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Homework answers / question archive / Submit Concept Maps here by due date - 23 concept maps are due

Submit Concept Maps here by due date - 23 concept maps are due

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Submit Concept Maps here by due date - 23 concept maps are due. PDF, doc, and docx will be the ONLY accepted formats, other formats will NOT be accepted for grading. Plagarism review is turned on for this assignment, remember to cite your sources in proper APA format (7th edition) if you are using direct quotes. Also, try to reword using your own words and still provide an in-text citation. There are 23 total concept maps due for this module (every disease exemplar in module 1). You just need one primary concept and then 2 more concepts (both with rationale of how they relate to the disease itself). Also, you need to use your own words the best you can when filling out etiology, patho, CM, risks, labs/diagnostics.

Name: ___________________________ Immunity Etiology #3 Pathophysiologic process #4 Risk Factors/Populations #6 Hypersensitivity Reaction I Clinical Manifestations #5 Labs/Diagnostic Tests #7 Nursing Concept #1 (2) mobility • Provide rationale for how this nursing concept links with concept #1 (1) Nursing Concept #1 (3) nutrition • Provide rationale for how this nursing concept links with concept #1 (1) Name: ___________________________ Immunity Etiology #3 Pathophysiologic process #4 Risk Factors/Populations #6 Hypersensitivity Reaction II Clinical Manifestations #5 Labs/Diagnostic Tests #7 Nursing Concept #1 (2) comfort • Provide rationale for how this nursing concept links with concept #1 (1) Nursing Concept #1 (3) coping • Provide rationale for how this nursing concept links with concept #1 (1) Name: ___________________________ Immunity Etiology #3 Pathophysiologic process #4 Risk Factors/Populations #6 Hypersensitivity Reaction III Clinical Manifestations #5 Labs/Diagnostic Tests #7 Nursing Concept #1 (2) tissue integrity • Provide rationale for how this nursing concept links with concept #1 (1) Nursing Concept #1 (3) cellular regulation • Provide rationale for how this nursing concept links with concept #1 (1) Name: ___________________________ Immunity Etiology #3 Pathophysiologic process #4 Risk Factors/Populations #6 Hypersensitivity Reaction IV Clinical Manifestations #5 Labs/Diagnostic Tests #7 Nursing Concept #1 (2) cellular regulation • Provide rationale for how this nursing concept links with concept #1 (1) Nursing Concept #1 (3) thermoregulation • Provide rationale for how this nursing concept links with concept #1 (1) Name: ___________________________ Immunity Etiology #3 Pathophysiologic process #4 Risk Factors/Populations #6 Acquired Immunodeficiency Syndrome AIDS Clinical Manifestations #5 Labs/Diagnostic Tests #7 Nursing Concept #1 (2) • Provide rationale for how this nursing concept links with concept #1 (1) Nursing Concept #1 (3) • Provide rationale for how this nursing concept links with concept #1 (1) Name: ___________________________ Concept #1 (1) Etiology #3 Pathophysiologic process #4 Risk Factors/Populations #6 Disease #2 Clinical Manifestations #5 Labs/Diagnostic Tests #7 Nursing Concept #1 (2) • Provide rationale for how this nursing concept links with concept #1 (1) Nursing Concept #1 (3) • Provide rationale for how this nursing concept links with concept #1 (1) Name: ___________________________ Immunity Etiology #3 Pathophysiologic process #4 Risk Factors/Populations #6 Systemic Lupus Erythematosus SLE Clinical Manifestations #5 Labs/Diagnostic Tests #7 Nursing Concept #1 (2) • Provide rationale for how this nursing concept links with concept #1 (1) Nursing Concept #1 (3) • Provide rationale for how this nursing concept links with concept #1 (1) Name: ___________________________ Fluid and Electrolytes balance Etiology #3 Pathophysiologic process #4 Risk Factors/Populations #6 Hyponatremia Clinical Manifestations #5 Labs/Diagnostic Tests #7 Nursing Concept #1 (2) • Provide rationale for how this nursing concept links with concept #1 (1) Nursing Concept #1 (3) • Provide rationale for how this nursing concept links with concept #1 (1) Name: ___________________________ Fluid and Electrolytes balance Etiology #3 Pathophysiologic process #4 Risk Factors/Populations #6 Hypernatremia Clinical Manifestations #5 Labs/Diagnostic Tests #7 Nursing Concept #1 (2) • Provide rationale for how this nursing concept links with concept #1 (1) Nursing Concept #1 (3) • Provide rationale for how this nursing concept links with concept #1 (1) Name: ___________________________ Fluid and Electrolytes balance Etiology #3 Pathophysiologic process #4 Risk Factors/Populations #6 Hypokalemia Clinical Manifestations #5 Labs/Diagnostic Tests #7 Nursing Concept #1 (2) • Provide rationale for how this nursing concept links with concept #1 (1) Nursing Concept #1 (3) • Provide rationale for how this nursing concept links with concept #1 (1) Name: ___________________________ Fluid and Electrolytes balance Etiology #3 Pathophysiologic process #4 Risk Factors/Populations #6 Hyperkalemia Clinical Manifestations #5 Labs/Diagnostic Tests #7 Nursing Concept #1 (2) • Provide rationale for how this nursing concept links with concept #1 (1) Nursing Concept #1 (3) • Provide rationale for how this nursing concept links with concept #1 (1) Name: ___________________________ Fluid and Electrolytes balance Etiology #3 Pathophysiologic process #4 Risk Factors/Populations #6 Metabolic Acidosis Clinical Manifestations #5 Labs/Diagnostic Tests #7 Nursing Concept #1 (2) • Provide rationale for how this nursing concept links with concept #1 (1) Nursing Concept #1 (3) • Provide rationale for how this nursing concept links with concept #1 (1) Name: ___________________________ Fluid and Electrolytes balance Etiology #3 Pathophysiologic process #4 Risk Factors/Populations #6 Metabolic Alkalosis Clinical Manifestations #5 Labs/Diagnostic Tests #7 Nursing Concept #1 (2) • Provide rationale for how this nursing concept links with concept #1 (1) Nursing Concept #1 (3) • Provide rationale for how this nursing concept links with concept #1 (1) Name: ___________________________ Fluid and Electrolytes balance Etiology #3 Pathophysiologic process #4 Risk Factors/Populations #6 Respiratory acidosis Clinical Manifestations #5 Labs/Diagnostic Tests #7 Nursing Concept #1 (2) • Provide rationale for how this nursing concept links with concept #1 (1) Nursing Concept #1 (3) • Provide rationale for how this nursing concept links with concept #1 (1) Name: ___________________________ Fluid and Electrolytes balance Etiology #3 Pathophysiologic process #4 Risk Factors/Populations #6 Respiratory Alkalosis Clinical Manifestations #5 Labs/Diagnostic Tests #7 Nursing Concept #1 (2) • Provide rationale for how this nursing concept links with concept #1 (1) Nursing Concept #1 (3) • Provide rationale for how this nursing concept links with concept #1 (1) Name: ___________________________ Intracranial regulation Etiology #3 Pathophysiologic process #4 Risk Factors/Populations #6 Delirium Clinical Manifestations #5 Labs/Diagnostic Tests #7 Pain • Provide rationale for how this nursing concept links with concept #1 (1) health promotion • Provide rationale for how this nursing concept links with concept #1 (1) Name: ___________________________ Intracranial regulation Etiology #3 Pathophysiologic process #4 Risk Factors/Populations #6 Seizure disorders Clinical Manifestations #5 Labs/Diagnostic Tests #7 Pain • Provide rationale for how this nursing concept links with concept #1 (1) health promotion • Provide rationale for how this nursing concept links with concept #1 (1) Name: ___________________________ Intracranial regulation Etiology #3 Pathophysiologic process #4 Risk Factors/Populations #6 Parkinson’s disease (PD) Clinical Manifestations #5 Labs/Diagnostic Tests #7 Pain • Provide rationale for how this nursing concept links with concept #1 (1) health promotion • Provide rationale for how this nursing concept links with concept #1 (1) Name: ___________________________ Intracranial regulation Etiology #3 Pathophysiologic process #4 Risk Factors/Populations #6 Amyotrophic lateral sclerosis (ALS) Clinical Manifestations #5 Labs/Diagnostic Tests #7 Pain • Provide rationale for how this nursing concept links with concept #1 (1) health promotion • Provide rationale for how this nursing concept links with concept #1 (1) Name: ___________________________ Intracranial regulation Etiology #3 Pathophysiologic process #4 Risk Factors/Populations #6 Traumatic Brain Injury Clinical Manifestations #5 Labs/Diagnostic Tests #7 • Provide rationale for how this nursing concept links with concept #1 (1) • Provide rationale for how this nursing concept links with concept #1 (1) Name: ___________________________ Intracranial regulation Etiology #3 Pathophysiologic process #4 Risk Factors/Populations #6 Spinal Cord injury Clinical Manifestations #5 Labs/Diagnostic Tests #7 • Provide rationale for how this nursing concept links with concept #1 (1) • Provide rationale for how this nursing concept links with concept #1 (1) Name: ___________________________ Intracranial regulation Etiology #3 Pathophysiologic process #4 Risk Factors/Populations #6 Meningitis Clinical Manifestations #5 Labs/Diagnostic Tests #7 • Provide rationale for how this nursing concept links with concept #1 (1) • Provide rationale for how this nursing concept links with concept #1 (1) Name: ___________________________ Intracranial regulation Etiology #3 Pathophysiologic process #4 Risk Factors/Populations #6 Encephalitis Clinical Manifestations #5 Labs/Diagnostic Tests #7 • Provide rationale for how this nursing concept links with concept #1 (1) • Provide rationale for how this nursing concept links with concept #1 (1) Pathophysiology Instructor: Dr. Crystal-Rae Evans, PhD, RN Immunity Disease Exemplars Hypersensitivity Reaction I ** Allergic Reactions or Anaphylaxis (severe form) ** Etiology: Exposure to foreign antigens (Allergens: cats, dogs, tree nuts, hormones (insulin) Pathophysiology: The reaction happens immediately. B-cells are stimulated (by CD4+ Th2 cells) to produce IgE antibodies specific to an antigen. The cellular component responsible for this reaction is the mast cell or basophil. Clinical Manifestations: Effects on the nose (rhinitis, inflammation, hay fever) airways (inflammation, constriction, asthma, throat irritation), and skin (eczema, hives and edema) **If untreated anaphylaxis or death could occur. Risk Factors/Populations at Risk: - Genetic (Atopy) - Autoimmune disorders/Compromised immune system - Allergies - Environmental factors - Children Labs/Diagnostic Tests: - Complete blood count - Assessment of Immunoglobulins - Skin prick test - Radioallergosorbent test: determine specific IgE antibodies https://www.youtube.com/watch?v=hWq_kdjRAP8 Hypersensitivity Reaction II ** Transfusion Reactions ** Tissue Transplant Rejection ** Platelet disorders ** Etiology: Immune reaction against a specific cell or tissue resulting in cellular lysis induced by the direct binding of antibody (IgG and IgM) to cell surface antigens. Pathophysiology: Cell surface antigens draw out antibodies response → Antibodies bind to cell → cell is lysed or complement components attract phagocytic cells → tissue damage by the release of proteolytic enzymes Clinical Manifestations: Urticaria, anaphylaxis, immediate drug reaction, hemolytic anemia, serum sickness, Neutropenia, Thrombocytopenia. Risk factors/Populations at risk: Environmental factors (drugs or their metabolites), autoimmune diseases (Autoimmune thrombocytopenic purpura, Graves disease, autoimmune hemolytic anemia) Labs/Diagnostic Tests: CBC with differential, coomb tests (hemolytic anemia), test number and sizes of bone marrow cells (where mature platelets are released), numerous in vitro tests: anti-CD16-coated plates, monoclonal antibody-coated target cells (monitor ADCC function of NK cells), Drug provocation test (DPT) if the hypersensitivity is believed to be from a drug https://www.youtube.com/watch?v=xVHkXNXrsbg Hypersensitivity Reaction II Hypersensitivity Reaction III **Type III is not organ specific and most commonly results in a vasculitis in the skin, kidney, or lungs. This takes hours to happen.** Etiology: Most are caused by antigen-antibody complexes that are formed in the circulation and are deposited in vessel walls or other tissues. Pathophysiology: The antibody (IgG, IgM) binds to soluble antigens that was released into blood or body fluids. This occurs when there is accumulation of immune complexes (antigen-antibody complexes) that have not been adequately cleared by innate immune cells, giving rise to an inflammatory response and attraction of leukocytes generally leading into immune complex diseases. Clinical Manifestations: Localized Arthus reaction (when caused by vaccines), Serum sickness. Type 3 reactions have a unique characteristic of clumping and dumping. Patients will show symptoms of fever, enlarged lymph nodes, rash and pain at inflamed sites. Risk Factors/Population at Risk: Autoimmune disorders (SLE), compromised immune system Labs/Diagnostic Test: There is no single test to determine a type 3 reaction https://www.youtube.com/watch?v=-_yUsZO6Vio Hypersensitivity Reaction IV **Contact sensitivity to poison ivy, metals (jewelry), and latex** ** Cell-mediated reaction** Etiology: T cells recognize foreign antigens on the surface of antigen presenting cells. Pathophysiology: Exposure to antigen→ 24-72 hours after exposure to antigen Tc (helper) cells attack and destroy cellular targets → Inflammation and breakdown of the antigen cell leads to tissue destruction. Clinical Manifestations: Contact dermatitis; pruritus, swelling/edema, rash, blisters, redness; anaphylaxis: difficulty breathing, shock, nausea and vomiting Risk Factors/Populations at Risk: Autoimmune Diseases (Grave’s disease, Hashimoto, Rheumatoid Arthritis, Lupus, and Type 1 Diabetes), Genetic, Contact with chemicals, Outdoor activity (ex. Plants), Cosmetics / ointments / topical medicines, Adhesives, Metals, Receiving Mantoux skin test to test for Tuberculosis, Skin graft (results in rejection) Labs/Diagnostic Tests: Patch Testing/Allergy Test https://www.youtube.com/watch?v=kQFmrQfBW5k Acquired Immunodeficiency Syndrome AIDS **Secondary immune deficiency** ** Blood-Borne Pathogen ** Etiology: HIV infects and destroys the CD4-positive Th cells which are necessary for the development of both plasma and cytotoxic T cells. HIV suppresses the immune system against itself which leads to the development of AIDS and suppresses development of immune responses against other pathogens and opportunistic microorganisms Pathophysiology: HIV attaches itself to CD4 and enters → HIV copies itself to make more virus → HIV and CD4 cell fight HIV damages CD4 cell → Young HIV leaves CD4 → HIV grows mature and goes off to invade more CD4 cells https://www.youtube.com/watch?v=GR8oOMifISM Clinical Manifestations: 1. Serologically negative—no detectable antibody 2. Serologically positive but asymptomatic—positive for antibody against HIV proteins 3. Early stages of HIV—mild and nonspecific symptoms a. Resemble influenza (sweats, chills, recurring fever, chronic diarrhea, swollen lymph, white spots/lesion on tongue/in mouth, fatigue, weakness, weight loss, rashes) b. Disappear after 1-6 weeks 4. AIDS—more serious signs and symptoms a. Atypical or opportunistic infections and cancers b. Debilitating chronic disease Acquired Immunodeficiency Syndrome AIDS Risk Factors/Populations at Risk: Unprotected sex, Sharing needles or contaminated medical injection tools, Use of blood/blood products, Mother to fetus transmission, African Americans and Latinos, Transgender individuals (male to female), Gay and bisexual men, Women affected by HIV/AIDs more often Labs/Diagnostic Tests: CD4 count < 200/mmg, CBC, HIV Viral load, Enzyme-linked immunosorbent assay (ELISA), Western blot antibody testing, CBC, Protein p24 (HIV antibody), Polymerase chain reaction, Clinical Symptoms** Systemic Lupus Erythematosus SLE ** Most common autoimmune disease, Chronic multisystem inflammatory disease** **Type II and III hypersensitivity reaction** Etiology: The causes of SLE are unknown but it can be linked to genetic, environmental and hormonal factors (CDC, 2018) Pathophysiology: Activation of T-helper and B cells → Production of autoantibodies that attack self antigens (such as nucleic acids and erythrocytes) → tissue damage. *Antibodies are attacking the body’s own tissues instead of foreign invaders* Risk Factors/Populations at Risk: • Females (9:1) more likely than males • 20-40 yrs • African American (8:1) more likely than whites • Autoimmune diseases in family Systemic Lupus Erythematosus SLE Clinical Manifestations Labs/Diagnostic Tests: Blood Tests • CBC (measures the number of RBC, WBC & platelets) • Antibody tests (finds out if your immune system is attacking healthy tissue) • Blood clotting time tests (to check for clotting problems) • Complement tests (checks for signs of inflammation) Urine Tests (detects problems with kidneys) Biopsies (checks tissue for any signs of inflammation and damage) (Lupus Foundation of America, 2020) Systemic Lupus Erythematosus SLE Khan Academy Video: Systemic Lupus Erythematosus (SLE) - causes, symptoms, diagnosis & pathology (11min) Pathophysiology Instructor: Dr. Crystal-Rae Evans, PhD, RN Fluid and Electrolyte Disease Exemplars Acid-Base Disease Exemplars Hyponatremia Etiology: Sodium level of 145 Types: I, Hypovolemic, Hypervolemic Isovolemic Risk Factors: advanced age, mental or physical impairment, uncontrolled diabetes, underlying polyuria disorders, diuretic therapy, nursing home residents, hospitalized patients Pathophysiology: High levels of ECF sodium → osmotic attraction of water → water goes out of cell → cell shrinkage Clinical Manifestations: • Neurologic changes: Confusion, Neuromuscular excitability, Hyperreflexia, Seizures, Coma • Thirst • Weight gain • Increased blood pressure Labs: Urine and plasma osmolality ;Urine and serum electrolytes Hypernatremia Hypokalemia Etiology and Risk Factors: Potassium level 45, pH 7.45) https://www.youtube.com/watch?v=Kw89JJZU3GA&list=PLQrdx7rRsKfXyEQ16C2E1zI6MLPFk0hSB& index=3 ME VISUAL Respiratory acidosis VS.Respiratory Alkalosis Pathophysiology Instructor: Dr. Crystal-Rae Evans, PhD, RN Neurologic Disease Exemplars Delirium Etiology: Acute confusional state → cognitive deficits caused by physiologic changes in the brain. Underlying physiological causes that are usually multifactorial in nature. Pathophysiology: *Limited understanding of pathogenesis* There is disruption in the right-upper middle temporal gyrus or left temporal-occipital junction and neurotransmitters (acetylcholine and dopamine). Associated with ANS overactivity and usually develops over 2-3 days. Clinical Manifestations: Disorientation, Hallucinations, Restlessness, Combative Behavior, Anxiety, Depression,Difficulty Concentrating, and Poor Appetite Risk Factors and Populations at risk: Surgery/Post-anesthesia, Geriatric population, Comorbid illnesses such as Dementia, Stroke or Parkinson’s Disease, Visual or Hearing Impairment, Past delirium episodes, Drug/ETOH withdrawal Labs/ Diagnostic Test: Mental status exam or confusion assessment method (CAM), Neurologic exam, Physical exam Seizure disorders Etiology: Often cause is unknown (idiopathic); electrolyte imbalances, congenital malformations, perinatal injury, trauma, myoclonic syndromes, infection, brain tumors, vascular disease, fever, drug abuse, genetics Pathophysiology: Abnormal discharge of electrical activity within the brain. When a sufficient number of neurons become overexcited, they discharge abnormally, which sometimes results in clinical manifestations (seizures) with alterations in motor function, sensation, autonomic function, behavior, and consciousness. If there is more than one unprovoked seizure, it is said the individual would have epilepsy. Risk Factors: Structural abnormalities of the brain, Hypoxia, Intracranial hemorrhage, CNS infection, Traumatic injury, Electrolyte imbalance, Inborn metabolic disturbances, Genetic/familial, High fever, Lack of sleep, Hyponatremia, Stroke, Brain tumor, Alcohol abuse (during withdrawal or extreme intoxication), Illegal drug use (such as amphetamines or cocaine), Environmental stimuli (i.e. blinking lights or loud music) Seizure Disorders TYPE GENERALIZED SEIZURE (4 types) CLINICAL MANIFESTATIONS Seizure activity starts in or involves both cerebral hemispheres; consciousness may be impaired; bilateral manifestations; may be preceded by an aura Tonic-Clonic Musculature stiffens followed by intense jerking as trunk and extremities undergo rhythmic contraction and relaxation Atonic Sudden, momentary loss of muscle tone, drop attacks Myoclonic Sudden, brief contractures of a muscle or group of muscles Absence Seizure Brief loss of consciousness with minimal or no loss of muscle tone; may experience 20 or more episodes a day that last approx. 5 to 10 seconds each; may have minor movement such as lip smacking or twitching of eyelids STATUS EPILEPTICUS Continuing or a recurrent seizure activity that recovery from the seizure activity is incomplete; unrelenting seizure activity can last 30 minutes or more; medical emergency that requires immediate intervention Seizure disorders Clinical Manifestations: Symptoms range from mild to severe depending on the type of seizure signs and symptoms could be temporary confusion, staring spell, loss of consciousness or awareness and uncontrollable jerking movements Preictal Phase: (The time before the seizure, last minutes to days) - Prodroma (Beginning phase) early signs are mood changes, behavioral changes, anxiety, difficulty sleeping Aura(partial seizure) is the early part of the seizure, early signs are odd smells, dizziness, numbness, “funny feeling” Ictal Phase (Middle phase/event of seizure) The time from the first symptom to end of seizure activity, common signs are loss of awareness, memory lapse, loss of muscle control - Tonic phase, the state of muscle contraction in which there is excessive muscle tone Clonic phase, the state of alternating contraction and relaxation of muscles Postictal Phase (Ending phase) is the recovery stage and time period immediately after the seizure activity, common signs are confusion, loss of conscious, sore muscles, fatigue, and exhaustion Seizure Disorders Seizure Disorders Labs/Diagnostic Tests ? A neurological exam ? Blood tests (electrolyte imbalance?) ? Lumbar puncture (CNS infection?) ? Electroencephalogram (EEG) ? CT scan ? MRI ? Single-Photon Emission Computerized Tomogra ? phy (SPECT) Parkinson’s disease (PD) Etiology: idiopathic disease, it can be the combination of gene, environmental and lifestyle influence which cause a loss of dopaminergic neurons in substantia nigra. Pathophysiology: degeneration of the basal ganglia → loss of dopaminergic neurons in the substantia nigra and dorsal striatum -> dopamine deficiency. Clinical manifestations: Not all but most people have these, symptoms are worsen over time. • at first: resting tremor, muscle rigidity, bradykinesia. • later on: postural disturbance. Risk factors: • some pesticides: cleaning chemicals • age: people >60 yrs old have a higher chance • history of concussions • gender: men have a little higher chance than women • heavy metals: Copper (Cu), Manganese (Mn), Lead (Pb) in industrial area. Labs/ Diagnostic tests: no specific test to confirm PD. A combination of: • Clinical history (based on symptoms worsen overtime, and eventually the loss of smell) • Neurological exams (physical exams): look for signs • Give medicine (L-dopa) that restores dopamine -> the medicine works -> they have PD. • Check with patients overtime to see how the symptoms worsen. Amyotrophic lateral sclerosis (ALS) Etiology: Neurodegenerative disorder that diffusely involves lower and upper motor neurons, resulting in progessive muscle weakness. (Amyotrophic) without muscle nutrition Pathophysiology: Degeneration of lower and upper motor neurons → Decrease in large motor neurons in spinal cord, brainstem, and cerebral cortex. Clinical Manifestations: • Common symptoms of ALS are heterogeneous, lower and upper motor neuron dysfunction. Muscle weakness beginning in the arms and legs. About 60% of individuals have spinal of ALS. • When ALS starts to progress the symptoms that will occur are muscle atrophy, spasticity, frontotemporal dementia, and loss of manual dexterity and gait. ALS with progressive bulbar palsy causes difficulty speaking and swallowing. Peripheral muscle weakness and atrophy usually occur within 1 to 2 years. Risk Factors/Populations at Risk: • Hereditary • Most common between ages of 40 and mid-60’s • More men develop ALS than women Labs/Diagnostic Tests: • Genetic testing • Electromyography and muscle biopsy examination Traumatic Brain Injury **CNS disorder** Etiology: TBI can be caused by a bump, blow, or jolt to the head that disrupts the normal function of the brain(CDC) Pathophysiology: Alteration in the brain function caused by an external force such as a motor vehicle accidents, falls, etc. Risk Factors: Athletes such as footballers, boxers; drunk drivers, males, infants-children under 4 years old, those at risk for falls (older adults and children), lower- and median-income families Labs/Diagnostic Tests: CT scan, MRI, intracranial pressure monitoring, Glasgow Coma Scale (GCS), speech and language tests, & cognition and neuropsychological tests Traumatic Brain Injury Clinical Manifestations: (some S&S may appear right away, others can take days or weeks to appear. Also depends on severity of injury. - Mild Traumatic Injury: Brief loss of consciousness (few mins/secs) or no loss, headache, nausea, vomiting, fatigue, drowsiness, problems with speech, sleeping more than usual or having difficulty sleeping, loss of balance, dizziness, sensory problems (blurred vision, ringing in ears, changes in smell and taste) mood and memory changes, difficulty concentrating. - Moderate to Severe Traumatic Injury: - LOC for several minutes to hours, persistent headache, continuous nausea & vomiting, convulsions and seizures, pupil dilation, clear fluids draining from nose and ears, difficulty waking from sleep, numbness in fingers and toes, loss of coordination, profound confusion, combative and unusual behaviors, difficulty with speech, coma Spinal Cord injury Etiology: Spinal cord injury can be a result of fracture or dislocation of the vertebrae due to traumatic injury, a severed or segmented spinal cord due to other penetrating injury. Pathophysiology: Primary: Initial mechanical trauma -> immediate tissue destruction Secondary: microscopic hemorrhage central grey matter->edema in white matter-> decrease vascular perfusion-> tissue death/loss function Vertebral: force of rapid acceleration, deceleration, or deformation occurring at impact → vertebrae destruction, inflammatory response, loss of function Clinical Manifestations: 1.Spinal shock: below the level of injury ceases with complete loss of reflex function, flaccid paralysis, absence of sensation,loss of bladder and rectal control , transient drop in blood pressure, and poor venous circulation.Also, individual assumes the temperature of air( poikilothermia) 2.Neurogenic shock:including vasodilation,hypotension,bradycardia,and failure of body temperature regulation. 3.Autonomic hyperreflexia(dysreflexia):includes paroxysmal hypertension(up to 300mm Hg,systolic), pounding headache, blurred vision,sweating above the level of the lesion with flushing of the skin, nasal congestion, nausea, piloerection cause by pilomotor spasm,and bradycardia(30 to 40 beats/min). Spinal Cord Injury Risk Factors/Population at risk: Male, between the ages of 16 and 30, older than 56, engaging in risky behavior, and having a bone or joint disorder Lab/ Diagnostic Test: Physical Examination: test sensory functions, muscle movement and strength, and reflexes through a physical examination), Imaging studies: X-ray, CT scan, or MRI Myelogram: assess muscle conduction and function Spinal Cord Injury Meningitis Etiology: can be caused by bacteria, viruses, fungi, parasites, or toxins. Inflammation of the brain or spinal cord. Pathophysiology: Bacteria enter blood stream/sinuses or ears/trauma (penetrating head wound) → neutrophils fight the infection → cytotoxic inflammatory agents → damage brain tissue → blood vessels are more permeable → CSF thickens → normal flow is impaired (hydrocephalus) and meningeal cells swell and exudate (increased intracranial pressure) - Can be acute/subacute/chronic Two most common types: - Bacterial (Infection of pia mater and arachnoid villi, subarachnoid space, ventricular system CSF) - Most common pathogens causing this are Meningococci (Neisseria Meningitidis) and Pneumococci (Streptococcus Pneumoniae). - Viral (limited to meninges - no identifiable bacteria in CSF) - Virus enters by crossing blood brain barrier, direct spread along peripheral nerves, or through choroid plexus epithelium. Clinical Manifestations: Same symptoms for both, but viral meningitis is usually milder. • • • • Signs of infection: Fever, tachycardia, chills, petechial rash Signs of increased ICP: Vomiting, Headache, Irritability, Seizures Decreased level of consciousness/confusion/delirium Stiff neck (nuchal rigidity) Meninges: Protective layers of brain and spinal cord Pia mater Dura mater Arachnoid Meningitis Risk Factors: • • • • • • Skipping vaccinations (children or adult) Age: Most cases of viral meningitis occur in children younger than 5. Bacterial meningitis is common in those under age 20. Living in a community setting: College students, living in dormitories. This is probably because the bacterium is spread by the respiratory route and spreads quickly through large group. Pregnancy: increases the risk of listeriosis. Compromised immune system: AIDS, alcoholism, diabetes, use of immunosuppressant drugs and other factors that affects your immune system. Removed spleen. Labs/Tests: Physical examination, blood cultures, nasopharyngeal smear, antigen tests, CSF analysis (determine causative organism, High WBCs and neutrophils, low glucose), CT scan, MRI, intracranial pressure monitoring, Glasgow coma test, speech and language tests, & cognition and neuropsychological tests Encephalitis Etiology: Caused by bites of mosquitoes, ticks or flies, and herpes simplex type 1. It can arise after recovery from viral infections such as rubella, varicella, rubeola, or yellow fever. Inflammation of the brain. Pathophysiology: Viruses gain access to the CNS through the bloodstream, olfactory bulb, or choroid plexus, or through an intraneuronal route from peripheral nerves → meningeal involvement is present in all encephalitides → widespread nerve cell degeneration → viruses cross into the BBB to neurons and disrupts functioning → inflammation, edema, necrosis with or without hemorrhage, and increased intracranial pressure develop Clinical Manifestations: Mild: Malaise, headache, body aches, nausea, vomiting Severe: Fever, difficulty with word finding, seizure activity, cranial nerve palsies, paresis and paralysis, involuntary movement, abnormal reflexes, and delirium or confusion progressing to unconsciousness. signs of ICP may be present. Risk Factors/Populations at risk: Young children, Older adults, Regions where mosquito and tick borne illnesses are popular, and seasonal (mosquito and tick borne illnesses are popular in the summer) Labs / Diagnostics: History and Physical CSF examination & culture (elevated WBCs, high protein) Labs (WBCs) CT scan or MRI (hemorrhage, edema) https://www.youtube.com/watch?v=LX5-dY9BV8Y Guillain-Barre Syndrome **Rare, acquired inflammatory disease-causing demyelination of the peripheral nerves** Etiology: The exact cause of GBS is unknown, but thought to be an autoimmune inflammatory response (humoral and cellular immunologic reaction); precipitating events (Camplyobacter jejuni 60%). Pathophysiology: Precipitating cause → axonal demyelination → nerve conduction stops or slows (peripheral nerves) → muscle weakness or loss of reflex response and/or paralysis (Motor neurons are affected more than sensory neurons) Clinical Manifestations **Progressive symptoms: weakness → paralysis ** Medical Emergency!! Acute onset, ascending motor paralysis Clinical manifestations are related to antibody subtypes: manifestations can include paresis of legs to complete quadriplegia, paralysis of eye muscles, respiratory insufficiency (20%), autonomic nervous system instability, sensory symptoms (pain, numbness, paresthesia): may progress to respiratory arrest of cardiovascular collapse. Risk Factors: Older age, respiratory or gastrointestinal infection, vaccinations (especially influenza and meningococcal), history of lymphoma, systemic lupus erythematosus, or HIV and AIDS, and recent surgery Labs/Diagnostic Tests: The clinical diagnosis of GBS needs to be confirmed by cerebrospinal fluid analysis and nerve conduction studies. Lumbar puncture is indicated in every case of suspected GBS (CSF - high protein). https://www.youtube.com/watch?v=6vYwVPQ77J4&t=29s https://www.youtube.com/watch?time_continue=6&v=4omfTbiB0kk&feature=emb_title ETIOLOGY CONCEPT HIV infects and destroys the CD4 positive Th cells which are necessary for the development of both plasma and cytotoxic T cells. HIV suppresses the immune system against itself which leads to the development of AIDS and suppresses the development of immune responses against other pathogens and opportunistic microorganisms. IMMUNITY PATHOPHYSIOLOGY HIV attaches itself to CD4 and enters -> HIV copies itself to make more virus -> HIV and CD4 cell fight HIV damages CD4 cell -> young HIV leaves CD4 -> HIV grows mature and goes off to invade more CD4 cells CLINICAL MANIFESTATIONS Early stages of HIV – mild/nonspecific symptoms (resembles influenza) AIDS AIDS – more serious s&S (4 stages), opportunistic infections at the end *Secondary immune deficiency* Muscle/joint pain, rash, nausea, vomiting, weight loss, diarrhea, viral infections, swollen lymph nodes, drowsiness LABS/DIAGNOSTIC TESTS RISK FACTORS CD4 count

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