Week 1 Intro to Patho and Infection SC (2) PDF

WELCOME TO NSG 302 Expectations Introductions Review of Syllabus Lecture Zia W. Massar, MS, AGACNP-BC, CCRN Mount Sinai Phillips School of Nursing NSG 302 CHAPTER 1 INTRODUCTION TO...

WELCOME TO NSG 302 Expectations Introductions Review of Syllabus Lecture Zia W. Massar, MS, AGACNP-BC, CCRN Mount Sinai Phillips School of Nursing NSG 302 CHAPTER 1 INTRODUCTION TO PATHOPHYSIOLOGY PATHOPHYSIOLOGY Foundational building block to future nursing courses Study of functional changes in the body caused by injury, disorder, or disease Homeostasis Related sciences  Pathology  Anatomy and physiology  Biology  Microbiology  Chemistry DISEASE Functional impairment of cells, tissues, organs, or organ systems Often used broadly to include:  Injuries  Disorders  Illnesses  Syndromes ASPECTS OF DISEASE PROCESS Etiology Pathogenesis Clinical Manifestations Diagnosis Prognosis Treatment PATHOGENESIS Origination and development of illness or disease Encompasses  From point at which disease process begins  To point when disease presents itself  Risk factors (modifiable vs. nonmodifiable) Goal of study is to prevent disease or facilitate early diagnosis and intervention ETIOLOGY Precise cause of disease Types  Pathogen: disease-causing microorganism  Multifactorial: having more than one cause  Idiopathic: no known cause  Nosocomial: caused by an infection received in a healthcare environment  Iatrogenic: caused inadvertently by medical treatment CLINICAL MANIFESTATIONS Presenting signs and symptoms of disease Signs vs. symptoms Local vs. systemic Acute vs. subacute vs. chronic Remissions vs. exacerbations Asymptomatic DIAGNOSIS AND TREATMENT Diagnosis  A label for a disease  Based on diagnostic criteria Prognosis  Prediction of how one will proceed through the disease process  Morbidity vs. mortality Treatment PATHOPHYSIOLOGY CONCEPT MAP INDIVIDUAL HEALTH Focuses on:  The whole person  The person’s perception of health and illness Continuum of health and illness  Health: perceived wholeness of body, mind, and spirit  Illness: a state resulting in suffering or distress Homeostasis POPULATION HEALTH Epidemiology  Incidence: the number of new cases arising in a population at risk during a specified time  Prevalence: a measure of existing disease in a population at a given point in time Classification of global disease  Endemic  Epidemic  Pandemic World Health Organization (WHO) LEVELS OF PREVENTION Primary prevention  Prevention of a disease from occurring Secondary prevention  Early detection of disease by screening Tertiary prevention  Rehabilitation of a patient to prevent complications or progression of disease EVIDENCE-BASED PRACTICE A way of caring for others that is cognizant of the most current research and knowledge in the health professions Characteristics  Goes beyond one piece of research  Encompasses totality of what is known through research and knowledge and practice of experts  Requires conscientious respect for human health variations HUMAN DIVERSITY Factors affecting pathogenesis:  Gender  Age  Race  Locale  Socioeconomic status  Ethnicity Zia W. Massar, MS, AGACNP-BC, CCRN Mount Sinai Phillips School of Nursing NSG 302 CHAPTER 2 ALTERED CELLS AND TISSUES REVIEW OF CELLULAR STRUCTURE AND FUNCTION Please review normal cell structure/function in Chapter 2  CELLULAR RESPONSE TO Atrophy STRESS Hypertrophy Hyperplasia Metaplasia Dysplasia CELLULAR INJURY AND DEATH Mechanisms of death  Apoptosis  Necrosis Causes of injury  Mechanical  Thermal  Chemical APPLICATION OF THE CONCEPTS OF ALTERATIONS IN CELLS AND TISSUES o Cerebral atrophy o Cardiac hypertrophy CEREBRAL ATROPHY PATHOPHYSIOLOGY Reduction in size of the cells in the cerebrum of the brain Progressive reduction in the size of the neurons Result of  Reduced stimulation  Injury CEREBRAL ATROPHY CLINICAL MANIFESTATIONS AND DIAGNOSTIC CRITERIAL Clinical Manifestations Diagnostic Criteria Focal Early identification of loss of  Localized to a particular region function Global Health History  Affecting the entire brain  Onset  Duration  Severity Neurologic examination Imaging Studies  PET scans  CT/MRI/SPECT CEREBRAL ATROPHY TREATMENT Prevention Interruption of injury process Slowing course of disease  CARDIAC HYPERTROPHY (HOCM) PATHOPHYSIOLOGY Increased cardiac muscle mass Etiology  Excessive cardiac workload  Increased functional demand  Inherited genetic trait 2 categories  Primary  Inherited  Secondary  Due to an underlying condition increasing left ventricular workload  Increase in left ventricular muscle mass results from an increase in myocardial cell size CARDIAC HYPERTROPHY CLINICAL MANIFESTATIONS & DIAGNOSTIC CRITERIA Clinical Manifestations Diagnostic Criteria Variable Genetic Testing  Mild to severe Hypertension (2º HOCM) Shortness of breath EKG, Echo Chest pain Reduced exercise tolerance Syncope (fainting) Ventricular arrhythmia Impaired cardiac function  Altered signals in the cells of the ventricle Heart murmur CARDIAC HYPERTROPHY TREATMENT Pharmacologic  Drugs that relax the ventricles  Drugs that reduce the workload of the heart  Decrease the pressure that the heart must pump against Surgical  Risky procedures  Alcohol Septal Ablation is alternative Nonpharmacologic: activity restriction Zia W. Massar, MS, AGACNP-BC, CCRN Mount Sinai Phillips School of Nursing NSG 302 CHAPTER 3 INFLAMMATION AND TISSUE REPAIR  LINES OF DEFENSE First: Skin and mucous membranes Second: Inflammatory response Third: Immune response ACUTE INFLAMMATION Triggered by tissue injury Goals of inflammation  Vascular Response: Increase blood flow to site  Cellular Response: Increase healing cells at site  Prepare for tissue repair VASCULAR RESPONSE Facilitated by chemical mediators Induces vasodilation and increases capillary permeability Objective is to get more blood flowing to the injured area INFLAMMATION CONCEPT MAP ACTIVE CELLS IN CELLULAR RESPONSE 32 COMMON BLOOD TESTS 33 CLINICAL JUDGMENT FOR INFLAMMATION/INFECTION What is pyrexia? What is leukocytosis? What could too high indicate? What could too low indicate? How do we assess health status using this level? What does an elevation in leukocytes, erythrocyte sedimentation rate (ESR), or CRP tell you about the location of acute or chronic inflammation? 34 MANIFESTATIONS OF INFLAMMATION Local manifestations  Heat  Pain  Edema  Redness Systemic manifestations  Fever  Leukocytosis  Body aches TREATMENT OF INFLAMMATION Reduce blood flow Decrease swelling Block the action of chemical mediators Decrease pain RICE HEALING AND TISSUE REPAIR Inflammatory phase  Acute inflammatory response  Seal the wound Proliferative phase  Clear the debris  Restore structural integrity Remodeling phase  Restore functional integrity  Remodeling PROMOTING PROPER WOUND HEALING Adequate nutrition Healing by intention  Primary  Secondary COMPLICATIONS OF HEALING Infection Ulceration Dehiscence Keloids Adhesions CHRONIC INFLAMMATION Recurrent or persistent inflammation lasting several weeks or longer Monocytes, macrophages, and lymphocytes more prominently involved Formation of granulomas and scarring often occur APPLICATION OF THE CONCEPTS OF INFLAMMATION Sinusitis (chronic & acute) Burns ACUTE SINUSITIS PATHOPHYSIOLOGY Blockage of ostia and outflow of mucus due to allergy, viruses, or other irritants Impaired clearance of mucus by cilia Altered mucus quality or quantity Lasting 4-8 weeks (subacute = 8-12 weeks)  ACUTE SINUSITIS CLINICAL MANIFESTATIONS & DIAGNOSTIC CRITERIA Clinical Manifestations Diagnostic Criteria Facial pain over sinus regions of  Clinical manifestations following face increasing with straining or upper respiratory infection, bending down symptoms lasting >10 days  Physical examination Fever  General laboratory tests Nasal congestion and/or excessive nasal discharge and postnasal o Erythrocyte sedimentation drainage rate (ESR) Persistent cough o C-reactive protein (CRP) test Fatigue o White blood cell (WBC) count  Sinus radiographs o Reveal opaque, mucus- filled sinuses ACUTE SINUSITIS TREATMENT Pharmacologic  Antibiotics  Antihistamines  Decongestants  Nasal sprays Surgical CHRONIC SINUSITIS PATHOPHYSIOLOGY Multifactorial  Environmental factors  Persistent infection  Allergens  Genetic factors  Metabolic abnormalities  Immune deficiencies Disruption of mucociliary clearance Symptoms lasting >12 weeks w/ or w/o flares of acute sinusitis CHRONIC SINUSITIS CLINICAL MANIFESTATIONS & DIAGNOSTIC CRITERIA Clinical Manifestations Diagnostic Criteria Nasal congestion Physical examination Nasal and postnasal discharge  Must have at least 2 present:  Anterior or posterior mucopurulent drainage Sore throat  Facial pain, pressure, fullness,  Hyposmia Foul breath, unpleasant taste  Nasal obstruction Low-grade fever +  Polyps in the nasal cavity or middle meatus - Fatigue, anorexia AND/OR-  Purulent mucus or edema in the middle meatus Chronic cough or ethmoid region Hyposmia (reduced ability to smell) Computed tomography (CT) scan  Might reveal changes to bones, air- Facial fullness, discomfort, pain, and headache fluid levels, mucosal thickening CHRONIC SINUSITIS TREATMENT Pharmacologic  Glucocorticoids  Antibiotics  Nasal saline irrigation Surgical BURNS PATHOPHYSIOLOGY Cause: direct contact with excessive heat or radiation, caustic chemicals, or electricity Result: acute inflammatory response Burn severity is correlated with exposure type and time  BURNS CLASSIFICATIONS & CLINICAL MANIFESTATIONS Superficial partial-thickness burns  Heat, swelling, pain, redness, loss of function Deep partial-thickness burns  Blistering, redness, heat, pain, edema, serous exudate Full-thickness burns  Redness, eschar, edema, exudate BURNS DIAGNOSTIC CRITERIA Rule of nines American Burn Association has designated criteria for distinguishing minor, moderate, and major burns based on  Wound depth  Surface area  Required level of treatment BURNS TREATMENT Moderate/Major burn: need to go to an Burn Center Remove source of injury and cool/rinse skin then dress them and change dressings q1-2d to aid in debridement Airway, breathing, circulation Fluids, nutrition, antibiotics, analgesics Wound management may include  Hydrotherapy  Skin grafting  CHAPTER 4 Zia W. Massar, MS, AGACNP-BC, CCRN Mount Sinai Phillips School of Nursing ALTERED IMMUNITY NSG 302 IMMUNE DEFENSE Third line of defense Recognition and neutralization of foreign substances Specific immune response Immunologic memory CELLULAR COMPONENTS OF IMMUNITY Lymphoid progenitor cells  T lymphocytes  Cytotoxic  Helper  Suppressor  B lymphocytes  Differentiate into plasma cells  Antibody production  Natural killer cells LYMPHATICS Important in establishing the immune response Central organs, bone marrow, and thymus Peripheral organs: spleen, lymph nodes, and lymphoid tissue IMMUNE PROCESSES Innate immunity  Nonspecific  Involves inflammatory processes  Initiates phagocytic process and stimulates the release of chemical mediators Adaptive immunity  Targeted to a specific antigen  Involves T and B lymphocytes  ADAPTIVE IMMUNITY Active immunity  Development of antibodies to an antigen  Achieved by having a specific disease or vaccine Passive immunity  Immunity transfer from host to recipient  Achieved via mother–infant transfer (placenta or breast milk) or injection of antibody Humoral immunity  B lymphocytes  Antibodies secreted from plasma cells IgA, IgD, IgE, IgG, IgM  Memory cells  Primary adaptive immune response  Activation with first recognition of a specific antigen  Secondary adaptive immune response  Reactivation with later recognition of the same antigen ADAPTIVE IMMUNITY ADAPTIVE IMMUNITY Cell-mediated immunity  Cytotoxic T lymphocytes: CD8  Helper T lymphocytes (TH1, TH2): CD4  Major histocompatibility complex (MHC)  MHC class 1 molecules (CD8)  MHC class 2 molecules (CD4)  Also known as human leukocyte antigen (HLA) PROCESS OF ALTERING IMMUNE FUNCTION Host defense failure  Antigenic variation Autoimmunity  Viral latency  Failure to distinguish self from  Immunodeficiency nonself  Causes damage to specific organs or Hypersensitivity to the entire system  Type 1 (immediate) hypersensitivity reaction Alloimmunity  Type II antibody-mediated  Graft rejection hypersensitivity reaction  Graft versus host disease  Type III immune complex–mediated reaction  Type IV cytotoxic T lymphocyte– mediated hypersensitivity reaction  Direct cell-mediated toxicity  Delayed hypersensitivity reaction IMMUNE RESPONSE MANIPULATION Treatment of maladaptive immune responses Immune response in disease management Immune response in the prevention of disease  Vaccines APPLICATION OF THE CONCEPTS OF ALTERATIONS IN IMMUNITY Acquired immunodeficiency syndrome (AIDS) Anaphylactic reaction Systemic lupus erythematosus (SLE) ACQUIRED IMMUNODEFICIENCY SYNDROME (AIDS) PATHOPHYSIOLOGY Altered host defense resulting from secondary immunodeficiency  Infection of CD4 helper T lymphocytes, dendritic cells, and macrophages with human immunodeficiency virus (HIV) Results in loss of cell-mediated and humoral immunity due to loss of CD4 TH1 lymphocytes Transmission:  Blood & body fluid  Perinatally  AIDS CLINICAL MANIFESTATIONS Generalized symptoms:  Fever  Lymphadenopathy  Sore throat  Joint/muscle pain Immunosuppression Opportunistic infections  Fungal infection  Pneumocystis jirovecii pneumonia Kaposi sarcoma AIDS DIAGNOSTIC CRITERIA & TREATMENT Diagnostic Criteria Treatment History and physical Antiretroviral therapy (ART) examination  Suppress viral load  Risk factors  Restore or preserve immune  Signs and symptoms of infection function  Reduce morbidity and mortality Laboratory analysis  Detection of antibodies to HIV Drugs used in combination  Reduce the development of  HIV viral load drug resistance  CD4 T helper lymphocyte cell counts Prophylaxis is the best treatment  PrEP (ART + preventive strategies) ANAPHYLACTIC REACTION PATHOPHYSIOLOGY Exaggerated systemic immune response due to a type 1 hypersensitivity reaction Triggers  Insect stings  Food allergies  Drug allergies Antigen exposure stimulates an IgE-mediated response in a previously sensitized individual. Degranulation of mast cells and basophils occurs locally, but leads to systemic responses via the bloodstream  Dilation of vascular smooth muscle  Constriction of bronchial smooth muscle  Increase in vascular permeability ANAPHYLACTIC REACTION PATHOPHYSIOLOGY ANAPHYLACTIC REACTION CLINICAL MANIFESTATIONS & DIAGNOSTIC CRITERIA Clinical Manifestations Diagnostic Criteria Phase 1  History and physical  Difficulty breathing examination  Skin flushing and urticaria  Allergy testing  Angioedema Phase 2  Difficulty breathing  Severe hypotension  Severe edema ANAPHYLACTIC REACTION TREATMENT Symptomatic  Drugs to relax bronchial smooth muscle  Drugs to constrict vascular smooth muscle  Drugs to limit bronchospasm  Limit inflammation  Airway management Preventative  Desensitization to allergen  Switch IgE response to IgG response  Bind allergen and prevent stimulation of IgE-mediated responses by skin injection in progressively larger doses  Change helper T lymphocyte effectors to down-regulate IgE response SYSTEMIC LUPUS ERYTHEMATOSUS (SLE) PATHOPHYSIOLOGY Type III hypersensitivity reaction Autoimmune response Involves responses by the innate and adaptive immune systems Chronic disease due to persistent antigen  Activation of B cells, producing antibodies  Activation of T cells, promoting inflammation Systemic condition  Autoantibodies targeted against the cell membrane, cytoplasm, and nucleus SLE PATHOPHYSIOLOGY  SLE CLINICAL MANIFESTATIONS & DIAGNOSTICS Specific to organs injured by inflammation and complex deposition Local  Skin, musculoskeletal, pulmonary, and kidney Systemic  Neurologic, pulmonary, hematologic, and cardiac disease  SLE DIAGNOSTIC CRITERIA AND TREATMENT Diagnostic Criteria Treatment History and physical  Pharmacologic examination o Anti-inflammatories Laboratory analysis o Disease-modifying  Antibodies against cell components and DNA antirheumatoid (DMARD)  Antinuclear antibodies (ANA) o Antimalarial  Extractable nuclear antigens (ENAs)  Inflammatory markers: complement o Immunosuppressants (C3 and C4) Must have clinical/immunologic signs of disease + positive ANA  CHAPTER 5 Zia W. Massar, MS, AGACNP-BC, CCRN Mount Sinai Phillips School of Nursing INFECTION NSG 302 INFECTION A state of cellular, tissue, and organ destruction resulting from invasion by microorganisms Penetration of three lines of defense Multiple drug-resistant microbes Globalization and spread of harmful microbes PATHOGENS Disease-causing microbe Factors affecting pathogenicity Mechanisms for causing  Virulence disease  Infectivity  Direct destruction of host  Toxigenicity cell by pathogen  Antigenicity  Interference with host cell’s metabolic function  Antigenic variability  Exposing host cell to  Pathogenic defense mechanisms toxins produced by  Coinfection pathogen  Superinfection PATHOGENS Types  Obligate versus facultative  Bacteria  Single-celled microorganisms  Aerobic or anaerobic  Viruses  Rickettsiae, mycoplasmas, and Chlamydiae  Fungi  Protozoa  Helminths CHAIN OF INFECTION PHASES OF ACUTE INFECTION Exposure Incubation Prodrome Acute clinical illness Convalescence  MANIFESTATIONS OF INFECTION Local Systemic  Heat  Fever  Incapacitation  Weakness  Pain  Headache  Edema  Malaise  Redness  Anorexia  Lymphadenitis  Nausea  Purulent exudate LABORATORY AND DIAGNOSTIC TESTS White blood cell count  Leukocytosis  Leukopenia Serum antibody levels Cultures Sensitivities TREATMENT OF INFECTION Antimicrobial drugs  Antibacterials  Antifungals  Antivirals Symptom reduction  Fluids  Rest  Analgesics  APPLICATION OF THE CONCEPTS OF INFECTION Influenza Acute pyelonephritis Viral hepatitis Bacterial meningitis Tuberculosis Tinea Urinary tract infection Malaria