NUR 3031 Patho Final Review Updated, Exams of Nursing

Download NUR 3031 Patho Final Review Updated and more Exams Nursing in PDF only on Docsity! 1 1  Cellular Injury Reversible  Although impairing cell function, does not result in cell death.  Two patterns under microscope: 1 Cellular swelling: occurs with impairment of Na+/K+ pump, usually as a result of hypoxic cell injury 2 Fatty change: linked to intracellular accumulations of fat; reversible, usually indicates severe injury. Irreversible  Cell death or necrosis can occur.  Apoptosis (Programmed cell death): a form of cell death necessary to make way for new cells; NORMAL PROCESS IN THE BODY  Necrosis: cell death and degradation; UNREGULATED death; cell swells and ruptures; inflammation results. Cells may undergo liquefaction, coagulation, infarction, or caseous necrosis Gangrene  Large area of necrotic tissue; Three types: 1 Dry gangrene: lack of arterial blood supply but venous flow can carry fluid OUT of tissue 2 wEt gangrene: lack of venous flow lets fluid ACCUMULATE in tissue (E fluid can ‘E’nter) 3 Gas gangrene: Clostridium infection produces toxins and bubbles Cellular stressors  Hypoxia: lack of oxygen in air, respiratory disease, ischemia, anemia, edema, or inability of cells to use oxygen. Causes: ATP DEPLETION or “POWER FAILURE”; AEROBIC metabolism STOPS, less ATP is produced, Na+/K+ pump is impeded, cell swells up, lactic acid is produced due to ANAEROBIC metabolism.  Heat and Cold: extremes of heat and cold cause damage to the cells Electricity: can cause extensive tissue injury and disruption of neural/ cardiac impulses Chemical agents: injures cell membrane, block enzymatic pathways, and disrupt osmotic/ionic balance Biologic agents: are able to replicate and continue to produce injurious effects Radiation: ionizing radiation, ultraviolet radiation, nonionizing radiation Nutritional imbalances: Nutritional excess/deficiency can predispose cells to injury Atrophy  decrease cell size causing reduce oxygen consumption and other cellular functions.  General causes: 1 Disuse: reduction in muscle use 2 Denervation: atrophy in muscles of paralyzed limbs 3 Loss of endocrine stimulation: in relationship with disuse atrophy 4 Inadequate nutrition and ischemia: cells decrease size and energy requirements due to lack of nutrition and oxygen. Hypertrophy  increase cell size and with it an increase in the amount of functioning tissue mass.  Pathogenic Hypertrophy: thickening of urinary bladder and myocardial hypertrophy. Hyperplasia  increase in the number of cells in an organ or tissue.  Occurs in tissues such as epidermis, intestinal epithelium, and glandular tissue.  2 types of PHYSIOLOGICAL HYPERPLASIA: 1 Hormonal hyperplasia: Breast and uterine enlargement during pregnancy, due to estrogen. 2 Compensatory hyperplasia: Regeneration of the liver that occurs after partial hepatectomy, or with the removal of a kidney.  Most forms on NONPHYSIOLOGICAL HYPERPLASIA are due to excessive hormonal or the effects of growth factors on target tissues. Metaplasia  Reversible change in which a cell type is replaced by another cell type, occurs in response to irritation 2 2 and inflammation. (‘M’ is like mix-and-match) Dysplasia  deranged cell growth of a specific tissue, results in cells that varies in size, shape, and organization  Strongly implicated as a precursor of cancer; reversible change Hypoxia  lack of oxygen supply to the tissue despite of good perfusion of blood. Ischemia  Decreased blood supply to a body organ or part usually due to functional constriction or obstruction.  ISCHEMIA commonly depends on blood flow through limited numbers of blood vessels and produces LOCAL TISSUE injury  IMMUNE DISORDERS AND IMMUNODEFICIENCY HIV  retrovirus selectively attacks CD4+ T lymphocytes; pt. infectious even when asymptomatic Unprotected sexual activity; blood, semen, vaginal fluids, oral intercourse; Contaminated blood; infected mother to child, breast milk, placenta, needles, blood transfusions Stage 1  Occurs shortly after infection, high viral load  Symptoms: flu like symptoms; GI issues; Lymphoadenopathy, rash; viral replication, CD4+ cell count Stage 2  Latent Period, lowest viral load  Symptoms: Asymptomatic of illness; CD4+ count drops progressively ; 200-499 cells/ᵤL; Risk for opportunistic infections; Inflammation in more than 2 areas for > 3 months Stage 3  AIDS phase, caused by HIV infection of cells, viral load increases, suppressed immune system and opportunistic infections, malignancies, wasting and CNS degeneration.  Symptoms: Occurs when CD4+ cell count is less than 200 cells  Respiratory: pneumocystis carinni pneumonia (PCP), pulmonary TB (can migrate anywhere in the body)  GI: esophageal candidiasis, CMV infection, herpes simple virus, diarreah, gastroenteritis Nervous System: taxoplasmosis (cat poo)  Malignancies: Kaposi sarcoma, non-hodgkins, lumphoma Diagnostic HIV tests 1. ELISA  enzyme-linked immunosorbent assay (ELISA) screens for HIV antibodies. 2. Western blot  test to confirm a positive Elisa test. 3. Polymerase Chain Reaction (PCR)  most accurate, most expensve Nursing Assessment Weight analysis, LOC, Reports of pain  Skin; palpation of lymph nodes, VS, lung sounds, oral cavity, rectal and vaginal exam  HEMATOLOGIC DISORDERS MVC  Normocytic: normal size; normal MVC  Macrocytic: large size; high MVC  Microcytic: small size; low MVC MCHC  Normochromic: normal amount of Hb; normal MCHC  Macrochromic: concentrated amount of Hb; high MCHC  Microchromic: diluted amount of Hb; low MCHC 5 5  Avascular necrosis of femoral head  Kidney infarcts (chronic kidney disease)  Osteomyelitis  Skin ulcers  Pallor, Jaundice  Fatigue and irritability. Diagnostic test  hemoglobin electrophoresis: determines presence hemoglobin S, CBC. Treatement Folic acid supplements and analgesics  Hydration therapy as well as scheduled transfusions decreases crisis episodes.  During a crisis, hydration to improve blood flow, reduce pain, prevent renal damage, O2, IV (narcotics)  Maintaining full immunization  Hydroxyurea inhibits DNA synthesis, reduces pain crisis. Increases RBC levels, acts as an anti- inflammatory inhibiting the production of WBCs.  Bone marrow or stem cell transplant; however risk of graft-versus-host disease. Megaloblastic Anemia  impaired DNA synthesis results in enlarged RBC’s due to vitamin B12 (cobalmin) and folic acid deficiency  causes pernicious anemia: inability to absorb vitamin B12 due to lack of intrinsic factor  Macrocytic (Larger than normal cell size), Normochromic (normal concentration of Hb)  Possibly destruction of the gastric mucosa, caused by the loss of parietal cells and production of antibodies that interfere with binding of vitamin B12 to intrinsic factor. Related Factors  Caused by gastrectomy, gastrojejunostomy, ileal resection and after gastric bypass surgery  Inflammation or neoplasms in the terminal ileum.  Malabsorption syndrome (poor absorption) Signs and Symptoms  Pallor, slight jaundice, nails  Weakness, fatigue and diarrhea  Smooth sore beefy red tongue  Disrupts function of peripheral nerves, spinal cord, and brain.  Parasthesias: numbness or tingling in the extremities  Proprioreception, may progress to imbalance and spinal cord damage.  dark stool because of blood, internal hemorrhage; most leading cause if IG bleed Treatment Life long parental (injection) or high oral Vitamin B12.  increase intake of foods such as eggs, meats, and dairys Diagnostic Test  CBC, MCV, MCHC, MCH Iron Deficiency Anemia inadequate iron supply due to excessive iron loss from bleeding, decreased dietary intake, or malabsorption.  impairs cellular division and maturation especially in rapidly proliferating RBCs  microcytic and microchromic  Iron is stored in body as ferritin  Women loose 15 mg monthly during menstruation (most common cause in women) GI bleeding is most common cause in men. Clinical Manifestation  poor cognitive, motor and emotional function; related to effects on brain development or 6 6 neurotransmitter function. Related Factors  Pregnancy, menstruation  Hemorrhage  Medication use (aspirin)  GI bleeds (peptic ulcer, intestinal polyps, hemorrhoids or cancer)  Eating disorders; Diets (cow’s milk for infants low in iron) Signs and Symptoms  develop slow until Hb drops to 7-8 g/dl; Fatigue and weakness, SOB, Hypoxia  Pallor (ear lobes, palms and conjunctiva)  Dyspnea; Tachichardia  Dysphagia and decreased acid secretion.  Brittle hair and nails  Cheilosis (cracks in corners of mouth)  Smooth tongue, dizziness  Pica (craving to eat unusual substances such as clay or starch) Treatment  Control chronic blood loss.  Increase dietary intake of iron, ferrous sulfate, oral replacement therapy.  Parental iron therapy may be used when oral forms are not tolerated or are ineffective.  Vitamin C enhances absorption  iron-rich foods (as beef, chicken, egg yolk, pork loin, turkey and whole grain breads and cereals). Polycythemia  Abnormally high RBC count: hematocrit >50%  overproduction of RBC’s, WBC’s, and platelets increasing blood viscosity, volume, congestion of tissues (live and spleen) causing acidosis, clotting, and thrombi  Absolute (PRIMARY) Polycythemia: most common in Caucasian men of European, jewish ancestry Neoplastic disease of bone marrow Thick, slow moving blood Secondary Polycythemia Physiologic increase in level of erythropoietin Compensatory response to hypoxia: High altitudes, chronic heart, lung disease and smoking  GI Disorders GERD  Gastric backflow into esophagus (reflux, heartburn or esophagitis) associated with weak or incompetent lower esophageal sphincter  Delayed gastric emptying contributes to reflux, esophageal mucosal injury may occur  Normally cleared and neutralized by esophageal peristalsis and salivary bicarbonate  Chronic inflammatory disease of the antrum and body of the stomach  H. pylori secretes urease which produces ammonia to buffer acidity of stomach; produces enzymes and toxins interfering with protection of the gastric mucosa against acid  The severity of the heartburn is not indicative of the extent of the mucosal injury Related Risk Factors  common problem in infants and children, occurs at least once a day in infants 0-3 months, by 6 months is less frequent  Hiatal hernia  Pregnancy  Obesity; Poor dietary habits, high fat diet  Esophageal structures or previous surgery  Smoking 7 7  Excessive caffeine intake  Gastroparesis (delayed gastric emptying time)  Vomiting, coughing, lifting or bending Signs and Symptoms  Most frequent is heartburn; frequently severe, 30–60 minutes after meal; evening onset  Belching and chest pain  Dyspepsia (burning, pain in epigastric, radiates to throat, shoulder, or back)  wheezing, chronic cough and hoarseness Diagnostic Test  Radiographic studies with barium, esophagoscopy and ambulatory esophageal pH monitoring.  pH probe test used to determine stomach pH (less than 4 = positive)  H. pylori can be detected by C urea breath test Treatment  Avoid large meals; eat sitting right up; foods that reduce esophageal pH(chocolate, fats, caffeine)  Avoid recumbent position several hours after a meal; avoid bending for long periods  Avoid alcohol use and smoking  Sleep with the head elevated  Lose weight if overweight  Antacids, and inhibitors of gastric acid. Histamine-2 (H2) antagonist inhibits gastric acid production  Treatment for h. pylori: PPI; Antibiotic therapy. Complication  Produces a cycle of hyperemia, edema, and erosion of the mucosal surface of the esophagus. Barrett’s esophagus (combination of scar tissue, spasm, and edema). • Produces narrowing of esophagus and causes dysphagia when lumen becomes constricted. • Diagnosis: endoscopic evidence of abnormal mucosa, and intestinal metaplasia.  Two types of esophageal cancer: adenocarcinoma (linked to gastroesophageal reflux and Barret esophagus) and squamous cell carcinoma (attributed to alcohol and tobacco use). Peptic Ulcer  Ulcerative disorder, upper gastrointestinal tract that’s exposed to acid-pepsin secretions  Most common forms of peptic ulcer are duodenal and gastric ulcers  Affects one or all layers of the stomach or duodenum.  Superficial ulcers are called erosions Deep lesions extend through musculature, penetrate blood vessels causing hemorrhage, can cause perforation of the stomach wall or intestines  Three main factors 1. Excessive acid: leads to a break or ulceration in mucosa of stomach or duodenum 2. Decreased mucus production: leaves mucosal cells unprotected from acid environment; hypoxia, shock, or severe burns can lead to injury of mucosa cells 3. Increased delivery of acid: irritated mucus layer because rapid movement of stomach content (dumping syndrome). The duodenum cannot keep up with it Gastric Ulcers  Ingestion of medications (NSAID), tobacco, caffeine, alcohol, H. pylori infection, chronic bile reflux (bile backs up into stomach) and increased HCL.  Occurs in older adults.  Food aggravates pain  Causes weight loss due to the aggravation by food  No pain at hours of sleep Duodenal Ulcer  Hypersecretion of pepsinogen, H. pylori infection.  Occurs in early adults pain when stomach is empty.  Weight gain  Pain at hours of sleep; food and antacids relieve pain 10 10  Whites have a higher risk  Family history  Stress Diagnostic Test  Physical exam and medical history  CBC (low RBC, Hgb, Hct)  Negative Stool Test  Biopsy  Sigmoidoscopy; Colonoscopy/ risk perforatin with severe disease  Barium Enema X-Ray  Computerized Tomography (CT) Scan Treatment  Medication Therapy to reduce symptoms Bulk free diet and a well- balanced nutritious diet  Avoid caffeine, lactose  Surgical Procedures  Monitor intake and output, administer iv fluids as ordered Pancreatitis  Reversible inflammatory process of pancreatic acini (functional units of exocrine pancreas)  Auto-digestion of tissue by inappropriately activated pancreatic enzymes  Begins with trypsin, trypsin activates other digestive enzymes causing pancreatic injury  May result in systemic illness and multisystem organ failure Related Factors  Gallstones (in the common duct)  Alcohol abuse and Infections (primary causes)  Hyperlipidemia, Hyperparathyroidism  Abdominal and surgical trauma  Drugs such as steroids and thiazide diuretics Signs and Symptoms Mild to severe abdominal pain: epigastric or peri-umbilical  Radiating to back, chest or flank  Fever, tachycardia, hypotension, respiratory distress, abdominal distention Diagnostic Test  Elevated C-reactive protein: more than 10 mg/dl  Hypocalcemia, hyperglycemia  Elevated serum amylase/lipase  Elevated WBC: higher that 12000/uL  Elevated serum bilirubin  Serum amylase and serum lipase: lab markers most commonly used • Amylase: most used to diagnosis acute pancreatitis. Serum amylase levels rise within the first 24 hrs. Remain elevated for 48 to 72 hrs. Urinary clearance of amylase is increased and is often measured. WBC count may be increased and hyperglycemia and elevated serum bilirubin level may be present. • Lipase: Are elevated during the first 24 to 48 hrs., but remains elevated for 5 to 14 days Complications Systemic inflammatory response (SIRS)  Acute respiratory distress syndrome (ARDS)  Fluid into retroperitoneal space  Pancreatic pseudocyst 11 11 Treatment Nothing by mouth Put fluid back into vascular bed Assessment of Liver Func. Serum aminotransferase levels are unique to liver function (hepatic cells). Cirrhosis  End stage chronic liver disease, liver tissue replaced by fibrous tissue, disrupt blood flow to vascular channels and biliary duct system  Predisposed to portal hypertension, associated with alcoholism, can also develop because other disorders (viral hepatitis, and biliary disease)  Accompanies metabolic disorders that cause the deposition of minerals in the liver.  Two disease: hemochromatosis (iron deposition) and Wilson diseases(cooper deposition) Laennec’s Cirrhosis (Alcoholics)  Alcohol is transformed to acetaldehyde, which alter hepatocyte function inhibiting removal of proteins from liver and alters metabolism of vitamins and minerals. Fat accumulates in liver, known as “fatty liver”.  Manifestations: Asymptomatic hepatomegaly to hepatic failure. Signs and Symptoms  Weight loss  Hepatomegaly  Splenomegaly  Late manifestations related to portal hypertension and liver cell failure.  Jaundice; abnormally high levels of bilirubin (>2.0)  Fetor hepaticus (musty sweet breath)  Vascular spiders, esophageal varices (enlarged veins)  Anemia: chronic blood loss  Hepatic encephalopathy (inability to get rid of ammonia) Symptoms: ALOC, confusion,  Hepatorenal syndrome Hepatitis  acute chronic inflammation of the liver caused by virus known as Hepatotropic virus  chronic alcoholism, drug toxicities, and autoimmune disorders.  Malaria, infectious mononucleosis, salmonellosis, & amoebiasis.  5 Types: A, B, C, D, E  Hepatitis A: up to a month incubation period • Contracted by the fecal–oral route for lack of hand hygiene • Contaminated food or water • Most common in children to spread • Having sex with someone who has the virus • Not chronic, Hep-A vaccine  Symptoms: fever, malaise, nausea, anorexia, abdominal discomfort, dark urine and jaundice (can last for 2 months or more) Hepatitis B: up to 6 months incubation period • Enters liver, invades cells and begins to multiply and this causes inflammation • Sexual contact (unprotected sexual intercourse,blood , saliva , semen or vaginal secretions) • Sharing needles or accidental needle sticks • Mother to child: during childbirth • Hep-B vaccine Symptoms: fever, fatigue, abdominal pain, nausea and vomiting, joint pain, jaundice, and clay colored stool  Hepatitis C: 2-26 weeks incubation period • Transmitted via Blood /serum 12 12 • Patient w/ organ transplants • Via Unprotected sex • Patients who undergo dialysis are in contact with blood. • No vaccine • Associated with liver cancer, failure and cirrhosis  Symptoms: fatigue, weight loss, anorexia, Jaundice  Hepatitis D: 30 days incubation period • Via Blood/serum • Symptoms similar to Hepatitis A • Can become chronic • Hep-B vaccine to prevent  Hepatitis E: 40 days incubation period • Contracted primarily by the fecal–oral route for lack of hand hygine • High mortality rate • No vaccine • Severe infections develop  Cardiac and Vascular Disorders Atherosclerosis  Most common cause of CAD, build up of plaque narrows arteries & leads to poor perfusion. Can rupture if plaque becomes unstable and clotting can occur.  Associated more with lifestyle, diet and high cholesterol  Blood vessel damage increases inflammatory response  Stable Plaque: white, shiny, fibrous, covers lipids; thrombosis & vessel constriction obstructs lumen and increases inadequate perfusion to distal tissues  Unstable Plaque: liquid lipid core (flappy, obstructs flow of blood), partially or completely blocks flow of artery, more severe, platelet adhesion & clot formation, ischemia & infarction  Final stage: calcification, hemorrhagic, ulceration, thrombosis, affects all layers of vessel  Endardorectomy: removal of plaque stent to open vessel Myocardial Infarction (MI)  Death of cells in myocardium usually related to prolonged or sever ischemia. Decrease in O2 may lead to cell death. Decreased stroke volume and cardiac output.  Pain (typical)-midsternal, radiating to jaw, abdomen, or shoulder; tightness, crushing feeling; not relieved with NTG and rest; may be pain free (silent MI). Males-back pain. Females-abdominal pain.  Sudden onset of pain, usually not associated with activity, may awaken in the middle of the night  Tachycardia, tachypnea, dyspnea, diaphoresis, nausea or vomiting, SOB  ECG changes-depressed or elevated S-T segment (most common), inverted T wave, formation of Q waves  Diagnostic tests: Troponin-Take these labs about 3 times or every 6-8 hours because the troponin might not have circulated completely in the first sample of blood.  Troponin above 0.01= positive= MI  Troponin below 0.01=negative= You can rule out MI (may just be angina)  A-fib is most common post MI; A-fib can cause patient to get blood clots  Treatment: MONA (Morphine, O2, Nitroglycerin, & Aspirin), stool softener, Beta Blocker, Ca+ channel blocker, anti-arrhythmic drug ACRONYM: MONA MORPHIN (DECREASE ANXIETY, LOWER BP), OXYGEN, NITROGLYCERIN (REDUCES CHEST PAIN DUE TO ISCHEMIA, DILATE THE VESSELS & INCREASE OXYGENATION, GETTING RID OF 15 15 Compensatory Mechanisms  When CO is insufficient to meet demands of body, may initially improve CO, eventually damages pump function  Stimulation of SNS: tissue hypoxia: increasing catecholamine’s  Stimulation of beta adrenergic & alpha adrenergic receptors: increase in HR  Activation of RAA system: when oliguria starts to kick in it decreases urine output. Reduced blood flow to kidneys activate RAA angiotensin II  vasoconstriction  aldosterone (NA & H2O retention), preload & afterload increase ventricular modeling  Natriuretic response: Atrial natriuretic peptide released where there is an increase in BP, cells in atria are enlarged; inhibit ADH, stretch wall of heart cause a natural diuretic effect. BNP is released from ventricles & promotes diuresis  Myocardial hypertrophy: (principal mechanism in compensation) enlargement of myocardium, thickening of walls of heart, causes changes in electrical currents and creates scar tissue. Part of the remodeling process- when LV enlarges, structures inside those chambers will change ex: valves can change due to this  Compensatory response of acute HF is tachycardia & HTN (doesn’t last forever) Hypertension (HTN)  a sustained BP that is 140mmHg or higher systolic and 90mmHg or higher diastolic Pathophysiology  Increased activity of RAA system. Renin is released into the bloodstream, which leads to a reduction of blood flow to kidneys, a fall in BP and decreased concentration of tubular Na+. Angiotensin I combines with rennin to form a nonpressor form of angiotensin I, which is converted in the lungs into Angiotensin II (vasoconstrictor) by the ACE enzyme. Angiotensin II causes the release of aldosterone, leading to the reabsorption of Na+ and water, further increasing the BP. Blood viscosity increases and blood becomes thicker. Primary Hypertension  (essential HTN) elevated BP with an unknown cause Secondary Hypertension  Elevated BP associated with a disease process or abnormality; such as: pulmonary, circulatory, renal diseases, endocrine issues, and medications Orthostatic Hypotension  syncope or dizziness with sudden position changes because of a drop in BP BP Classification Systolic Diastolic Normal Less than 120 And lesser than 80 Pre-hypertensive 120-139 Or 80-89 Stage 1 Hypertension 140-159 Or 90-99 Stage 2 Hypertension Greater than or equal to 160 Or greater than or equal to 100 Assessment  Edema, nutrition status, weight, medications, and social history. Assess BP: measure in each arm using 3 positions: lying, sitting & standing, note pulse pressure. Take BP 3 times in different visits to declare HTN Signs and Symptoms  Headache is the most common symptom, numbness & stress  Severe HTN: dizziness, nausea, vomiting, confusion (can signify encephalopathy), visual disturbances, renal insufficiency, aortic dissection, hypertensive crisis Risk Factors  Family history, age, maturation, and race: more prevalent in blacks, cholesterol  Monitor salt intake, modify pt diet, lifestyle, weight, exercise. Can’t modify-gender, age, or ethnicit. 16 16 Complications  Stroke, seizures, CHF, ventricular hypertrophy, damage to retina, renal insufficiency, aortic dissection, hypertensive crisis, brain bleed (aneurism)  Respiratory Disorders COPD  A group of pulmonary diseases of chronic nature, increased resistance to airway/airflow, Ex: Bronchitis, Emphysema, and Asthma  Hypercapnia: High CO2, increase in the arterial blood, drives COPDers breathing, which maintains. ABG’s reflect a high CO2 and low O2 Respiratory acidosis  Occurs in conditions that impair alveolar ventilation and cause an increase in serum PaCO2, hypercapnia, along with a decrease in pH Signs and Symptoms  Loss of weight, SOB, monitor diet and activity, ambulation (give them a rest period in between), encourage activity as much as you can  Patient with COPD cannot be given high levels of O2 because they can pass out. (O2 knocks out respiratory drive) & Hypercapnia is typical along with hypoxemia Diagnostic Tests  ABGs usually show hypercapnia and hypoxemia, FEV1 is decreased, CBC shows polycythemia Normal Adult Arterial Blood Gas Values: pH 7.35-7.45 PaCO2 35-45mmHg PaO2 80-100mmHg HCO3- (bicarb) 21-28 mEq/L O2 saturation (SaO2) 95-100% Emphysema  (Pink Puffers) Retaining CO2 , vasodilators make them appear pink, barrel chested, usually have chronic bronchitis  Loss of lung elasticity & enlargement of the of the air spaces distal to the terminal bronchioles that include alveolar wall and capillary bed destruction  Leads to increase in anterior posterior diameter of the chest cavity (barrel chest) b/c of the trapping of gas & lose the recoil of the lungs, Hyperinflation of lung  Changes result in dyspnea (SOB) & ↑ resp. rate  Mostly associated with smoking or chronic exposure to irritants  In an x-ray, the lungs flatten the diaphragm because they are hyper-inflated (they start to push the diaphragm down- this could be a problem because the diaphragm is used for breathing)  Tachycardia and tachypnea are compensatory  Increased levels of proteases (enzyme that breakdown protein & elastin) ↑ levels damage alveoli & small airways by breaking down elastin, alveolar sacs lose elasticity, Small airways collapse or become narrow, decreased area for effective gas exchange Signs and Symptoms  Use of accessory muscles, decreased breath sounds and air hunger. The more muscles you use, the more calories you burn that’s why patients are acidotic because they are burning a lot of oxygen and calories  Need 5 cm water of peep to keep alveoli inflated, bronchi open for good gas exchange 17 17 Chronic Bronchitis  inflammation of bronchi & bronchioles, caused by chronic exposure to irritants  Irritant triggers inflammation and lead to vasoconstriction, congestion, mucosal edema, and bronchospasms. A chronic cough and productive sputum are present for a minimum of 3 months for 2 consecutive years  Affects only airways not the alveoli  Chronic inflammation: ↑ number & size of mucous glands, ↑ mucous production, Bronchial wall thickens and causes ↓ airflow, blocks smaller airways; narrows larger ones  Hinders airflow & gas exchange related to mucous plugs & infection  PaO2 ↓ (hypoxemia); PaCO2 ↑ (resp. acidosis), Hypercapnia & Hypoxemia Asthma  Chronic inflammatory disorder of airways resulting in REVERSIBLE bronchial constriction and air hunger in response to triggers from a variety of sources Pathophysiology  when exposed to a trigger, hyperactivity of medium-sized bronchi causes release of histamines and other agents from mast cells that intensify inflammatory process and cause bronchospasms  Triggers/Predisposing factors: stress, allergens, cold temperature, high altitudes, strong odors, hormone changes, cigarette smoke and exercise  Allergens bind to specific Ab’s (IgE) Assessment  Patient reports of air hunger, chest tightness, anxiety, tachypnea, tachycardia, and lung sounds (wheezing, long expiratory effort, diminished breath sounds in lower airways). Mainly hear wheezing 20 20  Cytokine mediated response causes all the symptoms of hyperthyroidism Thyroid Storm Thyroid crisis or Thyrotoxicosis, life threatening condition.  Rare: seen in undiagnosed cases or inadequate treatment methods.  Precipitated by stress (infection, DKA, physical/emotional trauma, thyroidectomy) Signs and Symptoms Very high fever, extreme hyperthermia (102F-106F) Tachycardia, CHF, angina, agitation, restlessness, delirium, and seizures Nursing Management Elevate head of the bed to decrease eye pressure, monitor I&O’s, weight, dietary intake (require 4,000-5,000 Cal/day) Hypothyroidism hypometabolic state, decrease in O2 consumption by tissue and decreased heat production.  Hashimoto Thyroiditis: affects women 30-50 y/o, antibodies develop and destroy thyroid tissue  Primary: caused by congenital defects, loss of thyroid tissue from surgery or medications, iodine deficiency, or thyroiditis.  Secondary: peripheral resistance to thyroid hormones or pituitary TSH deficiency  Iodine deficiency results b/c of antithyroid drugs, lithium intake or inadequate iodine intake Signs and Symptoms Weakness, fatigue, weight gain, cold intolerance/dry skin, mental impairment or confusion, Decrease reflexes, puffy face, edema, hoarse voice, bradycardia, hypotension, goiter, Everything is decreased except weight! Nursing Management Intravenous glucose, monitor for hyperglycemia and hypoglycemia, monitor signs of digitalis Toxicity, daily weight  avoid: cabbage, carrots, spinach, turnips, and peaches, which inhibit TH utilization Myxedema hypometabolic state occurring w/ untreated hypothyroidism  CO2 retention, fluid and electrolyte imbalance, hypothermia  Accumulation of proteins in interstitial spaces causes an increase in interstitial fluids, causes mucinous edema (myxedema). Non-pitting edema is most common in pretibial & facial areas Myxedema Coma Hypothyroid crisis, rare and life-threatening, characterized by a severe hypometabolic state  S/S: lactic acidosis, hypoglycemia, hyponatremia, hypotension, bradycardia, CV prolapse, hypothermia, hypoventilation, and coma  cause due to inadequate thyroid replacement, infection, trauma, cold temp. exposure, CNS depressants  Diabetes Mellitus Glucose → Regulated by endocrine hormones of the pancreas  Beta cells secrete insulin (decrease glucose)  Alpha cells secrete glucagon (increase glucose)  Delta cells secrete somatostatin * Brain needs glucose, but cannot store which is why is so important * Hypoglycemic pts. may show signs similar to stroke due to the lack of glucose to the brain (no paralysis) * High sugar causes problems with healing, bacteria likes sugar. Glucocorticoids → secreted during stressful times, critical during periods of fasting and starvation * When steroids are given to pts, must monitor blood sugar, levels will go up! * Steroid used to septic pts. in shock! 21 21 Diabetes Mellitus → Abnormality in blood glucose regulation and nutrient storage, imbalance between insulin availability and insulin need. Different Types of Diabetes:  –Absolute deficiency of insulin (Type I)  –Resistance to the actions of insulin (Type II) * Fasting sugar should be 70-90; If sugar above 100 get a good history, assure they didn’t eat or drink anything * Pre-diabetes: impaired fasting plasma glucose most likely will lead Type II * Can represent:  Absolute insulin deficiency  Impaired release of insulin  Inadequate or defective insulin receptors  Production of inactive insulin or insulin that is destroyed before it can carry out its action Clinical Manifestations → Polyuria (excessive urination and loss of electrolytes) * Polydipsia (excessive thirst) * Polyphagia (excessive hunger) * Glucosuria * Weight loss (type 1) or gain (type 2) * Recurrent blurred vision (type 2) * Fatigue (type 1) * Nausea, vomiting, and abdominal pain (type 1) * Paresthesia (numbness and tingling of the extremities) * Skin infections (bacteria loves sugar) * Dehydration: Hemoconcentration; Hypovolemia (hypertension/ tachycardia); Hyperviscosity (prone to clotts!!!); Hypoperfusion; Hypoxia (especially to brain cells; confusion) Type 1 Diabetes → destruction of beta cells, an absolute insulin deficiency, leads to insulin dependence *Renal threshold: 180-200 mg/dL; when glucose exceeds the renal threshold it spills into urine, fluids follow glucose causing osmotic diuresis and polyuria * Etiology: genetics, environmental, or immunological factors that damage the beta cells * Prone to development of ketoacidosis, fatty acids converted to ketones (ABGs Test) * All pts. with type 1 require exogenous insulin replacement Type 2 Diabetes → Impaired beta cell function, decreased beta cell weight and insulin resistance. Long-standing insulin resistance, leading to beta cell exhaustion * Amyloid (abnormal protein) deposition in the beta cell can cause dysfunction. * May go undetected for years; most common in older adults, Overweight (Fat cells are very insulin resistance) * Increasing in children due to obesity  Type 2 diabetics can progress to Type 1 and become insulin dependent * Lipotoxicity: chronic elevation of free fatty acids can cause toxicity to beta cells Different Types of Diabetes/Secondary to Diabetes → Pancreatic disease * Endocrine disease (problem with adrenal gland) * Medication induced * Infection related * Gestational diabetes: glucose intolerance during pregnancy, if FPG > 126 or random > 200 22 22 Treatments → Insulin; Types: Short-acting (regular) - Intermediate-acting (NPH) - Long-acting (Lantus) * Insulin is administered via IV insulin, subcutaneously, insulin pump * Pancreas or islet cell transplantation Diabetic Ketoacidosis (DKA) → Primarily affects type 1 DM; Characterized by:  Hyperglycemia (> 250 mg/dL)  Ketosis (+ urine and serum ketones) * Life-threatening * cause by stress, infections, and pt. not compliant with treatment can lead to death Signs and Symptoms  Abdominal pain, nausea and vomiting, metabolic acidosis, fruity breath odor, kussmaul’s respirations, confusion, death Hyperosmolarity Hyperglycemic State → May occur with Type 2 DM; Characterized by:  Hyperglycemia (> 600 mg/dL)  Hyperosmolarity (plasma Osmolarity > 320)  Dehydration  Absence of ketoacidosis (can be present but not enough for ketoacidosis)  Depression of sensorium (lethargy) Hypoglycemia → Rapid onset, low blood sugar levels (give them Oj or sugar) they have to be able to swallow, if patient cannot swallow place sugar under the tongue; mostly seen in Type 2 ➔ Treatment: 15-20 gm glucose; Recheck glucose 15 min. after treating * cause by pt. taking their medication without eating, or by excessive exercise Diabetes Complications → Retinopathy: cataracts, glaucoma, optic nerve damage (cause vision loss) * Cardiovascular: atherosclerosis: inflammation and injury of vessels (CAD); MIs; sugars cause an inflammatory response and damage to vessels, and Hypertension * Genitourinary Dysfunction: Urine infections (good indication in males because they don’t get urine infections commonly); erectile dysfunction; edema; albuminuria; glomerulosclerosis; chronic kidney disease * Neuropathy: loss of sensation, dizziness and syncope (fainting) abnormal sensory and motor function; foot ulcers that can lead to infection; gangrene and possible amputation * Microangiopathy: Cerebral infarcts; hemorrhage Diagnostic Test → Impaired fasting plasma glucose * Fasting plasma glucose (FPG) should be < 100 mg/dL (normal)  FPG 100-120 mg/dL= “Pre-diabetes”. Treatment: calorie/weight reduction  FPG > 126 mg/dL = criteria for diagnosis of DM * Glycosylated hemoglobin (HbA₁c), reflects glucose control over the last 2-3 months, that’s how long glucose attaches to the Hb. Also tells you if pt has been complying with treatment:  –3.9 - 5.6 %= normal  –5.7 - 6.4 % = increased risk  –> 6.5 %= + DM  Urine test positive for glucose and Ketones  Disorders of Musculoskeletal Function Compound Fracture  Bone breaks through tissue, most prone to infections 25 25  Rigidity: Cogwheel (jerky catches when joint is moved), Lead pipe (smooth, stiff movement) Diagnosis  Physical assessment and HPI, rule out other etiology, PET scan and Dopamine challenge Treatment Drugs to increase dopamine levels, stimulate dopamine receptors or retard the breakdown of dopamine Nursing interventions Fall prevention, aspiration precautions and monitoring of vital signs Multiple Sclerosis  Demyelination of nerve fibers in white matter of the brain, spinal cord and optic nerve causes temporary, repetitive or sustained interruption in conduction of nerve impulses  Unknown etiology, possibly autoimmune or genetic basis or childhood viral infection  Most common demyelinating disorder, not curable but treatment can slow progression  Women affected twice as frequently than men, most prominent in European Americans w/ an age onset of 20-40 y/o  Lesions of MS macroscopically visible throughout the white matter (plaques); Oligodendrocytes are decrease in number or absent  Inflammation occurs around plaques as well as in normal tissue; astrocytes (gliosis) appear in lesions and scar tissue forms, replacing axons and leading to permanent disability. The term gliosis leads to the term sclerosis which means scarring  Characterized by exacerbations and remissions over many years in several different sites in the CNS Initially, there is normal or near-normal neurologic function between exacerbations. As the disease progresses, there is less improvement between exacerbations Signs & Symptoms  Visual disturbances/blindness (retrobullar neuritis), sudden progressive weakness of one or more limbs, spasticity of muscles, nystagmus, tremors, gait instability, fatigue, bladder dysfunction (UTI’s, incontinence), & depression Diagnosis  MRI, Lumbar Puncture for CSF (clonal IgG bands present), muscle testing Guillain-Barre Syndrome  Acute rapidly progressing inflammation of peripheral (polyneuropathy) motor and sensory nerves  Characterized by variable motor weakness and paralysis, paralysis ascends symmetrically from lower extremities. With excellent care has a 96% complete recovery  Seen mostly in 30-50 y/o in both genders  Results from immune mechanism causesing demyelination neuropathy, acute influenza- like illness before onset of symptoms, CMV, Epstein-Barr virus, C. jejuni, & Vaccination  Immune reaction triggered by viral illness or immunization, instead of antibody preventing invading organism, it has a damaging effect on peripheral nerve myelin; an IgM antimyelin antibody exists, lymphocytes are sensitized and aid in damaging myelin  Nerve impulses are slowed or stopped, muscles lose innervation and begin to waste. Signs & Symptoms  Weakness/paresis (partial paralysis), produces symmetrical flaccid paralysis, progressive ascending muscle weakness of the limbs requiring ventilator support, postural hypotension, arrhythmias, pain, diaphoresis, acute respiratory failure, dyspnea, diminished vital capacity, decreased O2 saturation, impaired eye movement, flushing, brady/tachycardia, heart block Diagnostic  electrolytes, ABG’s, nerve conduction tests, LP for CSF (elevated protein) Treatment  Support of vital signs, Plasmapheresis: monitor for complication b/c of loss of clotting factors, fluid and electrolyte imbalance, respiratory support, IV immunoglobulin may cause low-grade fever, 26 26 muscle aches, headache, acute renal failure (rare), & retinal necrosis Nursing Interventions  Cardiopulmonary assessment and support, prevent skin breakdown, med. administration  Acid-Base Balance and Electrolytes Acid-Base Balance  pH: indirectly measures H+ concentration & reflects balance between CO2 (regulated by the lungs), and HCO3¯ (regulated by the kidneys)  pH normal arterial blood values: 7.35-7.45  Measures the acidity or alkalinity of a fluid and represents the balance between the percentage of hydrogen ions & bicarbonate ions  Carbonic acid (H2CO3): an acid-molecule that releases, or donates, H+  Bicarbonate (HCO3-): a base-molecule that accepts H+ Acidosis  pH < 7.35, Contains greater amounts of H+, Results from too much CO2 or not enough HCO3ˉ Alkalosis  pH > 7.45, Contains lesser amounts of H+, Results from too much HCO3ˉ or not enough CO2 Respiratory System  Controls the regulation of CO2  Hyperventilation leads to “blowing off” CO2  Hypoventilation leads to “retaining” CO2  If CO2 is elevated, hydrogen ion concentration is elevated and pH decreases  Respiratory system is rapid acting but does not fully return pH to normal  Chemoreceptors in the medulla and pons ABG Testing  Provides values of acid-base balance, pt’s oxygenation status, and arterial blood gas  Values may determine if body/system is compensating  PaO2: 80-100 mm/Hg  pH: 7.35-7.45  PaCO2: 35-45 mmHg  HCO3: 22-26 mEq/L  Oxygen Saturation: 95-100% Oxygen Saturation  Gives you an idea about how the patient is breathing/oxygenating  Has absolutely nothing to do with acid base balance  Adequate saturation may not be indicative of adequate oxygenation Metabolic Acidosis  pH below 7.35 – normal pCO2 – HCO3 below 22  Compensatory mechanism: Increase in respiratory rate (Kussmaul’s respirations), “blow off” CO2 & H2CO3  Etiology: Diabetic ketoacidosis, lactic acid accumulation, starvation, renal failure, severe diarrhea, and increases in chloride  High Potassium Metabolic Alkalosis  pH above 7.45 – normal pCO2 – HCO3 above 26  Causes: Prolonged vomiting, gastric suctioning  Compensatory mechanism: Decrease in respiratory rate in order to increase CO2 and renal excretion of bicarbonate  Low Potassium Al(K)a(LO)sis Respiratory Acidosis  pH below 7.35 – pCO2 above 45 – normal HCO3 27 27  Increase in pCO2 and carbonic acid  Causes: Hypoventilation and a decrease in pH  Compensatory mechanism: Kidneys conserve bicarbonate and secrete hydrogen ion into the urine.  Etiology: Lung disease, Chest injury, Respiratory failure, Non functioning respiratory muscles, Sepsis, Airway obstruction, COPD Respiratory Alkalosis  pH above 7.45 – pCO2 below 35 – normal HCO3  Decrease in pCO2 and increase in pH  Causes: Hyperventilation, anxiety/panic attacks, fever  Pt’s usually on mechanical ventilation Isotonic Fluid Volume Deficit  Decrease in ECF, Decrease in circulating blood volume (Hypovolemia)  Loss of water results in loss of Na, Concentration of serum electrolytes remain the same Factors of Volume Loss  GI loss of fluids (due to: suction, fistulas, drainage tubes, vomiting, diarrhea)  Polyuria, Sweating, hemorrhaging  Endocrine disorders (adrenal insufficiency  decrease aldosterone levels)  ECF sequestration: when there is a movement of fluids from interstitial to extracellular and stay there such as Ascites Manifestations  Thirst, weight loss (1 L water = 1 Kg (2.2 lbs), renal water conservation, poor temp control, postural hypotension, weak but rapid pulse to compensate  Headaches and visual disturbances can occur  Anasarca (extreme generalized edema) Diagnosis and Treatment  Hx of patient complaints, weight loss (do daily weigh ins), I & O’s, vital signs, capillary refill will be poor w/ dehydration  Treat underlying cause: If bleeding first give Isotonic fluid with electrolytes 0.9% saline IV, then blood transfusion if necessary Volume Excess  (Ex: Cushings) Manifest as hypertensive w/ edema, sometimes with fluid in the lungs  Increase in interstitial and vascular volumes mostly related to Na and water retention  Renal dysfunction, Heart failure, Liver failure, Excess corticosteroids Manifestations  Weight gain, Edema, Increase CVP (place a direct line to measure), JVD  Full bounding pulse (not normal if laying in bed), Hemodilution, Pulmonary edema, SOB, Crackles and Ascites Diagnosis and Treatment  H & P, Monitor I & O’s, Fluid balance (restriction) 1L/1000ml, Sodium restriction, give potassium sparing Diuretics Regulation of Body Fluids  Fluid intake: 2200 to 2700 ml/day  Thirst-control center: the hypothalamus (thirst regulates intake)  Hormonal: Antidiuretic hormone (ADH), Renin-angiotensin-aldosterone mechanism, Atrial natriuretic peptide  Fluid output: Fluid is lost through kidneys, skin, lungs, and GI tract, Insensible loss of fluid through breathing and sweating (cannot be measured)  Goal is to maintain Homeostasis 30 30 hypoxia results  Decreased LOC is earliest sign of neurological deterioration  Neuronal death Brain Herniation  Cushing reflex (important indicator of increased ICP): Elevated MABP; Widening of pulse pressure; Reflex slowing of the heart rate (bradycardia)  Herniation: Displacement of brain tissue; Occurs with elevated ICP in one brain compartment causes shifting of the cerebral tissue toward an area of lower pressure Nursing Interventions  Monitor oxygenation, Monitor PC02, Maintain ABC’s, Positioning  Cluster care: everything done at once as fast as possible to avoid overstimulation the pt because stimulation causes more ICP  Prevent coughing, straining, Monitor VS, Medication administration, Lab value monitoring  De(cortic)ate: arms flexed to chest, corticospinal tract lesion  Decerebrate: arms extended away from chest, brainstem injury CVA/Stroke  Syndrome of acute focal neurologic deficits from a vascular disorder that injures brain tissue, causes abrupt loss of consciousness with resulting paralysis that may be temporary or permanent  Sometimes prior to having a stroke, there is an alarm phase: TIA (transient Ischemic attack lasting no more than 24 hrs) If symptoms last for more than 24 hrs then its considered a stroke TIA  Similar symptoms to a stroke but go away after 24 hrs (mimic a stroke w/o permanent paralysis) causes temporary interference in cerebral blood flow causing neurological dysfunction from local or retinal ischemia with clinical symptoms lasting less than one hour and w/o evidence of an acute infarction CVA Risk Factors  Age, Gender, Race, Family history, Hypertension (biggest cause of hemorrhagic stroke), Cigarette smoking, DM, Hyperlipidemia, Atrial fibrillation  Micro clots in the circle of Willis lead to a stroke (ischemic)  Incidence increases with age; African Americans have twice the risk of first-ever strokes as whites Men at greater risk than women at a younger age Ischemic strokes  Caused by an interruption of blood flow in a cerebral vessel and are the most common type of strokes, accounting for 70–80% of all strokes Pathophysiology  Cerebral Thrombus: (blood clot) that develops at the clogged part of the vessel most (large or small vessels), Atherosclerosis  Cerebral embolism: a blood clot that forms at another location in the circulatory system (heart & large artewries of chest & neck). Clot travels through the brain's blood vessels until it reaches vessels too small to let it pass. A second important cause of embolism is an irregular heartbeat (atrial fibrillation). It creates conditions where clots can form in the heart, dislodge and travel to the brain frequent site: MCA Treatment  Tissue Plasminogen Acting: for Ischemic strokes give w/in 4-6 hours, no strokes with in the last 6 months, the age of the person is important if 80 or older not given because they can bleed, anticoagulant therapy is ok (heparin, coumadin, lovenox)  Contraindicated: if you’ve had surgery with in the last 6 months, to pts with liver failure b/c they will increase bleeding, anemia pts, renal failure, and to pts w/ GI bleeds  Reperfusion by increasing blood pressure by giving them norepinephrine, see if the symptoms improve Hemorrhagic strokes  Caused by bleeding into brain tissue, usually from a blood vessel rupture caused by 31 31 hypertension, aneurysms, arteriovenous malformations (AVM), head injury, or blood dyscrasias (imbalance/disproportion of bodily fluids: phlegm, blood, & yellow & black bile)  AVM where the artery and the veins come together in the junction but are weakened. Its congenital Pathophysiology  Most frequent fatal stroke because it spreads quickly, Hemorrhage into brain tissue causes an irritation to the meninges that can lead to seizures, or compression of a tumor to the meninges. The actual hemorrhage causes a mass effect that shifts brain tissue or causes herniation  Pressure from supratentorial hematomas and the accompanying edema may cause transtentorial brain herniation compressing the brain stem and often causing secondary hemorrhages in the midbrain and pons. If the hemorrhage ruptures into the ventricular system (intraventricular hemorrhage), the blood may cause acute hydrocephalus Predisposing factors  Age, Hypertension, Aneurysm, Trauma, Tumors, AV malformations, Coagulopathy CVA Manifestations  sudden in onset, focal/one-sided, weakness of face/arm/leg, unexplained imbalance or unsteady gait, unilateral numbness, vision loss in one eye or to one side (L sided stroke will affect the same eye but opposing side of the body)  Language disturbances, expressive aphasia (they cant say the correct answer, it will be random words). Difficulty speaking understandably and comprehending speech; confusion between left and right; difficulty reading, writing, naming objects, and calculating if Wernicke’s area affected Diagnosis  CT scan (truly diagnoses the stroke), MRI, H & P Treatment  Stroke centers, reverse ischemia, reperfusion (to remove the clot) IVR (goes through the vessels) Nursing Interventions  Safe environment (semi-fowler position), monitor ABC’s, medication administration  Aspiration precautions (food/fluid into lungs they don’t cough because of the brain damage, short term: NG tube, long term: PEG), Sitter, get a really good report from nurse  Renal and Urinary Disorders Acute renal failure  due to drug overdoes (Cardizem), Antibiotics, Bacterimia, Iodine Contrast (HYDRATE PT> before during and after!) Reversible if recognized early and treated appropriately  Assess: preexisting renal insufficiency and diabetes and Elderly persons.  Nursing interventions: Close monitoring of urine output; Urine osmolality (earliest manifestation: inability to concentrate urine), urinary sodium concentration; Urinalysis; BUN, Creatinine (Creatinine will stay down but BUN will go up with dehydration, internal bleeding – hypovolemia) Diet; Fluid balance (I/O)  GFR main determinant Creatinine second best  Three categories of ARF 1. ARF Prerenal Etiology: Hypovolemia; Decreased vascular filling (shock); Heart Failure; Decreased renal perfusion due to vasoactive mediators, drugs, diagnostic agents; Most common; Marked decrease in renal blood flow; Reversible  Patho: Kidneys receive 20% of cardiac output; As renal blood flow falls, GFR falls; substances filtered by glomeruli is reduced; Oxygen consumption by Ischemic changes occur when blood flow falls to less than 25% of normal. 2. ARF Intrarenal Etiology of Acute Tubular Necrosis: Prolonged renal ischemia; Exposure to nephrotoxic drugs, metals, organic solvents; Intratubular obstruction 32 32 resulting from (Hemoglobinuria; Myoglobinuria (rabdo); Uric acid casts; Acute renal disease  Patho: destruction of tubular epithelial cells; Reversible: process depends on recovery of injured cells and regeneration of tubular cells; Nephrotoxic agents cause tubular injury by causing renal vasoconstriction, direct tubular damage or intratubular obstruction  Phases of Tubular Necrosis: • Onset or initiating phase: Lasts hours or days. From the onset of the precipitating event until tubular injury occurs • Maintenance phase: a marked decrease in the GFR • Recovery phase: Period during which repair of renal tissue takes place (pt starts producing urine again) 3. ARF Postrenal Etiology: Bilateral ureteral obstruction; Bladder outlet obstruction; Prostatic hyperplasia (most common cause) Patho: obstruction of urine outflow (Ureters; Bladder; Urethra); Both of the ureters must be occluded to produce renal failure Chronic kidney disease  End result of irreparable kidney damage; Develops over number of years  Caused by Hypertension, Diabetes mellitus; Polycystic kidney disease; Obstructions of the urinary tract; Glomerulonephritis; Cancers; Autoimmune disorders; Diseases of the heart or lungs; Chronic use of pain medication  loss of functioning nephrons; deterioration of glomerular filtration, deterioration of tubular reabsorptive capacity, and decline in endocrine functions of the kidney  Reduction of GFR reflects a corresponding reduction in number of functional nephrons proteinuria: measures nephron injury and repair  GFR is used to classify 5 stages: 1. Damage with normal or increased GFR 2. Mild reduction of GFR to 60–89 mL/min/1.73 m2 3. Moderate reduction of GFR to 30–59 mL/min/1.73 m2 (for 3 months or longer) 4. Severe reduction in GFR to 15–29 mL/min/1.73 m2 5. Kidney failure with a GFR < 15 mL/min/1.73 m2 , need for renal replacement therapy Clinical Manifestations  Accumulation of nitrogenous wastes, alterations in water, electrolyte, and acid-base balance. Metabolic Acidosis because kidneys unable to excrete H+ or make HCO3  Mineral and skeletal disorders  Anemia due to a lack of erythropoiesis and coagulation disorders  Hypertension and alterations in cardiovascular function  Gastrointestinal disorders  Neurologic complications  Disorders of skin integrity  Immunologic disorders  Azotemia: excess of urea or other nitrogenous wastes in the blood as a result of kidney insufficiency (high BUN)  Oliguria Disorders Due to Renal Failure  Anemia; Coagulopathies, HTN, Heart disease, Pericarditis, Impaired phosphate elimination, Hypocalcemia  Accumulation of Nitrogenous Waste: Azotemia (elevation of BUN, creatinine) Uremia (acid in the urine); Neuromuscular manifestations; GI manifestations Infection and Immune disorders