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NURS 611 EXAM 1 PATHOLOGY 400+ QUESTIONS AND CORRECT DETAILED ANSWERS ALREADY GRADED A+ (M, Exams of Pathophysiology

NURS 611 EXAM 1 PATHOPHYSIOLOGY 400+ QUESTIONS AND CORRECT DETAILED ANSWERS ALREADY GRADED A+ (MARYVILLE UNIVERSITY)

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NURS 611 EXAM 1
PATHOLOGY 400+
QUESTIONS AND CORRECT
DETAILED ANSWERS
ALREADY GRADED A+
(MARYVILLE UNIVERSITY)
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Download NURS 611 EXAM 1 PATHOLOGY 400+ QUESTIONS AND CORRECT DETAILED ANSWERS ALREADY GRADED A+ (M and more Exams Pathophysiology in PDF only on Docsity!

NURS 611 EXAM 1

PATHOLOGY 400 +

QUESTIONS AND CORRECT

DETAILED ANSWERS

ALREADY GRADED A+

(MARYVILLE UNIVERSITY)

[Document subtitle]

[DATE]

[COMPANY NAME] [Company address]

  1. Parasympathetic Nervous System Conserves energy and the body's resources; manages day-to-day needs of the body.
  2. Autonomic Nervous System Made up of parasympathetic and sympathetic nervous systems.
  3. Sympathetic Nervous System Responds to stress by preparing the body to defend itself (fight or flight). Releases catecholamines (epinephrine), mobilizes energy stores (glucose to muscles), decreases the release of insulin, redirects blood supply from the gut (decreases peristalsis) to the muscles (fight), heart, and lungs (increases diameter of bronchioles).
  4. What is the first defense of our bodies? Skin and mucous membranes.
  5. What is the purpose of the inflammatory process? To prevent infection of the injured tissue. If the epithelial barrier is damaged, then a highly efficient local and system response (inflammation) is mobilized to limit the extent of damage, to protect against infection, and to initiate the repair of damaged tissue.
  6. What are the 4 cardinal signs of infection? Edema, warmth, redness, and pain.
  7. Which type of White blood cell is the first to arrive at the site of infection? Leukocytes.
  8. Classifications of primary brain injury? Focal or diffuse.
  1. What causes sweating above the level of the injury in autonomic hyperreflexia? The spinal cord injury results in disturbed thermal control because the hypothalamus is unable to regulate body heat due to damaged sympathetic nervous system.
  2. What causes bradycardia in autonomic hyperreflexia? Stimulation of the carotid sinus to the vagus nerve causes the SA node to slow down to 30 - 40 bpm.
  3. Delirium Typically occurs in older adults. Onset is acute (common during hospitalization) and can last from hours to weeks; remits with treatment. Attention and orientation are impaired; thoughts are disorganized, and delusions, hallucinations, and illusions can occur.
  4. Common associated conditions with delirium Hospitalization, UTI, thyroid disorders, hypoxia, hypoglycemia, toxicity, fluid-electrolyte imbalances, renal insufficiency, trauma, multiple medications.
  5. Dementia Typically seen in older adults; onset is gradual with a slow decline. Duration can last from months to years. Early on, attention, orientation, perceptions, and behaviors are intact but deteriorate over time.
  6. Dementia is characterized by the deterioration in which abilities? Dementia is the progressive failure (an acquired deterioration) of many cerebral functions, including impairment of intellectual function with decreased orientation, memory, language, executive functions, and behavioral changes.
  7. What is the normal intracranial pressure (mm Hg)? 5 - 15 mm Hg.
  1. Alzheimer Disease Leading cause of dementia and severe cognitive dysfunction in older adults. Greatest risk factors: age and family history.
  2. Alzheimer disease cause and diagnosis Exact cause unknown. Diagnosis is made postmortem. Rule out other causes with clinical history, cognitive testing, course of illness, labs, and brain imaging. Genetic tests (PSEN1, PSEN2, APP) for early onset.
  3. Symptoms of Alzheimer Disease Memory loss, difficulty speaking, disorientation, poor judgment, problems with abstract thinking, misplaced belongings, personality changes, difficulty with routine tasks.
  4. How are strokes classified? According to pathophysiology: ischemic (thrombotic or embolic), global hypoperfusion (shock), intracerebral hemorrhage.
  5. Most common type of stroke? Ischemic (thrombotic or embolic). Many are classified as "undetermined" or "cryptogenic."
  6. Contributing factors for stroke Diabetes, HTN, high cholesterol, heart disease, PVD, polycythemia, thrombocytopenia, atrial fibrillation, smoking, inactivity, obesity, sleep deprivation, ethnicity.
  7. Most common location of a stroke? Middle cerebral artery.
  8. Greatest risk factor for stroke? Uncontrolled hypertension.
  1. MS prognosis 90% relapsing/remitting; 10% primary progressive. Progression accelerates as demyelination increases.
  2. Progression of MS Increased CNS damage, brain volume loss, disrupted ion channels, microglia activation.
  3. Myasthenia Gravis Chronic autoimmune disease targeting acetylcholine receptors at neuromuscular junctions.
  4. Onset of Myasthenia Gravis Usually insidious.
  5. Initial signs of Myasthenia Gravis Fatigue, weakness, especially in ocular muscles (diplopia, ptosis), worsening with activity, improving with rest.
  6. Progression of Myasthenia Gravis Facial, swallowing, speech muscles; possible respiratory distress.
  7. Strabismus Deviation of one eye from the other (misalignment).
  8. Diplopia Double vision.
  9. Nystagmus

Involuntary rhythmic eye movements.

  1. Amblyopia ("lazy eye") Reduced vision from abnormal visual development in childhood.
  2. In Myasthenia Gravis, patients may develop A leading to recurrent infections. Microaspirations.
  3. Ptosis Drooping eyelids.
  4. Clinical manifestations of Parkinson disease caused by dopamine deficit? Resting tremor, bradykinesia, rigidity, postural instability, facial mask, shuffling gait.
  5. Parkinson Disease (PD) Degeneration of basal ganglia, loss of dopaminergic neurons in substantia nigra.
  6. Characteristic PD features Resting tremor, shuffling gait, bradykinesia, muscle rigidity, facial masking.
  7. Balance issues in PD Postural instability, tendency to fall, spontaneous or pushed.
  8. Tremors in PD Resting tremor, pill-rolling.
  9. Atrophy of neurons in the A causes PD symptoms.

Rapid onset, steady, orbit/temple/cheek, tearing, runny nose, Horner syndrome.

  1. Tension Headache Gradual onset, steady, variable location, no associated features.
  2. Hormone peaking in the morning? Cortisol.
  3. Obstructive Sleep Apnea Syndrome (OSAS) Breathing disorder during sleep, upper airway collapse, reduced oxygen saturation, hypercapnia.
  4. Major risk factors for OSAS Obesity, male sex, older age, postmenopause (not on hormone therapy).
  5. What is the Apnea Hypopnea Index (AHI)? Number of apnea/hypopnea episodes per hour—severity index.
  6. Sleep issues in women Progesterone (respiratory stimulant) protective premenstrually; insomnia, restless legs, depression, hallucinations.
  7. Sleep issues in obesity Short, thick neck, airway collapse, impaired mechanics.
  8. Sleep issues in men Longer airway, snoring, apneas.
  9. Most common sleep disorder?

Obstructive sleep apnea.

  1. Effects of excess cortisol? Arthritis, immune suppression, decreased metabolism, depression, HTN, fatigue, migraines, reflux, hostility, hunger.
  2. Sleep deprivation effects? Disrupted circadian rhythm, cortisol dysregulation, increased BP and glucose, immune suppression.
  3. Leading cause of visual impairment? Glaucoma.
  4. Open Angle Glaucoma Most common, caused by chronic intraocular pressure, optic nerve damage, peripheral vision loss.
  5. What causes loss of visual acuity in glaucoma? Pressure on the optic nerve.
  6. Major categories of hearing loss? Conductive, sensorineural, mixed, functional.
  7. Functional hearing loss No organic basis; psychogenic.
  8. Mixed hearing loss Combination of conductive and sensorineural.

Thought disorder, break in reality, positive/negative symptoms.

  1. How is schizophrenia diagnosed? At least 2 symptoms (delusions, hallucinations, disorganized speech, behavior, negative symptoms) over 1 month, with disturbance >6 months.
  2. Neurobiology of schizophrenia Ventricular enlargement, cortical atrophy, reduced thalamic size.
  3. Positive symptoms of schizophrenia? Delusions, hallucinations, agitation, insomnia.
  4. Negative symptoms of schizophrenia? Flattened affect, alogia, anhedonia, avolition, asocial.
  5. What is anhedonia? Inability to feel pleasure or pain; detachment.
  6. Alogia Absence of spontaneous speech.
  7. Avolition Lack of goal-directed activity.
  8. Disorganized behaviors in schizophrenia Disorganized speech, thought, behavior, poor attention.
  9. Major depressive mood disorder (depression) S/S

Loss of interest, guilt, death wishes, fatigue, decreased concentration, sleep and appetite changes.

  1. Major Depressive Disorder (Unipolar) Persistent depressed mood, anhedonia, decreased activity, guilt, sleep, appetite, weight changes.
  2. Bipolar Disorder Bipolar I: manic episodes ± depressive; Bipolar II: hypomanic + depressive.
  3. Mania symptoms? Impairs functioning, psychosis, hospitalization.
  4. What causes edema during inflammation? Vasodilation increases blood flow and capillary permeability, leading to plasma leakage and swelling.
  5. Innate immunity includes which lines of defense? Natural barriers and inflammation.
  6. Natural barriers Physical, mechanical, biochemical; in place at birth.
  7. What happens if barriers are breached? Inflammation is activated to protect and heal.
  8. What is the inflammatory response? Rapid, nonspecific biochemical and cellular activation against tissue damage.

Pathogen-produced.

  1. Pyrogens Act on hypothalamus to raise body temperature.
  2. Endogenous pyrogen release? After phagocytosis, endotoxin exposure, or immune complexes.
  3. Benefit of fever? Some microbes are heat-sensitive, and fever enhances immune response.
  4. Function of opsonization? Tags pathogens for phagocyte destruction.
  5. Sequence of phagocytosis? Recognition (opsonization), engulfment, fusion, destruction.
  6. Acute inflammation and fever? Produced by hypothalamic effects of endogenous pyrogens.
  7. WBC differential and inflammation? Elevated neutrophils in early inflammation.
  8. Resolution and repair process? Healing begins during inflammation; can take up to 2 years.
  9. If damage is minor in resolution? Tissue regenerates, returning to normal.
  1. If damage is extensive? Infection, abscess, granuloma, or scar tissue; regeneration not possible.
  2. Impaired healing in older adults? Chronic illnesses, medications, poor nutrition.
  3. Cell primary defense against parasites? Eosinophils.
  4. Normal gut flora produce vitamin K for absorption of? Calcium, iron, magnesium.
  5. Headache that feels like a band around the head? Tension headache.
  6. What is an antibody? Proteins that protect against bacteria and viruses.
  7. Humoral immunity? Antibodies in blood that inactivate pathogens or activate other immune mediators.
  8. Cellular immunity? T cells attack infected or abnormal cells and secrete cytokines.
  9. Active acquired immunity? Produced by individual after exposure or vaccination; long-term memory.

Eliminate malignant and virus-infected cells.

  1. Which antibody indicates a typical primary immune response? IgM.
  2. Most susceptible to mucous membrane infections? Low IgA levels.
  3. Endogenous antigen example? Cancer cells.
  4. When are antibodies usually detectable after antigen exposure? Within 6 days.
  5. Vaccinations protect primarily through which immunoglobulin? IgG.
  6. How does aging affect T-cell activity? Decreased immune response, increased infection risk.
  7. Hypersensitivity causing allergic reactions? Type I (immediate, IgE-mediated).
  8. Class of immunoglobulin involved in type I hypersensitivity? IgE.
  9. Blood transfusion reactions are an example of? Alloimmunity.
  1. Type I hypersensitivity reactions? IgE, mast cells, allergic responses.
  2. Type II hypersensitivity reactions? Antibodies target specific cells (e.g., autoimmune hemolytic anemia).
  3. Type III hypersensitivity reactions? Immune complexes deposit in tissues (e.g., serum sickness, SLE).
  4. Raynaud phenomenon involves which hypersensitivity? Type III.
  5. Type IV hypersensitivity? Cell-mediated, no antibodies; contact dermatitis, graft rejection.
  6. Which reactions are antibody-mediated? Type I, II, III.
  7. Which reactions are T-cell mediated? Type IV.
  8. Systemic Lupus Erythematosus (SLE)? Chronic autoimmune disease with immune complex deposition causing tissue damage.
  9. Autoantibodies in SLE? Against DNA, erythrocytes, phospholipids, etc.