PATHOPHYSIOLOGY FINAL NUR 2063 FINAL EXAM TEST PP

PATHOPHYSIOLOGY FINAL NUR 2063 FINAL EXAM TEST PP Gastritis and Etiology and patho - CORRECT ANSWER-inflammation of stomach's mucolas lining (can involve entire stomach or region) can be acute or chronic. may be caused by h. pylori infection (imbeds in mucosal layer activating toxins and enzymes that cause inflammation. NSAIDS, chronic alcohol consumption, stress, trauma, burns, or infections, autoimmune conditions manifestations of gastritis - CORRECT ANSWER-indigestion, heartburn, epigastric pain, abdominal cramping, nausea, vomiting, anorexia, fever, malaise. hematemesis and dark, tarry stools indicate ulceration and bleeding. chronic gastritis increases risk for peptic ulcers, gastric cancer, anemia, and hemorrhage. gastritis diagnosis/treatment - CORRECT ANSWER-h&p, GI tract x ray, egd, serum h. pylori antibodies, h. pylori breath test, stool analysis (h. pylori and occult blood treatment-acute is self limiting ususally resolves meds-antacids, acid-reducing agents, and mucosal barrier agents other strategies include those for GERD (diet, small meals, antacids) Peptic ulcer disease (PUD) - CORRECT ANSWER-refers to erosive lesions affecting the muscularis mucosa of the stomach or duodenum. ulcers vary in size and severity, ranging from superficial erosions to complete penetration through GI tract wall peptic ulcer disease etiology and patho - CORRECT ANSWER-ETIOLOGY: most commonly H. pylori and NSAID use. PATHO: develops because of an imbalance between destructive forces and protective mechanisms PUD duodenal ulcers - CORRECT ANSWER-most commonly associated with excessive acid or H. pylori infections typically present with epigastric pain relieved in the presence of food PUD gastric ulcers - CORRECT ANSWER-less frequent-more deadly typically associated with malignancy and NSAIDS pain worsens with eating PUD Stress ulcers - CORRECT ANSWER-develop because of major physiological stressor on body due to local tissue ischemia, tissue acidosis, bile salts entering stomach, and decreased GI motility most frequently develop in stomach; multiple ulcers can form within hours of the precipitating event often hemorrhage is the first indication (vomiting blood or blood in stool) PUD manifestations/treatment - CORRECT ANSWER-epigastric, abd. pain, abd. cramping, heartburn, indigestion, chest pain, nausea/voimiting, melena (dark, tarry stools), fatigue, unexplained weight loss Treatment: same as gastritis: antacids, mucosal barrier agents, acid-reducing agents possible surgical repair Iron-deficiency Anemia - CORRECT ANSWER-Not enough iron for hemoglobin production erythrocytes pale and small Etiology: decreased iron consumption/absorption, increased bleeding manifestations in addition to "anemia": brittle nails, headache/irritability, pica, cyanosis of sclera of eyes, delayed healing Anemia - CORRECT ANSWER-common acquired or inherited disorder of erythrocytes that impairs the bloods oxygen-carrying capacity. ETIOLOGY: decrease in # of circulating erythrocytes, reduction in hemoglobin content, presence of abnormal hemoglobin MANIFESTATIONS: weakness, fatigue, pallor, syncope, dyspnea, tachycardia Pernicious anemia - CORRECT ANSWER-B12 deficiency or megaloblastic anemia large, immature erythrocytes. usually lack of intrinsic factor (protein necessary for b12 absorption in stomach) b12 is needed for cell division and maturity. too little b12 gradually causes neuro problems because of the breakdown in myelin, neuro effects may be seen before anemia is diagnosed. Additional manifestations: bleeding gums, diarrhea, impaired smell, DTR loss, anorexia, personality/memory changes, + babinski sign, stomatitis, paresthesia of hands and feet, unsteady gait aplastic anemia - CORRECT ANSWER-bone marrow fails to make enough blood cells leading to pancytopenia MANIFESTATIONS: general anemia, leukcytopenia, and recurrent infections can be caused by cancers, cancer treatment, pesticides Sickle cell anemia - CORRECT ANSWER-genetic, hemoglobin-s trait vs. gene crescent shape during times of hypoxia, can clump together and clog vessels. MANIFESTATIONS: swelling in hands and feet, sickle cell crisis, abd. pain, bone pain, jaundice, skin ulcers, stroke, chest pain tissue ischemia and necrosis. electrophoresis and stem cell transplant may cure thalassemia - CORRECT ANSWER-genetic, not RBC problem, hemoglobin problem. lack one or 2 proteins that make up hemoglobin MANIFESTATIONS: heart failure, splenomegaly, hepatomegaly, bone deformities, jaundice, fatigue, dyspnea Idiopathic thrombocytopenia purpura (ITP) - CORRECT ANSWER-hypocoagulopathy due to immune system destroying its own platelets (autoantibodies) Circulating IgG reacts with the platelets which are then destroyed in the spleen and liver. can be acute or chronic ETIOLOGY: idiopathic, autoimmune disease, live vaccines, immunodeficiency disorders, viral infections Manifestations: abnormal bleeding (petechiae, epistaxis [nose bleed], hematuria) ACUTE TREATMENT: glucocorticoid steroids, immunoglobulins, plasmapheresis and platelet pheresis CHRONIC TREATMENT: splenectomy, blood transfusions, immunosuppressants Thrombotic thrombocytopenia purpura - CORRECT ANSWER-coagulation disorter d/t deficiency of enzyme responsible for cleaving von Willebrand factor increased clotting which decreases available platelets --> bleeding under skin and purple colored spots called "purpura" manifestations: thrombi>thrombocytopenia>bleeding purpura, LOC changes, confusion, fatigue, fever Thrombocytopenia - CORRECT ANSWER-a condition in which there is an abnormally small number of platelets circulating in the blood hemostasis - CORRECT ANSWER-stoppage of bleeding 1. vasospasm (vasoconstriction)-brief reflex blood vessel narrows to decrease blood flow to injury and increase bp 2. platelet plug formation-involves activation, aggregation, and adherence of platelets into a plug that serves as a barrier against blood flowing out of vessel. 3 coagulation-or clotting changes blood into gel through cascade of events. fibrin mesh is cleaved from fibrinogen. fibrin acts like glue during clot formation holding the platelet plug together. Once blood flow is stopped tissue repair can begin parathyroid hormone (PTH) - CORRECT ANSWER-Works in opposite way to calcitonin to regulate serum calcium levels. PTH secreted with Ca levels drop. PTH increases osteoclast activity which releases Ca from bone. Also increases absorption of Ca in GI tract and kidneys. PTH also regulates phosphate levels by reducing renal reabsorption of phosphate in proximal tubule and increasing the uptake from the intestines and bones into blood hyperparathyroidism and etiology - CORRECT ANSWER-condition of excessive PTH production by parathyroid glands causes: tumors, hyperplasia, chronic hypocalcemia (renal failure) hyperparathyroidism manifestations/treatment - CORRECT ANSWER-osteoporosis, renal calculi, polyuria, abd. pain, constipation, fatigue, weakness, flaccid muscles, dysrhythmias, hypertension, depression, forgetfulness, Cushing's syndrome - CORRECT ANSWER-excessive cortisol that results from the increased ACTH levels Cushing's syndrome etiology - CORRECT ANSWER-iatrogenic from ingestion of glucocorticoid meds, adrenal tumors that secrete glucocorticoids, pituitary tumors that secrete ACTH and cortisol, and paraneoplastic syndrome (rare disorders triggered by abnormal immune response to a cancerous tumor called neoplasm) Cushing's syndrome treatment - CORRECT ANSWER-gradual tapering of any glucocorticoids tumors may need surgery and radiation meds to control cortisol production interventions to manage complications Cushing's manifestations - CORRECT ANSWER-moon face, obesity, buffalo hump, muscle weakness/wasting, delayed growth, acne, broad purple striae, thin bruisable skin, delayed healing, hyperpigmentation (due to ACTH), increased infections, osteoporosis, hirsutism (abnormail hair growth), glucose intolerance, hypertension, dyslipidemia, edema, hypokalemia, mood changes Growth Hormone (GH) - CORRECT ANSWER-stimulates cell growth and fat breakdown. primary targets are muscle and bone, where GH stimulates amino acid uptake and protein synthesis. Anterior Pituitary gland Type 1 diabetes mellitus, etiology - CORRECT ANSWER-develops when body's immune system destroys pancreatic beta cells. etiology-unknown, most likely viral or environmental trigger in genetically susceptible people. manifestations of diabetes mellitus - CORRECT ANSWER-polyuria, polydipsia, polyphagia hyperglycemia, glucosuria, weight loss, blurred vision, fatigue hypoglycemia manifestations - CORRECT ANSWER-weak, double or blurred vision, hunger, tachycardia, palpitations hyperglycemia manifestations - CORRECT ANSWER--urinary frequency, anorexia, dry mouth long term complications of diabetes mellitus - CORRECT ANSWER-hyperglycemia, DKA, hypoglycemia, heart disease, stroke, HTN, diabetic retinopathy, blindness, kidney disease, amputations, periodontal disease, preg complications, increase susceptibility to infections, erectile dysfunction. high blood glucose can harden vasculature Type 2 diabetes causes - CORRECT ANSWER-starts out as insulin resistance. ofter overweight treatment for diabetes mellitus - CORRECT ANSWER-Type 1 Insulin therapy Type 2 Lifestyle changes Oral drug therapy Insulin when the above no longer provide glycemic control Diabetes insipidus etiology - CORRECT ANSWER--almost half of the cases are idiopathic -The other half are usually attributed to head trauma resulting in damage to the pituitary gland or hypothalamus -Causes insufficient secretion of antidiuretic hormone (ADH) -This allows excessive water to be excreted by the kidneys Addisonian crisis/adrenal crisis - CORRECT ANSWER-onset of severe symptoms usually triggered by acute infection, trauma, surgery, or sodium loss. manifestations: profound fatigue, dehydration, vascular collapse (decreased BP), renal shut down, decreased serum Na, increased serum K Hyperthyroidism etiology - CORRECT ANSWER-excessive iodine, graves disease (autoimmune stimulates thyroid hormone production), thyroid tumors nonmalignant, goiter, inflammation, thyroid hormone replacement meds, high levesls of serum human chorionic gonadotropin