NURS3107 Pathophysiology Final Exam Study Guide Fall 2022 PDF

NURS3107-Pathophysiology Final Exam Study Guide Fall 2022 I. Cerebrovascular Accidents a. Ischemic = disruption of the blood supply caused by an obstruction, usually a thrombus or embolism, that causes infarcti...

NURS3107-Pathophysiology Final Exam Study Guide Fall 2022 I. Cerebrovascular Accidents a. Ischemic = disruption of the blood supply caused by an obstruction, usually a thrombus or embolism, that causes infarction of brain tissue b. Embolic = clots formed elsewhere in the body, often in the heart, travel to the brain c. Hemorrhagic = caused by bleeding into brain tissue, the ventricles, or subarachnoid space primary caused by vessel rupture due to HTN d. Thrombotic = blood clot develops in the arteries supplying blood to the brain due to conditions like atherosclerosis e. Clinical manifestations i. Hemiplegia = paralysis on one side of the body ii. Hemiparesis = weakness on one side of the body iii. Flaccidity = complete loss of muscle tone and the inability to move affected side of body iv. Ataxia = affects coordination and balance due to damage in cerebellum II. Multiple Sclerosis – demyelination of CNS a. Patho = progressive immune related demyelination disease of the CNS; T cells remain in the CNS and promote the infiltration of other agents that damage the immune system b. Clinical manifestations = disease is relapsing and remitting; has exacerbations and recurrences of symptoms, including fatigue, weakness, numbness, difficulty in coordination, loss of balance, pain, and visual disturbances c. Treatment = symptom management of muscle spasms, fatigue, ataxia, bowel and bladder control III. Myocardial Infarction a. Diagnostics = 12 lead EKG, cardiac labs, troponin and CK b. Risk factors i. Non-modifiable = male sex, postmenopausal female, and history of heart disease ii. Modifiable = smoking, high LDL, diabetes, elevated adrenaline (catecholamines), obesity, inactivity, lack of sleep, and hypertension IV. Atherosclerosis = the abnormal accumulation of lipid deposits and fibrous tissue within arterial walls and lumen a. In coronary atherosclerosis r/t CAD, blockages and narrowing of the coronary vessels reduce blood flow to myocardium; myocardial ischemia leads to necrosis if not treated V. Parkinson’s disease a. Clinical manifestations i. Cardinal = tremor, rigidity, bradykinesia/akinesia, postural instability  ii. Autonomic = sweating, drooling, flushing, orthostatic hypotension, gastric and urinary retention iii. Dysphagia – risk for aspiration pneumonia iv. Psychiatric changes = depression, anxiety, dementia, delirium, hallucinations b. Patho = slow, progressive neurologic movement disorder associated with decreased levels of dopamine; due to degeneration of storage cells in the substantia nigra in the basal ganglia VI. Peptic Ulcers a. Pathophysiology = erosion of mucous membrane due to an increased concentration of pepsin forms an excavation in the stomach, pylorus, duodenum, or esophagus; consists of both gastric and duodenal ulcers as mucosa can’t secrete enough mucous to act as a barrier --> mucosa then exposed to HCl and other irritating agents --> inflammation --> injury --> erosion b. Organisms that can cause PUD = H. pylori and chronic use of NSAIDs VII. Gout – inflammatory arthritis a. Patho = hyperuricemia causing urate crystal deposition and as they precipitate initiate an inflammatory response b. Clinical manifestations = accumulation of urate crystals called tophi, intense joint pain, tenderness, redness, warmth, and swelling VIII. Arterial blood gasses a. Respiratory acidosis = pH lower than 7.35 and CO2 more than 45 b. Respiratory alkalosis = pH greater than 7.45 and CO2 less than 35 c. Metabolic acidosis = pH lower than 7.35 – mostly seen in DKA d. Metabolic alkalosis = pH greater than 7.45 - hypokalemia IX. Pneumonia a. Clinical manifestations i. Pneumococcal = fever, chills, pleuritic chest pain, coughing, increase respiratory rate, and shortness of breath ii. Upper respiratory = congestion, sore throat, gradual and nonspecific HA, low grade fever, pleuritic chest pain, SOB, want to sit up, fatigue, purulent sputum b. Patho = alveoli develop an inflammatory reaction and exudates which interfere with diffusion of oxygen and CO2 as WBC migrate into alveoli; V/Q mismatch as ventilation is impaired eventually leading to arterial hypoxemia c. Labs/Diagnostics = chest X ray, blood culture, sputum culture d. Modifiable/non-modifiable Risk factors i. Conditions with mucus ii. Immunosuppression iii. Smoking iv. Immobility v. ETOH use vi. Age X. COPD – chronic obstructive pulmonary disease  a. Pathophysiology = progressive airflow limitation associated with an abnormal inflammatory response of the lungs to noxious particles or gasses i. Emphysema = loss of lung elasticity due to hyperinflation of alveoli and as alveoli collapse respiratory acidosis takes place due to CO2 not being able to be exhaled and O2 not inhaled ii. Chronic bronchitis = inflammation of the bronchi and bronchioles causing an increase in mucus cells producing a large amount of thick mucus; walls of bronchus hypertrophy causing narrowing of the airways and eventually obstruction that can lead to pulmonary HTN b. Clinical manifestations = chronic cough, sputum production, dyspnea on exertion, barrel chest, and clubbing c. Labs/Diagnostic tests = pulmonary function test (only way to diagnose COPD), chest X-ray to rule out other dx, and ABGs XI. Cirrhosis a. Clinical Manifestations = liver enlargement, portal obstruction, ascites, infection and peritonitis, varices, GI varices, edema, vitamin deficiency, anemia, mental deterioration b. Patho = excessive alcohol intake but can occur in people who do not consume any ETOH; ETOH cirrhosis is episodes of necrosis of the liver cells being replaced by scar tissue and as time goes there is more scar tissue than healthy tissue c. Hepatic encephalopathy i. Early signs = mental changes and motor disturbances ii. Hepatic insufficiency = inability of liver to detoxify toxic by-products of metabolism such as ammonia iii. Portosystemic shunting = collateral vessels develop element of the portal blood (laden with toxic substances) to enter systemic circulation d. Portal hypertension i. Patho = obstructed blood flow through the liver results in increased pressure throughout portal venous system ii. Results in ascites (fluid in abdomen causing constipation, pushing up on diaphragm, striae, difficulty walking) and esophageal varices e. Esophageal varices i. Clinical manifestations = hematemesis, melena, general deterioration, and shock ii. Patients with cirrhosis should undergo screening endoscopy q2-3 years, if they rupture could lead to aspiration increasing risk for apnea/infection XII. Crohn’s Disease a. Patho = transmural skip lesions that cause deep ulcerations between layers of edematous tissue creating a cobblestone appearance; with each exacerbation the intestines become more scarred which then leads to less ability to absorb nutrients – fistulas which are tracts b/w 2 or more body areas may develop b. Clinical manifestations = soft or semiliquid stool, nutritional deficiency, electrolyte imbalances, abdominal pain in RLQ  c. Area = anywhere in GI tract from mouth to anus but mostly in descending ileum and sigmoid colon XIII. Diverticulitis a. Patho = infection and inflammation of diverticula typically outside of the colon and is often referred to as outpouching; when food becomes entrapped in diverticula, it mixes with normal bacterial flora leading to a decreased blood supply that forms a mass called a fecalith or dried, hard, concrete-like stool b. Clinical manifestations = abdominal pain typically over sigmoid colon, fever or leukocytosis, flatulence, anorexia, abdominal bloating/distention, diarrhea, constipation, stool may contain mucus or blood i. In older patients they may present with a change in mental status, increased confusion, falling, and anorexia XIV. Diverticulosis a. Patho = multiple diverticula without inflammation b. Clinical manifestations = asymptomatic and might not even know they have it c. Diet recommendations = increase dietary fiber from raw fruits and veggies XV. Myasthenia Gravis – voluntary muscle weakness a. Clinical manifestations = initially symptoms involve ocular muscles; diplopia and ptosis – weakness of facial muscles, swallowing and voice impairment (dysphonia), generalized weakness b. Patho = antibodies directed at ACh at the myoneural junction impair transmission of impulses XVI. Peripheral arterial disease (PAD) a. Patho = progressive and chronic condition where the obstruction of blood flow through the large peripheral arteries cause a partial or total occlusion caused by a combination of atherosclerosis, inflammation, stenosis, embolus, and thrombus b. Priority clinical manifestations = reduced BP in ankle and intermittent claudication during exercise (relieved with rest) is expected but we want to monitor for signs of impaired circulation especially in the lower extremity such as blood clots XVII. Deep vein thrombosis (DVT) – blood clot in large vein usually in leg or pelvis a. Clinical manifestations = pain, swelling, tenderness, discoloration, redness (erythema), and warmth b. Risk factors = Virchow’s triad – stasis, vessel wall injury, hypercoagulability i. Injury, surgery, CVC, prolonged bedrest, pregnancy, age, cancer, chemotherapy, varicose veins, prior venous thrombosis, postpartum period, oral contraceptives, hormone therapy, immobility XVIII. Heart failure a. Clinical manifestations = signs r/t fluid overload or inadequate tissue perfusion b. Diagnostics = cardiac biomarkers such as troponin and CK, serum electrolytes, fasting lipid profile, LFT, and renal function tests; decreased Hgb and Hct c. Diet recommendation = low sodium to decrease circulatory blood volume  d. Patho = structural or functional cardiac disorder that impair the ability of the ventricles to fill or eject blood; problem with the contraction of the heart (systolic failure) or filling of the heart (diastolic failure) e. New York Heart Association Classification of Functional Status i. No symptoms with physical activity ii. Mild symptoms with ordinary activities iii. Marked limitation with physical activity but comfortable at rest iv. Severe limitation and distress with physical activity or rest f. Left sided i. Pulmonary congestion, crackles ii. S3 or “ventricular gallop” iii. Dyspnea on exertion (DOE) iv. Low O2 saturation v. Dry, nonproductive cough initially vi. Oliguria g. Right sided i. Viscera and peripheral congestion ii. Jugular vein distention iii. Dependent edema iv. Hepatomegaly v. Ascites vi. Weight gain XIX. Ulcerative colitis a. Clinical Manifestations = diarrhea with more than 20 stools per day, loss of fluid, blood, mucus, pus, pain and tenderness in LLQ, nutritional deficiency due to scar tissue; patients may manifest tenesmus which involves spasm of the anal sphincter and persistent desire to empty the bowel i. Crypt abscess = releases purulent discharge from the bowel mucosa b. Patho = inflammation affecting large intestine from rectum spreading upward to cecum; involves only mucosa and submucosa XX. Cholecystitis a. Patho = acute or chronic inflammation of the gallbladder caused by an obstruction of bile flow mostly by calculous cholecystitis (presence of gallstones); as blood vessels become compressed vascular supply is compromised allowing for gangrene with risk of perforation b. Most common bacteria = E. coli, klebsiella, streptococcus c. Clinical manifestations = pain, tenderness, rigidity of RUQ that can radiate to midsternal or right shoulder XXI. Rheumatoid Arthritis a. Clinical manifestations i. Local = joint pain, swelling, warmth, erythema, and decreased function; tends to self-immobilize and lead to contractures ii. Systemic = fever, weight loss, fatigue, anemia, lymph node enlargement, Raynaud’s phenomenon  b. Patho = chronic autoimmune inflammation and degeneration in synovial tissue generated by phagocytosis; enzymes in joint breakdown collagen cause edema-> proliferation of synovial membrane and pannus formation->pannus destroys cartilage and erodes to bone->lose joint motion, muscle degenerates, tendon and ligaments lose elasticity c. Diagnostics = rheumatoid factor present in 75% of cases, elevated ESR, RBC and C4 component decreased, C reactive protein and ANA may be positive, arthrocentesis cloudy milky or dark yellow synovial fluid i. X-rays = narrowed joint spaces and bony erosions XXII. Osteomyelitis a. Diagnostics = early x-rays, bone scans, MRI, leukocytosis, WBC, elevated ESR, wound and blood cultures b. Patho = infection typically due to MRSA that causes inflammation, increased vascularity, and edema leading to the thrombosis of vessels and eventually ischemia and bone necrosis i. If not treated, bone abscess can form, resulting in chronic osteomyelitis c. Clinical manifestations i. Systemic = sepsis – chills, fever, rapid pulse ii. Local = painful, swollen, extremely tender, pulsating pain, increases with movement iii. Chronic osteomyelitis = nonhealing ulcer, intermittent drainage of pus XXIII. Osteoporosis a. Patho = rate of osteoclasts greater than osteoblasts causing reduced bone mass, deterioration of bone matrix, and diminished bone architectural strength; bones become progressively porous, brittle, and fragile b. Clinical manifestations = bones fracture easily under stress; occur most commonly as compression fractures of the thoracic and lumbar spine, hip fractures, and Colles fractures of the wrist; deformities such as kyphosis and a protruding abdomen can occur producing pulmonary insufficiency and increasing risk for falls r/t balance issues c. Prevention = balanced diet high in calcium and vitamin D; use of calcium supplements to ensure adequate calcium intake, regular weight bearing exercises 20-30 mins/day to stimulate bone mineral density (BMD) d. Remember high risk of fractures i. Calcitonin = promotes bone formation; is decreased ii. Estrogen = inhibits bone breakdown; also decreases iii. PTH = increases bone turnover and resorption; production increases with aging XXIV. Neurotransmitters a. Acetylcholine = usually excitatory; parasympathetic stimulation of heart by vagal nerve b. Dopamine = usually inhibitory in substantia nigra and basal ganglia; affects behavior, attention, emotions, and fine movement  c. Norepinephrine = usually excitatory; sympathetic nervous system affects mood and overall activity XXV. Normal and abnormal lab values a. Sodium = 135-145 b. Potassium = 3.5-5.3 c. WBC = 4.5-11.1 d. Hgb i. Females = 11.7-15.5 ii. Males = 14-17.3 e. Hct i. Females = 36%-48% ii. Males = 42%-52% f. BUN = 8-21 g. Creat = 0.5-1.2 h. pH = 7.35-7.45 i. Co2 = 35-45 j. HC03 = 22-26 i. Less than 22 = acidosis ii. More than 26 = alkalosis k. TSH = 0.4-4.5 XXVI. Stages of CKD a. Normal GFR = 125 b. Stage 1 = GFR less than or equal to 90 c. Stage 2 = GFR 60-89 d. Stage 3 = GFR 30-59 e. Stage 4 = GFR 15-29 f. Stage 5 (end stage) = GFR less than 15 i. Clinical manifestation of CKD = increased serum creatinine, anemia, fluid retention (edema, CHF, ascites), and hypertension XXVII. Hypothyroidism a. Lab value trends = TSH high (more than 4.5) while T3 and T4 are low b. Clinical manifestations = decreased energy, increased sleep, fatigue, weight gain, decreased appetite, susceptibility to cold temps, hair loss, brittle nails, dry skin, voice changes, depression, lethargy, flat affect, myxedema coma c. Patho = characterized by thyroid deficiency caused by autoimmune disease known as Hashimoto’s, thyroid surgery, or radioactive iodine to treat hyperthyroidism XXVIII. Hyperthyroidism a. Lab value trends = TSH low (less than 0.4) while T3 and T4 are high b. Clinical manifestations = = exophthalmos, goiter, nervousness, rapid pulse, heat intolerance, tremors, flushed skin, warm soft, and moist, increased appetite, weight loss, elevated systolic BP, cardiac dysrhythmias  c. Patho = autoimmune disorder involving antibodies that bind to the thyroid gland resulting in the enlargement of the thyroid gland and hypersecretion of thyroid hormone XXIX. Chvostek = spasm of the facial muscle produced by sharply tapping over the facial in front of the parotid gland and anterior to the ear, suggestive of latent tetany in patients with hypocalcemia XXX. Trousseau = carpopedal spasm induced when blood flow to the arm is occluded using a BP cuff or tourniquet, causing ischemia to the distal nerves, suggestive sign for latent tetany in patients with hypocalcemia XXXI. Grave’s disease a. Patho = autoimmune disorder that causes hypersecretion of thyroid hormone b. Complication = thyroid storm causing hypermetabolic state XXXII. Renal calculi – consists of urolithiasis and nephrolithiasis a. Patho = calcium oxalate, calcium phosphate, uric acid, supersaturation, hypercalcemia, dehydration, medications b. Clinical manifestations = deep ache costovertebral region, hematuria, pyuria (elevated WBC in urine), radiating pain, N/V, diarrhea, ureteral colic c. Prevention strategies = increase fluid intake to 2.5-3 L daily, low sodium diet to prevent dehydration, pair food high in oxalate such as rhubarb, chocolate, tea, coffee, and nuts with calcium rich foods so they can bind together and be absorbed in the bloodstream instead of being deposited in the kidney XXXIII. Fluid volume deficits (FVD) - hypovolemia a. Clinical manifestations = weight loss, HR increases, BP decreases, decreased skin turgor, decreased urine output, increased urine specific gravity b. Causes = excessive loss of fluids, insufficient intake of fluid, or fluid shifts such as vomiting, diarrhea, and NG suction; additional causes include hemorrhage, DI, DKA, and adrenal insufficiency c. Third space fluid shifts = occurs when fluid leaves the vascular space and enters the space between cells becoming unavailable to support normal physiological activities; as fluid shifts into interstitial space, circulating blood volume decreases, resulting in a decrease in blood flow to the organs of the body i. Often seen in trauma, burns, cirrhosis, or right sided CHF XXXIV. Fluid volume excess (FVE) - hypervolemia a. Clinical manifestations = weight gain, increased HR and BP, crackles or wheezing, increased skin turgor, dependent edema, possible JVD, normal to low urine output, decreased urine specific gravity b. Causes = disease processes or conditions that result in retention of sodium and water such as cirrhosis, CHF, release of ADH and aldosterone, adrenal gland disorders, and use of corticosteroids; patients receiving sodium-containing fluids or salt in excessive amounts are also at risk XXXV. Functions of the kidney a. Urine formation b. Excretion of waste products c. Regulation of electrolytes  d. Regulation of acid-base balance e. Control of water balance f. Control of blood pressure g. Renal clearance h. Regulation of RBC production i. Synthesis of vitamin D to active form j. Secretion of prostaglandins XXXVI. Functions of: a. Insulin – secreted from beta cells in the islets of Langerhans in pancreas i. Transports and metabolizes glucose for energy ii. Stimulates storage of glucose in the liver and muscle iii. Signals the liver to stop the release of glucose iv. Enhances storage of dietary fat in adipose tissue v. Accelerates transport of amino acids into cells vi. Inhibits the breakdown of stored glucose, protein, and fat b. ADH (vasopressin) = increases water reabsorption by kidney c. Erythropoietin = protein produced in kidneys necessary for RBC production; in CKD erythropoietin is decreased causing anemia XXXVII. Cushing’s Disease a. Patho = overproduction of ACTH or corticosteroid medication causes an arrest of growth, obesity, musculoskeletal changes, along with glucose intolerance; excessive protein catabolism occurs producing muscle wasting and osteoporosis b. Clinical manifestations = muscle wasting, osteoporosis, kyphosis, backache, compression fractures of vertebrae, retention of sodium and water leading to HTN and CHF, possible development of hyperglycemia/overt diabetes i. Virilization often occurs where females take on masculine traits