Cardiac and Liver Medical Review Notes PDF

PREVIOUS EXAM - 4 (LOOK AT OLD NOTES !!!!) Insulin peaks Is min ○ For short-acting insulin, check blood glucose around 1000-1100. - ○ For long-acting insul...

PREVIOUS EXAM - 4 (LOOK AT OLD NOTES !!!!) Insulin peaks Is min ○ For short-acting insulin, check blood glucose around 1000-1100. - ○ For long-acting insulin, you can check blood glucose at regular intervals through the day, but there’s no specific peak time to monitor. - - - - & Dressing ○ Date time initial Chest tube ○ Monitor the Drainage System Water seal chamber: Acts as a one-way valve to let air out, but not back in. ○ TIDALING: Normal. bubble , pause, bubble , ○ Continuous bubbling: May indicate an air leak. pause - > wlbreathing Suction control chamber (if ordered): Usually filled with sterile water or uses wall suction to help pull out air/fluid. Assess Drainage Color, amount, and consistency: ○ Report >100 mL/hr of blood (post-op), sudden bright red, or * cloudy/purulent drainage. Mark and time output on the chamber regularly Keep It Below the Chest ○ Always keep the drainage system upright and below chest level to promote drainage by gravity. ○ Do not lift or clamp tubing unless ordered  Maintain Dressing and Insertion Site ○ Keep the dressing occlusive (airtight), dry, and intact. ○ Monitor for signs of infection: redness, swelling, drainage, fever. ○ Check for subcutaneous emphysema (air under the skin, feels like Rice* Krispies). Emergency Situations ○ If the tube gets pulled out: → Immediately cover the site with a sterile occlusive dressing (like petroleum gauze), tape on 3 sides to allow air to escape but not enter. - ○ If the system breaks: → Place the chest tube end in sterile water to create a temporary water seal Patient Care ○ Encourage deep breathing, coughing, and incentive spirometry to help lung expansion. ○ Reposition as needed, but don’t clamp the tube unless ordered. GLUCOSE + OXYGEN = CO2 AND WATER EKG Assess pt and leads S/S ○ HYPOTENSION ○ SOB ○ Chest pain ○ AMS ○ Pulses ○ Cap refill Sinus Rhythm Normal 60-100 Just monitor Sinus Brady Less than 60 Vagal stimulation Beta blockers Digoxin toxicity Increased ICP Treasons for brady ○ Notify doctor ○ Oxygen ○ Atropine!!! Or pacemaker Sinus Tachy > Greater than 100 calcium channel blockers betablockers Pain and anxiety and fever &reasonas Hypovolemia Pulmonary emboli MI Drugs PVC Wide bizarre QRS complex - Electrolyte imbalance bigeminy/trigening usually lowk orig Hypoxia Ischemia J reasons t ↓ ○ Notify PCP every other is every 2 PVC ○ Oxygen PVC ○ Medication - > A fib Atrial > 350 IRREGULAR- > inconsistent rhythm ○ HTN, ISCHEMIA, MI, CHF, COPD, EDEMA POST OP Notify PCP Oxygen CCB BB DIGOXIN ANTICOAGULANTS * Cardioversion if < 48hrs A flutter Atrial 250-350 - REGULAR OR IRREGULAR unique f waves saw footh ○ COPD, enlarged atria, pericarditis Notify PCP Oxygen CCB BB DIGOXIN ANTICOAGULANTS * Cardioversion V TACH 150-250 - (regular rhythm) SAME SHAPE REGULAR ○ HYPOKALEMIA OR MAGNESIUM ○ MI ○ CHF Treasons Oxygen Vital signs No pulse > DEFIB!!! THEN CPR Pulse > CARDIOVERSION FIRST ○ Amiodarone,B magnesium,Af or lidocaine SVT either or 150-250 Regular ○ Anxiety/caffeine ○ ○ ○ J Atrial enlargement Hyperthyroidism Toxicity - nicotine adenosine Oxygen VAGAL MANEUVER (cough and valsalva) Cardioversion unstable pts CCB OR BB  Torsade de Pointes 200-250 likee ile looks Irregular > VF OR ASYSTOLE MAGNESIUM *** V FIB CHAOTIC - no pulse or output ○ CAD, MI, TRAUMA, HYPOXIA, DRUG OD DEFIB!!! Be quick - ○ Then ACLS ○ IV- and INTUBATE Epinephrine, vasopressin, and amiodarone Asystole CPK IVintubate ↓ transc · pacing  H ○ Hypovolemia ○ Hypoxia ○ Acidosis from hydrogen ions ○ Hypoglycemia ○ Hypothermia T ○ Toxins ○ Tamponade ○ Tension pneumothorax ○ Thrombosis ○ Trauma CHECK FOR PULSE AND A DIFFERENT SECOND LEAD!!! ○ DO NOT SHOCK!!!! Start CPR, IV, INTUBATE Transcutaneous pacing early Tachycardia Fever Pain Anxiety Bladder 1. Heart Anatomy & Physiology – Know the Flow 4 Chambers: Right atrium → Right ventricle → Lungs Left atrium → Left ventricle → Body Valves: Tricuspid (RA → RV), Pulmonic, Mitral (LA → LV), Aortic Blood Flow Mnemonic: "Toilet Paper My Ass" = Tricuspid, Pulmonic, Mitral, Aortic RA-RV- > Lungs > LAtLV-tissues - Electrical Conduction System: SA node (pacemaker, 60–100 bpm) → AV node (slows down and allows ventricles to fill before contracting, 40–60 bpm) → Bundle of His → Purkinje fibers (stimulate ventricular contraction) Perfusion Basics: CO = HR x SV Normal EF (Ejection Fraction) = 55–70% Deoxygenated blood flows from the body into the right atrium, passes through the tricuspid valve to the right ventricle, and then to the lungs via the pulmonary artery for oxygenation. Oxygenated blood returns to the left atrium, passes through the mitral valve into the left ventricle, and is pumped through the aorta to supply the body. A – Assessment A Vitals, heart sounds (S3 = CHF!), edema, JVD, lung sounds (crackles), perfusion (cap refill), fatigue, chest pain, dyspnea. HX and modifiable risk factors D – Diagnosis Decreased cardiac output Impaired gas exchange Fluid volume excess Activity intolerance P – Planning Improve oxygenation & cardiac output Reduce fluid overload Promote rest and activity balance Prevent complications (dysrhythmias) I – Intervention Daily weights, I&Os Administer meds: ○ Antihypertensives (Lisinopril, Metoprolol) Reduce blood pressure to prevent damage to heart and blood vessels. ○ Diuretics (Furosemide): Reduce fluid overload in heart failure by increasing urine output. ○ Anticoagulants (Warfarin, Heparin): Prevent blood clot formation, reducing the risk of stroke/MI ○ Antiarrhythmics (Amiodarone): Used to manage arrhythmias and maintain normal heart rhythm. ○ Statins (Atorvastatin): Lower cholesterol levels to prevent atherosclerosis and reduce the risk of coronary artery disease. ○ Nitrates (Nitroglycerin): Vasodilators that relieve angina by increasing blood flow to the heart muscle. ○ Beta-Blockers (Metoprolol): Decrease heart rate and blood pressure, reducing the workload on the heart.  Monitor labs: BNP, K+, Mg++, troponin Elevate HOB, oxygen PRN, restrict fluids/sodium if ordered Educate on lifestyle changes (low Na+, smoking cessation, meds) E – Evaluation Improved breath sounds, stable vitals, decreased edema, better activity tolerance Diagnostic Tests – Cardiac Focus Test Purpose Notes ECG/EKG Rhythm & rate Look for ST elevation, arrhythmias Troponin I/T Cardiac muscle damage ↑ in MI; most specific BNP CHF marker (damage/failure) ↑ in fluid overload/heart failure < 100 = normal Echocardiogram Looks at EF, valves Noninvasive abnormalities, heart function Cardiac Cath Visualizes coronary arteries Risk of bleeding post-op (Angiography) and chambers; diagnose blockages Chest X-ray Size of heart, fluid in lungs Check for cardiomegaly Stress Test Assess heart under activity Treadmill or chemical test Cardiac Diseases – Compare & Contrast Disease Key S/S NCLEX Priorities CAD Angina, fatigue Nitro, lifestyle change, risk reduction MI Chest pain, SOB, N/V, MONA: Morphine, Oxygen, diaphoresis Nitro, Aspirin CHF (L vs R) L: crackles, SOB Daily weights, low Na+, meds R: JVD, edema  Arrhythmias (Afib, V Palpitations, dizzy, ↓ CO Monitor ECG, may need Tach) anticoagulants HTN Often silent; H/A, vision Lifestyle first, then meds changes (ACE/ARBs) Valvular disease Murmurs, fatigue May need surgical valve repair Cardiomyopathy Fatigue, dyspnea Leads to HF, monitor EF CHF – Interprofessional & Nursing Management Interventions: Low sodium diet Fluid restriction (if ordered) Daily weights – report ↑ of 2–3 lbs overnight O2 therapy as needed and elevate HOB Meds: ACE inhibitors, diuretics, beta-blockers, digoxin Team Involvement: Dietician – Na+ restriction education PT/OT – promote mobility with fatigue management Pharmacist – med reconciliation, side effect education Social work – follow-up resources, home health support Chronic Cardiac Disease – Clinical Manifestations & Management Chronic Issues: Angina, fatigue, orthopnea, paroxysmal nocturnal dyspnea, edema, decreased exercise tolerance Management Includes: Regular follow-ups Medication adherence Fluid and dietary control Monitoring for s/s of decompensation Emotional support & education  Infective Endocarditis (IE) Definition ○ Infection of the inner lining of the heart (endocardium) and heart valves Causes/Risk Factors: ○ Bacterial infection, especially Staphylococcus aureus and Streptococcus viridans. ○ Risk factors include intravenous drug use, recent dental procedures, presence of artificial heart valves, and previous history of endocarditis. Signs and Symptoms: ○ Fever, chills, fatigue, malaise, night sweats. normality SIS ○ Heart murmurs (new or changing).* ○ Janeway lesions (painless spots on palms and soles) and Osler’s nodes (painful nodules bleeding wor ○ on fingers and toes). throug body ○ Splinter hemorrhages (under nails), petechiae, and Roth spots (retinal hemorrhages). - - - Diagnosis: ○ Blood cultures to identify the pathogen. ○ Echocardiogram to visualize vegetation on valves. Treatment: ○ Long-term IV antibiotics ○ Surgery may be needed if there is valve damage or persistent infection. Angina Pectoris Definition ○ Chest pain or discomfort due to inadequate oxygen supply to the ○ heart muscle (myocardial ischemia). Types: ○ Stable Angina: Occurs with exertion and relieved by rest or nitroglycerin. ○ Unstable Angina: Occurs at rest, more severe, and not relieved by nitroglycerin; may indicate impending myocardial infarction. Signs and Symptoms: ○ Chest pain or pressure, often described as squeezing, heaviness, or burning. ○ Pain may radiate to the neck, jaw, shoulder, or arm. ○ Dyspnea, sweating, nausea. Diagnosis: ○ ECG, stress testing, and coronary angiography. Treatment: ○ Nitroglycerin to relieve pain. ○ Antiplatelets (aspirin) to reduce clotting risk. ○ Beta-blockers and calcium channel blockers to reduce heart workload. Congenital Heart Defects (CHD) Definition: Structural abnormalities in the heart present from birth that affect blood flow. Examples: ○ Atrial Septal Defect (ASD), Ventricular Septal Defect (VSD), Tetralogy of Fallot, Patent Ductus Arteriosus (PDA). Signs and Symptoms: ○ Cyanosis (for defects causing right-to-left shunt). ○ Fatigue, dyspnea, poor growth, and frequent respiratory infections. ○ Heart murmurs detected on auscultation. Diagnosis: Echocardiogram, chest X-ray, and sometimes cardiac MRI or catheterization. Treatment: ○ Mild defects may close on their own or require monitoring. ○ Surgical repair for more severe defects. ○ Medications like diuretics or ACE inhibitors in some cases. Acute Coronary Syndrome (ACS) Definition: A range of conditions associated with sudden, reduced blood flow to the heart, including unstable angina, NSTEMI, and STEMI. Signs and Symptoms: Severe, persistent chest pain or pressure. Pain radiating to jaw, neck, arm. Diaphoresis, dyspnea, nausea, and fatigue. Diagnosis: ECG changes (ST-segment elevation in STEMI). Elevated cardiac biomarkers (troponin, CK-MB). Treatment: MONA (Morphine, Oxygen, Nitroglycerin, Aspirin). Reperfusion therapy: PCI (angioplasty) or thrombolytics. Anticoagulants, beta-blockers, ACE inhibitors, and statins. Left-Sided Heart Failure lungs Definition: Left ventricle fails to pump blood effectively, causing fluid backup into the lungs. Signs and Symptoms: wake up to SoB Dyspnea, orthopnea, paroxysmal nocturnal dyspnea. Pulmonary congestion (crackles, cough). ~ Fatigue, cyanosis, and tachycardia.to compensate Diagnosis: Echocardiogram, chest X-ray, BNP levels. Treatment: ACE inhibitors, diuretics, beta-blockers, and lifestyle changes. ↓ workload , fluid  Right-Sided Heart Failure Peripheral Definition: Right ventricle fails to pump blood effectively, leading to systemic venous congestion. Signs and Symptoms: Peripheral edema, ascites, hepatomegaly, and jugular venous distention (JVD). Weight gain and anorexia. Diagnosis: Same as left-sided heart failure; echocardiogram and BNP levels. Treatment: Diuretics, ACE inhibitors, beta-blockers, and managing underlying causes ○ pulmonary hypertension Myocardial Infarction (MI) Definition: impeding doom ○ Death of heart muscle tissue due to prolonged lack of blood supply, often caused - by a blockage in coronary arteries. Signs and Symptoms: ○ Severe chest pain, radiating to arm, neck, or jaw. ○ Sweating, nausea, shortness of breath, and anxiety. ○ May also present with “silent” symptoms, especially in diabetic patients. Diagnosis: ○ Elevated cardiac biomarkers (troponin, CK-MB). ○ ECG changes (ST elevation for STEMI). Treatment: Immediate care: MONA (Morphine, Oxygen, Nitroglycerin, Aspirin). Reperfusion (angioplasty or thrombolytics). Beta-blockers, ACE inhibitors, and anticoagulants. Ethical Dilemmas – Heart Transplant & Research Common Ethical Topics: Donor eligibility & allocation – who gets on the transplant list? Compliance questions – should noncompliant patients still qualify? Cost vs benefit – especially in older adults or those with poor support Case Study #1 Heart Failure Key Symptoms Fatigue with light activity likelya Paroxysmal nocturnal dyspnea (awakens gasping for air) 8 lb weight gain in 2 weeks 4+ pedal and pretibial edema Bilateral lung crackles Question 2: At Most Risk For Fluid volume overload Electrolyte imbalance (from diuretics and digoxin) Question 3: Most Concerning Lab Value Potassium → critical to monitor with digoxin therapy due to risk of toxicity with hypokalemia Question 4: Teaching Plan (Select All That Apply) Weigh yourself daily at the same time and in the same clothes Limit sodium to no more than 2g/day Report a 1 lb weight gain in 1 day or 3 lbs in 1 week Take prescribed medications even if feeling better Do not: Increase fluid intake Limit exercise unless prescribed Eat high-potassium foods unless directed Question 5: Nursing Actions for New Orders Educate the client about stopping digoxin Instruct the client to begin the new medication (sacubitril/valsartan) today Ask dietitian to meet with the client Determine if the client owns a scale for daily weights Do not: Question the new medication unless unclear Advise an additional diuretic dose Request potassium supplement without indication Case Study #2 – Suspected MI Presentation Chest pain radiating to left arm Took aspirin before arrival ECG: ST elevation in V3/V4 (anterior leads) - Troponin levels elevated Question 2: Condition Differentiation ST elevation → STEMI ○ Likely due to coronary artery blockage or rupture  Troponin elevation without ST changes → NSTEMI Question 4: Medication Orders – Indicated or Not Enoxaparin → indicated CIPTOUST Metoprolol → indicated HiN Tenecteplase → indicated (thrombolytic) clotbust Morphine → indicated (pain relief, preload reduction) pain Question 5: Medication Timing Tenecteplase should be given within- 30 minutes of arrival ("door-to-needle" time) Other meds (like metoprolol, enoxaparin) may follow based on protocol Question 6: Reassessment Findings After Tenecteplase Improved: chest pain decreased, O2 saturation improved, HR and BP improved slightly Unchanged: O2 saturation remained stable at 92–95% Surgical - 9 Assessment (Surgical Patients) Baseline vitals (before surgery) Allergies, medication history, NPO status Physical assessment (focus on surgical site area) Pain level and location Emotional state (anxiety, understanding of procedure) Lab values (e.g., H&H, electrolytes, coagulation studies) Interventions (Pre- and Post-Op) Pre-op teaching (IS, TCDB, mobility, expectations) Verify consent signed NPO status maintained Start IV line, administer pre-op meds Skin prep as ordered Post-op: monitor vitals frequently Pain management (meds, positioning, non pharm methods) Promote early ambulation Encourage incentive spirometry, deep breathing Maintain wound care and drain care What is PACU? What Do They Do? PACU = Post Anesthesia Care Unit Nurses monitor pts immediately after surgery Assess airway, breathing, circulation (ABCs) Monitor VS, O2 sats, LOC, pain Manage post-anesthesia effects (e.g., nausea, shivering) Communicate with OR & floor nurse for handoff Post-Op Signs/Symptoms & Treatment Pain → treat with analgesics Nausea/vomiting → antiemetics (ondansetron) Hypoxia → oxygen, monitor RR & sats Bleeding → check surgical site, reinforce dressing, notify surgeon Low urine output ( I - Anatomy and physiology. S-3kg pibilable ○ RUQ below diaphragm - Liver Largest abdominal organ “Fat/Protein/Carbs Metabolism, Regulation of circulation blood, functions volume, filtering, clotting, and drug detoxification” ○ Carbohydrates Glucose levels normal 13 % of blood Stored as glycogen but released by liver uses- from digestive when needed (GLYCOGENOLYSIS) Filter blood coming - the rest Gluconeogenesis; amino acids to glucose tract before moving it to Fat: Of the body hence why high fat Energy and produces bile foods cause bile Protein: ammonia to urea (amino waste toxic to N issues nontoxic) Vitamins: iron ○ Maintaining normal levels of fat vitamins and iron # Albumin - spandex keeps the fluid part of your blood from proteins build leaking out of your blood vessels (the tubes vessels your blood flows through) and into other tissues - Bile Salt that helps with digestion > fatty acids, cholesterol, and fat vitamins - ○ Bilirubin - pigment -  - ven Coagulation factors from Vitamin K Blood volume reservoir and filter ○ Right side HF > takes one liter by ↓ a be distending for circulating volume nepate ○ CIRRHOSIS - liver damage so no L nein iron storage > iron deficiency anemia ○ Kupffer Cells help filter bacteria from blood and located in sinusoids Drug Metabolism supply blood supply Elimination of Bile - nutrient rich blood from to kidneys TWO LOBES ○ Right - 2 digestive tract Caudate and Quadrate ○ Left Enclosed in visceral peritoneal cavity and covered by Glisson’s capsule Hepatic duct Lobule = functional unit of liver - moves bile 11 ○ Cylinder shaped created by liver cell down to the S I- I ○ Surrounds a central vein with portal triads > portal vein, hepatic artery, and bile duct ○ Allows continuous exposure of hepatic cells to blood small interfine Blood enters sinusoids (blood vessel = oxygen and gall bladder nutrients) from portal vein and hepatic artery ↳ brak o fats shelps PORTAL TO CENTRAL ○ Portal venules supply to the blood that flows by the hepatic digestion cellular plates and ultimately into central vein LFT liver function tests ○ Bilirubin - PIGMENT HEME > brown of poop - - ↳ Jaundice = obstruction and exceeds 3 mg/dL ○ Enzymes - ALT, ALP, AST - - - Less than 1 = acute hepatitis Greater than 1 = cirrhosis Rises with damages to other organs ○ Proteins ○ Clotting Gallbladder Diagnosis ↳ joins R lube stines - bil until needed for fat digection - Bil from : influenced by cholecytokinin hormone  Assess ○ SUPINE POSITION INSPECT Skin and nails > jaundice/clubbing Distended abd Auscultation Bruit - hepatitis Palpate Enlarged liver > meet downwards and at fingertips JVD = HEPATIC PORTAL HTN Tenderness = hepatitis or CHF Percussion 5th intercostal space then downward DULLNESS = LIVER PRESENCE normal rexpected ○ Measure span of dullness = checking for enlargement LIVER SPAN Average size for women: 14-15 cm ; 3 pounds Average size for men: 15-16 cm ; 3 pounds Meds ○ Lactulose = hepatic encephalopathy by reducing ammonia ○ Diuretics = reduce fluid overload and ascites ○ Vitamin K = clotting factor ○ Antiviral (Tenovir and Entacavir) = viral hepatitis ○ Corticosteroids = reduce inflammation for autoimmune hepatitis ○ Acetylcysteine = antidote for acetaminophen OD and protect liver cells Avoids hepatotoxic drugs like NSAIDS  ROLE OF NURSES IN THE CARE OF PATIENTS WITH DECOMPENSATED CIRRHOSIS Holistic patient centered approach Assessment of frailty and risk of falls ○ Frailty is linked to faster disease progression, poor quality of life, and lower survival rates. The liver frailty index, which includes grip strength, chair stands, and balance. Key interventions to improve frailty include proper nutrition and moderate exercise, areas where nurses can play a key role. Frailty increases the risk of falls, which is also associated with hepatic encephalopathy. Nurses should identify patients at higher risk of falls and discuss preventive strategies with patients and caregivers. Counselling about healthy lifestyle, diet, and self-management ○ Nutritional counseling is crucial for patients with cirrhosis due to common issues like sarcopenia, frailty, and the need to reduce sodium intake in those with ascites or edema. A multidisciplinary team is essential to help ensure patients meet the goals of adequate calorie and protein intake. Nursing role in management of complications of cirrhosis ○ Nurses play a key role in caring for hospitalized patients with decompensated cirrhosis by conducting thorough assessments. This includes monitoring signs of disease progression (e.g., fluid buildup, jaundice), preventing risks (e.g., delirium, malnutrition), and addressing symptoms like pain, breathlessness, and anxiety. Understanding the patient's experience, including psychosocial factors such as fears and increased dependence, is essential for comprehensive care The role of specialist nurses in liver diseases NURSING CARE OF PATIENTS WITH COMPENSATED CIRRHOSIS L cirrhosis in the absence of ascites, variceal bleeding, or hepatic encephalopathy Diet education: High protein, low fat, moderate sodium and increased fiber. Encourage moderate exercise. Immunizations: review immunization history and perform hepatitis A & B titers Mandatory immunizations include COVID-19 Pneumococcal pneumonia Influenza Tetanus Medication Education: Pt is advised to avoid NSAIDs, aspirin, and acetaminophen Screening: The nurses role includes scheduling screenings and surveillance during an endoscopy  Counselling about healthy diet and lifestyle ○ focusing on high protein, low fat, low/moderate sodium, and increased fiber. ○ Nurses should encourage moderate exercise as physical activity can help prevent sarcopenia and improve the progression of cirrhosis. Education about cirrhosis and its potential complications ○ Providing education can help patients and caregivers recognize complications early and seek medical attention. One key complication, variceal hemorrhage, can be effectively prevented with beta-blockers or endoscopic variceal band ligation. Assisting in treating the cause of cirrhosis ○ For alcohol-related cirrhosis, nursing interventions in primary care can support patients in achieving abstinence and adhering to alcohol dependence treatments, such as acamprosate. Nurses should also collaborate with alcohol treatment facilities and address social stigma. For non-alcoholic fatty liver disease, nurses should focus on encouraging weight loss and addressing stigma related to being overweight. A Mediterranean or plant-based diet, reduced caloric intake, and an* exercise program can help achieve a weight loss of over 10%, improving liver health by reducing steatosis, inflammation, and fibrosis. Screening for gastroesophageal hepatocellular carcinoma ○ Endoscopy should be performed at the time of initial diagnosis of cirrhosis. If no mem - varices are found, a follow-up endoscopy should be done in 3 years. For small varices, a repeat endoscopy should be scheduled in 1 to 2 years. Non-selective beta-blockers should be prescribed for patients with small or large varices, unless contraindicated. Nurses play a key role in educating patients on how to monitor beta-blocker therapy, including tracking resting heart rate and blood pressure, and informing them about potential side effects like hypotension, dizziness, and cold extremities. Immunization ○ Mandatory vaccines for patients include COVID-19, pneumococcal pneumonia, influenza, and tetanus. Serologic testing for hepatitis A and B should be done to check for previous exposure, and the respective vaccines should be administered if the patient is negative for anti-HAV and anti-HBc antibodies. Medication counseling ○ Nurses play a crucial role in reviewing medications and improving medication adherence during both initial and follow-up visits, including via telehealth. Patients should be advised to avoid NSAIDs and aspirin, and use acetaminophen (up to 2g daily) as an alternative. Patients with active alcohol use should be informed of the increased risk of liver toxicity with acetaminophen. Fluoroquinolones, penicillins, and cephalosporins are generally safe antibiotics, and statins at lower doses, along with oral hypoglycemic agents or insulin for diabetes, are acceptable.  Caring for comorbidities ○ Comorbidities may include features of the metabolic syndrome, namely obesity, diabetes, hypertension, and cardiovascular disease. This section is a reminder about the liver and its physiological functions including metabolic, hematologic, and production of bile. Think about functions such as blood volume reservoir, blood filter, blood clotting factors, and drug metabolism and detoxification. Anatomy: Largest internal organ, located in RUQ under the diaphragm. Made of lobes; functional units = lobules. Gets blood from the hepatic artery (oxygen) and portal vein (nutrients from GI tract). Physiology: Metabolism of carbs, proteins, fats. Detoxifies meds and toxins. Produces bile → helps digest fats. Synthesizes albumin & clotting factors. Stores vitamins A, D, E, K, and B12. Converts ammonia → urea for excretion. Nursing Process for Liver Disease Assessment: Fatigue, jaundice, ascites, RUQ pain, bleeding. ↑ Labs: ↑ AST/ALT, bilirubin Vitamin K & ○ ammonia; ↓ albumin, platelets. Diagnosis: Risk for bleeding, Imbalanced nutrition, Excess fluid volume, Impaired skin integrity. Planning/Intervention: Monitor labs & weight. Low-sodium, high-calorie, low-protein (if ammonia ↑). * Administer lactulose (↓ ammonia), diuretics, vit K.* Evaluation: Improved energy, labs stabilizing, less ascites, ammonia levels down. Diagnostic Testing for Liver LFTs: AST, ALT, ALP, bilirubin, albumin. ○ ALT = liver damage specific to the liver * ○ AST = liver damage specific for other organs like heart kidneys pancreas brain* PT/INR: prolonged if the liver is damaged > blood isn’t clotting quick enough Ammonia: ↑ with hepatic encephalopathy.  Ultrasound: check structure. CT/MRI: tumor, abscess, cirrhosis. KUB XRAY HIDA Scan Comparing Types of Liver Disease Disease Cause Key Features Hepatitis (A–E) Viral Inflammation, fatigue, jaundice Cirrhosis Chronic damage Scarring, portal HTN, ascites NAFLD Obesity, DM Fat in liver, silent at first Alcoholic Liver Disease ETOH abuse Steatosis (overload of fat) → hepatitis → cirrhosis Cirrhosis Assessment: ○ Jaundice, ascites, spider angiomas, hepatomegaly ○ Fatigue, easy bruising, GI bleeding, confusion (hepatic encephalopathy) ○ Labs: Elevated liver enzymes (AST, ALT), bilirubin, INR, low albumin Nursing Interventions: ○ Diet: Low sodium, high protein, high fiber (individualized based on condition) ○ Fluid management: Monitor for ascites, administer diuretics, restrict fluids as needed ○ Monitor for complications: Hepatic encephalopathy, variceal bleeding, and infection ○ Educate: Avoid alcohol, medication adherence, and signs of complications Hepatic Encephalopathy LIFE THREATENING D reached brain , ammonia can A complication of liver failure that leads to accumulation of toxic waste (Ammonia) KILL the brain Can be caused: insidiously, exacerbated by an acute aka kill pt illness or infection, GI bleed (blood is swallowed and broken down creating an increased amount of toxic waste) Manifestations: AMS, asterixis, ataxia, may have seizures, coma, death The patient may be agitated, slow at answering you ASTERIXIS → flapping tremor or relaxing of muscle while using it kinda opposite of intent  DX HIGH serum ammonia levels * Treatment: Lactulose → increased ammonia excretion in the stool! (acidic pH) SE: runny stools (titrate it until they have a bowel movement) Give nasally or rectally Rifaximin: an abx that literally kills the bacteria in the bowel that produces ammonia (late-stage use) IV fluids, supportive care Hepatomegaly S/S ○ Abdominal discomfort or pain RUQ ○ Fullness or bloating ○ Fatigue or weakness ○ Jaundice ○ Nausea or loss of appetite ○ Edema and Ascites TX ○ Hepatitis - antiviral ○ Fatty Liver Disease - lifestyle modification ○ ALD - alcohol cessation Avoid alcohol, healthy weight, eat liver friendly food (low sat fat and high in fiber) 2. Hepatitis (A, B, C) Assessment: ○ Jaundice, malaise, fever, dark urine, clay-colored stools ○ History of exposure, risk factors (e.g., unprotected sex, IV drug use) factor determining ○ Labs: Elevated ALT, AST, bilirubin, specific hepatitis antibodies Nursing Interventions: ○ Rest and support during acute phase ○ Education: Safe practices to prevent transmission (e.g., hand hygiene, vaccination) ○ Manage pain: Analgesics and antiemetics as needed ○ Vaccination: Administer vaccines (HAV, HBV) if applicable 3. Fatty Liver Disease (NAFLD/NASH): an accumulation of fat in the liver in individuals who consume little to no alcohol. This fat buildup leads to inflammation and liver cell damage, a condition known as non-alcoholic steatohepatitis (NASH), which is a more severe form of NAFLD and has a higher risk of progressing to cirrhosis. Assessment: NAFLD - NASH yairr. Often asymptomatic, may present with mild fatigue, discomfort in RUQ ○ Risk factors: Obesity, diabetes, hyperlipidemia Labs: Elevated liver enzymes (ALT, AST), insulin resistance ○ Nursing Interventions: Promote weight loss: Encourage a healthy diet (Mediterranean/plant-based), exercise Manage comorbidities: Diabetes, hyperlipidemia Educate: Avoid alcohol, lifestyle modifications 4. Alcoholic Liver Disease Assessment: ○ History of heavy alcohol use, jaundice, ascites, varices ○ Labs: Elevated liver enzymes (AST > ALT), elevated bilirubin Nursing Interventions: ○ Abstinence: Support alcohol cessation, collaborate with addiction services Reversible; first stage ○ Medications: Disulfiram, acamprosate for alcohol dependence, corticosteroids Pentoxifylline for second stage alcoholic hepatitis ○ Monitor for liver failure and complications (bleeding, encephalopathy) ○ Nutrition: High-protein, low-fat, non fatty diet ○ Transplant 5. Liver Cancer (Hepatocellular Carcinoma) loss Assessment: Livers is + weight ○ Unexplained weight loss, RUQ pain, jaundice ○ Risk factors: Chronic liver disease (e.g., cirrhosis, hepatitis B/C) zweig ascites usually ○ Labs: Elevated AFP (alpha-fetoprotein), imaging studies (CT, MRI) Nursing Interventions: ○ Supportive care: Pain management, nausea control ○ Post-surgical care: Monitor for complications (infection, bleeding) ○ Educate: Treatment options (surgery, chemo, liver transplant) 6. Portal Hypertension ○ Assessment: HiN- rupture Ascites, splenomegaly, variceal bleeding (vomiting blood) - of ducts/vessels Labs: Elevated portal vein pressure, low platelets Nursing Interventions: ○ Monitor for variceal bleeding: Prophylactic beta-blockers, endoscopic ligation ○ Fluid management: Diuretics for ascites, manage electrolyte imbalances ○ Educate: Avoid NSAIDs, alcohol, and seek medical attention for bleeding General Nursing Considerations for All Liver Diseases Assess for complications: Hepatic encephalopathy, variceal bleeding, ascites, infection Monitor vital signs: Especially for signs of bleeding or infection Pain management: Use appropriate analgesics, avoid NSAIDs Patient education: Alcohol avoidance, medication adherence, vaccination, dietary management Multidisciplinary care: Work with dietitians, social workers, addiction specialists, and hepatologists as needed Interprofessional & Nursing Management Non-Alcoholic Liver Disease (NAFLD/NASH) Lifestyle change: weight loss, low-fat diet, exercise. Control DM, cholesterol. Nurses: education & monitoring labs. Alcoholic Liver Disease Stop alcohol completely. Vitamins: thiamine, folate. Possible detox support, social work, psych. Nurses: Monitor for withdrawal, bleeding, nutrition. Team includes: GI, hepatology, dietitian, pharmacist, psych, social work. The article titled "From NAFLD to MAFLD: Nurse and Allied Health Perspective," authored by Michelle Clayton and colleagues, discusses the renaming of non-alcoholic fatty liver disease (NAFLD) to metabolic (dysfunction) associated fatty liver disease (MAFLD). This change aims to better reflect the disease's association with metabolic dysfunction. The authors, including nurse and allied health practitioners, express support for this redefinition, believing it will enhance nurse-patient communication, improve patient care, and reduce healthcare system burdens  Ideally, going for-ward, the change to MAFLD would improve the dialogue between treating healthcare professionals and patients and may help bridge the gap (health literacy), with increase awareness of MAFLD will continue to improve among providers and the public, so that patients can be risk strati-fied and appropriately counselled on interventions that are likely to improve metabolic and liver health. ○ CV HEALTH Unlike NAFLD, which defines fatty liver disease by the absence of alcohol use, MAFLD shifts the focus to the metabolic factors that contribute to liver disease. Clinical Manifestations & Management of Cirrhosis Manifestations: Jaundice, ascites, spider angiomas, varices, fatigue. Decompensated signs: hepatic encephalopathy (confusion, asterixis: flapping tremor), GI bleed, edema, hepatorenal syndrome. Management: Lactulose for ammonia. ○ Lactulose is also used to reduce the amount of ammonia in the blood of patients with liver disease. It works by drawing ammonia from the blood into the colon where it is removed from the body. Diuretics (spironolactone). ascites Paracentesis for ascites. Beta-blockers to prevent variceal bleeding. treats portalin ○ By lowering portal pressure and reducing the risk of varices becoming distended and fragile, beta-blockers help prevent variceal bleeding, which can be life-threatening. Nutrition: low sodium, soft protein if encephalopathy. ○ A low-sodium diet helps control ascites and edema, and protein management is critical in controlling ammonia levels and preventing further brain impairment. Ethical Dilemmas in Liver Transplant Arises from issues related to limited organ availability and prioritization criteria, substance abuse hx, adherence to post-transplant care, resource allocation, and decisions aggressive treatment, and palliative care Dilemmas: Who qualifies for a transplant? (e.g., former alcohol use, relapse risk). Limited organs vs. high demand. Equity in access (insurance, social factors). Nursing Role: Advocate for fair access. Participate in transplant research to improve outcomes. LIVER end Post-Liver Transplant: Can the Client Self-Care? ARE THEY GONNA STOP THE BEHAVIORS THAT CAUSED THEM TO LOSE THEIR LIVER IN THE FIRST PLACE? AND CAN THEY TAKE CARE OF THAT ORGAN? Alcoholism should not define someone’s lives especially young It is not about judgement This involves adhering to medication regimens, attending regular follow-up appointments, maintaining a healthy lifestyle, and being vigilant about signs of organ rejection or infection. Post-transplant care includes: Lifelong immunosuppressants → must take exactly as ordered. Infection prevention (hand hygiene, avoid crowds). immunocompromised Regular labs & appointments. Monitor for signs of rejection: fever, RUQ pain, jaundice, dark urine. Nursing Role: Educate, reinforce adherence, monitor for complications, connect with the transplant team. 8 - Neuro Assessment – FAST & Focused LOC (Level of Consciousness): Alert and Oriented to person, place, time, and situation Use Glasgow Coma Scale (GCS): Eye (4), Verbal (5), Motor (6) = /15 Alert → Confused → Lethargic → Stuporous → Comatose Pupils: PERRLA = Pupils Equal, Round, Reactive to Light and Accommodation Motor & Sensory Check: Strength: grip, push/pull Sensation: light touch, pain, temperature Drift test: lift arms/legs – do they drift? Reflexes: deep tendon - patellar and babinski’s sign Romberg: finger to nose Speech glossopharyngeal Cranial Nerves: facial Lvagal optic occulomotor Know basics of CN 2 (vision), 3 (pupil reaction), 7 (facial symmetry), 9/10 (gag), 12 hypoglossal (tongue) FAST for stroke: 3 3 On occasion ↳ offactory-smen · optic-vision-eyes Face droop -6 occulomotor our i Arm weakness trochlear eyes - Speech slurred ↓ trigeminal-ceek/forches Time to call 911 3 3 acts 6. abducens-eyes funny 7 facial-facetast Anatomy & Physiology of Neuro System ve & Vestibulocochlear-hearing glossopharyngeal-s Vehicle 10vagus-miss. que any 11. accessory-shoulders now 12 hypoglossal tongue - - CNS (Central Nervous System) Brain & spinal cord Brain parts: ○ Cerebrum – thinking, movement ○ Cerebellum – balance/coordination ○ Brainstem – HR, breathing, consciousness ○ Meninges – protective layers CSF (Cerebrospinal Fluid) – cushions brain & removes waste PNS (Peripheral Nervous System) Nerves outside brain/spinal cord Includes cranial nerves & spinal nerves Autonomic Nervous System Sympathetic ("fight or flight") Parasympathetic ("rest and digest") Common Neurological Diseases Disease Hallmark Signs Notes Stroke (CVA) FAST signs, hemiparesis Ischemic (blood clot in brain) or (one side weakness), hemorrhagic (ruptured blood vessel > hem-severe headache bleeding in the brain) Seizures/Epilepsy Jerking, LOC Keep patients safe from injury, no Absence: sudden lapses in restraints or objects in mouth, TURN attention TO SIDE !!!! time it Focal: unusual sensation, meds = anticonvulsants repetitive movements (carbamazepine, phenytoin) Meningitis Fever, stiff neck, Bacterial = urgent! photophobia Parkinson’s Tremor, rigidity, slow Low dopamine; fall risk movement Multiple Sclerosis (MS) Muscle weakness, vision Autoimmune; attacks protective sheath issues of nerves Alzheimer’s Memory loss, confusion Progressive, safety is key TBI (Traumatic Brain LOC, behavior changes Monitor ICP, seizure risk Injury) Neuro Medications Drug Class Example Used For Watch For Anticonvulsants Phenytoin, Levetiracetam Seizures Continuous cardiac (Keppra) monitoring, Gingival hyperplasia (Dilantin), drowsiness Dopaminergics Carbidopa-Levodopa Parkinson’s Orthostatic hypotension, (Sinemet) dyskinesia > SAFETY FOR FALL RISK Anticholinesterase Donepezil (Aricept) Alzheimer’s GI upset, bradycardia Steroids Dexamethasone Cerebral GI bleed, ↑ BG think what MOM took edema Osmotic Diuretics Mannitol ↓ ICP Monitor I&Os, electrolytes (K+) Antibiotics Ceftriaxone Meningitis Finish the full course, watch for allergies!! Benzodiazepines Lorazepam (Ativan) Acute Sedation, respiratory seizures depression Neuro Patients (ADPIE) A – Assessment LOC, GCS, pupils, motor/sensory, vital signs, headache, nausea, seizure activity. D – Diagnosis Risk for falls, Impaired mobility, Risk for aspiration, Acute confusion, Knowledge deficit. P – Planning Prevent injury, maintain airway, promote orientation, seizure precautions, medication safety. I – Intervention Neuro checks q2-4h Fall precautions Reorient pt frequently HOB ↑30° (if ICP risk)  Seizure precautions: pad bed, O2/suction at bedside Administer meds safely and on time E – Evaluation Pt maintains orientation/safety, no new deficits, seizure-free, tolerates meds Parkinson’s Disease: a chronic, progressive neurodegenerative disorder affecting motor control due to dopamine depletion in the neurons of the brain. Pathophysiology Dopamine (inhibitory neurotransmitter) is reduced. Acetylcholine (excitatory neurotransmitter) is unopposed. This imbalance causes tremors, rigidity, and bradykinesia. Etiology & Risk Factors idiopathic, but some links to: ○ Age >60 ○ Male sex ○ Family history ○ Exposure to pesticides/herbicides ○ Repeated head trauma Classic Symptoms : TRAP Tremor Resting tremor, often "pill-rolling" Rigidity "Cogwheel" stiffness, resistance to passive movement Akinesia/Bradykinesia Slowed movement, shuffling gait Postural instability Poor balance, risk for falls Other signs: Mask-like facial expression lost muscle control of fact Soft, slurred speech Drooling Dysphagia Depression and dementia (later stages) Diagnosis Based on clinical presentation (no definitive test)  Response to dopaminergic medications (Levodopa trial) MRI/CT to rule out other causes Pharmacologic Management Drug Class Examples Action Dopaminergic Levodopa/Carbidopa Increases dopamine availability Dopamine Ropinirole, Stimulate dopamine receptors agonists Pramipexole MAO-B Selegiline, Prevent dopamine breakdown inhibitors Rasagiline COMT inhibitors Entacapone Prolong Levodopa effect Anticholinergics Benztropine Reduce tremors/rigidity (not first-line for elderly due to confusion risk) Nursing Considerations: ABC SAFETY AND FALL RISK AND EXERCISE Monitor for orthostatic hypotension Fall risk precautions Monitor swallowing → risk of aspiration Offer small, frequent, high-calorie meals Encourage fiber and fluids → prevent constipation Administer meds on time to maintain consistent dopamine levels Educate about on/off effect (fluctuations in symptom control with Levodopa) Patient Teaching Use assistive devices for mobility (canes, walkers) Rock side to side to initiate movement ("freezing" episodes) Practice ROM exercises to maintain flexibility Promote speech therapy if dysarthria present Encourage occupational therapy for ADLs Avoid high-protein meals when taking Levodopa (interferes with absorption) Complications Dysphagia → aspiration pneumonia Immobility → skin breakdown, contractures, DVT  Depression and cognitive decline Medication tolerance over time (less effective) CASE STUDY FOR PARKINSON What factors could be a cause of Joshua’s high blood pressure? Parkinson’s disease progression: As Parkinson’s disease progresses, it contributes to orthostatic hypotension or elevated blood pressure. Medication side effects: Some medications used to manage Parkinson’s disease (e.g., levodopa) may contribute to elevated blood pressure or interfere with its regulation. Environmental stressors: The change in living environment, such as moving into the nursing home, can be a stressor that might elevate blood pressure. Pain or discomfort: Parkinson’s disease can lead to muscle stiffness or discomfort, which can contribute to elevated blood pressure. Dehydration or lack of proper nutrition: These could also be factors, especially with the recent change in environment and care. What things can you assess with Joshua to get more information about his current state? Orthostatic blood pressure measurements: Measure his blood pressure in both lying and standing positions to assess for orthostatic hypotension, which is common in Parkinson’s disease. Heart rate and rhythm: Take his pulse to assess for irregularities, as Parkinson’s can sometimes cause arrhythmias. Symptoms of dizziness or lightheadedness: Ask Joshua about any episodes of dizziness, which may suggest orthostatic hypotension or medication side effects. Pain assessment: Given that Parkinson’s disease causes muscle rigidity, assess for pain or discomfort that could elevate his blood pressure. Medication review: Review his current medications for any that might be contributing to the elevated blood pressure or causing adverse effects. What nonpharmacological steps can Joshua take to lower his blood pressure? Dietary changes: Encourage a heart-healthy diet, such as the DASH (Dietary Approaches to Stop Hypertension) diet, which emphasizes fruits, vegetables, whole grains, and low-fat dairy. Physical activity: Encourage regular, light physical activity that is safe for his mobility, such as walking or chair exercises, which can help manage blood pressure. Stress management: Techniques like deep breathing, meditation, or guided relaxation may help reduce stress, a potential contributor to elevated blood pressure.  Adequate hydration and nutrition: Ensure that he is drinking enough fluids and receiving proper nutrition to avoid dehydration, which can affect blood pressure regulation. Regular monitoring of blood pressure: Encourage frequent blood pressure checks to track any changes and adjust interventions accordingly. What general information will you share with Joshua’s family to promote his CV health? Regular blood pressure monitoring: Emphasize the importance of monitoring Joshua’s blood pressure regularly to identify any changes or trends. Diet and nutrition: Share information about the importance of a low-sodium, high-potassium diet and encourage heart-healthy food choices to support cardiovascular health. Physical activity: Discuss the importance of maintaining physical activity within his abilities, as it helps control blood pressure and improves overall well-being. Medication adherence: Explain the role of prescribed medications for managing blood pressure and the importance of compliance, if Joshua changes his mind about taking medications. Stress management techniques: Offer guidance on relaxation and stress-reduction strategies to help lower his blood pressure. Symptom recognition: Educate his family on symptoms of high or low blood pressure, including dizziness, headaches, or fainting, so they can be vigilant and intervene appropriately. Amyotrophic Lateral Sclerosis (ALS) Definition: A progressive neurodegenerative disease that affects motor neurons, leading to muscle weakness and atrophy. Signs and Symptoms (S/S): ○ Muscle weakness, twitching, spasticity, and eventual loss of motor control. ○ Difficulty speaking, swallowing, and breathing ○ Cognitive function is typically unaffected. Interventions: ○ Provide assistive devices for mobility and communication as needed. ○ Support respiratory function, often with non-invasive ventilation. ○ Educate family on progressive nature of ALS and prepare for end-of-life decisions. Riluzole: Slows disease progression slightly. no cure , just slow it Edaravone: May slow progression in some patients. Symptomatic management: Pt will diefrom ALS. ○ Includes muscle relaxants for spasticity and medications for pain management.atsomepoint  Medications ○ Stroke: tPA: For ischemic stroke if given within the therapeutic window to dissolve clots. Antiplatelet agents (e.g., aspirin) and anticoagulants (e.g., warfarin) to prevent future clots in ischemic stroke. ○ Antihypertensives: For hemorrhagic stroke to manage blood pressure. Reduction of Risk Potential (RRP) Focus: Prevent complications or deterioration in clinical settings. Tips: Memorize early vs late signs of complications ○ hypoxia = restlessness first, cyanosis later). Flashcards for tubes/drains/wounds – what's normal output for a chest tube? What does cloudy urine mean? Physiological Adaptation Tips: Practice linking symptoms + pathophysiology + priority intervention. → Ex: CHF = fluid overload → crackles/SOB → furosemide & elevate HOB. Review ABGs, acid-base, ventilator settings, and ICP/CVP values. Go over med-surg “zebras” like SIADH vs. DI, Addison’s vs. Cushing’s. Health Promotion & Maintenance Focus: Prevention, screenings, growth/development, vaccines, education. Tips: Know your immunization schedule (e.g., DTaP, MMR, HPV, flu). Use growth/development mnemonics for kids (Erikson, milestones). Screening ages: mammogram = 40, colonoscopy = 45, PSA = 50. Teach lifestyle changes in simple terms: low-sodium diet, smoking cessation, exercise. Match education to the client’s developmental level (you wouldn’t teach a toddler the same way as a teen). Psychosocial Integrity Focus: Coping, mental health, therapeutic communication, grief, abuse. Learn stages of grief and appropriate nursing responses for each. Know signs of abuse, neglect, or trauma—and when/what to report. Be present, not prescriptive.” The patient needs support more than solutions.