NUR 250 Pathophysiology Exam PDF

Pathophysiology Exam Two Exemplars SENSORY PERCEPTION Conductive Hearing Loss Pathophysiology Impact outer and middle ear structures (sound is processed normally in the inner ear,...

Pathophysiology Exam Two Exemplars SENSORY PERCEPTION Conductive Hearing Loss Pathophysiology Impact outer and middle ear structures (sound is processed normally in the inner ear, but it is no longer as loud as it should be when it reaches the inner ear) Manifestations Cerumen impaction, otosclerosis (abnormal bone growth), otitis media, Diagnostic Hearing tests, possible MRI, CT Procedures & Labs Therapeutic/Medical Drain fluid from middle ear, reconstructive surgery, earwax removal, hearing aid, Interventions cochlear implant Sensorineural Hearing Loss Pathophysiology Damage to the structures of the inner ear; frequency and sound can no longer be accurately processed or transmitted to auditory cortex Manifestations Ototoxic drugs, Autoimmune disorders, Noise Diagnostic Hearing tests, possible MRI, CT Procedures & Labs Therapeutic/Medical Stop ototoxic drugs, hearing aids, cochlear implants Interventions Spinal Cord Injuries Pathophysiology Usually a secondary injury, Calcium influx into cells, inhibiting impulse conduction Expected Findings ↑ ischemia, ↑ lipids released from spinal cord, ↑ vasospasm, inflammatory process: endothelial damage, ↑ vascular permeability, edema, inflammatory cells Risk Factors Injuries to the head, neck, and spine Associated Spinal Shock: temporary loss of spinal reflex activity below injury level, interruption Complications of sympathetic outflow Hypotension, ↓ vascular resistance, vascular dilation, bradycardia Central Cord Syndrome: ↓ strength, ↓ pain, ↓ temperature sensation in upper extremities  Anterior Cord Syndrome: damage to corticospinal and spinothalamic pathways, loss of motor function, pain, and temperature distal to injury (still can feel vibrations and positions) Brown-Sequard Syndrome: Damage to one half of spinal cord Loss of motor function on SAME side as injury to cord Loss of pain, temp, and sensation on OPPOSITE side as injury to cord Diagnostic MRI, CT Procedures & Labs Therapeutic/Medical Surgery? Interventions Autonomic Dysreflexia Pathophysiology Massive, uncompensated cardiovascular response to stimulation of sympathetic nervous system (may occur after spinal shock resolves) Manifestations Usual trigger is distended bladder/bowel which triggers baroreceptors, which triggers PNS. PNS causes bradycardia and flushing, neuronal message cant pass through spinal cord injury, so vessels vasoconstrict. BP shoots into 300s, which risks cerebral hemorrhage Risk Factors Spinal cord injuries, spinal shock Diagnostic Bladder scan Procedures & Labs Therapeutic/Medical Remove tight clothing, try to relieve bladder/bowel, decrease blood pressure Interventions Cataracts Pathophysiology Cloudy or opaque discoloration of an otherwise clear lens Manifestations Symptoms gradual in onset, slow decrease in acuity, cloudy/burring vision Risk Factors Age, UV light Diagnostic Eye exam Procedures & Labs Therapeutic/Medical Surgery, artificial lens Interventions Glaucoma Pathophysiology A group of diseases resulting in increased intraocular pressure; leads to slow, painless loss of vision due to too much production of aqueous humor, or poor drainage Expected Findings Open Angle: either too much aqueous humor or does not drain fast enough; no symptoms or warning signs in early early; peripheral vision affected in late stage  Closed-Angle: treated a an emergency, outflow is stopped due to angle between iris and cornea; dilated pupil unreactive to light, redness, pain, vomiting, blurred vision with halos; can occur after administration of dilating eye drops in patients with preexisting open angle Risk Factors Old age, genetics, comorbidity, decreased corneal thickness Diagnostic Eye exam, look at inner eye pressure Procedures & Labs Therapeutic/Medical Medications (pilocarpine, echothiophate, timolol), laser treatment, surgery Interventions Macular Degeneration Pathophysiology Macula, central part of retina, degenerates resulting in loss of central vision Expected Findings Dry: most common, less severe, blurry or wavy central vision with normal peripheral vision Wet: severe, new blood vessels form around macula and cause bleeding, scarring, and atrophy (irreversible) Risk Factors Age, genetics, smoking, hypertension, obesity, hyperlipidemia Diagnostic Eye exam Procedures & Labs Therapeutic/Medical No treatment, infection prevention Interventions Special combo of vitamins/minerals can help reduce progression? Diabetic Retinopathy Pathophysiology Change in blood vessels over time due to diabetes (damages retina) Expected Findings Nonproliferative: elevated blood glucose over long period of time; walls of vessels weaken and leak fluid into macula Proliferative: tiny new vessels grow into vitreous humor disrupting humor flow (comes after nonproliferative) Risk Factors Poor control of diabetes, high BP, high cholesterol, tobacco use Diagnostic Eye exams Procedures & Labs Therapeutic/Medical Management of diabetes Interventions Retinal Detachment Pathophysiology Retina separates from underlying structure; can occur secondary to cataract surgery, proliferative diabetic retinopathy, and trauma Expected Findings Sudden onset of floaters, flashes of light, or veils falling over vision Risk Factors Age, genetics, myopathy, injury, Diagnostic Eye exam Procedures & Labs Therapeutic/Medical Surgery Interventions INTRACRANIAL REGULATION Traumatic Brain Injury (TBI) Pathophysiology Primary: occurs at the moment of direct mechanical injury Secondary: the biochemical and cellular response to the initial trauma Expected Findings Primary: fractures, hematoma, contusions, lacerations, concussions, shearing, and hemorrhaging Secondary: ischemia, neuronal death, cerebral swelling, inflammation Risk Factors Falls, age, risky behavior Diagnostic Procedures MRI, CT & Labs Therapeutic/Medical Rest, Surgery, Medication Interventions Epilepsy Pathophysiology Abnormal electrical activity in the brain, involuntary change in body movements, sensation, awareness, and behavior Expected Findings Febrile: occurs in children due to rapid temp rising above 102, causing a lower seizure threshold; only last a few minutes; acute illness Simple Partial: affects a limited area of brain, loss of motor control without affecting awareness Complex Partial: affects a limited area of brain, behavior changes, memory, and consciousness are impaired for several hours Absence: blank stare, unresponsive to environment, cessation of motor activity, typical has an aura Tonic-Clonic: most common, no aura, increased metabolic demands, hypoxia, hyperventilation, eyes roll back Tonic: muscle rigidity, arms and legs extend with jaw clenched  Clonic: alternating period of muscle contraction and relaxation Status Epilepticus: involves continuous seizure activity with only short periods of calm between seizures (can cause death, lots of continuous brainwave dysfunction) Risk Factors Genetics, head trauma, tumors, brain infections, SES (malnutrition), developmental Diagnostic Procedures ECG, MRI, CT, Neuro exam, PET & Labs CBC/CMP, Chemistry panel, Serum prolactin Therapeutic/Medical Anticonvulsants, nerve stimulations, surgery, behavioral/lifestyle changes Interventions Meningitis Pathophysiology Inflammation of the protective membranes covering the brain and spinal cord (can be viral, bacterial, fungal, parasitic, or noninfectious) Expected Findings Systemic infection (fever, tachycardia), meningeal irritation (headache, photophobia, nuchal rigidity), decreased consciousness, focal deficits and seizures, projectile vomiting, papilledema (swelling of optic disc from high ICP) Risk Factors AIDS, alcohol abuse, immunocompromised Diagnostic Procedures Lumbar puncture to test CSF & Labs Kernig’s sign: pain with leg lifted up Brudzinski’s sign: flex head, knees come up too Therapeutic/Medical Bacterial: treat with antibiotics (difficult) Interventions Viral: treat symptoms Vaccines Hydrocephalus Pathophysiology Excessive amount of CSF in cranial vault caused by lesions that obstruct flow of CSF from ventricles or problems with resorption of CSF Expected Findings Mental impairment, incontinence, unstable gait, enlarged skull in children because their heads are not fused yet Risk Factors Tumor infection or idiopathic (seen in older adults) Diagnostic Procedures CT/MRI & Labs Therapeutic/Medical VP Shunt to drain into stomach Interventions Hematoma Pathophysiology Epidural: arterial bleed between skull and dura mater, caused by skull fracture/contusion  Subdural: venous bleed between dura and arachnoid mater due o the tearing of veins Expected Findings Epidural: Brief loss of consciousness, then lucid; rapid deterioration, from drowsy to coma Subdural: N/V, seizure, weakness Acute: slow bleed, due to trauma or spontaneous, occurs within 14 days of injury Chronic: brain atrophy from alcohol abuse/age, tension on veins cause bleeding, occurs after 14 days of injury Risk Factors Age, anticoagulants, trauma to head Diagnostic Procedures CT/MRI, EEG, CSF analysis & Labs Therapeutic/Medical Vaccines, surgery, medications Interventions COGNITION Alzheimers Pathophysiology Long term decrease in acetylcholine, an accumulation of abnormal plaques and protein clumps in neurons, loss of gray matter, most common form of dementia Expected Findings Memory loss (hippocampus affected first), decreased cognition, language dysfunction, poor judgment, behavioral issues Early stage: delayed short-term memory, forgetfulness, losing objectives Intermediate stage: loss of long-term memory, irritability, delusions, wandering, depression (usually when diagnosis will occur) Late stage: mental capacity severely deteriorated, unable to perform ADLs, combative and agitation can occur Risk Factors Genetics, environmental, age Diagnostic Procedures Labs, Brain scans, Mental status exam & Labs Therapeutic/Medical Cholinesterase inhibitors can possibly help in the beginning, but there is no Interventions treatment Dementia Pathophysiology Chronic disorder of mental processes marked by memory impairment, personality changes, and impaired reasoning Cognitive impairment is a sign of disease, not aging Decrease in number of neurons with age Risk Factors Genetic links, familial pattern involves mutation of amyloid precursor protein genes, vascular disorders, brain injuries Diagnostic Procedures CT/MRI, Mental status exam & Labs Therapeutic/Medical Patient safety precautions, no treatment Interventions Delirium Pathophysiology Not well understood, acute confused mental state Expected Findings Disorientation, rapid speech, sudden onset, intense mood swings, can occur over hours to days Risk Factors Drugs, dehydration, infections (Pneumonia, UTIs), recent surgery, underlying diseases (dementia), fatigue/decreased sleep, age, inflammation, idiopathic Diagnostic Procedures Mental status exam/level of consciousness exam & Labs Therapeutic/Medical CT, MRI, CBC for infections, urine test (drugs) Interventions Stroke (Cerebral Vascular Accident) Pathophysiology Irreversible, evidence of tissue infarction Ischemic: Interruption in blood supply to a region of the brain, focal neurologic deficits present, atherosclerosis leads to injury on vessel wall; WBCs proliferate at site leading to blockage Hemorrhagic: bleeding of a vessel, can be caused by aneurysms or AVMs Expected Findings Ischemic: facial drooping, speech difficulty, paralysis of one side Thrombus: slower to develop, caused by atherosclerosis Embolus: rapidly formed clot, caused by atrial fibrillation Hemorrhagic: ↑ ICP Intracerebral: bleeding into brain tissue Intraventricular: bleeding into ventricles Extracerebral: bleeding into surrounding membranes Risk Factors Age, family history, chronic disease (diabetes, heart disease, high blood pressure, high cholesterol, smoking, alcohol Uncontrolled hypertension is major risk for hemorrhagic stroke! Diagnostic Procedures CT scan immediately/ MRI (takes long) & Labs Therapeutic/Medical Ischemic: blood thinners to break up clot Interventions Hemorrhagic: management of blood pressure, oxygenation, glycemic control, and maintaining expected ICP range (diuretics) Surgery (either) Medications: fibrinolytic therapy (ischemic) , antipsychotics for delirium  PSYCHOBIOLOGY Schizophrenia Pathophysiology Enlarged ventricles, widened fissures and sulci, decreased temporal and frontal lobe volume, asymmetry of lobes, volume reduction sometimes seen in hippocampus, amygdala, basal ganglia, and thalamus Phases: premorbid, prodromal, acute onset, progressive, chronic First Hit: Developmental defects in neuron or synapse formation sensitizes the brain to react differently than a “normal” brain to stresses (either biological or environmental) Second Hit: Stress during adolescence triggers abnormal response within brain that initiates and perpetuates injury and concurrent psychosis Expected Findings Hallucinations, delusions, social isolations, violence, inappropriate affect, bizarre behavior, apathy, autism, faulty perceptions Positive symptoms: additions (hallucinations, thought disorder) Negative symptoms: diminished (avolition, poverty of speech) Risk Factors Genetic influences (correlated with autism) Mental illness (often comorbid) Neurotransmitter abnormality: dopamine, norepinephrine, serotonin, GABA (dopamine causes language issues) Impairment in immunity: increased cytokine levels, illness, stress, exacerbate condition Diagnostic Procedures MRI/CT, CBC, Norepinephrine, Dopamine, GABA, Serotonin, Psych evaluation & Labs Therapeutic/Medical Antipsychotics, CBT Interventions Major Depressive Disorder Pathophysiology Persistent feelings of sadness and loss of interest in life (MDD: 2+ weeks) Neural mechanisms that filter info become biased in favor of negative information ↓ norepinephrine (apathy, fatigue), ↓ serotonin (mood, optimism), ↓ dopamine, ↑ cortisol, ↑ CRF Desensitized negative feedback receptors HPA axis (stress), Amygdala (suicide) Expected Findings Depressed mood, weight loss, fatigue, poor concentration, decreased appetite, sleep disturbance, suicidal thoughts Risk Factors Genetics, anxiety disorders, substance abuse, chronic mental illness, chronic stress Diagnostic Procedures CRF, Cortisol, screenings (PHQ9), EEG, MRI/CT & Labs Therapeutic/Medical Therapy, antidepressants, lifestyle changes, support system Interventions Bipolar Pathophysiology Prefrontal cortex smaller in size and decreased functioning, changes in receptor sensitivity, inability to get glutamate back into cells ↑ norepinephrine in mania ↓ norepinephrine in depression Dysregulation of serotonin and dopamine Kindling: gradual worsening of manic episodes over time due to ↓ threshold Expected Findings Bipolar 1: one or more manic or mixed episodes & MDD Bipolar 2: one or more MDD episodes & hypomania Cyclothymic: alternating periods of hypomanic and depressive symptoms not significant enough to meet criteria for hypomania or depression Mania: persistently elevated or irritable mood and increased energy; flight of ideas, delusions/hallucinations may occur; follows emotional trigger Hypomania: symptoms not as severe as mania, patient may not notice change but others do Risk Factors Genetics (biggest predictor), stressful life events, ↑ norepinephrine, small PFC Diagnostic Procedures Physical and psychological exams & Labs Therapeutic/Medical Mood stabilizers, depression medication Interventions Anxiety Pathophysiology Sense of dread without any apparent stimulus, leads to negative coping mechanisms, ↓ GABA receptors in brain, ↓ in serotonin HPA axis imbalance: inappropriate activation of norepinephrine in locus coeruleus and Imbalance between norepinephrine and dopamine, glutamate, and CRH GAD: Worry generates restlessness, fatigue, irritability, tension, limbic system and midbrain involved, ↓ GABA, ↑ Norepinephrine, worry centered Can evolve into OCD and phobic disorders Expected Findings Somatic responses: palpitations, sweating, rapid breathing (GABA)  Avoidance: social interactions, relationships, opportunities for growth Consolidation: fearful stimuli stored in amygdala Reconsolidation: fearful memory is activated and reinforced, creating a long term fearful memory, fear grows stronger Caudate nucleus: plays role in avoidance Drives behavior based on recall of past successful outcomes; if this area does not function well, recall is impaired and only negative aspects are focused on Amygdala: plays role in fear overactive and over responsive in anxiety Risk Factors Traumatic events, genetics Diagnostic Procedures Psychological evaluation & Labs Therapeutic/Medical Anxiety medication, CBT Interventions Panic Disorder Pathophysiology Sudden episodes of intense fear that results in increased sympathetic function, chronic disorder ↓ GABA, ↑ Norepinephrine (fight/flight), ↑ Glutamate Expected Findings Palpitations, sweating, feelings of unreality, avoidance of situation, episodes which occur without warning, feeling of impending doom, numbing, paresthesias Individual truly believes death is imminent because of physical symptoms Risk Factors Genetics, abuse, smoking, anxiety Diagnostic Procedures Psych evaluation & Labs Therapeutic/Medical CBT, psychotherapy, medications Interventions Post Traumatic Stress Disorder (PTSD) Pathophysiology Traumatic event beyond the realm of normal human experience, consolidation-reconsolidation, Hyper-responsiveness of the amygdala occurs (suicidal thoughts) Expected Findings Memory: flashbacks, intrusive thoughts, impaired memory Cognition: difficulty concentrating, hypervigilance Sleep disturbances & Somatic problems High suicide rates due to not seeking help Risk Factors Experiencing or witnessing a traumatic event Diagnostic Procedures Psych evaluation & Labs Therapeutic/Medical Anxiety/depression medication, CBT, exposure therapy Interventions Addiction Pathophysiology Recurrent use of substance such that the individual experiences clinical and functional impairment and inability to manage responsibilities of daily life Binge and intoxication: ↑ dopamine; activation of brain’s reward system Preoccupation: decreased function of prefrontal cortex Withdrawal: increased sensitivity to stress and negative emotions Alteration of nucleus accumbens and amygdala Expected Findings Alcohol ↑ GABA, ↑ Dopamine, ↓ Glutamate Quit cold turkey: rebound overstimulation can lead to seizures, tremors, hallucinations Tobacco Rapidly absorbed in pulmonary circulation, circulated to brain Binds to nicotinic cholinergic receptors, ↑ Dopamine ↑ Epinephrine in SNS, vasoconstriction increases stress on cardiovascular Vasoconstriction + Stress + Hypertension = MI Opioids Interact at opioid receptor systems, rapid dependance Potent depressive effects on nervous system Overdose – overall depression of systems: ↓ respiratory rate, sedation or coma ○ Push fentanyl too fast: rigid chest syndrome Risk Factors Psychiatric comorbidity Diagnostic Procedures History/Physical, CT/MRI, SPECT, PET & Labs Labs: substance use (liver enzymes, etc.) Therapeutic/Medical Cognitive-behavioral therapy, Medications, Support groups/treatment – substance Interventions use disorders Obsessive-Compulsive Disorder Pathophysiology Recurring unwanted thoughts, ideas, or sensations (obsessions) that make them feel driven to do something repetitively (compulsions) Dysfunction leads to overactive circuits that fail to integrate cognitive, emotional, and emotional responses to sensory input; rumination Expected Findings ↓ serotonin, ↑ cortisol, ↑ frontal lobe activity, ↑ metabolic rates in PFC, basal ganglia abnormalities Increased frontal lobe activity: guilt, intense affect, worry Risk Factors Genetics, presence of other mental health conditions, stress, age, gender Diagnostic Procedures PET Scans (show high metabolic rate in PFC) Therapeutic/Medical Medication therapy Interventions ADD/ADHD Pathophysiology Trouble paying attention, difficulty finishing tasks, distracted, overly active (ADHD only) Expected Findings Impaired functioning, difficulty at school, home, or with others, excessive talking, impulsivity, risk-taking behavior, restlessness Risk Factors Idiopathic, possible genetic links, maternal alcohol use/tobacco use, premature delivery, environmental factors Diagnostic Procedures Psychological evaluation, ADD/ADHD exam Therapeutic/Medical Behavioral medications (adderall, ritalin) Interventions