COLLEGE OF NURSING NURS 364 FINAL EXAM STUDY GUIDE FOR COMPREHENSIVE PORTION 2024 LATEST U, Exams of Nursing

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COLLEGE OF NURSING NURS 364 FINAL EXAM STUDY GUIDE FOR COMPREHENSIVE PORTION 2024 LATEST UPDATED QUESTIONS AND ANSWERS GRADED 100 % PASS *NOTE: THIS STUDY GUIDE IS NOT INCLUSIVE OF ALL CONTENT ON EXAM Cell Adaptation, Injury, and Death -Be able to define and know examples of: Atrophy, Hyperplasia, Hypertrophy, Metaplasia, and Dysplasia • Atrophy o A decrease in cell size and a more efficient level of function ▪ Examples • Disuse: Reduced skeletal muscle use -> Broken Arm • Denervation: More extreme disuse in paralyzed limbs or muscle groups with decreased innervation • Loss of endocrine stimulation: Reduced activity from reduced stimulation e.g. estrogen in menopause • Inadequate nutrition: Triggers decreased activity as means of survival • Ischemia/Decreased blood flow: Decreases nutrient and oxygen availability • Hyperplasia o Increase in the number of cells ▪ Examples • Physiologic o Hormonal: Breast and uterine enlargement in pregnancy o Compensatory: Liver regeneration • Non-Physiologic o BPH: Linked to changes in testosterone o Endometrial hyperplasia: Estrogen o Warts: Growth factor from viruses (sometimes dysplastic) • Hypertrophy o Increased cell size and ultimately tissue mass ▪ Examples • Normal Physiologic o Weight-baring exercise: Depletes ATP and stretches muscle fibers, triggers hypertrophy for additional actin and myosin filaments and increased ATP synthesis o Organ/Tissue removal (Kidney removal) • Abnormal Pathologic o Long-standing hypertension ▪ Increased workload required to pump blood against elevated arterial pressure ▪ Progressive concentric increase in left ventricular muscle mass ▪ Increased oxygen demand ▪ Perpetuated by decreased end diastolic volume/decreased stroke volume • Metaplasia o One mature cell (epithelial or mesenchymal) type is replaced by another cell type ▪ Example NURS 364 - Final Exam Study Guide. • Patients with chronic GERD: normal squamous epithelium of lower esophagus are replaced with columnar epithelium o Barrett’s Esophagus o Gastric reflux • Dysplasia o Cell growth in a tissue that varies in cell size, shape, and organization ▪ Examples • Cervical cell dysplasia o Pap smear o Infection with human papilloma virus -What occurs to a cell during a hypoxic injury? Why does cell swelling occur? • Causes: Ischemia, decreased oxygen in the air, decreased production of RBCs, Cardiovascular diseases, and Respiratory Diseases • Swelling: Lacking ATP the sodium-potassium pump shuts down which causes swelling due to the excess sodium because sodium follows water -What is the difference between apoptosis and necrosis? Apoptosis Necrosis Cell Size Reduced (Shrinkage) Enlarges (Swelling) Cell Nucleus Fragmentation Nuclear Dissolution (Karyolysis) Plasma Membrane Intact Disrupted Cell Content Intact or Apoptotic bodies May leak out of cell Presence of adjacent inflammation No Frequent Physiologic or Pathologic Role Often Physiologic Pathologic Genetics -What is the difference between expressivity and penetrance? What are some examples of each? • Expressivity is the degree to which a gene is expressed in the phenotype o Marfan Syndrome • Penetrance is the ability of a gene to express its function o Huntington’s disease -What is trisomy? Monosomy? What are examples of each? What is the risk of trisomy (i.e. Down syndrome) related to? • Trisomy o More than 2 chromosomes in a pair ▪ Ex. Down Syndrome (Trisomy 21) • Risks o Intellectual Disability o Congenital Heart Defects o Increased Risk of Alzheimer’s disease o Characteristic Physical features • Monosomy o Only one chromosome present in a chromosome pair ▪ Ex. Turner Syndrome -Autosomal Dominant Disorders: What are the chances of inheritance? • 50% chance of inheritance NURS 364 - Final Exam Study Guide. -Define self-tolerance. What happens when self-tolerance is lost? • Ability of the immune system to recognize self-produced antigens as a non-threat while appropriately mounting a response to foreign substances • Genetic susceptibility and environmental factors appear to play a role and infections may contribute to development or exacerbations of autoimmunity -What is the clinical course of an HIV infection? How does it progress to AIDS? • Clinical course o Acute Phase (or primary infection) may have symptoms similar to flu or mononucleosis with fever, fatigue, myalgias, sore throat, night sweats, lymphadenopathy, rash, headache o Latency: The initial symptoms resolve and are followed by an asymptomatic period where virus is replicating slowly o AIDS: CD4+ T cell count less than 200 cells/mm or presence of AIDS-defining conditions (such as opportunistic illnesses or AIDS-related malignancies) • Progress o HIV is an RNA from DNA o Infections CD4+ T cells, macrophages, and dendritic cells o HIV attaches to the cell and the contents of the viral core enter into the host cell o HIV changes RNA to DNA using reverse transcriptase enzyme and is able to integrate into the host DNA o This new DNA undergoes transcription to form a single strand mRNA to direct production of new viruses o The mRNA is translated to create polyprotein chains for the new virus which then migrate to cell membrane and bud off from the cell -> extensive viral budding can lead to cell death -What are opportunistic infections in AIDS? • Pneumonia: pneumocystis jiroveci • CMV infection • Herpes virus infection • Toxoplasmosis infection of brain Neoplasia -Differentiate between benign and malignant tumors Tumors Benign Malignant Characteristics of Tumor Cells Well differentiated and resemble original cells Undifferentiated with anaplasia and little resemblance to original tissue Rate of Growth Usually progressive and slow Variable and depends on the level of differentiation Local Invasion Grow by expansion but do not invade surrounding tissue usually encapsulated Grows by invasion and sends out processes that infiltrate surrounding tissues Ability to Metastasize (Secondary Tumor Breaks off and imbeds somewhere else) Does NOT metastasize Can metastasize through blood or lymph channels Nomenclature Often “-oma”, “adenoma”, “fibroma”, or “glioma” Carcinoma or Sarcoma Ex. “adenocarcinoma” “fibrosarcoma” “glioblastoma” NURS 364 - Final Exam Study Guide. -What is anaplasia? • Lack of differentiation, Pleiomorphic “Graded”, Genetic Instability -Define the term metastasis. By what routes does cancer metastasize? • Metastasis is a secondary tumor development in a different area from the primary tumor • Lymphatic Spread: Through lymph nodes that drain the tumor area • Hematogenous Spread: Through blood system; through blood vessels -What is a proto-oncogene? Oncogene? Tumor suppressor gene? How do these relate to cancer development? • Proto-oncogene: Normal genes that tell us to proliferate • Oncogene: Genes that tell us to proliferate uncontrollable • Tumor suppressor genes are genes that suppress the growth of tumors • Proto-oncogenes-> mutation -> from oncogenes -> Underactivity of tumor suppressor genes -> inactivation leads to unregulated growth o Pressing full on the gas (produces a lot of cells) -> Cutting the breaks -What is cachexia? • Weight loss and wasting of body fat and muscle tissue with anorexia and fatigue/weakness -What is a Paraneoplasic syndrome? Provide some examples. • Manifestations of cancer at sites other than the tumor site o Examples ▪ Endocrinologic (Hormones) • SIADH: Due to production and release of ADH by tumor o Associated with small cell lung cancer • Cushing Syndrome: Due to production and release of ACTH by tumor o Associated with small cell lung cancer • Hypercalcemia: Due to release of polypeptide factor closely related to Parathyroid H ▪ Hematologic: Ex. Venous Thrombosis ▪ Neurologic: Ex. Myasthenia -How is dysplasia different from cancer? Consider the example of HPV that we discussed. • Even though cells appear abnormal they DO NOT indicate cancer • Cell growth in a tissue that varies in cell size, shape, and organization o Pap smear White Blood Cell Disorders -Define neutropenia. What does neutropenia increase the risk for? • Neutropenia is abnormally low amount of neutrophils (Less than 1500/uL) • Increased risk for developing an infection -Leukemias: -How is Leukemia classified? • Often classified according to the o Predominant cell type: Lymphocytic (B-cells, T-cells, NK cells) or Myelocytic o Acute or Chronic ▪ Acute: Usually undifferentiated or immature Cells (Blast Cells) ▪ Chronic: More differentiated cell but does not function normally; slower progression -What are some major manifestations of leukemia? What causes these symptoms to occur? • Acute Leukemia: Abrupt Onset NURS 364 - Final Exam Study Guide. o Manifestations: Fatigue due to Anemia, Fever due to Infection, Bleeding due to Thrombocytopenia, Night Sweats, Weight Loss, Pain in bones and joints (Overcrowding of Leukemia Cells), Lymphadenopathy, Splenomegaly, Hepatomegaly, Elevated uric acid levels, Possible Leukocytosis, May have CNS involvement • Chronic Leukemia o Manifestations: Often asymptomatic at first with slow and insidious progression, Isolated increase in lymphocytes, Lymphadenopathy, Increased risk for infection due to decreased humoral immune response (can’t produce antibodies) -What is the difference between the symptoms in acute and chronic leukemias? • Acute Leukemia symptoms occur abruptly while chronic symptoms occur slowly and over time -What is a “blast crisis?” • Terminal blast phase and “blast crisis” in which there is evolution to acute leukemia -Lymphoma: know definition of lymphoma • Tumors that develop from malignant lymphocytes -Hodgkin Lymphoma: what is the defining cell involved in Hodgkin lymphoma? • Special type of lymphoma featuring an abnormal cell known as a Reed-Sternberg Cell which is a painless enlargement of a single node or group of nodes -Multiple Myeloma: -What cells are affected by multiple myeloma? o Multiple Myeloma o B Cell malignancy of terminally differentiated Plasma Cells o Occurs most frequently in adults over 60 o Risk factors: immune disorders, ionizing radiation, occupation exposures to chemicals ▪ associated with Agent Orange exposure in Vietnam War o Patho: o Proliferation of malignant plasma cells in the bone marrow ▪ Malignant myeloma cause abnormal secretion of cytokines including IL-6 which leads to increased osteoclast activity—leading to _Breakdown of bone o Malignant myeloma cells release abnormal proteins (paraprotein): ▪ M Protein ▪ Free Ig light chain ( Bence Jones Protein ) that can be detected in the blood and urine and damage renal tubular cells o Normal antibody production is diminished or absent NURS 364 - Final Exam Study Guide. -Calcium imbalances: why would end stage kidney disease lead to hypocalcemia? • Inability to activate vitamin D Acid-Base Imbalances -How can the lungs respond to compensate for changes in pH? • Increased ventilation -> Increased PaCO2 -> 45<; Hyperventilation • Decreased ventilation -> Decreased PaCO2 -> >35 -How do the kidneys respond to compensate for changes in pH? Does this happen as quickly as lung responses? • Can regulate HCO3- and H+ in response to changes in pH • This response is slower -How does H+/ K+ exchange buffer pH? • When excess H+ is in the bloodstream (ECF), it moves into the cell (ICF) and K+ comes out of the cell into the ECF (bloodstream) -> leads to an increase K+ into bloodstream • When excess K+ is in the bloodstream (ECF) it moves into body cells (ICF) and H+ moves into the ECF (bloodstream)-> leads to an increase of H+ in the bloodstream and a decreased pH -What conditions can lead to respiratory acidosis? How does compensation occur? • Conditions o Acute Disorders of ventilation ▪ Airway obstruction, Chest wall injury, Respiratory muscle weakness, Decreased ventilation from CNS injury or narcotics, Lung disease o Chronic Disorders of ventilation ▪ COPD o Increased CO2 production ▪ Fever • Compensation o In acute respiratory acidosis compensation is not effective because kidneys take time to compensate o In chronic respiratory acidosis the kidneys will conserve HCO3- and eliminate H+ in urine -What conditions can lead to respiratory alkalosis? How does compensation occur? • Conditions o Increased ventilation from disorders ▪ Hypermetabolic states (fever, anemia) ▪ Anxiety/panic disorders • Compensation o Often occurs suddenly, so a decrease in bicarbonate level may not be able to occur o When chronic: renal compensation occurs with decreased H+ excretion and bicarbonate absorption -What conditions lead to metabolic acidosis? How does compensation occur? What are Kussmaul’s respirations? • Conditions o Increased production of metabolic acids ▪ Lactic acidosis: produced as a bi-product of shock or hypoxemia ▪ Ketoacids: such as in diabetes mellitus or starvation o Decreased renal function: Kidney’s ability to excrete acids and retain bicarbonate is impaired o Increased bicarbonate loss: Severe diarrhea because intestinal secretions have high HCO3- • Compensation NURS 364 - Final Exam Study Guide. o Body compensates for decrease in pH by increasing the respiratory rate in an attempt to decrease PaCO2 (and subsequently H2CO3) levels -What conditions lead to ? How does compensation occur? • Conditions o Excessive bicarbonate base: due to excess oral ingestion of bicarbonate antacids (like Alka- Seltzer) o Loss of acids: prolonged vomiting or continuous NG suctioning causing loss of HCl o Diuretics o Hypokalemia: due to attempts at renal compensation and intracellular shifts of H+ and K+ • Compensations o Increased inhibits respiratory center leading to decrease in rate/depth ventilation to try and retain CO2 Endocrine: -ADH Disorders: differentiate between DI and SIADH. • DI the body makes or is able to use too little ADH • SIADH the body makes too much ADH -Describe how each disorder affects the: serum sodium, serum osmolality, urine output, and urine osmolality. SIADH DI Urine Output Decreased: Low Increased: High Urine Osmolality Increased: High Decreased: Low Serum Sodium Decreased: Low Increased: High Serum Osmolality Decreased: Low Increased: High -Growth hormone: what is the difference in growth hormone excess in an adult vs in a child? • In Children o Epiphyseal plates have no closed ▪ Excessive skeletal growth-> termed Gigantism • Body height can 8 or 9 feet, bones • In Adults o Epiphyseal plates have closed ▪ GH and IGF-1 -> connective tissue proliferation and increased cytoplasmic matrix and bony proliferation -> termed Acromegaly • Enlarged hands/feet, facial changes, forehead -Thyroid: -Identify the symptoms of hypothyroidism and hyperthyroidism (Think about the function of thyroid hormone in the body) • Hypothyroidism o Manifestations ▪ Hypometabolic state • Cold intolerance, Weight gain, Constipation, Decreased HR, Lethargy, Tiredness, Decreased body temperature ▪ Goiter may or may no be present ▪ Myxedema: non-pitting edema resulting from altered compositions of dermis and other tissues; due to deposits of mucopolysaccharides and proteins in connective tissues • Especially apparent around eyes, hands, feet o Enlargement of tongue • Hyperthyroidism NURS 364 - Final Exam Study Guide. o Manifestations ▪ Nervousness, Irritability, Fatigability, Restlessness, Weight loss, Heat intolerance, Excessive sweating, Tachycardia, Palpitations, Exophthalmos -What is Hashimoto’s thyroiditis? What is Graves’ Disease? • Hashimoto’s Thyroiditis: Autoimmune destruction of thyroid gland (most common in US); Type 2 Hypersensitivity • Graves’ Disease: Autoimmune disorder with abnormal stimulation of thyroid by thyroid- stimulating antibodies (TSH receptor antibodies) -In primary hypothyroidism, what would be the expected TSH level? • Increased TSH and Low TH -What is a myxedema coma? What disorder is it a complication of? • Complication of Hypothyroidism o Life-threatening and end-stage expression of hypothyroidism o Manifestations: Coma, Hypothermia, Cardiovascular collapse, Hypoventilation, Hypoglycemia, Lactic acidosis -What is thyroid storm? What disorder is it a complication of? • Complication of Hyperthyroidism o Extreme and life-threatening form of thyrotoxicosis o Manifestations: very high fever, tachycardia, heart failure, agitations, restlessness, deliruim -Parathyroid glands: If there is hyperparathyroidism what would happen to the calcium level? What would happen to the bones? • Increased concentration of calcium may promote kidney stones • Excess bone resorption can lead to pathologic fractures; osteopenia -Adrenal glands -Primary Adrenocortical insufficiency (Addison’s Disease): -Why is there hyperpigmentation of the skin? • Increased ACTH causes Hyperpigmentation of the skin (ACTH is similar to melanocyte stimulating hormone) o Skin becomes bronze -What hormones are deficient in Addison’s disease? What are some manifestations? • Decreased adrenal cortical hormones o Manifestations ▪ Glucocorticoid (Cortisol) Deficiency: poor response to stress • Hypoglycemia, weakness, lethargy, fever, GI symptoms, Weight loss ▪ Mineralocorticoid (aldosterone) Deficiency: causes increased urinary loss of Na+, Cl-, H2O and retention of K+ • Dehydration -> Orthostatic hypotension o If severe -> Cardiovascular collapse and shock -Why could sudden withdrawal of a long term glucocorticoid medication (ex. Prednisone) lead to adrenal insufficiency? • No endogenous glucocorticoid secretion -What is an adrenal crisis? • Life-threatening complication of Adrenal Insufficiency -Cushing Syndrome/Cushing Disease occur from an excess of which hormone? What are some manifestations? • Glucocorticoid Excess o Manifestations NURS 364 - Final Exam Study Guide. -How does acute pyelonephritis differ from lower urinary tract infection? • Acute pyelonephritis o Infection of the renal pelvis and interstitium o Causes: ▪ Obstructive uropathy with static urine allowing bacterial growth ▪ Vesicoureteral reflux ▪ Neurogenic bladder ▪ Pregnancy o Patho: ▪ Infection ascends from lower urinary tract o Manifestations: ▪ Fever, Chills, Flank or groin pain, CVA (Costo Vertebral Angle) tenderness ▪ Sometime lower urinary symptoms • Lower Urinary Tract Infection o Defenses: ▪ Wash out phenomenon: Ureters, Bladder and Urethra constantly flushed with urine, difficult for pathogens to establish ▪ Bladder lining: Barrier to protect against invasion ▪ Immune Response o Risk Factors: ▪ More common in women ▪ Improper hygiene • Irritating bath products • Sexual Intercourse • Contraceptive diaphragms ▪ In older men enlargement of prostate increases risk ▪ For both males and females • Urinary catheterization, diabetes, dehydration increase risk ▪ Urinary catheterization is most common cause of nosocomial UTI in hospitalized patients o Causes: ▪ E.coli (origination from bowel) is the most common cause of UTI o Symptoms: ▪ Frequency, Urgency, Dysuria, Hematuria, Urinary retention ▪ No fever may indicate-pyelonephritis or sepsis ▪ May have atypical symptoms in older adults o Labs ▪ Nitrites ▪ Leukocyte Esterase ▪ Detection of WBC (pyuria) ▪ WBC activity -What is an important cause of UTI in hospitalized patients? • Urinary catheterization is most common cause of nosocomial UTI in hospitalized patients -Describe the following types of incontinence: stress, urge, functional. • Stress o Involuntary loss of urine in the absence of detrusor muscle action when intravesical pressure exceeds urethral closure pressure ▪ Risk Factors • Women, Weak pelvic floor, aging, childbirth NURS 364 - Final Exam Study Guide. o Example: Leakage of urine with coughing, sneezing, laughing • Urge o Urinary incontinence associated with strong desire to void o Urgency and frequency of urination associated with hyperactivity or the detrusor muscle • Functional o Due to immobility or dementia ▪ Individual’s inability to locate, reach, or receive assistance in reaching an appropriate place to void Cardiovascular Disorders -Venous Disorders -Why does hyperpigmentation of the skin occur in chronic venous insufficiency? • Brown hyperpigmentation o Of skin due to hemosiderin deposits d/t red blood cell breakdown ▪ Statis dermatitis -What is a DVT? What are the 3 categories of factors that lead to the development of DVT? What are some examples in each category? What is the most serious complication of a DVT? • DVT is a thrombus in a deep vein, usually in the lower extremities • Virchow’s Triad o Venous stasis: Bedrest, Immobility o Vessel wall injury: Trauma, Venipuncture, Surgery, Diabetes mellitus, Hypertension o Hypercoagulable states: Malignancy, Smoking, Genetics, Oral contraceptives, Pregnancy • Manifestations: DVTs are often asymptomatic; if symptoms occure they depend on location of DVT o Pain o Leg swelling-usually unilateral o Warmth/Erythema o If embolization occurred S/S of pulmonary embolism could be present -Arterial disorders -Hypertension -What is hypertension a leading risk factor for? • Cardio Vascular Disorders -What are examples of target organ damage from hypertension? • Hypertensive Emergency -Describe orthostatic hypotension. What are some causes of orthostatic hypotension? • Abnormal drop in blood pressure that occurs with standing after sitting or being supine • Causes: o Reduced blood volume o Drug-induced o Aging o Immobility o Autonomic nervous system dysfunction -Hyperlipidemia: What is the difference between LDL and HDL? • LDL o Low-Density Lipoprotein ▪ Also referred to as bad cholesterol • Main carrier of cholesterol • Elevations in LDL associated with increased risk for atherosclerosis o Can enter vessel wall and become oxidized NURS 364 - Final Exam Study Guide. • HDL o High-Density Lipoprotein ▪ Often referred to as good cholesterol • Carriers cholesterol from peripheral tissues to liver • HDL levels are inversely related to risk for atherosclerosis o Other: Chylomicrons, Very-low density lipoprotein, Intermediate- density lipoprotein -Atherosclerosis -What are the risk factors for atherosclerosis? • Non-modifiable o Age o Male sex: until post-menopause when risk for males and females tends to equalize o Genetic lipid disorders o Family history • Modifiable o Cigarette smoking o Obesity o Hypertension o Hyperlipidemia ▪ Elevated LDL-C and low HDL-C o Others: Inflammation -Describe the process involved in the development of atherosclerosis. What initiates it? • Initiation: Injury to the endothelium due to factors such as hypertension, smoking, inflammation, etc. • Monocytes adhere to endothelium and migrate into the intima and transform to macrophages -> engulf LDL particles -Peripheral Arterial Disease: What is intermittent claudication? • Pain with walking, typically the calf -Aortic Aneurysm/Dissection -What is the difference between an aortic aneurysm and an aortic dissection? • Aortic Aneurysm o Is the pathological outpouching or dilation of the wall of a vessel due to weakening of the vessel wall • Aortic Dissection o Tear in the intimal layer of the vessel that allows blood to enter the vessel wall -What contributes to the progression and growth of an aneurysm? • Vessel Tension -What are the manifestations of an aortic dissection? • Abrupt excruciating, tearing or ripping pain usually upper back or chest • S/S of ischemia, shock, syncope, MI, bowel ischemia, paraplegia -Coronary Artery Disease -What are the risk factors for CAD? What normally causes CAD? • Risk Factors o D • Most common cause is Atherosclerosis -What is an unstable coronary plaque? • -What is angina pectoris? What causes angina? • Chest pain that is associated with myocardial ischemia NURS 364 - Final Exam Study Guide. -Shock States -What is shock? What are some common features of all forms of shock? • Shock is a clinical syndrome and described as: Acute failure of circulatory system to supply peripheral tissues and organs with an adequate blood supply • Multiple classifications of shock exist, but all shock states have some common features: o Inadequate tissue and organ perfusion o Altered cell metabolism and function o Compensatory response to these derangements -What are the cell changes that occur in response to shock states? • Ineffective oxygen delivery to the cells causes cells to enter anaerobic metabolism and resultant production of lactic acid -Why is lactic acid formed in shock states? • Decreased ATP production occurs leading to NA+/K+- ATPase membrane pump dysfunction resulting in cell accumulation of sodium, cell edema, and increased membrane permeability -What are the body’s general compensatory mechanisms to shock? • Sympathetic Nervous System Response o Tachycardia, Increased cardiac contraction, Vasoconstriction • Increased renin release o Aldosterone (Sodium and water retention) -Describe hypovolemic shock. What conditions can contribute to this? • Occurs due to an acute loss of 15% or more of circulating blood volume (blood or fluid) • Hemorrhage, volume depletion, dehydration, shifting of fluid out of vascular spaces -What is cardiogenic shock? What can cause it? • Heart fails to pump sufficiently to meet the body’s needs • Low CO leading to hypoperfusion despite adequate volume • Manifestations o Fluid volume retention, low urine output, signs of poor perfusion -Explain the mechanism involved in distributive shocks. What types of shock are classified as “distributive?” • Vasodilatory shock which is characterized by loss of vessel tone with displacement of vascular volume away from the heart and central circulation -What can trigger anaphylactic shock? What are the manifestations of this shock? • Severe allergic reactions • Manifestations o Difficulty breathing, wheezing o Flushing, warmth, itching, urticaria -How does neurogenic shock differ from the other forms of shock? • Caused by decreased sympathetic control of blood vessel tone due to a defect in the vasomotor center of brainstem or sympathetic outflow to vessels • Etiology: Spinal cord injury • Mechanism: Wide-spread vasodilation occurs but HR is often low; skin is warm and dry -What causes septic shock? What type of shock is this? • A subset of sepsis with profound circulatory, cellular and metabolic abnormalities that are associated with greater risk for mortality compared to sepsis alone • Clinically, septic shock is usually when the patient requires a vasopressor to maintain adequate mean arterial pressure after receiving adequate fluid volume Pulmonary Disorders -What can increase the risk of developing pneumonia? NURS 364 - Final Exam Study Guide. • Immunocompromised -Do patients with TB always have symptoms? If someone has latent TB can they develop active disease? • No • Yes, active once immune system becomes impaired -Lung Cancers: What is the leading risk factor for lung cancer in the US? What are some symptoms? • Smoking • Symptoms o Cough, Shortness of Breath, Wheezing, Pain o Hemoptysis due to erosion of the blood vessels o Hoarseness or pleural pain or effusion -Why is epiglottitis potentially life-threatening? • Medical emergency due to risk for airway obstruction and asphyxia -> death • Collapse of airway -What is the difference between hypoxemia and hypercapnia? • Hypoxemia o Reduction in the PO2 of arterial blood ▪ Respiratory alkalosis • Hypercapnia o Increase in PCO2 of arterial blood ▪ Respiratory acidosis -Pleural Disorders -Describe pleuritic chest pain • Unilateral pain that is abrupt in onset and worsens with breathing or coughing -What is a pleural effusion? What type of fluid can accumulate in a pleural effusion? • Abnormal fluid collection in the pleural space • Serous Transudate, Exudate, Empyema, Hemothorax -What is a pneumothorax? What are manifestations of a pneumothorax? • Air in the pleural space o Manifestations ▪ Spontaneous • Primary: Often occurs in tall, thin people and increased risk in smokers • Secondary: Associated with underlying lung disease especially emphysema ▪ Traumatic • Other complications and possibly a hemothorax -How does tension pneumothorax affect cardiac output? What are the manifestations? • Compression of vena cava resulting in decreased venous return and decreased cardiac output • Manifestations o Tachypnea, dyspnea o Asymmetric chest expansion; diminished or absent breath sounds on affected side o Hypoxemia with large pneumothorax o Tension pneumothorax ▪ Mediastinal shift including the vena cava opposite side ▪ Distention of neck veins ▪ Signs of shock -Obstructive Disorders -Asthma: what changes occur in the airways during an asthma attack? Manifestations? • Common pathway is exaggerated hypersensitivity response to stimuli • Manifestations: Depends on severity o Wheezing and chest tightness; expiration in prolonged due to airway obstruction NURS 364 - Final Exam Study Guide. o Prolonged attack leads to hyperinflation of the lungs o Increased work of breathing with use of accessory muscles with tachypnea, dyspnea and fatigue o Symptoms of anxiety o Hypoxemia and hypercapnia may result -COPD -What is the leading cause of COPD? • Smoking -Obstruction is worse during which phase of the respiratory cycle in COPD? • Obstruction is worse with expiration -Describe the characteristic lung changes occurring in emphysema. • Characterized by loos of lung elasticity, and abnormal enlargement of gas exchange airways with destruction of alveolar walls and capillary beds -How does α1-antitrypsin deficiency lead to emphysema? • Breakdown of elastin and alveolar wall by proteases—especially elastase -What are the characteristic lung changes that occur in chronic bronchitis? • Airway obstruction of major and small airways -Cystic Fibrosis: How does CF affect the respiratory system? • Respiratory manifestations due to accumulation of viscid mucus and impaired mucociliary clearance o Predisposition to infection especially with P. aeruginosa o Chronic bronchitis and bronchiolitis that can progress to bronchiectasis -Interstitial Lung Diseases: In general, what changes occur to the lungs in interstitial lung diseases if prolonged? • Persistence of injurious agent causes accumulation of inflammatory and immune cells -Disorders of pulmonary circulation -What do pulmonary emboli most commonly result from? How does a PE affect perfusion? What are symptoms of a PE? • Most arise from DVT • Absent blood flow to part of lung causes ventilation without perfusion (V/Q mismatch) • Manifestations o Dyspnea, tachypnea, pleuritic chest pain, cough, tachycardia, anxiety o If large could be severe pulmonary hypertension and shock -How can pulmonary hypertension lead to right-sided HF? • Pulmonary vasoconstriction due hypoxia -What is cor pulmonale? • Right sided heart failure resulting from primary lung disease or pulmonary hypertension -What is ARDS? As ARDS progresses, what happens to the PO2? • Clinical syndrome with rapid onset of dyspnea, hypoxemia, and pulmonary infiltrates • Diffuse alveolar damage causes fluid accumulation, inactivation of surfactant, and formation of hyaline membrane that is fibrous and impervious to gas exchange Musculoskeletal Disorders -What is an open or compound fracture? • Open fracture bone fragments have broken through the skin • Compound fracture haven’t broken through the skin -What is compartment syndrome? What is the hallmark manifestation of this? • Increased pressure within a limited space, in this case a muscle compartment • Manifestations: Pain out of proportion to original injury or physical findings