NUR 3031 Pathophysiology Final Review, Exams of Pathophysiology

Download NUR 3031 Pathophysiology Final Review and more Exams Pathophysiology in PDF only on Docsity! NUR 3031 Pathophysiology Final Review Updated 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 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. 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: Cellular stressors Hypertrophy 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. Reversible change in which a cell type is replaced by another cell type, occurs in response to irritation and inflammation. (‘M’ is like mix-and-match) deranged cell growth of a specific tissue, results in cells that varies in size, shape, and organization Strongly implicated as a precursor of cancer; reversible change lack of oxygen supply to the tissue despite of good perfusion of blood. Decreased blood supply to a body organ or part usually due to functional constriction or obstruction. ISCHEMIA commonly depends on blood flow through limited numbers of blood vessels and produces LOCAL TISSUE injury IMMUNE DISORDERS AND IMMUNODEFICIENCY HIV retrovirus selectively attacks CD4+ T lymphocytes; pt. infectious even when asymptomatic Unprotected sexual activity; blood, semen, vaginal fluids, oral intercourse; Contaminated blood; infected mother to child, breast milk, placenta, needles, blood transfusions Stage 1 Occurs shortly after infection, high viral load Symptoms: flu like symptoms; GI issues; Lymphoadenopathy, rash; viral replication, CD4+ cell count Stage 2 Latent Period, lowest viral load Symptoms: Asymptomatic of illness; CD4+ count drops progressively ; 200-499 cells/ᵤL; Risk for opportunistic infections; Inflammation in more than 2 areas for > 3 months Stage 3 AIDS phase, caused by HIV infection of cells, viral load increases, suppressed immune system and opportunistic infections, malignancies, wasting and CNS degeneration. Symptoms: Occurs when CD4+ cell count is less than 200 cells Respiratory: pneumocystis carinni pneumonia (PCP), pulmonary TB (can migrate anywhere in the body) GI: esophageal candidiasis, CMV infection, herpes simple virus, diarreah, gastroenteritis Nervous System: taxoplasmosis (cat poo) Malignancies: Kaposi sarcoma, non-hodgkins, lumphoma Diagnostic HIV tests 1. ELISA enzyme-linked immunosorbent assay (ELISA) screens for HIV antibodies. 2. Western blot test to confirm a positive Elisa test. 3. Polymerase Chain Reaction (PCR) most accurate, most expensve Nursing Assessment Weight analysis, LOC, Reports of pain Skin; palpation of lymph nodes, VS, lung sounds, oral cavity, rectal and vaginal exam Metaplasia Dysplasia Hypoxia Ischemia 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) Lung infarcts (pneumonia, acute chest syndrome) Pigment gallstones Avascular necrosis of femoral head Kidney infarcts (chronic kidney disease) Osteomyelitis Skin ulcers Pallor, Jaundice Fatigue and irritability. Diagnostic tes t hemoglobin electrophoresis: determines presence hemoglobin S, CBC. Treatement Folic acid supplements and analgesics Hydration therapy as well as scheduled transfusions decreases crisis episodes. During a crisis, hydration to improve blood flow, reduce pain, prevent renal damage, O2, IV (narcotics) Maintaining full immunization Hydroxyurea inhibits DNA synthesis, reduces pain crisis. Increases RBC levels, acts as an anti inflammatory inhibiting the production of WBCs. Bone marrow or stem cell transplant; however risk of graft-versus-host disease. Megaloblastic Anemia impaired DNA synthesis results in enlarged RBC’s due to vitamin B12 (cobalmin) and folic acid deficiency causes pernicious anemia: inability to absorb vitamin B12 due to lack of intrinsic factor Macrocytic (Larger than normal cell size), Normochromic (normal concentration of Hb) Possibly destruction of the gastric mucosa, caused by the loss of parietal cells and production of antibodies that interfere with binding of vitamin B12 to intrinsic factor. Related Factors Caused by gastrectomy, gastrojejunostomy, ileal resection and after gastric bypass surgery Inflammation or neoplasms in the terminal ileum. Malabsorption syndrome (poor absorption) Signs and Symptoms Pallor, slight jaundice, nails Weakness, fatigue and diarrhea Smooth sore beefy red tongue Disrupts function of peripheral nerves, spinal cord, and brain. Parasthesias: numbness or tingling in the extremities Proprioreception, may progress to imbalance and spinal cord damage. dark stool because of blood, internal hemorrhage; most leading cause if IG bleed Treatment Life long parental (injection) or high oral Vitamin B12. increase intake of foods such as eggs, meats, and dairys Diagnostic Test CBC, MCV, MCHC, MCH Iron Deficiency Anemia inadequate iron supply due to excessive iron loss from bleeding, decreased dietary intake, or malabsorption. impairs cellular division and maturation especially in rapidly proliferating RBCs microcytic and microchromic Iron is stored in body as ferritin Women loose 15 mg monthly during menstruation (most common cause in women) GI bleeding is most common cause in men. Clinical Manifestation poor cognitive, motor and emotional function; related to effects on brain development or neurotransmitter function. Related Factors Pregnancy, menstruation Hemorrhage Medication use (aspirin) GI bleeds (peptic ulcer, intestinal polyps, hemorrhoids or cancer) Eating disorders; Diets (cow’s milk for infants low in iron) Signs and Symptoms develop slow until Hb drops to 7-8 g/dl; Fatigue and weakness, SOB, Hypoxia Pallor (ear lobes, palms and conjunctiva) Dyspnea; Tachichardia Dysphagia and decreased acid secretion. Brittle hair and nails Cheilosis (cracks in corners of mouth) Smooth tongue, dizziness Pica (craving to eat unusual substances such as clay or starch) Treatment Control chronic blood loss. Increase dietary intake of iron, ferrous sulfate, oral replacement therapy. Parental iron therapy may be used when oral forms are not tolerated or are ineffective. Vitamin C enhances absorption iron-rich foods (as beef, chicken, egg yolk, pork loin, turkey and whole grain breads and cereals). Polycythemia Abnormally high RBC count: hematocrit >50% overproduction of RBC’s, WBC’s, and platelets increasing blood viscosity, volume, congestion of tissues (live and spleen) causing acidosis, clotting, and thrombi Absolute (PRIMARY) Polycythemia: most common in Caucasian men of European, jewish ancestry Neoplastic disease of bone marrow Thick, slow moving blood Secondary Polycythemia Physiologic increase in level of erythropoietin Compensatory response to hypoxia: High altitudes, chronic heart, lung disease and smoking GI Disorders GERD Gastric backflow into esophagus (reflux, heartburn or esophagitis) associated with weak or incompetent lower esophageal sphincter Delayed gastric emptying contributes to reflux, esophageal mucosal injury may occur Normally cleared and neutralized by esophageal peristalsis and salivary bicarbonate Chronic inflammatory disease of the antrum and body of the stomach H. pylori secretes urease which produces ammonia to buffer acidity of stomach; produces enzymes and toxins interfering with protection of the gastric mucosa against acid The severity of the heartburn is not indicative of the extent of the mucosal injury Related Risk Factors common problem in infants and children, occurs at least once a day in infants 0-3 months, by 6 months is less frequent Hiatal hernia Pregnancy Obesity; Poor dietary habits, high fat diet Esophageal structures or previous surgery Smoking Excessive caffeine intake Gastroparesis (delayed gastric emptying time) Vomiting, coughing, lifting or bending Signs and Symptoms Most frequent is heartburn; frequently severe, 30–60 minutes after meal; evening onset Belching and chest pain Dyspepsia (burning, pain in epigastric, radiates to throat, shoulder, or back) wheezing, chronic cough and hoarseness Diagnostic Test Radiographic studies with barium, esophagoscopy and ambulatory esophageal pH monitoring. pH probe test used to determine stomach pH (less than 4 = positive) H. pylori can be detected by C urea breath test Treatment Avoid large meals; eat sitting right up; foods that reduce esophageal pH(chocolate, fats, caffeine) Avoid recumbent position several hours after a meal; avoid bending for long periods Avoid alcohol use and smoking Sleep with the head elevated Lose weight if overweight Antacids, and inhibitors of gastric acid. Histamine-2 (H2) antagonist inhibits gastric acid production Treatment for h. pylori: PPI; Antibiotic therapy. 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 Risk Factors usually before age of 30; can occur at any age Whites have a higher risk Family history Stress Diagnostic Test Physical exam and medical history CBC (low RBC, Hgb, Hct) Negative Stool Test Biopsy Sigmoidoscopy; Colonoscopy/ risk perforatin with severe disease Barium Enema X-Ray Computerized Tomography (CT) Scan Treatment Medication Therapy to reduce symptoms Bulk free diet and a well- balanced nutritious diet Avoid caffeine, lactose Surgical Procedures Monitor intake and output, administer iv fluids as ordered Pancreatitis Reversible inflammatory process of pancreatic acini (functional units of exocrine pancreas) Auto-digestion of tissue by inappropriately activated pancreatic enzymes Begins with trypsin, trypsin activates other digestive enzymes causing pancreatic injury May result in systemic illness and multisystem organ failure Related Factors Gallstones (in the common duct) Alcohol abuse and Infections (primary causes) Hyperlipidemia, Hyperparathyroidism Abdominal and surgical trauma Drugs such as steroids and thiazide diuretics Signs and Symptoms Mild to severe abdominal pain: epigastric or peri-umbilical Radiating to back, chest or flank Fever, tachycardia, hypotension, respiratory distress, abdominal distention Diagnostic Test Elevated C-reactive protein: more than 10 mg/dl Hypocalcemia, hyperglycemia Elevated serum amylase/lipase Elevated WBC: higher that 12000/uL Elevated serum bilirubin Serum amylase and serum lipase: lab markers most commonly used • Amylase: most used to diagnosis acute pancreatitis. Serum amylase levels rise within the first 24 hrs. Remain elevated for 48 to 72 hrs. Urinary clearance of amylase is increased and is often measured. WBC count may be increased and hyperglycemia and elevated serum bilirubin level may be present. • Lipase: Are elevated during the first 24 to 48 hrs., but remains elevated for 5 to 14 days Complications Systemic inflammatory response (SIRS) Acute respiratory distress syndrome (ARDS) Fluid into retroperitoneal space Pancreatic pseudocyst 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) 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), jugular neck vein distention, abdominal assessment, activity tolerance. 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 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 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 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 Signs and Symptoms Cor Pulmonale Signs and Symptoms 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 confusion. Cachexia, malnutrition, cyanosis, arrhythmias, & sudden cardiac death Compensatory Mechanisms When CO is insufficient to meet demands of body, may initially improve CO, eventually damages pump function Stimulation of SNS: tissue hypoxia: increasing catecholamine’s Stimulation of beta adrenergic & alpha adrenergic receptors: increase in HR Activation of RAA system: when oliguria starts to kick in it decreases urine output. Reduced blood flow to kidneys activate RAA angiotensin II vasoconstriction aldosterone (NA & H2O retention), preload & afterload increase ventricular modeling Natriuretic response: Atrial natriuretic peptide released where there is an increase in BP, cells in atria are enlarged; inhibit ADH, stretch wall of heart cause a natural diuretic effect. BNP is released from ventricles & promotes diuresis Myocardial hypertrophy: (principal mechanism in compensation) enlargement of myocardium, thickening of walls of heart, causes changes in electrical currents and creates scar tissue. Part of the remodeling process- when LV enlarges, structures inside those chambers will change ex: valves can change due to this Compensatory response of acute HF is tachycardia & HTN (doesn’t last forever) Hypertension (HTN) a sustained BP that is 140mmHg or higher systolic and 90mmHg or higher diastolic Pathophysiology Increased activity of RAA system. Renin is released into the bloodstream, which leads to a reduction of blood flow to kidneys, a fall in BP and decreased concentration of tubular Na+. Angiotensin I combines with rennin to form a nonpressor form of angiotensin I, which is converted in the lungs into Angiotensin II (vasoconstrictor) by the ACE enzyme. Angiotensin II causes the release of aldosterone, leading to the reabsorption of Na+ and water, further increasing the BP. Blood viscosity increases and blood becomes thicker. (essential HTN) elevated BP with an unknown cause Elevated BP associated with a disease process or abnormality; such as: pulmonary, Primary Hypertension Secondary Hypertension circulatory, renal diseases, endocrine issues, and medications 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 Or greater than or to 160 equal to 100 Assessment Edema, nutrition status, weight, medications, and social history. Assess BP: measure in each arm using 3 positions: lying, sitting & standing, note pulse pressure. Take BP 3 times in different visits to declare HTN Signs and Symptoms Headache is the most common symptom, numbness & stress Severe HTN: dizziness, nausea, vomiting, confusion (can signify encephalopathy), visual disturbances, renal insufficiency, aortic dissection, hypertensive crisis Risk Factors Family history, age, maturation, and race: more prevalent in blacks, cholesterol Monitor salt intake, modify pt diet, lifestyle, weight, exercise. Can’t modify-gender, age, or ethnicit. 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 Occurs in conditions that impair alveolar ventilation and cause an increase in serum PaCO2, hypercapnia, along with a decrease in pH 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 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 95-100% Orthostatic Hypotension Respiratory acidosis Signs and Symptoms Diagnostic Tests Viruses, bacteria, fungi, protozoa or parasites. Most common bacteria to cause it: Streptococcus pneumonia Get flu vaccine! Ask patient if they had it, if not must ask them if they want it. Must get the flu shot every year. Pneumonia vaccine is every 5 years Assessment Cough, productive septum or mucous, fever, tachycardia, lung sounds: Rails and Rhonchi Chest x-ray, labs : WBC (if elevated=infection), sputum testing, culture and sensitivity, blood culture (3x, in 3 spots for consistency) Treatment put patient on oxygen due to SOB, antibiotics, deep breathing, facemask O2 is considered a drug, you need an order unless it is an emergency situation. Adrenal Cortex Hypofunction → destruction of adrenal glands due to trauma, infection, hemorrhage into gland, AIDS, drugs, cancer, or sudden stress resulting in chronic adrenocortical hormones insufficiency and decreased production of cortisone, aldosterone, and androgens → Hyperpigmentation from ↑ACTH levels causing bronze pigment. (lack of feedback inhibition) Mineralocorticoid deficiency (aldosterone): cause low NA+, low Cardiac Output, high K+; Dehydration (Water follows solute causing Hypovolemia and hypotension) Weakness, fatigue; CV collapse; orthostatic pressure Glucocorticoid deficiency: Hypoglycemia; Lethargy, weakness; Fever; GI symptoms 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. immediate IV glucocorticoid replacement and fluids with Na+ (isotonic solution 0.9% Na+CL) → 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 → 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 Causes Diagnostic Test Addison’s Disease Signs and Symptoms Cushing syndrome 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 thyroid gland from long acting thyroid stimulator (LATS) Seen most often in women under 40 y/o Cytokine mediated response causes all the symptoms of hyperthyroidism Thyroid Storm Thyroid crisis or Thyrotoxicosis, life threatening condition. Rare: seen in undiagnosed cases or inadequate treatment methods. Precipitated by stress (infection, DKA, physical/emotional trauma, thyroidectomy) Signs and Symptoms Very high fever, extreme hyperthermia (102F-106F) Tachycardia, CHF, angina, agitation, restlessness, delirium, and seizures Nursing Management Elevate head of the bed to decrease eye pressure, monitor I&O’s, weight, dietary intake (require 4,000-5,000 Cal/day) Hypothyroidism hypometabolic state, decrease in O2 consumption by tissue and decreased heat production. Hashimoto Thyroiditis: affects women 30-50 y/o, antibodies develop and destroy thyroid tissue Primary: caused by congenital defects, loss of thyroid tissue from surgery or medications, iodine deficiency, or thyroiditis. Secondary: peripheral resistance to thyroid hormones or pituitary TSH deficiency Iodine deficiency results b/c of antithyroid drugs, lithium intake or inadequate iodine intake Signs and Symptoms Weakness, fatigue, weight gain, cold intolerance/dry skin, mental impairment or confusion, Decrease reflexes, puffy face, edema, hoarse voice, bradycardia, hypotension, goiter, Everything is decreased except weight! Nursing Management Intravenous glucose, monitor for hyperglycemia and hypoglycemia, monitor signs of digitalis Toxicity, daily weight avoid: cabbage, carrots, spinach, turnips, and peaches, which inhibit TH utilization Myxedema hypometabolic state occurring w/ untreated hypothyroidism CO2 retention, fluid and electrolyte imbalance, hypothermia Accumulation of proteins in interstitial spaces causes an increase in interstitial fluids, causes mucinous edema (myxedema). Non-pitting edema is most common in pretibial & facial areas Myxedema Coma Hypothyroid crisis, rare and life-threatening, characterized by a severe hypometabolic state S/S: lactic acidosis, hypoglycemia, hyponatremia, hypotension, bradycardia, CV prolapse, hypothermia, hypoventilation, and coma cause due to inadequate thyroid replacement, infection, trauma, cold temp. exposure, CNS depressants Diabetes Mellitus Glucose → Regulated by endocrine hormones of the pancreas Beta cells secrete insulin (decrease glucose) Alpha cells secrete glucagon (increase glucose) Delta cells secrete somatostatin → Brain needs glucose, but cannot store which is why is so important → Hypoglycemic pts. may show signs similar to stroke due to the lack of glucose to the brain (no paralysis) → High sugar causes problems with healing, bacteria likes sugar. Glucocorticoids → secreted during stressful times, critical during periods of fasting and starvation → When steroids are given to pts, must monitor blood sugar, levels will go up! → Steroid used to septic pts. in shock! → 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 Diabetes Mellitus Secondary: predisposing conditions, eg: congenital or acquired defects of joint structures, trauma, metabolic disorders, or inflammatory diseases. Most prevalent form of arthritis, leading cause of pain and disability in elderly Signs & symptoms Usually involves hand, knee, hip, foot, spine unilateral joint pain aggravated by movement, stiffness of joint Numbness/tingling at night Limited movement Herberden’s nodes (hard nodules in DIP) and Bouchard’s nodes (hard nodules in PIP) resulting in joint deformity chronic, systemic, autoimmune disease with inflammation of the joints and deformities. Most common in females Unknown cause; however evidence shows progression is related to autoimmune process Systemic complications include extrasynovial rheumatoid nodules. Altered immune response; Synovial inflammation (where joints articulate) Activation of CD4+ helper T cells, cytokine release, antibody formation Positive rheumatoid factor (IgRF) in 70-80% of cases, found in the blood, synovial fluid, and synovial membrane. Tests also for antricyclic citrullinated peptide antibodies (anti-CCP) more specific diagnostic marker Morning stiffness, Simultaneous Destructive changes irreversible Swan neck, Ulnar drift (joint deformities), Boutonniere deformities Rheumatoid nodules: found on the olecranon bursae or extension of forearm Characterized by remission and exacerbations; chronic inflammation of bilateral joints and surrounding structures Morning stiffness at least 1 hour for at least 6 weeks Swelling of three or more joints for at least 6 weeks Swelling of wrist, metacarpophalangeal, proximal interphalangeal joints for 6 or more wks Rheumatoid nodules, Serum RF+ Fatigue, Weakness, Anorexia, Weight loss, Low-grade fever, Vasculitis and Anemia Kidneys may get inflamed & not able to urinate Neurological Disorders chronic disorder of peripheral nervous system affecting transmission of nerve impulses to muscles, causing muscle weakness and fatigue that increases w/exertion and improves w/rest Autoimmune disease caused by loss of acetylcholine receptors in neuromuscular junction Three underlie cause of loss of acetylcholine receptors function: 1) Complement-mediated injury to postsynaptic muscle membrane. 2) Accelerated acetylcholine receptor degradation by receptor specific antibodies. 3) Blockade of the receptor by antibodies attached to the acetylcholine-binding sites. Associated w/ continued production of autoantibodies by thymus gland in 75% of cases Slow onset, precipitated by emotional stress, hormonal disturbances (pregnancy, menses, Rheumatoid Arthritis Signs and Symptoms Myasthenia Gravis 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 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 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) 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. 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 Cholinergic Crisis Nursing Assessment/Management Parkinson’s Disease Signs & Symptoms 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 Weight loss, constipation, dysphagia, orthostatic hypotension, depression, and dementia Rigidity: Cogwheel (jerky catches when joint is moved), Lead pipe (smooth, stiff movement) Diagnosis Physical assessment and HPI, rule out other etiology, PET scan and Dopamine challenge Treatment Drugs to increase dopamine levels, stimulate dopamine receptors or retard the breakdown of dopamine Nursing interventions Fall prevention, aspiration precautions and monitoring of vital signs Demyelination of nerve fibers in white matter of the brain, spinal cord and optic nerve causes temporary, repetitive or sustained interruption in conduction of nerve impulses Unknown etiology, possibly autoimmune or genetic basis or childhood viral infection Most common demyelinating disorder, not curable but treatment can slow progression Women affected twice as frequently than men, most prominent in European Americans w/ an age onset of 20-40 y/o Lesions of MS macroscopically visible throughout the white matter (plaques); Oligodendrocytes are decrease in number or absent Inflammation occurs around plaques as well as in normal tissue; astrocytes (gliosis) appear in lesions and scar tissue forms, replacing axons and leading to permanent disability. The term gliosis leads to the term sclerosis which means scarring Characterized by exacerbations and remissions over many years in several different sites in the CNS Initially, there is normal or near-normal neurologic function between exacerbations. As the disease progresses, there is less improvement between exacerbations Visual disturbances/blindness (retrobullar neuritis), sudden progressive weakness of one or more limbs, spasticity of muscles, nystagmus, tremors, gait instability, fatigue, bladder dysfunction (UTI’s, incontinence), & depression Diagnosis MRI, Lumbar Puncture for CSF (clonal IgG bands present), muscle testing Acute rapidly progressing inflammation of peripheral (polyneuropathy) motor and sensory nerves Characterized by variable motor weakness and paralysis, paralysis ascends symmetrically from lower extremities. With excellent care has a 96% complete recovery Seen mostly in 30-50 y/o in both genders Results from immune mechanism causesing demyelination neuropathy, acute influenza like illness before onset of symptoms, CMV, Epstein-Barr virus, C. jejuni, & Vaccination Immune reaction triggered by viral illness or immunization, instead of antibody preventing invading organism, it has a damaging effect on peripheral nerve myelin; an IgM antimyelin antibody exists, lymphocytes are sensitized and aid in damaging myelin Nerve impulses are slowed or stopped, muscles lose innervation and begin to waste. Multiple Sclerosis Signs & Symptoms Guillain-Barre Syndrome 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 H & P, Monitor I & O’s, Fluid balance (restriction) 1L/1000ml, Sodium restriction, give potassium sparing Diuretics Fluid intake: 2200 to 2700 ml/day Thirst-control center: the hypothalamus (thirst regulates intake) Hormonal: Antidiuretic hormone (ADH), Renin-angiotensin-aldosterone mechanism, Atrial natriuretic peptide Fluid output: Fluid is lost through kidneys, skin, lungs, and GI tract, Insensible loss of fluid through breathing and sweating (cannot be measured) Goal is to maintain Homeostasis Sodium 135-145 mEq/L, it is the most abundant cation in ECF Functions: maintains water balance, nerve impulse transmission, regulate acid-base balance, and participate in cellular chemical reactions. Regulated by dietary intake & aldosterone secretion Most sodium losses occur in the kidneys. Small amount (<10%) lost in the GI tract Hyponatremia Sodium loss < 135 mEq/L (GI, renal, and skin losses) Causes: pshychogenic polydipsia; water intoxication; SIADH Signs/Symp: N/V, abdominal cramping, edema, disorientation, convulsions and coma Hypernatremia Excess salt intake, aldosterone secretions, DI, increased sensible & insensible water loss, and water deprivation. Administration of NaHCO3- during cardiopulmonary arrest can cause hypernatremia Signs/Symp: Thirst (sticky mucosa, swallowing becomes difficult), dry & flushed skin, dry & sticky m.m., postural hypotension, fever, agitation, decreased reflexes, convulsions, restlessness, & irritability. Potassium Maintains many body functions: transmission & conduction of nerve impulses, normal cardiac conduction, skeletal/smooth muscle contraction, and regulates metabolic activities. Also regulates acid-base balance; necessary for the kidneys to concentrate urine. Remember that the cell is full of potassium Hypokalemia caused by: K+ wasting diuretics, polyuria, GI losses (vomiting, diarrhea, NG/colostomy outputs), alkalosis, treatment of DKA with insulin. Most of the causes of hypokalemia are medications, NG tubes, diarrhea, vomiting, and alkalosis Skeletal muscle weakness U wave/ ECG changes: ↓K decreases the resting membrane potential, causing prolonged PR interval, and prolonged relative refractory pd which causes ST segment depression, flattened T wave, and presence of a U wave Diagnosis and Treatment Regulation of Body Fluids Constipation, ileus Toxic effects of digoxin Irregular, weak pulse Orthostatic hypotension Numbness (paresthesias) Hyperkalemia due to: Renal failure, fluid volume deficit, massive cellular damage (burns & trauma), Acidosis especially DKA Rapid infusion of stored blood; during a transfusion, if blood sits out for too long it releases potassium. Must be given with in 3-5 hrs max & keep refrigerated Hemolosis can occur while drawing blood and it’s due to the cells splitting open Use of K+ sparing diuretics, and salt substitutes because they contain a lot of potassium chloride Signs/Symp: ECG changes (tall, tented/peaked T wave), paresthesias, muscle weakness, abdominal cramping diarrhea, and hyponatremia Calcium 8.5 – 10.5 mg/dL, 50% bound to bound to albumin, 40% free ionized. Functions: bone & teeth formation, blood clotting, hormone secretion, cardiac conduction, nerve impulse transmission, & muscle contraction. PTH & Vitamin D responsible for maintenance, “Parathyroid pulls… Calcitonin keeps” 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 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 Brain death CPP 0 – 40 mmHg Intra ventricular catheter tells ICP; Tissue perfusion inadequate leads to cellular hypoxia results Decreased LOC is earliest sign of neurological deterioration Neuronal death Cushing reflex (important indicator of increased ICP): Elevated MABP; Widening of pulse pressure; Reflex slowing of the heart rate (bradycardia) Herniation: Displacement of brain tissue; Occurs with elevated ICP in one brain compartment causes shifting of the cerebral tissue toward an area of lower pressure Monitor oxygenation, Monitor PC02, Maintain ABC’s, Positioning Cluster care: everything done at once as fast as possible to avoid overstimulation the pt because stimulation causes more ICP Prevent coughing, straining, Monitor VS, Medication administration, Lab value monitoring De(cortic)ate: arms flexed to chest, corticospinal tract lesion Decerebrate: arms extended away from chest, brainstem injury CVA/Stroke Syndrome of acute focal neurologic deficits from a vascular disorder that injures brain tissue, causes abrupt loss of consciousness with resulting paralysis that may be temporary or permanent Sometimes prior to having a stroke, there is an alarm phase: TIA (transient Ischemic attack lasting no more than 24 hrs) If symptoms last for more than 24 hrs then its considered a stroke Cerebral Perfusion Pressure Brain Herniation Nursing Interventions Patho: obstruction of urine outflow (Ureters; Bladder; Urethra); Both of the ureters must be occluded to produce renal failure 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 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 Anemia; Coagulopathies, HTN, Heart disease, Pericarditis, Impaired phosphate elimination, Hypocalcemia Accumulation of Nitrogenous Waste: Azotemia (elevation of BUN, creatinine) Uremia (acid in the urine); Neuromuscular manifestations; GI manifestations Infection and Immune disorders Sodium and water balance; Potassium balance (90% of potassium excretion is by kidneys); Acid-base balance: kidneys regulate blood pH by eliminating H+ ions produced in metabolic processes and by regenerating bicarbonate. Treatment can interfere with the absorption, distribution, and elimination of drugs Altered drug absorption: antacid treatment Altered metabolism: Result of less protein-bound drugs; Increased intermediates of drug metabolism Alterations in dosage may be required. Treatment Treating urinary tract infections promptly Chronic kidney disease Clinical Manifestations Disorders Due to Renal Failure Avoiding medication with renal-damaging potential Controlling blood pressure Controlling blood sugar in persons with diabetes Stopping smoking Sensory Glacoma Chronic, increased intraocular pressure, if untreated can lead to ischemia and degeneration of retina and optic nerve, loss of vision and blindness. Caused by alterations in resorption of aqueous humor Normal IOP: 12-21 mmHg Primary Cause: Anatomically predisposed eyes without other pathology; Risk factors: > 40 years, Juvenile onset, Black race; Family history, and Chromosome 1 abnormality Secondary Cause: Inflammatory processes, Trauma, Lens changes, Intraocular tumors, HTN, DM Type 2 Aqueous humor fills anterior and posterior chambers of the eye. Intraocular pressure results from a balance of several factors: Rate of aqueous humor production; Resistance to flow; Rate of removal by drainage system Two types: Open Angle and Close Angle Most common; Asymptomatic/chronic; Impaired outflow results from impair drainage system. The iridocorneal angle remains open. Trabecular meshwork abnormality decreases rate of aqueous humor reabsorption causing gradual buildup of aqueous humor Results in: damage to the optic nerve, peripheral visual loss, Intraocular pressure (tonometry) is present but not only diagnostic factor, Visual field exam also used. S/S: Tunnel Vision (first signs), dull eye pain > 20 minutes, blurred vision, inability to detect colors, headaches. Common in adults >60 Occlusion of the anterior chamber angle by the iris, impaired outflow results form occlusion of the iridocorneal angle; impairing access to the drainage system. Risk factors: Pre-existing shallow anterior chamber, Pupillary dilation, Inherited anatomic defect, Asia/Inuit descent Manifestations: eye and face pain, Blurred or iridescent vision, Relieved by sleep, severe headache with N/V, red eyes and hazy cornea, halos around light, fixed dilated pupil nonreactive to light Open Angle Closed Angle