre/Post Op Care: Pre- Education, informed consent, blood work, vitals, NPO, aspirin, IV hydration (fluoro is hard on the kidneys. Balance with HF!), EKG Post- EKG, pulse check (distal to cath site; pedal), blood work (inflammatory markers and cardiac enzymes may be elevated), hydration, vitals, activity restriction, close monitoring of cath site for hematoma Nursing Management Assess for: C hest Pain E pigastric Discomfort N ausea and Vomiting D iaphoresis S yncope S OB P ain between shoulders/jaw line Illicit Drug use, COLDSPA (especially for women), vitals (bradycardia, hypotension), temperature of extremities, capillary refill Labs: Ca, cardiac enzymes, renal function, HbA1C, lipids, electrolytes (esp. Mg and K), ECG (12-lead) ST segment Actions; Comfort- Aspirin [only drug with clear benefits] Reduce the Clot- Aspirin and Statins Decrease Work of the Heart- BBs/CCBs, O Older Adults; Risk factor reduction, modify physical activity to limitations, medication regimen (complex), incorporate caregivers in teaching Know when to call 911! 90 minutes door to balloon Medications  Reduce Clot Formation o Statins o Fibric Acids o Nicotinic Acid o Bile Acid Sequestrants o Platelet Inhibitors (i.e. Aspirin, Plavix)  Decrease Work of the Heart (HR and/or BP) o Beta Blockers o Calcium Channel Blockers o Vasodilators Nitroglycerin ; Vasodilator Side Effects- Drops BP (sometimes HR), headache, syncope Route: Sublingual Q5 min x 3 doses Patch DDIs: Other vasodilators [Viagra] > hypotension Chest pain relieved by Nitro may be more likely to be chronic and stable. Interventions Lifestyle; Clarify personal values, set realistic goals Physical Fitness; Weight reduction. Goal BMI< 25kg/m Reduction of >10% in systolic BP Increase in HDL (more in men) FITT Formula- 30 mins most days plus weight training 2 days a week Nutrition Therapy;  Saturated fats and cholesterol Red meat, egg yolks, whole milk Complex carbs and fiber Omega-3 fatty acids Smoking cessation

Valvular Heart Disease Terminology Stenosis: Stiffening and thickening of the valve. Narrow opening obstructs flow. Regurgitation: Leaky valve allows blood to flow in the wrong direction. Prolapse: Valve leaflets do not lay correctly and are bulging. Infection/Infective Endocarditis: Heart valves grow “vegetation” Often occurs due to bacteria that colonize the teeth. Abx may be necessary to prophylactically to treat patients prior to dental procedures to prevent IE. Teaching includes maintenance of good oral hygiene and informing healthcare provider about hx prior to any dental or invasive procedure. Clinical Manifestations: [Resembles Heart Failure]  SOB  Edema  Angina  Syncope  Dysrhythmia  Palpitations  Dizziness  Fatigue  Weight gain Mitral Valve Stenosis: Increased pressure in left atrium. Backflow into lungs causing pulmonary congestion. Clinical Manifestations-  Exertional dyspnea  Loud S  Murmur; Regurgitation usually systolic  Fatigue  Palpitations  Hoarseness, hemoptysis  Chest pain, seizures/stroke Aortic Valve Stenosis: [Most prevalent valve disorder] Congenital stenosis usually discovered in childhood, adolescence, or young adulthood. Can also be degenerative or caused by rheumatic fever. Causes left ventricle to become enlarged (hypertrophy) so that the ventricle can force the valve open. Eventually leads to heart failure. Poor prognosis if symptomatic and not corrected. Use Nitroglycerin cautiously; Reduced preload and BP/can worsen chest pain Clinical Manifestations-  Murmurs o Caused by force of blood through stenosed/regurgitant valve o Systolic, diastolic, or continuous o Aortic stenosis usually systolic and turbulent o Regurgitation usually diastolic Risk Factors Infectious diseases Congenital defects Degenerative changes Pregnancy Smoking HTN, HLD Typical Causes MI HF Congenital Defects Degenerative Changes CVD Risk Factors

Valvular Disease Diagnostics and Procedures Diagnostics  EKG  Echocardiography - watch the valves open and shut under ultrasound  CXR- look for hypertrophy  Stress testing  Cardiac Cath Nursing Management Assess For: S OB A ngina D ysrhythmia E dema S yncope F atigue W eight Gain P alpitations D izziness Vitals: [HR, BP, temp, SpO2] EKG [Especially atrial fibrillation] Perfusion: Skin color, cap refill, temperature, pulses Breath Sounds: [Expect congestion] Activity Intolerance Heart Sounds Labs: [ INR for patients on warfarin ] Actions: Medications Fluid Restriction Nutrition Education If mechanical valve, Coumadin teaching  Watch green leafy veggies  Bleeding risks  Must be adherent to avoid stroke Medications  Decrease workload o Beta Blockers o Calcium Channel Blockers  Reduce Volume (Preload) and Congestion o Diuretics CAUTION: Aortic Stenosis is preload dependent = Volume is needed for enough pressure to get through the valve Cardiogenic shock and death can result from diuresing a patient with aortic stenosis Surgical Management  Open Heart Valve Replacement/Repair o Mechanical (artificial)  Last longer, risk of thromboembolism, require long-term anticoagulation o Biologic (tissue)  Bovine, porcine, human. No anticoagulation required. Less durable  Transcatheter Aortic Valve Replacement (TAVR)  Balloon Valvuloplasty o Palliative o May not have lasting result  Commissurotomy o Splits fused leaflets  Annuloplasty o Reconstructive repair to the aortic or mitral ring/root Surgical Considerations Risks to Consider:  Frailty  Smoking, COPD  Pulmonary hypertension  Liver disease  Stroke  Anemia  Mechanical valves require anticoagulation with warfarin (usually)

Module 6: Cardiac Conditions Part II

A group of diseases in which the structure or function of the myocardium is impaired or weakened. Types of Cardiomyopathy Dilated Hypertrophic Restrictive Arrhythmogenic Right Ventricular Cardiomyopathy (ARVC): Mixed [Compensatory] -Heart muscle becomes thickened, enlarged, and stiff. -Contraction not typically weakened. -Filling impaired due to obstruction by the hypertrophic myocardium. [Compensatory] -Least common type of CM. -Stiffness of ventricular wall (d/t myocardial fibrosis, hypertrophy, and infiltration)

• Impaired diastolic filling and stretch ; systolic function remains unaffected (EF may be normal) [Fat cardiomyopathy] -Familial incidence in more than 50% of patients, generally with an autosomal dominant mode of inheritance. -Family screening may reveal ARVC, but often sudden death is the first sign of ARVC with the diagnosis made postmortem. As compensatory systems are increasingly used to make up for anatomical changes, the heart is weakened and we have heart failure. [Dilated and hypertrophic] Causes:  Cardiogenic Agents- alcohol, cocaine, doxorubicin  CAD- HTN  Genetic  Metabolic Disorders  Muscular Dystrophy  Myocarditis  Pregnancy  Valve Disease Causes:  Aortic Stenosis  Genetic  HTN Causes:  Specific etiology unknown  Secondary causes; Amyloidosis  Endomyocardial Fibrosis Neoplastic Tumor  Post-Radiation Therapy  Sarcoidosis  Ventricular Thrombus Causes:  Fatty infiltration of the right ventricle  Genetic Cardiomyopathy

An abnormal clinical syndrome involving inadequate cardiac pumping/filling resulting in insufficient blood supply/oxygen to tissues. Supply of adequately oxygenated blood < demand of the body.  Pump cannot keep up Frank Starling Law: Etiology: HF is caused by any condition that interferes with mechanisms that regulate cardiac output. Primary Causes- Conditions that directly damage the heart. Precipitating Causes- Conditions that increase the workload of the ventricles. Classification:  Systolic V. Diastolic  Left-sided v. Right-sided  HFrEF (<45%) v. HFpEF (>45%)  NY Heart Assoc. Functional Classes 1-4 (4 is worst) o Can vary with treatment  Stages A-D (D is worst) o Progressive, can’t go back to A once at C  Increased ventricular end-diastolic volume produces increased stroke volume.  Heart muscle force varies with ventricular wall fiber tension, which is a function of length  Therefore, there is an amount of stretch in the ventricle when it can no longer squeeze efficiently, resulting in decreased stroke volume with larger end-diastolic volume  heart failure. Risk Factors: Primary- HTN CAD Contributing- Advanced Age Diabetes Tobacco Use Obesity High Serum Cholesterol Preload: Volume coming into ventricles (end diastolic pressure) Increased In: Hypervolemia Regurgitation of cardiac valves Afterload: Resistance left ventricle must overcome to circulate blood. Increased In: HTN Vasoconstriction

Heart Failure

Counterregulatory Mechanisms  Natriuretic Peptides Released in response to overstretching of ventricle BNP and pro-BNP Cause diuresis, vasodilation, and lowered BP Usually elevated during decompensated HF events  Nitric Oxide Relaxes arterial smooth muscle, resulting in vasodilation and decreased afterload Compensatory Mechanisms  Sympathetic Nervous System Activation Catecholamine release: Epi, Nor-Epi, Dopamine Vasoconstriction increases HR, BP, RR until it can’t anymore Increases contractility Not effective for long term compensation  Neurohormonal Responses Kidneys aren’t getting perfused to kidneys/adrenals release RAAS, ADH Endothelin Proinflammatory cytokines  Dilation : Occurs when pressure in left ventricle elevates  Hypertrophy : Due to overwork of heart muscle

Clinical Manifestations of Heart Failure Left-Sided Heart Failure Right-Sided Heart Failure Results from left ventricular dysfunction Blood backs up into left atrium and pulmonary veins  increased pulmonary pressure causes fluid leakage  pulmonary congestion and edema  SOB/dyspnea  Crackles  Poor color, weak pulses, cool extremities  Orthopnea  Nocturia “Cold and Wet” Results from right ventricular dysfunction Blood backs up into the right atrium and venous circulation  JVD  Hepatomegaly, Splenomegaly  Vascular congestion of GI tract  Ascites  Nausea and anorexia  Peripheral edema “Warm and Dry” Both  Depression  Fatigue  Decreased function status Heart Failure Complications Pulmonary edema Renal failure and/or multi-organ failure Advanced heart failure Dysrhythmias Left ventricular thrombus

Cardiac Resynchronization Therapy Intra-Aortic Balloon Pump

Heart Failure Disease Trajectory

Nursing Management Assess For:

F atigue

A ctivity Limits

C hest Congestion/Cough

E dema

S OB

Vitals, Breath Sounds, SpO2, EKG, Skin, Cough, Orthopnea, Activity Intolerance, I’s&O’s, Labs, Mood, Social Support Actions: Administer meds Obtain labs Electrolytes  Na, K Renal Function  BUN, Cr BNP Hepatic Function  ALT, AST Oxygen therapy Encourage physical and emotional rest Structured exercise program Nutrition and fluid management Daily weights [ Concern with weight gain > 2-3 lbs/day or 5 lbs in a week ] Fluid Restriction if required, < 2L/day Teaching Med management Rest and activity Low Na Diet: 2-3g a day. DASH Diet Daily Weights Sx checklist Medications

C ardiac Glycosides

A CE Inhibitors

V asodilators

A RBs

B eta Blockers

D iuretics

Goal: Improve CO Challenge: Don’t Overdo It! Maintain electrolyte balance Maintain perfusion Keep vitals stable Chronic Interventions: AICD Pacemaker Ventricular Resynchronization Therapy (CRT) Advanced Interventions: IV Inotropes Intra-Aortic Balloon Pump Left Ventricular Assist Device Cure:* Transplant- Gold Standard Mechanical Circulatory Support- LVAD, Total Artificial Heart Diagnostics  Echocardiography- TEE and TTE  CXR  ECG  Stress Test  Cardiac Cath  BNP (NT-proBNP) [Measures overstretching of ventricles, HF]  ABGs  Cardiac MRI Chronic HF Management Main Treatment Goals: Treat underlying cause, maximize CO, alleviate sx, improve ventricular function, improve QOL, preserve target organ function, improve mortality and morbidity. Digoxin: Inotropy helps with contractility. Risk of toxicity especially with K (consider when giving Lasix) Toxicity: change in mental status, nausea, vomiting

Module 7: GI, Cholecystitis, & Hepatitis

Cause: Unknown. Genetic overactive immune response to GI bacteria. Response to triggers (physical/emotional stress; infection, medication, smoking) Types of Inflammatory Bowel Disease Chron’s Disease Ulcerative Colitis Can affect anywhere from mouth to anus, but most commonly affects terminal ileum and colon Transmural  Affects all layers of bowel  Can penetrate bowel wall “Skip Lesions” (Patchy) Deep ulcerations with scarring after repeated ulcerations Causes malabsorption of nutrients 5-6 soft, loose non-bloody stools/day Cobblestone appearance of mucosa Complications: Bowel wall penetration [Fistulas, Abscesses, Peritonitis] Strictures, Adhesions, Small Bowel Cancer Affects large intestine (Small intestine involvement rare) Involves only mucosa and submucosa Spreads uniformly , beginning at rectum to cecum Diarrhea : 10-20 stools per day, several liters of fluid loss per day Blood, pus, and mucus are common Tenesmus: Feeling the need to poop with empty bowels Crypt Abscess: Abscess filled with pus Ulcerated areas lead to scar tissue formation Malabsorption from scar tissue and frequent diarrhea Complications: Abscesses, Hemorrhage, Colon Cancer Toxic Megacolon: Colonic dilation > 5cm; requires colectomy Diagnosis:  Colonoscopy: Visualize bowel wall and detect mucosal changes  Inflammation, stricture, fistulae  Barium Enema: Used when endoscopy is unavailable. Can determine depth of disease involvement  Lab Tests: CBC, BMP, Serum Albumin, Stool Samples (pathogens) Medication: Anti-inflammatories [5-aminosalicyclates], Glucocorticoids, Antibiotics, Biologic Therapies [Remicade], Immunomodulators, Antidiarrheals Nutrition: Identify and treat deficiencies, B12 injections/liquid vitamin supplements, monitor albumin levels, parenteral nutrition Avoid: Milk, gluten, caffeine, citrus, carbonated drinks, nuts, seeds, popcorn, alcohol Surgical Management: Chron’s Disease: Reserved for failed medical management and complications Disease frequently recurs after surgery [not curative] Ulcerative Colitis: Surgery is curative Extraintestinal manifestations continue

EMERGENCY

Colectomy Persistent diarrhea Abdominal pain/cramps Weight loss Fluid imbalances (r/t diarrhea) Malnutrition (r/t diarrhea) RED: High fever, sudden/general abdominal pain, s/sx of anemia or severe dehydration YELLOW: Changes in bowel habits/weight GREEN: Baseline Inflammatory Bowel Disease

“ Outpouching ”: Decreased fiber, slow stool transit time, thickened colon wall causes intraluminal pressure from constipation and straining, leading to formation of diverticula. If food becomes trapper, or a fecalith forms, inflammation or infection occurs  Diverticulitis Clinical Manifestations:  Fever  LLQ or middle abdominal pain  Altered bowel habits: Constipation/diarrhea  Cramping Complications:  Perforation  Abscess  Fistula formation  Bleeding Diagnosis: Abdominal X-Ray : To investigate abdominal pain CT Scan: To confirm and differentiate diagnosis. Shows bowel thickening and diverticula. Very similar appearance to carcinoma (r/o with biopsy) Barium Enema CONTRAINDICATED! [Could rupture diverticula]

Diverticulitis

Diverticulum: Small, pouch-like protrusion/herniation of the intestinal tract, most commonly the colon More common in elderly and men Causes: lack of dietary fiber, obesity, sedentary lifestyle Extraluminal  Occurring outside the colon May be acute or chronic Nursing Management: Assess For: Vitals r/t inflammation & infection Decreased Serum K r/t NG tube decompression I’s&O’s Pain [if generalized, suspect rupture/peritonitis] Mental status change in older adults Interventions: Administer ordered Abx, IV fluids NG tube to low suction Provide oral care Education:  daily fiber [limit during flares] Avoid nuts, seeds, etc. Maintain healthy BMI Complete Abx course Medical Management: Outpatient: Diet: High fiber, eliminate nuts, seeds, etc. Uncomplicated Flares: Broad-spectrum Abx, clear liquid diet until sx subside, lower fiber diet Inpatient: IV fluids NPO for bowel rest, NG tube for bowel decompression Pain control (opioids) Avoid laxatives and enemas RED: High fever, severe abd pain > 3 days, GI bleed, multiple comorbidities, immunocompromised YELLOW: Abd pain, change in bowel habits GREEN: Baseline

Risk Factors:  Personal or family hx of colorectal cancer or adenomatous polyps  IBS > 10 years  Lynch syndrome  Physical inactivity, BMI > 30  Diet high in red meat, processed meat, or fat  Smoking, ETOH use  Advanced age  DM Pathophysiology: Most are adenocarcinomas; originate in glandular cells of internal organs Most common metastasis is the liver [may also metastasize to lung, brain, bones, adrenals] Screening Options Not High Risk High Risk Age 45-75: High-sensitivity FOBT annually, Sigmoidoscopy every 5 years, Colonoscopy every 10 years Age 76-85: Do not screen routinely Age >85: Do not screen Begin before age 45 or screen more often Strong family/personal hx of colon cancer/polyps Personal hx of IBS, or radiation to abd/pelvis Medical Management Chemotherapy: Used for tumors that can’t be completely removed. Recommended for Stage II and III Radiation Therapy: Preoperatively to reduce tumor size. Palliative to control pain, hemorrhage, bowel obstruction, or lung metastasis Surgical Management [Preferred Tx] Used to remove the tumor, affected portion of colon, margins, and adjacent lymph nodes Colectomy: Excision of all or part of colon Hemicolectomy: Excision of half or less of the colon (left or right) Abdominoperineal Resection: Affected colon and rectum are removed, and anus is closed. Ileostomy is permanent. Nursing Management Assess For: Vitals, Pain, Bowel Habits, N/V, I’s&O’s, Incision/Stoma, Coping, Knowledge Interventions: Measure I’s&O’s, Manage Sx, Manage Drain/NGT

Colorect

al

Cancer

Cancer of the rectum and large intestine Third most common cancer, second leading cause of death in the US With early detection, most curable of all cancers Clinical Manifestations:  Insidious in early disease, often ignored  Unexpected weight loss  Fatigue  Change in bowel regularity/appearance  Red or black stool  Abdominal pain and/or distention  Feelings of incomplete evacuation after BM

Promote Activity, Diet/Fluid Status, Referrals [social work, home health, palliative care] The Liver: Receives 25% of cardiac output  Hepatic portal vein, hepatic artery Functions: Blood storage; Blood Filtration/Detox; Production of Bile; Metabolism of Carbs/Fats/Proteins; Synthesis and Management of Clotting Factors; Storage of Vitamins Viral Hepatitis Risk Factors:  ETOH Abuse  Toxins  Exposure  Living in high risk areas Pathophysiology: Exposure to virus  Inflammation of liver cells.  Limits ability of liver to detoxify  Limits production of proteins  Limits production of clotting factors  Alters ability to store vitamins, fat, sugars Types of Hepatitis Type Route of Transmission Source of Virus Acute or Chronic Available Vaccine Hepatitis A Fecal-oral Feces, contaminated water, food Acute [~8 weeks] Yes Hepatitis B Percutaneous or mucosal Blood, body fluids Chronic* Yes Hepatitis C Percutaneous or mucosal Blood, body fluids, needles, sharp instruments Chronic* No Hepatitis D Percutaneous or mucosal Blood, body fluids, needles, sharp instruments Acute Yes Hepatitis E Fecal-oral Feces Acute No Hepatitis G Infected blood or blood products Infected blood or blood products Acute No RED: Change in mental status, profound weight loss, high fever for several days YELLOW: Any change in symptoms (weight, jaundice, etc.) GREEN: Baseline *Can be asymptomatic!  Abd pain  Irritability  Pruritis  Malaise  Fever  N/V  Jaundice  Elevated AST, ALT, bilirubin, ammonia  Decreased albumin Clinical Manifestations

Viral

Hepatiti

s

Hepatitis C: Caused by childbirth, contaminated needles. [less likely sex, but still possible] Acute or Chronic: 85% become chronic with cirrhosis within 20-30 years High Risk: Baby Boomers born from 1940- d/t reuse of glass and needles in healthcare Guidelines: one-time screening for all adults > 18 with repeat screening for high risk [Can be cured with PO Antivirals!] Most common indication for liver transplantation Hepatitis B: Acute or Chronic: 95% of infants, 2-5% adults become chronic High-carrier areas: Sub-Saharan Africa, South Sudan Transmission: Childbirth (high carrier areas), unprotected sex, IVDU (US) High risk patient with chronic HBV should be screened every 6-12 months for HepC Risk Factors: high prevalence region, risk behavior, HepC or HIV, living with someone with HBV, inmates [Routine screening] Causes 1/3rd^ of liver cirrhosis and ½ of HCC cases Those with liver disease and risk for occupational exposure should be vaccinated Vaccination is the best defense! Hepatitis A: Caused by poor food handling, contact with infected persons, unsanitary conditions. Sx: [usually mild, sometimes asymptomatic] Abrupt onset of fever, anorexia, N/V, malaise, abd pain, myalgia, urticaria, cough, hepatosplenomegaly. 4-30 days later; Clay colored stools, rise in serum bilirubin, jaundice Those with liver disease should be vaccinated

Medical Management  Vaccination  Viral Suppression: PO antivirals, Pegylated Interferon Injections  Regular f/u to monitor liver function Surgical Management  Liver Transplant: Primarily through cadaver donor o Living Donor: One lobe o Complications: Rejection and infection Nursing Management Assess For: Vital Signs, Serum Liver Enzymes, Bilirubin Color of Skin/Sclera Nutritional intake, I’s&O’s, Daily weights Interventions: Administer meds as ordered, antiemetics Small, frequent meals and supplements Low fat diet, moderate protein intake Encourage activity as tolerated with rest periods Complications  Fulminant Viral Hepatitis: Acute Liver Failure Severe, rapidly progressing, life threatening Encephalopathy, bleeding  Liver Cirrhosis: Fibrosis  Liver Failure Causes Esophageal Varices  Hepatic Encephalopathy  Hepatocellular Carcinoma Diagnostics  History: Risk Factors  Physical Exam: Swollen, tender liver  Serology studies to identify virus/antibodies: HIGH VALUE Alanine Transaminase (ALT)- enzyme releases by liver d/t inflammation Aspartate Transaminase (AST)- Enzyme released by heart/kidneys d/t organ damage Bilirubin, total - Byproduct of RBC breakdown, cleared by liver Bilirubin, direct - Bilirubin that travels to small intestine; liver not clearing effectively Ammonia- Waste product from protein breakdown in the gut, cleared by the liver NO CHANGE Bilirubin, indirect - Caused by destruction of Hgb in RBC; indicates hemolytic anemia LOW VALUE Albumin - Protein made by liver Follow up studies to determine acute vs. chronic  Ultrasound: Identify inflamed liver and large areas of scar tissue  CT or MRI: Identify Cancer  Liver biopsy: Determine presence and extent of damage

Inflammation of the gallbladder caused by obstruction of bile flow Calculous Cholecystitis: With Stones Acalculous Cholecystitis: Without Stones Cholelithiasis: Gall Stones The Gall Bladder: Bile produced in liver  Travels to gall bladder where it’s stored Bile travels from gall bladder to duodenum [stimulated by cholecystokinin] Bile: Digestive enzyme that breaks down fats Pathophysiology: Acalculous Calculous Biliary Stasis : Slowing or stopping of flow of bile Decreased contractility of gallbladder Spasms in sphincter of Oddi Formation of gallstones in gallbladder Stones block cystic duct or common bile duct

Cholecy

stitis

Risk Factors Obesity/rapid weight loss Weight loss surgery High fat diet Pregnancy Genetics Medications (estrogen, octreotide, cholesterol- lowering) Five F’s: Fair, Fat, Female, Fertile, Forty+ RED: Peritonitis [sudden generalized abd pain, high fever] YELLOW: Changes in weight > 10% or symptoms GREEN: Baseline Diagnosis  WBC : Elevated r/t inflammation  Liver Enzymes : [AST/ALT, Bilirubin] Elevated r/t blockage of bile flow through ducts  Abd X-Ray : o Detect calcified gallstones  Abd Ultrasound : o Presence of gallstones & thickened (inflamed) gallbladder  Abd CT : o Visualize entire abd and detect gallstones  Hepatobiliary Iminodiacetic Acid (HIDA) Scan: o Nuclear medicine scan that detects bile flow  Endoscopic Retrograde Cholangiopancreatography (ERCP): o Diagnostic- visualize biliary tree and pancreatic ducts o Interventional- can place drain Medical Management  NPO Status Prevents release of cholecystokinin [reduced colicky pain]  IV Hydration, correction of fluid/electrolyte imbalance  Pain Management, IV Abx  Meds to “dissolve” gallstones; Ursodiol , Actigall , Chenodiol Take meds for 2 years. Stones come back with breaks in therapy.  Diet Avoid: fatty/fried foods, ice cream/dairy, red meats, heavy ETOH Encourage: low saturated fat (rice, potatoes, pasta, yogurt, fruits, lean meat, whole grains) Surgical Management  Laparoscopic Cholecystectomy : [Most Common]  Open Cholecystectomy : complications like perforated gallbladder, previous abd surgeries, morbid obesity  Biliary Drainage Tube : “T Tube” Placed for ~2 weeks during surgery or ERCP Nursing Management Vitals, Serum Electrolytes, WBC, Liver Enzymes/Bilirubin, Skin Turgor, Pain, Abd Assessment, Daily Weight, I’s&O’s, Nutrition Maintain NPO, Promote Semi-Fowler’s BR, NG Tube to Suction NO FAT IN DIET AFTER CHOLECYSTECTOMY Inflammation and Pain in gallbladder Clinical Manifestations Asymptomatic RUQ Pain “colicky” [intermittent/radiate to back r/t stone movement] Fever & Tachycardia [with infection] + Murphy’s Sign [pain with RUQ palpation upon deep inspiration] Possibly Jaundice N/V Uncomplicated: 1-4 day recovery Complications: Perforation Gangrene Sepsis; 60% mortality