NUR 2063 Pathophysiology Exam 3 Review Complete & Latest Update

NUR 2063 Pathophysiology Exam 3 Review Complete Primary Brain Injury: occurs as a direct result of the initial insult Secondary Brain Injury: progressive damage resulting from the body’s physiological response to the initial insult Reperfusion Injury: occurs when blood flow is reintroduced to previously ischemic but viable cells. Free radicals are generated, which damage cell structures. Inflammatory cells are recruited to the area and may increase edema, blood vessels, and contribute to free radical production. Intracranial Pressure: pressure exerted by the contents of the cranium, and it normally ranges from 0-15mm Hg. Elevated ICP may occur in most types of acute brain injury, and is associated with impaired neurologic function attributable to compression of brain structures. The volume of the cranium is made up of three components: brain tissue, cerebrospinal fluid (CSF), and blood. Causes of Increased ICP: stroke, trauma, tumors, hemorrhage, infection, ischemia, necrosis, edema, but many other primary and secondary disorders can cause significant elevations in ICP. They all affect the volume of CSF, blood, or brain tissue. An increase in brain tissue volume commonly occurs from conditions that cause cerebral edema. Edema of brain tissues is due to accumulation of fluid in interstitial or intracellular spaces. Signs of Increased ICP: Manifestations of elevated ICP include headache, vomiting, and altered level of consciousness (drowsiness), blurry vision, edema of optic disk (papilledema). As ICP rises to higher levels, the level of sciousness decreases and pupil responsiveness to light becomes impaired. Prolonged elevations of ICP are thought to damage brain structures by compressing the blood supply and causing ischemia. Glasgow Coma Scale: used to assess LOC with greater reliability among different observers in acutely brain-injured patients. [Eye Opening] 4- spontaneously 3- to speech 2- to pain 1- never [Verbal Response] 5- oriented 4- confused speech 3- inappropriate 2- incomprehensible sounds 1- none [Motor Response] 6- obeys commands 5- localizes pain 4- withdrawal 3- abnormal flexion 2- extension 1- none Ischemic Stroke: associated with atherosclerosis Hemorrhagic Stroke: major risk factor is HTN ⇒A stroke is a term applied to cerebrovascular events that result in a localized area of CNS infarction and was previously termed cerebrovascular accident (CVA). The term brain attack has been popularized to educate the public. The symptoms of stroke usually are sudden in onset and may include the following: 1) numbness or weakness of the face, arm, or leg, especially affecting only one side of the body, 2) confusion, trouble in speaking or in understanding others, 3) visual disturbances in one of both eyes 4) dizziness, loss of balance, and difficulty walking and 5) severe headache. Meningitis: most common sequela to microbial invasion of the CNS. Most frequently it is bacterial in origin, but it can also be viral or fungal. Encephalitis: inflammation of the brain caused by a variety of agents including viruses, bacteria, fungi, and parasites. Seizure Disorder: seizures are a transient neurologic event of paroxysmal abnormal or excessive cortical electrical discharges that are manifested by disturbances of skeletal motor function, sensation, autonomic visceral function, behavior, or consciousness. Seizures are diagnosed by an EEG, neuro exam, physical and pt’s hx. Generalized seizures [entire brain surface is affected] absence (petit mal), atypical absence, atonic (drop attack), clonic, tonic, generalized tonic-clonic (grand mal) Partial seizures [part of brain surface is affected] simple partial (no impairment of consciousness during seizure), complex partial (impairment of consciousness during seizure), with secondary generalization (onset begins as simple partial and then progresses to impairment of consciousness) Cerebral palsy: refers to a diverse group of crippling syndromes that appears during childhood and involves permanent, nonprogressive damage to the developing brain. Damage occurs in the upper motor neurons that control voluntary and involuntary muscle movement. Etiologic factors include prenatal infections or diseases of the mother; mechanical trauma to the head before, during, or after birth; or exposure to nerve-damaging poisons or a period of reduced oxygen supply to the brain. S/S Anaphylactic Shock: Bronchoconstriction, peripheral dilation increased capillary permeability Coronary Arteries: supply oxygenated blood to the myocardium Cardiogenic Shock: caused by severe ventricular dysfunction Kidney Cells: secrete renin to increase blood pressure when arterial pressure declines Left-sided Heart Failure: manifestations include dyspnea Malignancies of blood-forming tissues: include non-specific or no symptoms Arterial Blood Gas (ABG): PaCO2= Partial pressure of carbon dioxide in arterial blood, Normal PaCO2 is 35–45 mm Hg; PaO2= Partial pressure of oxygen in arterial blood, Normal PaO2 is 80–100 mm Hg; Ex: pH 7.4, PaCO2 40, PaO2 90, HCO3 24 Complication with anemia: tissue hypoxia; restore tissue oxygenation Tension Pneumothorax: develops when the air in the pleural space begins to exert a positive pressure on lung and mediastinal structures. A deviated trachea and decreased or absent breath sounds may occur. Arterial blood gas values can deteriorate rapidly. Tension pneumothorax is detectable by chest radiography. Hypoventilation: symptoms from increased carbon dioxide in the alveoli Metabolic acidosis: respiratory compensation is hyperventilation. condition that tends to cause a relative excess of any acid except carbonic acid Respiratory acidosis: is a condition that tends to cause an excess of carbonic acid; caused by factors that impair the respiratory excretion of carbonic acid. Carbonic acid is excreted by the lungs in the form of carbon dioxide and water during exhalation; compensatory response to respiratory acidosis is increased renal excretion of metabolic acid Metabolic alkalosis: is a condition that tends to cause a relative deficit of any acid except carbonic acid. Metabolic alkalosis may be caused by an increase in base (bicarbonate), by a decrease in acid, or by a combination of the two. Compensatory response to metabolic alkalosis is hypoventilation Respiratory alkalosis: is a condition that tends to cause a carbonic acid deficit. caused by hyperventilation; too much carbonic acid is excreted 3.25% $ Exam 2 review Gastritis: inflammation of the lining of the stomach; caused by ingestion of toxins such as alcohol, aspirin, or other irritating substances or may occur as a consequence of viral, bacterial, or autoimmune illnesses; chronic gastritis is promoted by H. pylori, which is usually the result of a primary inflammatory disorder such as Crohn’s disease GERD: the backflow of gastric contents into the esophagus through LES (lower esophageal 0sphincter); is a function of a multifactorial process; it alters the closure strength and efficacy of the LES or increases intraabdominal pressure may predispose an individual to GERD; closure strength of LES may be adversely affected by the intake of fatty foods, caffeine, alcohol, cigarette smoking, sleep position, or obesity as well as certain medications including progesterone-containing birth control, narcotics, benzos, calcium channel blockers, and theophylline; manifestations include heartburn, regurgitation, chest pain, and dysphagia; untreated GERD causes complications such as esophageal strictures, Barrett esophagus, and pulmonary symptoms related to reflux esophagitis such as cough, asthma, and laryngitis Peptic Ulcer Disease: Refers to disorders of the upper GI tract caused by the action of HCL acid and pepsin. These disorders are characterized by injury to the mucosa of the esophagus, stomach, or duodenum and may range from a slight irritation to severe ulceration. The GI mucosa is continuously exposed to caustic substances, and mucosal health depends on a number of protective mechanisms. The presence of an intact gastric mucosal barrier and the ability of the mucosa to renew its epithelium serve to protect it against injury. On the other hand, the presence of hydrochloric acid, which potentiates the actions of pepsin and other injurious substances such as aspirin and NSAIDs, will promote injury to the mucosa. PUD thus is the result of an excess of factors that tend to injure the mucosa relative to factors that protect it. H. pylori has a key role in promoting both gastric and duodenal ulcer formation. Manifestations of PUD include epigastric burning pain that is usually relieved by the intake of food (especially dairy products or antacids.) Other symptoms may include nausea, abdominal upset (dyspepsia), and chest discomfort. A significant proportion of ulcers are asymptomatic, and life-threatening complications, such as GI bleeding, may occur in pts with no warning. Pseudomembranous Colitis: AKA Antibiotic-Associated Colitis; an acute inflammation and necrosis of the large intestine caused by Clostridium difficile, usually affecting the mucosa but sometimes extending to other layers. Exposure to abx is the major factor predisposing to the development of this disorder, and patients with cancer or who have undergone abdominal surgery are at particular risk. Crohn’s disease: AKA regional enteritis or granulomatous colitis is an inflammation of the GI tract that extends through all layers of the intestinal wall Example: abd pain in RLQ with a palpable mass, reflecting significant ileocecal involvement; bloody stool Cause: result primarily from a process in which the lymphoid and lymphatic structures of the GI tract become blocked. Subsequent engorgement and inflammation of surrounding tissue lead to the development of deep linear ulcers in the bowel wall. Eventually, all layers of the GI tract wall may become involved, and the portion of intestine that is affected may become thickened by fibrous scar tissue. Deep fissures may develop into fistulas, which may extend into adjacent tissue of other organs such as the bladder wall or even the skin. One of the cardinal features of Crohn disease on histopathologic analysis is granulas, which is generally diagnostic of this disorder. Ulcerative Colitis (UC): an inflammatory disease of the mucosa of the rectum and colon. Example: Manifestations of UC are the result of these processes and include abdominal pain, diarrhea, and rectal bleeding. Bleeding occurs as a result of mucosal destruction and ulceration, as well as damage to newly developed granulation tissue. Diarrhea is a result of the mucosal destruction in the colon, which leads to decreased ability of the bowel to absorb water and sodium and thus to an increased volume of fluid in the intestinal contents. Cause: begins as an inflammation at the base of the crypts of Lieberkuhn. Damage to the crypt epithelium results, with eventual invasion of leukocytes and the formation of abscesses in the crypts. When multiple abscesses form in close proximity and begin to coalesce, large areas of ulcerations develop in the epithelium. Celiac Disease: AKA celiac sprue is characterized by an intolerance of gluten, a protein in wheat and wheat products. Celiac sprue is an immune disorder triggered by exposure to gliadin (a specific wheat gluten) in genetically predisposed persons. Example:.intestinal biopsy to show typical pathologic manifestation, new blood tests that assay for anti-tissue transglutaminase antibody and the more specific immunoglobulin. Cause: Environmental, genetic, and immune factors play pivotal roles in determining the nature of symptoms. The main pathologic finding is villus atrophy, with a decrease in the activity and amount of surface epithelial enzymes. The resulting malabsorption of ingested nutrients may promote malnutrition and severe debilitation. Appendicitis: S&S: Manifestations include generalized periumbilical pain accompanied by nausea and occasionally, diarrhea. The pain is often described as migrating or localizing to the lower right abdomen (McBurney point) because of distention of the serosa from inflammatory edema, at which time fever usually manifests. Assessment: CT scan or U/S Bowel/Intestinal Obstruction: partial or complete blockage of the intestinal lumen of the small or large bowel. Mechanical obstructions are caused by blockage of the intestine by adhesions, hernia, tumor, inflammation, stricture (as in Crohn’s disease), impacted feces, volvulus, or intussusception. Functional obstruction or ileus refers to the loss of propulsive ability by the bowel and may occur after abdominal surgery or in association with hypokalemia, peritonitis, severe trauma, spinal fractures, ureteral distention, and the administration of medications such as narcotics. Ogilvie syndrome, also known as intestinal pseudo obstruction, is a rare severe motility problem characterized by recurrent bouts of ileus. Liver Disease: S&S: weakness, fatigue, anorexia, weight loss, muscle wasting (failure of multiple metabolic functions), fever (liver inflammation, decreased reticuloendothelial function with increased risk of infection), bruising, increased bleeding (thrombocytopenia secondary to splenic enlargement, decreased synthesis of clotting factors), palmar erythema, cutaneous spider telangiectases, irregular menses, gynecomastia, erectile dysfunction, female body hair distribution in men, testicular atrophy (altered metabolism of sex hormones, chronic debilitation), hepatic encephalopathy (abnormal protein metabolism), fetor heapticus (decreased detoxification), pruritis (decreased bile salt excretion), cyanosis (arteriovenous shunts in lungs, liver), jaundice (biliary obstruction, decreased bilirubin synthesis, decreased bilirubin excretion), hyperdynamic circulation, wide pulse pressure, tachycardia (generalized vasodilation possibly mediated), ascites, peripheral edema (portal hypertension, sodium and water retention, low serum albumin secondary to decreased hepatic synthesis), splenomegaly (portal hypertension), hepatomegaly (cirrhosis where liver may be small, hepatitis, vascular congestion, bile duct obstruction, infection, benign infiltrative disease like fatty liver, amyloidosis, or hemochromatosis, malignant infilrative disease like metastatic cancer, lymphoma, large space-occupying lesion such as neoplasm or abscess), varices (esophageal, gastric, rectal, ectopic) or abnormal abdominal vascular pattern (caput medusae, umbilical buit) (portal hypertension with collateral blood flow around hepatic blockage), osteomalacia, hypocalcemia, night blindness, coagulopathy (fat-soluble vitamin malabsorption and loss of fat-soluble vitamin reserves A, D & K, loss of vitamin K metabolism), anemia (multifactorial including blood loss, chronic disease, vitamin B12 deficiency, spenic sequestration), leukopenia (hypersplenism secondary to portal hypertension), hypoglycemia (altered glycogenolysis, gluconeogenesis), hyperglycemia (portosystemic shunting with delayed hepatic uptake of absorbed glucose), hypercholesterolemia (obstructive jaundice with decreased cholesterol excretion) Gallstones: Formation: depends on 3 factors: 1) supersaturation of bile with cholesterol, 2) nucleation of crystals and 3) hypomotility (stasis of bile within the gallbladder), allowing stone growth; absorption of water concentrates the bile resulting in sludging and increasing the risk of crystal formation and stones. Lecithin is an important component of bile that helps keep cholesterol from precipitation into crystals. Crystals of cholesterol may initiate gallstone formation. The relative concentrations of cholesterol, lecithin, and bile acids appear to determine the likelihood of