NUR 3031 Patho Final Exam Review-latest Update with Complete Solutions, Exams of Nursing

Download NUR 3031 Patho Final Exam Review-latest Update with Complete Solutions and more Exams Nursing in PDF only on Docsity! NUR 3031 Patho Final Exam Review-latest Update with Complete Solutions ê Cellular Injury Reversible à Although impairing cell function, does not result in cell death. à 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 à Cell death or necrosis can occur. à Apoptosis (Programmed cell death): a form of cell death necessary to make way for new cells; NORMAL PROCESS IN THE BODY à Necrosis: cell death and degradation; UNREGULATED death; cell swells and ruptures; inflammation results. Cells may undergo liquefaction, coagulation, infarction, or caseous necrosis Gangrene à 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 (Eà fluid can ‘E’nter) 3 Gas gangrene: Clostridium infection produces toxins and bubbles Cellular stressors à 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. à 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 à decrease cell size causing reduce oxygen consumption and other cellular functions. à 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 à increase cell size and with it an increase in the amount of functioning tissue mass. à Pathogenic Hypertrophy: thickening of urinary bladder and myocardial hypertrophy. Hyperplasia à increase in the number of cells in an organ or tissue. à Occurs in tissues such as epidermis, intestinal epithelium, and glandular tissue. à 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. à Most forms on NONPHYSIOLOGICAL HYPERPLASIA are due to excessive hormonal or the effects of growth factors on target tissues. Metaplasia à Reversible change in which a cell type is replaced by another cell type, occurs in response to irritation Non-Hodkin Lymphoma à malignant transformations of either T or B cells during differentiation in peripheral lymphoid tissue. Originates outside the lymph and distributes rapidly. à The NHLs are multicentric, spread early to several lymphoid tissues throughout the body specially liver, spleen, and bone marrow. à linked to viral/bacterial infections, environmental agents, immunodeficiency, and autoimmune disorders à MORE AGGRESSIVE, B cell malignancy affects T cells and macrophages à DOES NOT HAVE REEDSTERNBERG CELLS à Most common in men between 50 – 70 à Common in pts. with HIV, chronic immunosuppressive therapy after organ transplantation, and with acquired or congenital immunodeficiency. Signs and Symptom à Painless lymphodenopathy (cervical usually first, then axillary, and the inguinal) à Fever, Night sweats à Dyspnea à Renal failure à Weight loss Diagnostic Test and Treatments à Lymph node biopsy and immunophenotyping to determine the lineage and clonality à Bone marrow biopsy, blood studies, chest and abnormal CT scans, MRI à Staging the disease is important to determine the treatment ê Anemias Hemolytic Anemia àPremature destruction of red blood cell; Retention of iron from hemoglobin destruction à increase in Erythropoisis, normocytic and normochromic red cells à Intrinsic: with in, defect of red cell membrane à Extrinsic: defect outside (drugs, bacteria, toxins, trauma) à Heart or valve malfunction à Sepsis: microorganism can lead to RBC destruction Sickle cell decreased plasma oxygen hemoglobin S causes RBC to elongate, clump together obstructing bloodflow, or adhering to the vessel endothelium causing ischemia, thrombosis or tissue infarction. à With normal oxygenation, sickled RBCs resume their normal shape. à Common sites obstructed: abdomen, chest, bones, and joints à caused by hypoxia, low environmental and/or body temperature, excessive exercise, high altitudes or inadequate oxygen during anesthesia, and stress. à caused by blood viscosity, decreased plasma volume, infection, dehydration, and/or increased hydrogen ion concentration (pH/acidosis). à Acidosis reduces affinity of hemoglobin for oxygen, increasing sickling. à Repeated episodes of sickling and unsickling weaken cell membranes, causing them to hemolyze (breakdown) and be removed. Episodes can last 4-6 days. à Acute chest syndrome: atypical pneumonia from pulmonary infarction characterized by infiltrates, shortness of breath, fever, chest pain, and cough Signs and Symptoms à Strokes (another mayor complication) à Retinal infarcts (blindness) à Lung infarcts (pneumonia, acute chest syndrome) à Pigment gallstones à Avascular necrosis of femoral head à Kidney infarcts (chronic kidney disease) à Osteomyelitis à Skin ulcers à Pallor, Jaundice à Fatigue and irritability. Diagnostic test à hemoglobin electrophoresis: determines presence hemoglobin S, CBC. Treatement Folic acid supplements and analgesics à Hydration therapy as well as scheduled transfusions decreases crisis episodes. à During a crisis, hydration to improve blood flow, reduce pain, prevent renal damage, O2, IV (narcotics) à Maintaining full immunization à Hydroxyurea inhibits DNA synthesis, reduces pain crisis. Increases RBC levels, acts as an anti- inflammatory inhibiting the production of WBCs. à Bone marrow or stem cell transplant; however risk of graft-versus-host disease. Megaloblastic Anemia à impaired DNA synthesis results in enlarged RBC’s due to vitamin B12 (cobalmin) and folic acid deficiency à causes pernicious anemia: inability to absorb vitamin B12 due to lack of intrinsic factor à Macrocytic (Larger than normal cell size), Normochromic (normal concentration of Hb) à 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 à Caused by gastrectomy, gastrojejunostomy, ileal resection and after gastric bypass surgery à Inflammation or neoplasms in the terminal ileum. à Malabsorption syndrome (poor absorption) Signs and Symptoms à Pallor, slight jaundice, nails à Weakness, fatigue and diarrhea à Smooth sore beefy red tongue à Disrupts function of peripheral nerves, spinal cord, and brain. à Parasthesias: numbness or tingling in the extremities à Proprioreception, may progress to imbalance and spinal cord damage. à dark stool because of blood, internal hemorrhage; most leading cause if IG bleed Treatment Life long parental (injection) or high oral Vitamin B12. à increase intake of foods such as eggs, meats, and dairys Diagnostic Test à CBC, MCV, MCHC, MCH Iron Deficiency Anemia inadequate iron supply due to excessive iron loss from bleeding, decreased dietaryintake, or malabsorption. à impairs cellular division and maturation especially in rapidly proliferating RBCs à microcytic and microchromic à Iron is stored in body as ferritin à Women loose 15 mg monthly during menstruation (most common cause in women) GI bleeding is most common cause in men. Clinical Manifestation à poor cognitive, motor and emotional function; related to effects on brain development or neurotransmitter function. Related Factors à Pregnancy, menstruation à Hemorrhage à Medication use (aspirin) à GI bleeds (peptic ulcer, intestinal polyps, hemorrhoids or cancer) à Eating disorders; Diets (cow’s milk for infants low in iron) Signs and Symptoms à develop slow until Hb drops to 7-8 g/dl; Fatigue and weakness, SOB, Hypoxia à Pallor (ear lobes, palms and conjunctiva) à Dyspnea; Tachichardia à Dysphagia and decreased acid secretion. à Brittle hair and nails à Cheilosis (cracks in corners of mouth) à Smooth tongue, dizziness à Pica (craving to eat unusual substances such as clay or starch) Treatment à Control chronic blood loss. à Increase dietary intake of iron, ferrous sulfate, oral replacement therapy. à Parental iron therapy may be used when oral forms are not tolerated or are ineffective. à Vitamin C enhances absorption à iron-rich foods (as beef, chicken, egg yolk, pork loin, turkey and whole grain breads and cereals). Polycythemia à Abnormally high RBC count: hematocrit >50% à overproduction of RBC’s, WBC’s, and platelets increasing blood viscosity, volume, congestion of tissues (live and spleen) causing acidosis, clotting, and thrombi à Absolute (PRIMARY) Polycythemia: most common in Caucasian men of European, jewish ancestry à Neoplastic disease of bone marrow à Thick, slow moving blood Secondary Polycythemia à Physiologic increase in level of erythropoietin à Compensatory response to hypoxia: High altitudes, chronic heart, lung disease and smoking ê GI Disorders GERD à Gastric backflow into esophagus (reflux, heartburn or esophagitis) associated with weak or incompetent lower esophageal sphincter à Delayed gastric emptying contributes to reflux, esophageal mucosal injury may occur à Normally cleared and neutralized by esophageal peristalsis and salivary bicarbonate à Chronic inflammatory disease of the antrum and body of the stomach à 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 à The severity of the heartburn is not indicative of the extent of the mucosal injury Related Risk Factors à common problem in infants and children, occurs at least once a day in infants 0-3 months, by 6 months is less frequent à Hiatal hernia à Pregnancy à Obesity; Poor dietary habits, high fat diet à Esophageal structures or previous surgery à Smoking Complications à fluid and electrolyte imbalance as well as dehydration due to diarreah à Deficiency in absorption of folic acid, calcium and vitamin D à Anal fissure, abdominal abscess, fistula, intestinal obstruction. Signs and Symptoms Intermittent diarrhea, colicky pain (usually in lower right quadrant) à Exacerbation/remission à Nausea, vomiting, weight loss caused by anorexia, loss of appetite. à Low grade fever à Malaise à Urgency at night to defecate à Joint pain/ swelling à Tenesmus (pain passing stool) à Swollen gums/ mouth ulcers à Steatorrah due to malnutrition Diagnostic Test Colonoscopy or sigmoidoscopy, eteroscopy à Albumin level low, CBC (elevated WBC, low RBC, Hgb and Hct) à Electrolyte (hypocalcemia) à High ESR à Stool cultures à CT scan of abdomen à Barium enema (reveals characteristics skip lesions) or upper GI series Treatement à No cure, treatment focuses on preventing complications. à Promote healing and maintain adequate nutrition. à Surgery, resection of damage bowel, drainage of abscesses, or repair fistula tracts. à Fluid replacement to correct dehydration, TPN (total parenteral nutrition) may be added. à Give low residue, low fat, high protein, and high calorie diet. à lifestyle management to reduce stress Ulcerative Colitis à Nonspecific inflammation of the colon, mucosa disease, can be cured by colectomy à Confined to the rectum and colon, Its an Chronic inflammatory bowl disease (IBD) à Begins in rectum, spreads proximally affecting mucosal layer, can extend to submucosal layer à 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 à Pseudopolyps develop Related Factors à Causes uncertain; virus or bacterium may trigger ulcerative colitis. à Possible that inflammation may come from an autoimmune reaction à Heredity or stress. Complications à Intestinal obstruction, dehydration, fluid and electrolyte imbalances, malabsorption, iron- deficiency anemia à Diarrhea for days/months, stools contain blood and mucous, nocturnal diarrhea. à Fecal incontinence à Anorexia, weakness, fatigue à Risk for: Toxic megacolon, cancer of the colon à Abdominal pain, nausea and vomiting, urge to defecate Risk Factors à usually before age of 30; can occur at any age à Whites have a higher risk à Family history à Stress Diagnostic Test à Physical exam and medical history à CBC (low RBC, Hgb, Hct) à Negative Stool Test à Biopsy à Sigmoidoscopy; Colonoscopy/ risk perforatin with severe disease à Barium Enema X-Ray à Computerized Tomography (CT) Scan Treatment à Medication Therapy to reduce symptoms Bulk free diet and a well- balanced nutritious diet à Avoid caffeine, lactose à Surgical Procedures à Monitor intake and output, administer iv fluids as ordered Pancreatitis à Reversible inflammatory process of pancreatic acini (functional units of exocrine pancreas) à Auto-digestion of tissue by inappropriately activated pancreatic enzymes à Begins with trypsin, trypsin activates other digestive enzymes causing pancreatic injury à May result in systemic illness and multisystem organ failure Related Factors à Gallstones (in the common duct) à Alcohol abuse and Infections (primary causes) à Hyperlipidemia, Hyperparathyroidism à Abdominal and surgical trauma à Drugs such as steroids and thiazide diuretics Signs and Symptoms Mild to severe abdominal pain: epigastric or peri-umbilical à Radiating to back, chest or flank à Fever, tachycardia, hypotension, respiratory distress, abdominal distention Diagnostic Test à Elevated C-reactive protein: more than 10 mg/dl à Hypocalcemia, hyperglycemia à Elevated serum amylase/lipase à Elevated WBC: higher that 12000/uL à Elevated serum bilirubin à 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) à Acute respiratory distress syndrome (ARDS) à Fluid into retroperitoneal space à Pancreatic pseudocyst 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 à End stage chronic liver disease, liver tissue replaced by fibrous tissue, disrupt blood flow to vascular channels and biliary duct system à Predisposed to portal hypertension, associated with alcoholism, can also develop because other disorders (viral hepatitis, and biliary disease) à Accompanies metabolic disorders that cause the deposition of minerals in the liver. à Two disease: hemochromatosis (iron deposition) and Wilson diseases(cooper deposition) Laennec’s Cirrhosis (Alcoholics) à 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”. à Manifestations: Asymptomatic hepatomegaly to hepatic failure. Signs and Symptoms à Weight loss à Hepatomegaly à Splenomegaly à Late manifestations related to portal hypertension and liver cell failure. à Jaundice; abnormally high levels of bilirubin (>2.0) à Fetor hepaticus (musty sweet breath) à Vascular spiders, esophageal varices (enlarged veins) à Anemia: chronic blood loss à Hepatic encephalopathy (inability to get rid of ammonia) Symptoms: ALOC, confusion, à Hepatorenal syndrome Hepatitis à acute chronic inflammation of the liver caused by virus known as Hepatotropic virus à chronic alcoholism, drug toxicities, and autoimmune disorders. à Malaria, infectious mononucleosis, salmonellosis, & amoebiasis. à 5 Types: A, B, C, D, E à 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 à 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 à Symptoms: fever, fatigue, abdominal pain, nausea and vomiting, joint pain, jaundice, and clay colored stool à Hepatitis C: 2-26 weeks incubation period • Transmitted via Blood /serum Left Sided Heart Failure à 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 à fatigue, SOB, pulmonary emboli, activity intolerance, dizziness, syncope, dyspnea, cough, pulmonary edema, S3 heart sounds, decreased urine output Right Sided Heart Failure à (aka Cor Pulmonale) caused by pulmonary hypertension (cor pulmonale) and left HF à Most common cause of Right sided HF is Left sided HF Cor Pulmonale à 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 à SOB, fatigue, waking up at night. Increased venous pressure causes abdominal organ congestion and peripheral edema à Patient who is ambulatory you will see lower extremity edema à Patient who is bedridden = sacral and/or scrotal edema à Liver engorgement will lead to RUQ pain. You will also see Jugular Vein distention High output failureà 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 à Fluid retention and Edema, nocturia, oliguria, ascites, Respiratory: dyspnea, orthopnea, exertional dyspnea, PND (parosoxymal nocturnal dyspnea) fatigue, weakness, & mental confusion. Cachexia, malnutrition, cyanosis, arrhythmias, & sudden cardiac death Compensatory Mechanisms à When CO is insufficient to meet demands of body, may initially improve CO, eventually damages pump function à Stimulation of SNS: tissue hypoxia: increasing catecholamine’s à Stimulation of beta adrenergic & alpha adrenergic receptors: increase in HR à Activation of RAA system: when oliguria starts to kick in it decreases urine output. Reduced blood flow to kidneys activate RAAà angiotensin II à vasoconstriction à aldosterone (NA & H2O retention), preload & afterload increase ventricular modeling à 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 à 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 à Compensatory response of acute HF is tachycardia & HTN (doesn’t last forever) Hypertension (HTN) à a sustained BP that is 140mmHg or higher systolic and 90mmHg or higher diastolic Pathophysiology à 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 à (essential HTN) elevated BP with an unknown cause Secondary Hypertension à Elevated BP associated with a disease process or abnormality; such as: pulmonary, circulatory, renal diseases, endocrine issues, and medications Orthostatic Hypotension à 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 à 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 à Headache is the most common symptom, numbness & stress à Severe HTN: dizziness, nausea, vomiting, confusion (can signify encephalopathy), visual disturbances, renal insufficiency, aortic dissection, hypertensive crisis Risk Factors à Family history, age, maturation, and race: more prevalent in blacks, cholesterol à Monitor salt intake, modify pt diet, lifestyle, weight, exercise. Can’t modify-gender, age, or ethnicit. Complications à Stroke, seizures, CHF, ventricular hypertrophy, damage to retina, renal insufficiency, aortic dissection, hypertensive crisis, brain bleed (aneurism) ê Respiratory Disorders COPD à A group of pulmonary diseases of chronic nature, increased resistance to airway/airflow, Ex: Bronchitis, Emphysema, and Asthma à Hypercapnia: High CO2, increase in the arterial blood, drives COPDers breathing, which maintains. ABG’s reflect a high CO2 and low O2 Respiratory acidosis à Occurs in conditions that impair alveolar ventilation and cause an increase in serum PaCO2, hypercapnia, along with a decrease in pH Signs and Symptoms à Loss of weight, SOB, monitor diet and activity, ambulation (give them a rest period in between), encourage activity as much as you can à 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 à 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 à (Pink Puffers) Retaining CO2 , vasodilators make them appear pink, barrel chested, usually have chronic bronchitis à Loss of lung elasticity & enlargement of the of the air spaces distal to the terminal bronchioles that include alveolar wall and capillary bed destruction à 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 à Changes result in dyspnea (SOB) & ↑ resp. rate à Mostly associated with smoking or chronic exposure to irritants à 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) à Tachycardia and tachypnea are compensatory à 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 à 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 à Need 5 cm water of peep to keep alveoli inflated, bronchi open for good gas exchange à 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 à Mineral and glucocorticoid replacement ê 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 à monitor I&O’s and cardiac rhythm ê 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 à Elevated serum thyroid antibodies, T3 Signs & Symptoms excessive stimulation of the Sympathetic (adrenergic) branch of the CNS causing cardiac activity and reflexes. à 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 thyroid gland from long acting thyroid stimulator (LATS) à Seen most often in women under 40 y/o à Cytokine mediated response causes all the symptoms of hyperthyroidism Thyroid Storm Thyroid crisis or Thyrotoxicosis, life threatening condition. à Rare: seen in undiagnosed cases or inadequate treatment methods. à 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. à Hashimoto Thyroiditis: affects women 30-50 y/o, antibodies develop and destroy thyroid tissue à Primary: caused by congenital defects, loss of thyroid tissue from surgery or medications, iodine deficiency, or thyroiditis. à Secondary: peripheral resistance to thyroid hormones or pituitary TSH deficiency à 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 à avoid: cabbage, carrots, spinach, turnips, and peaches, which inhibit TH utilization Myxedema hypometabolic state occurring w/ untreated hypothyroidism à CO2 retention, fluid and electrolyte imbalance, hypothermia à 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 à S/S: lactic acidosis, hypoglycemia, hyponatremia, hypotension, bradycardia, CV prolapse, hypothermia, hypoventilation, and coma à cause due to inadequate thyroid replacement, infection, trauma, cold temp. exposure, CNS depressants ê Diabetes Mellitus Glucose → Regulated by endocrine hormones of the pancreas ê Beta cells secrete insulin (decrease glucose) ê Alpha cells secrete glucagon (increase glucose) ê 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! Diabetes Mellitus → Abnormality in blood glucose regulation and nutrient storage, imbalance between insulin availability and insulin need. Different Types of Diabetes: ê – Absolute deficiency of insulin (Type I) ê – 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: ê Absolute insulin deficiency ê Impaired release of insulin ê Inadequate or defective insulin receptors ê 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 à 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 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 à Women affected more than men before 40; same in puberty and after 40, higher in men after age 50 à 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 à 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 à 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 à Severe muscle weakness, caused by overmedication à Signs: cramps, diarrhea, bradycardia & bronchial spasm w/ increased pulmonary secretions and risk of respiratory compromise Diagnosis à 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 à Neurological and musculoskeletal assessment, aspiration precautions à Usually pts are intubated, educate on incentive spirometer afterwards à Medications: Anticholinesterases & immunosuppressants à Plasmapheresis (exchange blood plasma): removes IgG antibodies à Thymectomy (removal of thymus gland) Parkinson’s Disease à degenerative of basal ganglia function known by: “resting” (nonintentional) tremors, bradykinesia (slow sometimes frozen movement), and muscle rigidity or stiffness à Second most neurodegenerative disease, begins after 50 y/o increasing by 4-5% in those greater than 85 y/o à Dopamine levels that inhibit motor activity deplete, acetylcholine is not inhibited so it increases excitation leading to Parkinson’s symptoms à Develops from a postencephalatic syndrome à Side effect of therapy with antipsychotic drugs that block dopamine receptors à Toxic reaction to a chemical agent à Outcome of severe carbon monoxide poisoning Causes à Primary: unknown but believed to be caused by environmental interaction and genetic factors à Secondary: linked to infection, neoplasms, encephalitis, intoxication with carbon monoxide, manganese and mercury. The use of antipsychotic drugs, hypoxia & cerebral ischemia. Signs & Symptoms à 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 à 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 when changing positions), unsteady shuffling gait à Weight loss, constipation, dysphagia, orthostatic hypotension, depression, and dementia à Rigidity: Cogwheel (jerky catches when joint is moved), Lead pipe (smooth, stiff movement) Diagnosis à Physical assessment and HPI, rule out other etiology, PET scan and Dopamine challenge Treatment àDrugs to increase dopamine levels, stimulate dopamine receptors or retard the breakdown of dopamine Nursing interventions àFall prevention, aspiration precautions and monitoring of vital signs Multiple Sclerosis à 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 à Unknown etiology, possibly autoimmune or genetic basis or childhood viral infection à Most common demyelinating disorder, not curable but treatment can slow progression à Women affected twice as frequently than men, most prominent in European Americans w/ an age onset of 20-40 y/o à Lesions of MS macroscopically visible throughout the white matter (plaques); Oligodendrocytes are decrease in number or absent à 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 à 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 à 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 à MRI, Lumbar Puncture for CSF (clonal IgG bands present), muscle testing Guillain-Barre Syndrome à Acute rapidly progressing inflammation of peripheral (polyneuropathy) motor and sensory nerves à Characterized by variable motor weakness and paralysis, paralysis ascends symmetrically from lower extremities. With excellent care has a 96% complete recovery à Seen mostly in 30-50 y/o in both genders à Results from immune mechanism causesing demyelination neuropathy, acute influenza- like illness before onset of symptoms, CMV, Epstein-Barr virus, C. jejuni, & Vaccination à 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 à Nerve impulses are slowed or stopped, muscles lose innervation and begin to waste. Signs & Symptoms à 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 à electrolytes, ABG’s, nerve conduction tests, LP for CSF (elevated protein) Treatment à 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, muscle aches, headache, acute renal failure (rare), & retinal necrosis Nursing Interventions à Cardiopulmonary assessment and support, prevent skin breakdown, med. administration ê Acid-Base Balance and Electrolytes Acid-Base Balance à pH: indirectly measures H+ concentration & reflects balance between CO2 (regulated by the lungs), and HCO3¯ (regulated by the kidneys) à pH normal arterial blood values: 7.35-7.45 à Measures the acidity or alkalinity of a fluid and represents the balance between the percentage of hydrogen ions & bicarbonate ions à Carbonic acid (H2CO3): an acid-molecule that releases, or donates, H+ à Bicarbonate (HCO3-): a base-molecule that accepts H+ Acidosis à pH < 7.35, Contains greater amounts of H+, Results from too much CO2 or not enough HCO3¯ Alkalosis à pH > 7.45, Contains lesser amounts of H+, Results from too much HCO3¯ or not enough CO2 Respiratory System à Controls the regulation of CO2 à Hyperventilation leads to “blowing off” CO2 à Hypoventilation leads to “retaining” CO2 à If CO2 is elevated, hydrogen ion concentration is elevated and pH decreases à Respiratory system is rapid acting but does not fully return pH to normal à Chemoreceptors in the medulla and pons ABG Testing à Provides values of acid-base balance, pt’s oxygenation status, and arterial blood gas à Values may determine if body/system is compensating à PaO2: 80-100 mm/Hg à pH: 7.35-7.45 à PaCO2: 35-45 mmHg à HCO3: 22-26 mEq/L à Oxygen Saturation: 95-100% Oxygen Saturation à Gives you an idea about how the patient is breathing/oxygenating à Has absolutely nothing to do with acid base balance à Adequate saturation may not be indicative of adequate oxygenation Metabolic Acidosis à pH below 7.35 – normal pCO2 – HCO3 below 22 à Compensatory mechanism: Increase in respiratory rate (Kussmaul’s respirations), “blow off” CO2 & H2CO3 à Etiology: Diabetic ketoacidosis, lactic acid accumulation, starvation, renal failure, severe diarrhea, and increases in chloride à High Potassium Metabolic Alkalosis à pH above 7.45 – normal pCO2 – HCO3 above 26 à Causes: Prolonged vomiting, gastric suctioning à Compensatory mechanism: Decrease in respiratory rate in order to increase CO2 and renal excretion of bicarbonate à Low Potassium Al(K)a(LO)sis Respiratory Acidosis à pH below 7.35 – pCO2 above 45 – normal HCO3 Hypocalcemia à due to: rapid administration of blood containing citrate à hypoalbuminemia, hypoparathyroidism, vitamin D deficiency, alkalosis, pancreatitis, CRF, and chronic alcoholism à 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 à due to: Hyperparathyroidism, Cancer, Paget’s disease, Osteoporosis, prolonged immobilization, and thiazide diuretics à Signs/Symp: Anorexia, abdominal pain & constipation, muscle weakness, hypoactive reflexes, lethargy, flank pain (if kidney stones), ECG: shortened QT & ST segment Magnesium à the second most abundant cation in ICF; Regulated by dietary intake, renal mechanisms, and actions of PTH. à Functions: Speeds up enzyme reactions during carbohydrate metabolism, helps produce ATP, important in protein synthesis, and affects cardiac and skeletal muscle excitability à Potassium and Magnesium are parallel Hypomagnesemia à due to: inadequate intake, inadequate absorption, and excessive loss from GI tract or urinary system; Alcoholics. à Similar to hypocalemia; The 3 Ts (tremors, twitching, tetany) & hyperactive DTRs (deep tendon reflexes), positive Chvostek’s & Trousseau’s sign à CNS irritation, lethargy, confusion, seizures, Dysrhythmias, and N/V à Acronym: STARVED: Seizures; Tetany; Anorexia & arrhythmias; Rapid heart rate; Vomiting Emotional lability; Deep tendon reflexes increased Hypermagnesemia à due to renal failure or excessive intake à hypoactive DTRs, weakness, drowsiness, decreased rate/depth of respirations, bradycardia, hypotension, and flushing of the skin à Signs/Symp: Acronym: RENAL: Reflexes decreased (plus weakness & paralysis); ECG changes (bradycardia) and hypotension; Nausea & Vomiting; Appearance flushed; Lethargy (plus drowsiness and coma) ê Traumatic Brain Injury ICP à 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 productionof 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 à Decadrone is given to reduce inflammation but to decrease degradation of the tissue & shift fluid to release the pressure à 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 à 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 à Brain death CPP 0 – 40 mmHg à Intra ventricular catheter tells ICP; Tissue perfusion inadequate leads to cellular hypoxia results à Decreased LOC is earliest sign of neurological deterioration à Neuronal death Brain Herniation à Cushing reflex (important indicator of increased ICP): Elevated MABP; Widening of pulse pressure; Reflex slowing of the heart rate (bradycardia) à 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 à Monitor oxygenation, Monitor PC02, Maintain ABC’s, Positioning à Cluster care: everything done at once as fast as possible to avoid overstimulation the pt because stimulation causes more ICP à Prevent coughing, straining, Monitor VS, Medication administration, Lab value monitoring à De(cortic)ate: arms flexed to chest, corticospinal tract lesion à Decerebrate: arms extended away from chest, brainstem injury CVA/Stroke à 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 à 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 à 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 à Age, Gender, Race, Family history, Hypertension (biggest cause of hemorrhagic stroke), Cigarette smoking, DM, Hyperlipidemia, Atrial fibrillation à Micro clots in the circle of Willis lead to a stroke (ischemic) à 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 à 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 à Cerebral Thrombus: (blood clot) that develops at the clogged part of the vessel most (large or small vessels), Atherosclerosis à 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 à 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) à 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 à Reperfusion by increasing blood pressure by giving them norepinephrine, see if the symptoms improve Hemorrhagic strokes à Caused by bleeding into brain tissue, usually from a blood vessel rupture caused by hypertension, aneurysms, arteriovenous malformations (AVM), head injury, or blood dyscrasias (imbalance/disproportion of bodily fluids: phlegm, blood, & yellow & black bile) à AVM where the artery and the veins come together in the junction but are weakened. Its congenital Pathophysiology à 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 à 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 à Age, Hypertension, Aneurysm, Trauma, Tumors, AV malformations, Coagulopathy CVA Manifestations à 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) à 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 à CT scan (truly diagnoses the stroke), MRI, H & P Treatment à Stroke centers, reverse ischemia, reperfusion (to remove the clot) IVR (goes through the vessels) Nursing Interventions à Safe environment (semi-fowler position), monitor ABC’s, medication administration à 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 ê Renal and Urinary Disorders Acute renal failure à due to drug overdoes (Cardizem), Antibiotics, Bacterimia, Iodine Contrast (HYDRATE PT> before during and after!) Reversible if recognized early and treated appropriately à Assess: preexisting renal insufficiency and diabetes and Elderly persons. à 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) à GFR main determinant Creatinine second best à 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 à 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