NUR 3031 PATHO FINAL REVIEW UPDATED 2023-2024, Exams of Nursing

Download NUR 3031 PATHO FINAL REVIEW UPDATED 2023-2024 and more Exams Nursing in PDF only on Docsity! 1 NUR 3031 PATHO FINAL REVIEW UPDATED 2023-2024  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. 2 NUR 3031 PATHO FINAL REVIEW UPDATED 2023-2024 Metaplasia  Reversible change in which a cell type is replaced by another cell type, occurs in response to irritation 5 NUR 3031 PATHO FINAL REVIEW UPDATED 2023-2024 Hypercoagulability  Increased platelet function  Diabetes Mellitus: if they develop CHF at risk for clots.  Smoking and oral contraceptives directly correlated in developing clots  Arterial Thrombi, Atherosclerosis, atrial fibrillation, blood clots arise from heart cause strokes, and murmurs  Venous Thrombi: incompetent valves w/in veins Thrombocytopenia  Platelet less than 100,000, most common cause of abnormal bleeding and loss of bone marrow function occurs  Excessive consumption of platelet (DIC chews up platelets, usually occurs from sepsis)  Excessive pooling of platelets in spleen  Causes: drug induced Thrombocytopenia; Heparin Induced Thrombocytopenia (HIT); Patients allergic to heparin: platelets drop by more than 10%; Immune Thrombocytopenia Purpura (ITP) Signs and Symptoms  mucus membranes bleeding: nose, mouth, GI, and uterine cavity. Occurs in small vessels  Acute ITP most common bleeding disorder in children  Chronic ITP most common in adults  Excess destruction of platelets by body, platelet production decreased 1-3 days  Petechiae (purplish red spots), Purpura (purple areas of bruising in large areas) DIC Disseminated intravascular coagulation; complication of other disorders, bleeding and clotting at the same time, seen in septic pts or severe trauma, cancers, and hematologic conditions  Treated w/ heparin as blood is transfused as well Post partum: amniotic emboli can occur along with DIC H1N1 also caused DIC in some pts Hodkin Lymphomareplacement of normal cell by Reedsternberg cells, mutation of T- lymphocyte.  starts in single lymph node and spreads to neighboring lymph node. Eventually infiltrates liver, spleen, lungs, bone marrow, and ureters.  2 Categories: 1. Nodular lymphocyte predominant Hodgkin lymphoma, unique form that exhibits a nodular growth pattern 2. Classical Hodgkin lymphoma is characterized by clonal proliferation of typical mononuclear Hodgkin cells  Unknown etiology, but exposure to carcinogens and viruses, genetics and immune mechanisms has been proved to be the involved.  Common in early adulthood (15-40) and in older adulthood (>55); Most common in men Signs and Symptoms  Painless enlargement of a single node or group of nodes; initial lymph above the diaphragm  Chest discomfort with cough and dyspnea.  Fever, night sweats  Weight loss  Pruritus (itching)  Advance stages of HL: liver, spleen, lungs, digestive tract, and CNS are involved. Diagnostic Test  presence of Reed Sternberg cells in biopsy  CT scans of chest and abdomen.  Thrombocytosis, leukocytosis, eosinophilia, elevated erythrocyte sedimentation rate (ESR), 6 NUR 3031 PATHO FINAL REVIEW UPDATED 2023-2024 elevated alkaline phosphatase 7 NUR 3031 PATHO FINAL REVIEW UPDATED 2023-2024 Non-Hodkin Lymphoma  malignant transformations of either T or B cells during differentiation in peripheral lymphoid tissue. Originates outside the lymph and distributes rapidly.  The NHLs are multicentric, spread early to several lymphoid tissues throughout the body specially liver, spleen, and bone marrow.  linked to viral/bacterial infections, environmental agents, immunodeficiency, and autoimmune disorders  MORE AGGRESSIVE, B cell malignancy affects T cells and macrophages  DOES NOT HAVE REEDSTERNBERG CELLS  Most common in men between 50 – 70  Common in pts. with HIV, chronic immunosuppressive therapy after organ transplantation, and with acquired or congenital immunodeficiency. Signs and Symptom  Painless lymphodenopathy (cervical usually first, then axillary, and the inguinal)  Fever, Night sweats  Dyspnea  Renal failure  Weight loss Diagnostic Test and Treatments  Lymph node biopsy and immunophenotyping to determine the lineage and clonality  Bone marrow biopsy, blood studies, chest and abnormal CT scans, MRI  Staging the disease is important to determine the treatment  Anemias Hemolytic Anemia Premature destruction of red blood cell; Retention of iron from hemoglobin destruction  increase in Erythropoisis, normocytic and normochromic red cells  Intrinsic: with in, defect of red cell membrane  Extrinsic: defect outside (drugs, bacteria, toxins, trauma)  Heart or valve malfunction  Sepsis: microorganism can lead to RBC destruction Sickle cell decreased plasma oxygen hemoglobin S causes RBC to elongate, clump together obstructing blood flow, or adhering to the vessel endothelium causing ischemia, thrombosis or tissue infarction.  With normal oxygenation, sickled RBCs resume their normal shape.  Common sites obstructed: abdomen, chest, bones, and joints  caused by hypoxia, low environmental and/or body temperature, excessive exercise, high altitudes or inadequate oxygen during anesthesia, and stress.  caused by blood viscosity, decreased plasma volume, infection, dehydration, and/or increased hydrogen ion concentration (pH/acidosis).  Acidosis reduces affinity of hemoglobin for oxygen, increasing sickling.  Repeated episodes of sickling and unsickling weaken cell membranes, causing them to hemolyze (breakdown) and be removed. Episodes can last 4-6 days.  Acute chest syndrome: atypical pneumonia from pulmonary infarction characterized by infiltrates, shortness of breath, fever, chest pain, and cough Signs and Symptoms  Strokes (another mayor complication)  Retinal infarcts (blindness) 10 NUR 3031 PATHO FINAL REVIEW UPDATED 2023-2024 Clinical Manifestation  poor cognitive, motor and emotional function; related to effects on brain development or 11 NUR 3031 PATHO FINAL REVIEW UPDATED 2023-2024 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 12 NUR 3031 PATHO FINAL REVIEW UPDATED 2023-2024  Esophageal structures or previous surgery  Smoking 15 NUR 3031 PATHO FINAL REVIEW UPDATED 2023-2024 Related Factors  H. pylori  Aspirin and other NSAIDs  Prior history of peptic ulcer  Warfarin, Corticosteroid drugs  Smoking (impairs healing)  Zollinger/ellison syndrome Clinical Manifestations  Burning, gnawing, cramp-like, rhythmic  Pain in small area near midline in epigastrium near xiphoid  May radiate below costal margins, into back or to right shoulder Complications Hemorrhage, perforation and penetration and gastric outlet obstruction.  Bleeding may be sudden, severe, insidious producing only occult blood in stool (Melena). Diagnostic Test  Bloodwork for electrolytes  Laboratory findings of occult blood in the stools indicate bleeding.  Test for presence of h pylori antibodies  Endoscopy; X-ray studies with a contrast medium such as barium. Treatment  Antibiotics to eradicate H. pylori  Medications to relieve symptoms and healing the ulcer crater.  Avoid aspirin and NSAID  Inhibition of gastric acid  Most ulcers heal within a matter of weeks. Irritable Bowl Syndrom (IBS)  Reduced of intestinal motor & sensory function  RELIEVED WITH DEFECATION Crohns Disease  Recurrent, granulomatous type of inflammatory response, can affect any area of GI  Slowly progressive, relentless and often disabling disease Most affected: distal small intestine (ileum) and proximal colon.  More often lesions in ascending colon and terminal ileum  Is a chronic inflammatory bowel disease (IBD)  Cause is unknown, body’s immune system attacks and destroys healthy body tissues  Local lesions: involves all intestinal wall layers; wall contains shallow long ulcers with long or short areas of stricture.  Skip lesions: involve some areas of bowel but not all areas  Involvement of submucosal layers causes Granuloma (tumor like growth), gives tissue a cobblestone appearance due to  Ongoing chronic inflammation of the gastrointestinal tract.  Malabsorption, also abscesses may develop, fistula between infected area, bladder or other area of intestine. Scar tissue may interfere w/ movement of chime, perforation or obstruction occurs. Risk Factors Genes/ family history; Jewish descents (higher risk)  Women more than men. (20s-30s at risk)  Environmental factors  Hormonal 16 NUR 3031 PATHO FINAL REVIEW UPDATED 2023-2024  Dietary antigen or microbial agent, smoking  Allergy or immune disorder; Body reacts to normal bacteria in intestines. 17 NUR 3031 PATHO FINAL REVIEW UPDATED 2023-2024 Complications  fluid and electrolyte imbalance as well as dehydration due to diarreah  Deficiency in absorption of folic acid, calcium and vitamin D  Anal fissure, abdominal abscess, fistula, intestinal obstruction. Signs and Symptoms Intermittent diarrhea, colicky pain (usually in lower right quadrant)  Exacerbation/remission  Nausea, vomiting, weight loss caused by anorexia, loss of appetite.  Low grade fever  Malaise  Urgency at night to defecate  Joint pain/ swelling  Tenesmus (pain passing stool)  Swollen gums/ mouth ulcers  Steatorrah due to malnutrition Diagnostic Test Colonoscopy or sigmoidoscopy, eteroscopy  Albumin level low, CBC (elevated WBC, low RBC, Hgb and Hct)  Electrolyte (hypocalcemia)  High ESR  Stool cultures  CT scan of abdomen  Barium enema (reveals characteristics skip lesions) or upper GI series Treatement  No cure, treatment focuses on preventing complications.  Promote healing and maintain adequate nutrition.  Surgery, resection of damage bowel, drainage of abscesses, or repair fistula tracts.  Fluid replacement to correct dehydration, TPN (total parenteral nutrition) may be added.  Give low residue, low fat, high protein, and high calorie diet.  lifestyle management to reduce stress Ulcerative Colitis  Nonspecific inflammation of the colon, mucosa disease, can be cured by colectomy  Confined to the rectum and colon, Its an Chronic inflammatory bowl disease (IBD)  Begins in rectum, spreads proximally affecting mucosal layer, can extend to submucosal layer  may feature small hemorrhages and abscesses, inflammation is confluent and continuous, leads to formation of crypt abscesses; may become necrotic; ulcerations are fibrotic in later stages  Pseudopolyps develop Related Factors  Causes uncertain; virus or bacterium may trigger ulcerative colitis.  Possible that inflammation may come from an autoimmune reaction  Heredity or stress. Complications  Intestinal obstruction, dehydration, fluid and electrolyte imbalances, malabsorption, iron- deficiency anemia  Diarrhea for days/months, stools contain blood and mucous, nocturnal diarrhea.  Fecal incontinence  Anorexia, weakness, fatigue  Risk for: Toxic megacolon, cancer of the colon  Abdominal pain, nausea and vomiting, urge to defecate 20 NUR 3031 PATHO FINAL REVIEW UPDATED 2023-2024  Pancreatic pseudocyst 21 NUR 3031 PATHO FINAL REVIEW UPDATED 2023-2024 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 22 NUR 3031 PATHO FINAL REVIEW UPDATED 2023-2024  Hepatitis C: 2-26 weeks incubation period • Transmitted via Blood /serum 25 NUR 3031 PATHO FINAL REVIEW UPDATED 2023-2024 ISCHEMIA), ASPRIN (PREVENTS PLATELETS FROM ADHERING) Angina  Chest pain caused by myocardial ischemia from reduced blood flow or oxygen supply compared to demand. Maybe reversible or temporary  Reduced O2 causes anaerobic metabolism and lactic acid build up  Silent ischemia caused by a decrease of O2 w/o warning signs of pain. Episodes may be shorter and may involve less myocardial tissue. Increased in pts with decreased pain transmission, sensory denervation, and autonomic neuropathy (clients who have diabetes) Stable Angina (most common)  Caused by a specific amount of activity and is predictable; relieved with rest and nitrates. Partial occlusion, remove the stressor and symptoms should subside Unstable Angina (most concerning)  pain increases in frequency and severity as well as duration over time; it’s unpredictable and occurs with decreasing levels of activities even with rest. Plaque is rupturing through the intimal layers or occluding the vessel Prinzmetals (variant)  Occurs without identified cause (variant because anything can cause it) may occur at same time each day or awaken a person from their sleep (at rest, minimal activity, and nocturnally). May intensify or worsen over the years but does not have the same concern as unstable angina.  Usually caused by coronary spasms, where atherosclerosis is present, however can occur in absence of disease. May occur d/t a hyperactive sympathetic nervous response, calcium defect in smooth muscle, disturbances in the production and release of nitric oxide, imbalance of endothelium-derived relaxing and contracting factors. Signs and symptoms  Pressure or heaviness in chest, diaphoresis, light-headedness, hypotension, pulse changes, pain may radiate to arms, jaw, abdomen, or back, deviated ST segment on EKG.  Men: angina on back and Women: stomach  Streptokinase: “clot busters” (actually gets rid of clot)  Punumbra: associated to heart & brain tissue. It’s the area of tissue that is surrounded by ischemic tissue, the punumbra is what we try so hard to save  Troponin levels must be less than 0.01 (normal) (maybe related due to renal disease too) Congestive Heart Failure  The heart’s inability to pump sufficiently to meet the body’s metabolic needs, causing decreased tissue perfusion. Decreased CO leads to decreased renal perfusion. Activation of the RAA mechanism causes vasoconstriction and stimulates production of aldosterone and ADH. Cause BP to increase.  May be acute (pulmonary edema or cardiogenic shock) or chronic heart failure  Ejection fraction: % of blood ejected from heart during systole, normal: 55-70% (the kidneys is the first thing affected by ejection fraction, less urine output & accumulation of fluid w/ edema in periphery), less than 40% means heart is not contracting enough, means there’s decreased tissue perfusion and blood may be accumulating in pulmonary vessels Causes  MI, HTN, CAD, kidney failure, cardiomyopathy, valve disorders, H2O intoxication, inflammatory conditions Management  Diuretics, Beta Blockers, Nitrate, I&O, Daily weight Assessment  VS, cardiac monitor, heart rhythm, pulse quality, respiratory status, heart sounds (S3 & S4, murmur), 26 NUR 3031 PATHO FINAL REVIEW UPDATED 2023-2024 jugular neck vein distention, abdominal assessment, activity tolerance. 27 NUR 3031 PATHO FINAL REVIEW UPDATED 2023-2024 Left Sided Heart Failure  More common than right side (left usually goes first), results from ventricular wall damage, blood backs up to the lungs, Impaired left ventricular filling results in congestion and increased pulmonary artery pressures; “Left and “Lung, the fluid “backs up” to lungs Signs and Symptoms  fatigue, SOB, pulmonary emboli, activity intolerance, dizziness, syncope, dyspnea, cough, pulmonary edema, S3 heart sounds, decreased urine output Right Sided Heart Failure  (aka Cor Pulmonale) caused by pulmonary hypertension (cor pulmonale) and left HF  Most common cause of Right sided HF is Left sided HF Cor Pulmonale  Right sided heart failure due to pulmonary causes. Right ventricular distention leads to blood accumulation in systemic veins; “Right and “Rest of body; fluid “backs-up” to rest of body Signs and Symptoms  SOB, fatigue, waking up at night. Increased venous pressure causes abdominal organ congestion and peripheral edema  Patient who is ambulatory you will see lower extremity edema  Patient who is bedridden = sacral and/or scrotal edema  Liver engorgement will lead to RUQ pain. You will also see Jugular Vein distention High output failure Heart is overworking trying to produce a higher ejection fraction, most seen w/ metabolic problems as in anemia, Paget’s disease & thyrotoxicosis. It’s the least common of heart failure Clinical Manifestations  Fluid retention and Edema, nocturia, oliguria, ascites, Respiratory: dyspnea, orthopnea, exertional dyspnea, PND (parosoxymal nocturnal dyspnea) fatigue, weakness, & mental 30 NUR 3031 PATHO FINAL REVIEW UPDATED 2023-2024  Monitor salt intake, modify pt diet, lifestyle, weight, exercise. Can’t modify-gender, age, or ethnicit. 31 NUR 3031 PATHO FINAL REVIEW UPDATED 2023-2024 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 32 NUR 3031 PATHO FINAL REVIEW UPDATED 2023-2024 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 35 NUR 3031 PATHO FINAL REVIEW UPDATED 2023-2024 Addisonian Crisis→ acute cortisol insufficiency during stress (ex: surgery and pregnancy) or when corticosteroid therapy is abruptly stopped, can cause circulatory collapse, shock, and death. 36 NUR 3031 PATHO FINAL REVIEW UPDATED 2023-2024  immediate IV glucocorticoid replacement and fluids with Na+ (isotonic solution 0.9% Na+CL) Signs and Symptoms → Neurological (neurosis, depression); Cardiovascular (hypotension, EKG changes: Peaked T- wave due to Hyperkalemia); Musculoskeletal (weakness, fatigue); Integumentary (hyperpigmentation of skin) GI (diarrhea, nausea, vomiting, anorexia); Reproductive (decreased libido, little pubic hair); Metabolic increased K+, hyponatremia, hypoglycemia, weight loss) Nursing Management → Monitor for signs of dehydration; Maintain high Na+, Low K+ diet * Teach client to carry medical alert identification  Mineral and glucocorticoid replacement  Adrenal Cortex Hyperfunction Cushing syndrome → hypercortisolism causing an increase in glucogenesis (glucose synthesis) * Primary cushing: caused by adrenal tumor (increases cortisol) * Secondary cushing: disorder of pituitary or hypothalamus (increases ACTH) * Iatrogenic cushing: most common cause of cushing, results by long term glucocorticoid therapy Signs and Symptoms → Neurological (psychosis, loss of memory, depression, poor concentration); Cardiovascular (HTN, dysrhythmias); GI (peptic ulcers); Musculoskeletal (muscle weakness and wasting, osteoporosis, “buffalo” hump, abdominal obesity); Integumentary (ecchymosis, hirsutism, abdominal purple striae, poor wound healing, thin skin, acne); Renal (glycosuria, polyuria, polydipsia, renal calculi); Reproductive (decreased libido, impotence, amenorrhea, male characteristics in females); Metabolic (High Na+, low K+, edema, moon face, weight gain) Nursing Management → monitor for Addisonian crisis caused by drug therapy * Priority nursing diagnoses: excess fluid volume; risk for infection; risk for injury; activity tolerance; anxiety; deficient knowledge; risk for impaired skin integrity  monitor I&O’s and cardiac rhythm  Disorders of the Thyroid Hyperthyroidism hyperfunction of thyroid gland leading to high levels of TH circulating in the body causing an increase in metabolic function. Disorder: Grave’s disease, Adenomas, Thyroid Storm, and Iodine containing agents Caused by autoimmune response, excess secretion of TSH, neoplasm, or excess intake of Thyroid medication  Elevated serum thyroid antibodies, T3 Signs & Symptoms excessive stimulation of the Sympathetic (adrenergic) branch of the CNS causing cardiac activity and reflexes.  Thyroxine: increased metabolism, weight loss, and psychological symptoms Emotional liability, agitation, SOB, exophthalmos (protrusion of eyes), increased reflexes, tachycardia, thin hair/skin, diarrhea, muscle weakness, fatigue, flushed skin, goiter, hyperthermia, Everything is elevated except weight! Graves Disease Most common cause of Hyperthyroidism, autoimmune disorder, responds to stimulation of 37 NUR 3031 PATHO FINAL REVIEW UPDATED 2023-2024 thyroid gland from long acting thyroid stimulator (LATS)  Seen most often in women under 40 y/o 40 NUR 3031 PATHO FINAL REVIEW UPDATED 2023-2024 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 41 NUR 3031 PATHO FINAL REVIEW UPDATED 2023-2024 * Gestational diabetes: glucose intolerance during pregnancy, if FPG > 126 or random > 200 42 NUR 3031 PATHO FINAL REVIEW UPDATED 2023-2024 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 45 NUR 3031 PATHO FINAL REVIEW UPDATED 2023-2024  Associated w/ continued production of autoantibodies by thymus gland in 75% of cases  Slow onset, precipitated by emotional stress, hormonal disturbances (pregnancy, menses, 46 NUR 3031 PATHO FINAL REVIEW UPDATED 2023-2024 thyroid disorders), infections/vaccinations, trauma and surgery, temperature extremes, excessive exercise, drugs that block or decrease neuromuscular transmission (opiods, sedatives, barbiturates, alcohol, quinidine, anesthetics), & thymus tumor  Women affected more than men before 40; same in puberty and after 40, higher in men after age 50  Lambert-Eaton myasthenic syndrome: develops in association with neoplasms (small-cell carcinoma of the lungs) Signs & Symptoms mild diplopia, unilateral ptosis; may also involve face, jaw, neck and hip. Severe weakness affects muscles of swallowing, chewing and speech impairment  Respiratory distress manifested by tachypnea, decreased depth, abnormal ABG’s, O2 sat. < 92%, decreased breath sounds, bowel and bladder incontinence, paresthesias, and pain b/c of generalized weakness Myasthenia Crisis  Sudden motor weakness; risk of respiratory failure and aspiration; most often caused by not enough medication, infection, emotional upset, pregnancy, and alcohol ingestion Cholinergic Crisis  Severe muscle weakness, caused by overmedication  Signs: cramps, diarrhea, bradycardia & bronchial spasm w/ increased pulmonary secretions and risk of respiratory compromise Diagnosis  Tensilon test: allows voluntary muscle contraction (tensilon allows acetylcholine to bind to receptors to temporarily improve symptoms); ABG’s and pulmonary function test Nursing Assessment/Management  Neurological and musculoskeletal assessment, aspiration precautions  Usually pts are intubated, educate on incentive spirometer afterwards  Medications: Anticholinesterases & immunosuppressants  Plasmapheresis (exchange blood plasma): removes IgG antibodies  Thymectomy (removal of thymus gland) Parkinson’s Disease  degenerative of basal ganglia function known by: “resting” (nonintentional) tremors, bradykinesia (slow sometimes frozen movement), and muscle rigidity or stiffness  Second most neurodegenerative disease, begins after 50 y/o increasing by 4-5% in those greater than 85 y/o  Dopamine levels that inhibit motor activity deplete, acetylcholine is not inhibited so it increases excitation leading to Parkinson’s symptoms  Develops from a postencephalatic syndrome  Side effect of therapy with antipsychotic drugs that block dopamine receptors  Toxic reaction to a chemical agent  Outcome of severe carbon monoxide poisoning Causes  Primary: unknown but believed to be caused by environmental interaction and genetic factors  Secondary: linked to infection, neoplasms, encephalitis, intoxication with carbon monoxide, manganese and mercury. The use of antipsychotic drugs, hypoxia & cerebral ischemia. Signs & Symptoms  nonintentional tremor of thumb and first finger as if rotating small object (pill rolling), may begin in one hand w/ tremor spreading to arm then the other arm and later the head  Bradykinesia and loss of automatic movement, characteristics: mast-like face w/ staring gaze, soft monotone voice, drooling, impaired balance and loss of righting reflex (correcting posture 47 NUR 3031 PATHO FINAL REVIEW UPDATED 2023-2024 when changing positions), unsteady shuffling gait  Weight loss, constipation, dysphagia, orthostatic hypotension, depression, and dementia 50 NUR 3031 PATHO FINAL REVIEW UPDATED 2023-2024 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 51 NUR 3031 PATHO FINAL REVIEW UPDATED 2023-2024 Respiratory Acidosis  pH below 7.35 – pCO2 above 45 – normal HCO3 52 NUR 3031 PATHO FINAL REVIEW UPDATED 2023-2024  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, 55 NUR 3031 PATHO FINAL REVIEW UPDATED 2023-2024  PTH & Vitamin D responsible for maintenance, “Parathyroid pulls… Calcitonin keeps” 56 NUR 3031 PATHO FINAL REVIEW UPDATED 2023-2024 Hypocalcemia  due to: rapid administration of blood containing citrate  hypoalbuminemia, hypoparathyroidism, vitamin D deficiency, alkalosis, pancreatitis, CRF, and chronic alcoholism  Signs/Symp: Numbness & tingling of fingers and circumoral (around mouth) region; Hyperactive reflexes, positive Trousseau’s (hand cramping when taking BP) and positive Chvostek’s (facial twitching when assessing Trigeminal V) sign, tetany, muscle cramps, fractures (if chronic). ECG: prolonged ST & QT waves Hypercalcemia  due to: Hyperparathyroidism, Cancer, Paget’s disease, Osteoporosis, prolonged immobilization, and thiazide diuretics  Signs/Symp: Anorexia, abdominal pain & constipation, muscle weakness, hypoactive reflexes, lethargy, flank pain (if kidney stones), ECG: shortened QT & ST segment Magnesium  the second most abundant cation in ICF; Regulated by dietary intake, renal mechanisms, and actions of PTH.  Functions: Speeds up enzyme reactions during carbohydrate metabolism, helps produce ATP, important in protein synthesis, and affects cardiac and skeletal muscle excitability  Potassium and Magnesium are parallel Hypomagnesemia  due to: inadequate intake, inadequate absorption, and excessive loss from GI tract or urinary system; Alcoholics.  Similar to hypocalemia; The 3 Ts (tremors, twitching, tetany) & hyperactive DTRs (deep tendon reflexes), positive Chvostek’s & Trousseau’s sign  CNS irritation, lethargy, confusion, seizures, Dysrhythmias, and N/V  Acronym: STARVED: Seizures; Tetany; Anorexia & arrhythmias; Rapid heart rate; Vomiting Emotional lability; Deep tendon reflexes increased Hypermagnesemia  due to renal failure or excessive intake  hypoactive DTRs, weakness, drowsiness, decreased rate/depth of respirations, bradycardia, hypotension, and flushing of the skin  Signs/Symp: Acronym: RENAL: Reflexes decreased (plus weakness & paralysis); ECG changes (bradycardia) and hypotension; Nausea & Vomiting; Appearance flushed; Lethargy (plus drowsiness and coma)  Traumatic Brain Injury ICP  Normal Cranial Cavity: Blood: 10%; Brain tissue: 80%; CSF: 10% Normal ICP: 0-15 mm Hg Monro-Kellie Hypothesis: brain compensatory mechanism of blood and CSF, body will slow down production of CSF if there is not enough room in the brain, same with the blood the body will send less blood to the brain. Brain tissue is unable to compensate  Decadrone is given to reduce inflammation but to decrease degradation of the tissue & shift fluid to release the pressure  Compensatory mechanisms: Normal shunting of CSF into subarachnoid space (most common); Increase absorption of CSF; decrease absorption of CSF; venous blood may be shunted to allow expansion Cerebral Perfusion Pressure  difference between the mean arterial blood pressure (MABP) and the ICP (CPP= MABP-ICP) Normal CPP: 70-100 mm Hg; Brain ischemia is present when CPP 40 – 60 mm Hg 57 NUR 3031 PATHO FINAL REVIEW UPDATED 2023-2024  Brain death CPP 0 – 40 mmHg  Intra ventricular catheter tells ICP; Tissue perfusion inadequate leads to cellular 60 NUR 3031 PATHO FINAL REVIEW UPDATED 2023-2024 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. 61 NUR 3031 PATHO FINAL REVIEW UPDATED 2023-2024 2. ARF Intrarenal Etiology of Acute Tubular Necrosis: Prolonged renal ischemia; Exposure to nephrotoxic drugs, metals, organic solvents; Intratubular obstruction 62 NUR 3031 PATHO FINAL REVIEW UPDATED 2023-2024 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)