NUR 2063 / NUR2063 F Final Exam Focused Review (Latest 2022 / 2023): Essentials of Pathoph, Study Guides, Projects, Research of Nursing

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NUR 2063 Module 7, 8, 9 Focused Review • 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 -Oxygen re-enters cells, behave as free-radicals, mediates inflammation, compounds problem • Broca’s aphasia -(verbal motor/expressive) consists of poor articulation and sparse vocabulary • Guillain-Barre Syndrome (peripheral nerve demyelination, ascending paralysis) -Immunologic basis -Demyelination of peripheral nerves -History of recent viral or bacterial illness followed by ascending paralysis -Severe cases- respiratory muscle weakness accompanies limb and trunk symptoms. -Usually have full recovery • Multiple sclerosis patho (CNS demyelination, young adults) -Chronic demyelinating disease of the CNS that primarily affects young adults o Autoimmune disorder that results in inflammation and scarring (sclerosis) of myelin sheaths covering nerves; slowly progressive -Demyelination can occur throughout the CNS but often affects the optic and oculomotor nerves and spinal nerve tracts, slow/impair nerve conduction -Marked by exacerbations and remissions; exacerbated by heat, infection, trauma, stress • S/s of a concussion (mTBI) (no brain damage, LOC affected <30 minutes) -Alteration or LOC (<30 minutes) but no evidence of brain damage on CT -Headache, n/v, dizziness, fatigue, blurred vision, cognitive, and emotional disturbances • Cerebral Palsy (childhood, upper motor neuron damage/S.A.D. classification) -Diverse group of crippling syndromes that appear during childhood and involve permanent, nonprogressive damage to motor control areas of the brain o Damage in upper motor neurons that control voluntary and involuntary muscle movement o Symptoms remain for life. -Classified on the basis of neurologic signs and symptoms, with the major types involving spasticity, ataxia, dyskinesia, or a mix of one or more of the three • Cranial nerves (pupillary response + eye movements) -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 o Avoid triggers o Environmental control ▪ 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) ▪ 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) o Contralateral tracheal shift (massive effusion) • Pneumothorax (pleural cavity air, hyperresonance, sudden chest pain/affected side) o Accumulation of air in the pleural space o Primary pneumothorax ▪ Spontaneous ▪ Occurs in tall, thin men 20 to 40 years ▪ No underlying disease factors ▪ Cigarette smoking increases risk. o Secondary pneumothorax ▪ Result of complications from preexisting pulmonary disease -Clinical manifestations o Small pneumothoraces (<20%) are usually not detectable on physical examination. o Tachycardia o Decreased or absent breath sounds on affected side. o Hyperresonance o Sudden chest pain on affected side o Dyspnea o Tension and large spontaneous pneumothorax are emergency situations. ▪ Severe tachycardia ▪ Hypotension ▪ Tracheal shift to contralateral (opposite) side ▪ Neck vein distention ▪ Hyperresonance ▪ Subcutaneous emphysema • Respiratory center (medulla oblongata +pons) -Region in medulla oblongata and pons responsible for mechanisms/neural control of respiration (levels of o2 and co2 in blood) • Types of obstructive pulmonary disorders (P.A.W.) -Obstruction from conditions in the wall of the lumen (asthma, acute/chronic bronchitis) -Obstruction resulting from increasing pressure around the outside of the airway lumen (emphysema) -Obstruction of the airway lumen (bronchiectasis, bronchiolitis, cystic fibrosis, ATO, croup, epiglottitis) • Lab values -pH 7.35-7.45 -PaCO2 35-45 -HCO3 22-25 -PaO2 80-100 • Emphysema (pink puffer, changes to alveolar walls, irreversible, clubbing, barrel chest, no cough, pursed lips) -Type A COPD -“Pink puffer”, associated with chronic bronchitis -Destructive changes of the alveolar walls without fibrosis -Abnormal enlargement of the distal air sacs 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