Traumatic Brain Injuries: Types, Mechanisms, Diagnosis, and Complications, Exams of Nursing

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NUR 2063 Module 7, 8, 9 Focused Review Exam Questions and Answers 2024 • Brain abscess s/s (infection, pus) Signs of infectious etiology, localized collection of pus -Stiff neck, headache, intracranial pressure, change in LOC, vision/speech/behavior changes • Priority assessments ABC’s (airway, breathing/respiratory, circulation/cardiovascular), level of consciousness • Glascow coma scale Used to assess LOC in acutely brain-injured patients, eye opening/arousal-directed responses/motor reactions, under 8 is severe, over 12 is mild • Mechanisms of spinal cord injuries Hyperflexion (forward), hyperextension (backward), compression • Decorticate vs decerebrate posturing Decorticate=abnormal flexor (arms/hands up on chest), decerebrate=abnormal extension (arms/hands at sides) • Meningitis (S.P. bacteria in CNS) -Bacteria usually reach the CNS via the bloodstream or extension from cranial structures like sinuses or ears. -Most common bacteria are Streptococcus pneumoniae. -Bacteria invade leptomeninges; accumulation of inflammatory exudate can result in obstructive hydrocephalus (excess fluid in head). -Classic presentations: headache, fever, stiff neck (meningismus), and signs of cerebral dysfunction (confusion, delirium) • Types of traumatic brain injuries LOCATION: Primary=focal (coup), polar (coup countercoup)(acceleration/deceleration, injury to polar sides), diffuse (widespread) MECHANISM: Concussion, contusion, intracranial hematomas=epidural, subdural, subarachnoid SEVERITY: Secondary Injury=ischemia (decreased blood flow), hypoxic events (decreased blood oxygenation), vasogenic/neurogenic edema • Focal (coup) brain injuries -Localized to site of impact -Decreased LOC, muscle weakness, cranial nerve dysfunction • Difference between hemorrhagic stroke and thrombotic/embolic stroke (ischemic) as well as diagnosis -Ischemic strokes result from sudden occlusion of a cerebral artery secondary to thrombus formation or embolization -Thrombotic strokes associated with atherosclerosis and coagulopathies- clot traveled to brain -Hemorrhage within the brain parenchyma , usually occurs secondary to severe, chronic hypertension (secondary injury, morbidity much higher) -CT, MRI, LOC • Increased intracranial pressure s/s -Headache, vomiting, and altered level of consciousness (drowsiness) -Blurry vision and edema of the optic disk (papilledema) -As ICP rises to higher levels, LOC decreases, pupil responsiveness to light becomes impaired; altered respiratory patterns and unresponsive to stimulation; unable to move, verbalize, or open the eyes • Activities that cause traumatic brain injuries Transportation-related accidents, falls, firearms, sports-related accidents • Differences between subarachnoid hemorrhage, epidural hematoma, subdural hematoma Subarachnoid: (berry aneurysm/circle of willis/thunderclap) -Collection of blood between arachnoid membrane and the pia mater -Caused by rupture of bridging veins that pass through the subarachnoid space -More commonly associated with rupture of cerebral aneurysms or arteriovenous malformations; arterial in origin -Blood spreads throughout CSF, causing meningeal irritation, hydrocephalus, headache, vasospasms, ischemia Epidural: (lens/arteries/trauma/lucid interval before rapid deterioration) o Avoid triggers o Environmental control -Pupillary responses for CN II and III. Eye movements controlled by CN III, IV, and VI may be impacted by increased ICPs • Spina Bifida (folic acid, protrusion of neural tube) -Developmental anomaly characterized by defective closure of the bony encasement of the spinal cord (neural tube) through which the spinal cord and meninges may or may not protrude -Etiology: environmental factors (especially lack of folate/folic acid) and genetics -Clinical manifestations: saclike cyst filled with CSF, spinal cord, and/or meninges; permanent neurologic damage resulting in motor weakness or paralysis and sensory deficit below the level of the spinal defect • ALS s/s (weakness/wasting/atrophied extremities, upper first) -Weakness and wasting of the upper extremities usually occur first, followed by impaired speech, swallowing, and breathing -Clinical manifestations: weakness, atrophy, cramps, stiffness, irregular twitching of muscles, hyperreflexia in weak, atrophied extremity (highly suggestive) • How to reduce risk of stroke -Manage hypertension, DM, hyperlipidemia, smoking • Status epilepticus -Continuing series of seizures without a period of recovery between episodes; can be life- threatening and cause brain damage • Pulmonary embolism (high right side BP, from veins, SOB sudden, ABG values decline, Virchow’s) -Pulmonary embolism results in elevated right-sided heart pressures, but left-sided pressures remain normal to low. Pulmonary emboli are usually generated in the veins of the lower extremities in patients with immobility, trauma, or hypercoagulable states. Pulmonary embolism is manifested as sudden, severe dyspnea and deteriorating arterial blood gas values. -DVT, embolic strokes associated with atrial fibrillation/cardiac dysfunction -Virchow’s triad are factors predisposing clients to thrombus formation and include: 1) venous stasis; 2) hypercoagulability; and 3) damage to the vessel wall. -Presentation of symptoms include restlessness, apprehension, anxiety, dyspnea, tachycardia and tachypnea. Pain is also noted in a majority of clients. If untreated, the client may experience heart failure, shock and respiratory arrest. • Treatment of asthma ▪ Dust control, removal of allergens, air purifiers, air conditioners o Preventive therapy ▪ Stop smoking, avoid second-hand smoke, aerosols, odors, early treatment for respiratory infections o Desensitization (allergen specific immunotherapy) o Medications ▪ O2 therapy, small-volume nebulizers, B2 agonists, corticosteroids, leukotriene modifiers, mast cell inhibitors o For status asthmaticus (severe attack unresponsive to routine therapy) ▪ Epinephrine, subcutaneous terbutaline, aminophylline, intravenous corticosteroids (mainstay of therapy); oxygen therapy with or without mechanical ventilation • Choking (Acute tracheobronchial obstruction) -Complete or partial -Heimlich • Bronchitis s/s Acute: usually mild and self-limiting, cough (productive or nonproductive), low-grade fever, substernal chest discomfort, sore throat, postnasal drip, fatigue Chronic: typical patient is overweight, associated with emphysema, SOB on exertion, excessive sputum, chronic cough (more severe in morning), edema, hypervolemia, cyanosis • Polycythemia Vera (liver + spleen congestion, increase in all cells) -Neoplastic transformation of bone marrow stem cells -Absolute increase in RBC mass, leukocytosis, thrombocytosis; increased uric acid because of excess proliferation; oxygen saturation normal. -The liver and spleen become congested, which increases the risk of clots, acidosis, and organ infarction, anemia, and acute myeloid leukemia • Cor pulmonale (right-sided heart enlargement) causes -Lung disorders: pulmonary hypertension, COPD, emboli, cystic fibrosis, sleep apnea, pulmonary diseases that increase right ventricular afterload -Condition that occurs when the right ventricle hypertrophies, systolic ejection click • Adult acute respiratory distress syndrome s/s -History of a precipitating event that has led to a low blood volume state (“shock” state) 1 or 2 days prior to the onset of respiratory failure o Early ▪ Sudden marked respiratory distress ▪ Slight increase in pulse rate ▪ Dyspnea ▪ Low PaO2 ▪ Shallow, rapid breathing o Late ▪ Tachycardia ▪ Tachypnea ▪ Hypotension ▪ Marked restlessness ▪ Frothy secretions ▪ Crackles, rhonchi on auscultation ▪ Use of accessory muscles ▪ Intercostal and sternal retractions ▪ Cyanosis • Pleural effusion (pleural cavity pus/fluid, decreased percussion + tactile fremitus) -Pathologic collection of fluid or pus in pleural cavity as a result of another disease process -Clinical manifestations o Vary depending on cause and size of effusion o May be asymptomatic with <290 mL of fluid in pleural cavity o Dyspnea (SOB) o Decreased chest wall movement o Pleuritic pain (sharp, worsens with inspiration) o Dry cough o Absence of breath sounds o Dullness to percussion (primary finding) o Decreased tactile fremitus over affected area (primary finding) • Extrinsic vs intrinsic asthma o Intrinsic: non-allergic, adult onset o Extrinsic: allergic, pediatric onset • Purpose of hemoglobin -Oxygen transport protein in RBCs • Surfactant and prematurity (IRDS, before 30 weeks, lung inflation difficulty) IRDS: needs surfactant (lowers surface tension in the lungs/makes lungs more difficult to inflate),less than 30 weeks at higher risk • Complete blood count -RBCs, WBCs, and platelets -detects anemia, infection, leukemia • DIC (Disseminated Intravascular Coagulation)(bleeding + clotting, shock risk) -Acquired hemorrhagic syndrome in which clotting and bleeding occur simultaneously -Causes may include: trauma, malignancy, burns, shock, and abruptio placentae -Widespread clot formation in small vessels; clotting factors and platelets consumed resulting in excessive bleeding, hemorrhagic shock • Sickle cell crisis patho, how to prevent (stem cell transplant) (C.H.I. F.A.D.) -Major medical event, complication can be hemolytic or vascular -Treatment of choice is stem cell transplant (cures), death if no/unsuccessful transplant -Prevent dehydration, infection, fever, acidosis, hypoxemia, and cold exposure • Initial symptoms of malignancies o Malaise, weakness o Unexplained fever, night sweats o Recurrent infections o Enlarged, nontender lymph nodes (lymphadenopathy) with lymphoma and some leukemias o Very high total white blood cell count or the presence of abnormal cell types • Absolute anemia -Actual decrease in numbers of red cells o Decreased production o Increased destruction • Anemia -Deficit of red blood cells, low oxygen-carrying capacity leads to hypoxia (deficient tissue O2) • Thrombocytopenia (decreased platelets, bleeding) -Prone to bleeding, deficient number of circulating platelets • Chronic Myeloid Leukemia (Philadelphia, BCR/ABL, splenomegaly, poor survival) -Characterized by malignant granulocytes that carry the Philadelphia chromosome (Ph+), fusion protein (bcr/abl) -High granulocyte count on CBCs and splenomegaly -Does not respond well to chemotherapy, poor overall survival • aPTT (activated partial thromboplastin time) -Assesses the intrinsic/coagulation pathway -clot formation time using activator • Jaundice -Yellowing of skin due to high bilirubin levels found in RBCs • Hodgkin’s disease (malignant, lymph nodes, Reed-Sternberg, B cells, predictable) -Malignant disorder of the lymph nodes o Characterized by Reed–Sternberg cells o Originate from B cells in germinal centers of lymph nodes ▪ Malignant but grow/spread in predictable way; sets HD apart from other lymphomas, usually metastasizes along contiguous lymphatic pathways -A: absence of clinical symptoms -B: symptoms present at time of staging o Loss of more than 10% body weight o Unexplained fevers o Night sweats • Erythropoietin (erythrocyte production hormone, kidneys) -Hormone from kidneys that stimulates erythrocyte production • Hematemesis -vomiting of blood -associated with bleeding in upper GI • Allogenic transplants -Stem cells from closely matched relative • Multiple Myeloma (adults 40+, malignant, Bence-Jones, hypercalcemia, bone lesions) -Malignant disorder of mature, antibody-secreting B lymphocytes (plasma cells) -Occurs exclusively in adults; usually >40 years; median age 65 years, men > women -Malignant plasma cells invade bone and form multiple tumor sites -May also target other tissues, including lymph nodes, liver, spleen, and kidneys -Bence Jones protein: confirms diagnosis, accumulates in kidneys and damage them -Hypercalcemia, bone lesions (most clinical manifestation caused by bone/renal damage) • Neutropenia (low neutrophils, infections, bacterial sepsis) -Prone to infections, low neutrophil count, type of leukopenia, high risk of bacterial sepsis • Erythrocytes and their function -Transport oxygen to tissues and removes carbon dioxide/waste from tissues, balance/buffer blood pH -gas transport to/from tissue cells and lungs • Plasma proteins (F.A.G., blood volume/fluid/pressure regulation) -Albumin, globulin, fibrinogen -Blood clotting factors=proteins in inactive state -Regulates blood volume, fluid balance, and colloid osmotic pressure