Cellular Injury & Adaptation Module Topics PDF

Module Topics Cellular Injury & Adaptation Wound Healing...

Module Topics Cellular Injury & Adaptation Wound Healing Infectious Disease Immunity, Inflammation Immune System Disorders and Infectious Disorders Shermel Edwards-Maddox PhD, RN, CNE, CHSE, RN-BC Types of Cellular Homeostasis Adaptations This is a dynamic steady state at which the body Atrophy maintains itself at a relatively constant composition. Hypertrophy A well-functioning cell can maintain homeostasis. When cells have challenges, stress or injuries, they Hyperplasia must: Metaplasia Adapt with compensatory changes Dysplasia Develop maladaptive changes Reverse the damage Neoplasia In circumstances of overwhelming insult, cell injury or cell death can occur. Ex: brain cells vs. skeletal muscle cells in aerobic environments.  Hypertrophy- Atrophy- Decrease in Cell Size Increase in Cell Size Cell reverts to a smaller size in response to Increase in individual cell size that changes in metabolic requirements or their results in an enlargement of environment. functioning tissue mass Results from: Can lead to greater metabolic demand Disuse or diminished workload and energy needs. Lack of nerve stimulation (paralysis) Example: Loss of hormonal stimulation The heart cells increase in size in response to hypertension due to greater workload Inadequate nutrition because of greater peripheral resistance Decreased blood flow (ischemia) Aging Hyperplasia - Metaplasia- Cells Increase in the Replaced by Another Number of Cells Type of Cell Increased mitotic activity Replacement of one cell type by another cell type Results in increased tissue/organ mass Results of: Cells genetic reprogramming in Example: response to a change in Pregnancy increases environmental conditions. demand of milk Chronic inflammation production (lactation), Example: which causes GERD- Normal squamous hyperplasia of breast epithelial cells transform in milk glands and tissue columnar like cells. mass  Neoplasia- Dysplasia- Deranged Unfavorable New Cellular Growth Growth Altered cellular growth Usually disorganized and lack Often caused by: normal cell function Precancerous condition Usually cancerous, continue to Chronic inflammation grow and grow Watch carefully because very often Can break away and travel will develop into neoplasia Neoplasm = tumor Can be benign or malignant Causes of Cellular Injury/Damage Apoptosis Hypoxic cell- oxygen deprivation Free radicals- (oxidative stress) Known as programmed cell death Physical agents- shearing against endothelium in HTN Can be triggered by cellular injury or it can be Chemical- high glucose causes glycosylation of endothelium genetically programmed: Example of cellular injury: Infectious agents- Helicobacteria erodes gastric mucosa A cell that has become cancerous and needs to be destroyed Injurious immunological reactions – allergic reactions Example of genetically programmed: Genetic defects – mutated DNA results in mutated proteins Ovaries undergo apoptosis in females aged 55 Nutritional imbalances - high LDL cholesterol deposits on endothelial wall Cells that fail to undergo apoptosis can give rise to certain cancers, tumors, and detrimental hyperplastic arteriosclerosis cell changes. Example: Prostate cancer is theorized to arise from cells that lose their apoptotic function.  Inflammation & The Inflammatory Response Inflammation is a protective, coordinated response of the body to an injurious agent. Can be acute or chronic Commonly termed “itis” The major aims of inflammation: Inflammation and The Wall-off the area of injury Inflammatory Response Prevent spread of the injurious agent Bring the body’s defenses to the region under attack Cardinal Signs of 3 Stages of Acute Inflammation Inflammatory Response Rubor (redness) 1. Vascular Permeability Tumor (swelling) 2. Cellular Chemotaxis Calor (heat) 3. Systemic Responses Dolor (pain) Loss of function Stage 1: Vascular Stage 2: Cellular Permeability Chemotaxis Blood vessels dilate at the site of injury Chemical signals are sent to both help amplify Caused by inflammatory mediators and stop the inflammation process. (ex. histamine, nitric oxide, and Cytokines- inflammatory mediators released bradykinin) by WBCs This permeability permits: Examples include tumor necrosis factor (TNF-alpha) and interleukins (ILs). Fluids, white blood cells (WBCs), and platelets to travel out to the site of Cytokines amplify or deactivate injury or infection. inflammation Fluid to flow out of the blood vessels to the injured tissues, causing Acute Phase Proteins- released by the liver swelling under direction of cytokines Examples include C-reactive protein (CRP), fibrinogen, and serum amyloid A. Influence the inflammatory process by stimulating, modulating, and deactivating the reaction. Stage 3: Systemic Response Clinical Manifestation: Fever Fever is a protective mechanism Microbial organisms, bacterial products, and cytokines all act as As a result of acute inflammation, patients may pyrogens  substances that cause fever. experience: Fever Pyrogens activate prostaglandins to reset the hypothalamic Pain temperature-regulating center in the brain to a higher level. General malaise Fever can reach levels high enough to cause seizures and brain Lymphadenopathy Anorexia damage. Sleepiness Recommended to keep fever below 102°F through the use of Lethargy antipyretic medications such as aspirin, ibuprofen, or Anemia acetaminophen. Weight loss These medications inhibit prostaglandin formation and, thus, This systemic response is caused by inflammatory mediators released from WBCs: reduce fever. Ex: Prostaglandins, Leukotrienes, Tumor necrosis factor (TNF-alpha), Interleukins (Ils), Histamine, Bradykinin Pause and Reflect Potential Complication: Reye’s Syndrome How does fever vary in Typically occurs after a viral illness (particularly an upper respiratory tract infection, influenza, varicella, or the geriatric population gastroenteritis) and is associated with the use of aspirin during the illness. compared to adults or In ages 18 years or younger children? Affects liver and the neurological system Symptoms: Nausea and vomiting Change in mental status Weakness Vision and hearing changes Agitation/ Seizures Treatment: supportive measures Particular attention paid to control of increased intracranial pressure (ICP) Assessment of the Immune System Types of WBC’s Granulocytes Agranulocytes Determined by a CBC (complete blood count) via venipuncture Neutrophils Monocytes (macrophages) Examines amounts of leukocytes and other white blood cells Eosinophils Lymphocytes During inflammation  increased number of WBCs from bone marrow into bloodstream Basophils Normal range = 4,000 – 10,000 cells/ml Leukopenia= less than 4,000 cells/ml Leukocytosis= greater than 10,000 cells/ml Leukemoid reaction = greater than 50,000 cells/ml WBC’s and the Immune Response CBC Interpretation Neutrophils are “first responders” – on scene within 24- 28 hours Is this client experiencing an Begin phagocytosis but have a short life acute inflammatory span (hours to days) response? Immature neutrophils = bands Why or why not? Monocytes are activated after 24-48 hours Macrophages remove foreign material, cellular debris Long life span, weeks to months Wound Healing Divided into multiple phases: 1. Hemostasis 2. Inflammation 3. Proliferation, granulation tissue formation, and epithelialization 4. Wound contraction and remodeling Wound Healing Factors that Affect Wound Healing Nurse’s Role In Wound Healing Nutrition Dressing Changes – keeping area clean Oxygenation Lab values- albumin, pre-albumin Circulation Tight glycemic control (avoid high blood glucose levels) Immune strength Diabetes; weakens healing Nutrition- encourage high protein diet Use of corticosteroids; diminishes healing Nutrition- encourage supplementation (zinc, vitamin C) Use of immunosuppressant agents Ambulation – to increase circulation and perfusion Contamination Turning bed bound patients every 2 hours Surgically inserted devices Off loading weight Obesity Age Complications of Wound Healing Contractures: inflexible shrinkage of wound Keloid: hyperplasia of Dehiscence: opening of tissue that pulls the scar tissue a wound’s suture line edges toward the center of the wound Stricture: an abnormal Fistula: an abnormal Evisceration: opening of narrowing of a tubular connection between wound with extrusion of body passage from the two epithelium-lined tissue and organs formation of scar tissue organs or vessels Adhesions: internal scar Infectious Diseases tissue between tissues or organs Normal Flora vs. Pathogens Opportunistic vs. Nosocomial Normal flora do not cause infection when they Infections remain within the strict boundaries of their anatomic niche in the body. Opportunistic infection caused by a microorganism that flourishes because of a host’s deficient immune system. Ex. E. coli in the intestines Ex: widespread candida infection in patient with AIDS. Nosocomial infection caused by microorganisms inherent to However, if normal flora bacteria invade the health-care facility environment; hospital-acquired noncolonized areas of the body, they can infection. cause infection. Nosocomial infections may be difficult to treat because they are often caused by antibiotic-resistant bacteria. Ex. E. coli in the urethra/bladder Commonly caused by Staphylococcus aureus Ex: Ventilator associated pneumonia (VAP) in intubated patients Two Levels of Defense Innate Immunity Adaptive Immunity Portals of Entry Nonspecific mechanism that defends the Specific mechanism that develops with Skin body against all types of pathogens exposure to antigens and targets immediately; 1st line of defense precise pathogens; 2nd line of defense Respiratory Tract Ex: Barriers including skin, mucous Ex: T lymphocytes and B lymphocytes, Gastrointestinal (GI) Tract membranes, phagocytic cells, ciliated which have memory for specific Genitourinary (GU) Tract cells, neutrophils, and mediators of antigens Blood-Blood Transmission inflammatory reactions Maternal-Fetal Transmission *Pathogens often enter the body of the host through the same route they exited the reservoir  5 Stages of Infection Incubation Organism begins active replication without symptoms in Laboratory Tests the host Host is highly contagious, not aware of illness CBC with differential Prodromal Stage Initial appearance of symptoms Gram stain (bacteria) Vague symptoms: malaise, headache, fatigue Host is highly contagious Culture (urine, stool, sputum, wound) Acute Stage Biopsy Host experiences full infectious disease with rapid proliferation of pathogen Antibody titer Defenses are in full force, inflammation reaction is fully engaged Polymerase chain reaction (PCR) detects Symptoms are heightened; still contagious genetic material Convalescent Stage Body’s attempt to eliminate the pathogen Resolution of symptoms begins Resolution Stage Total elimination of pathogen; no signs or symptoms Prevention of Illness Through Common Bacterial Immunization Infectious Diseases Prevention of infectious disease through Staphylococcal administration of vaccines is the most Streptococcal efficient method of controlling contagious disease. Mycoplasma Psuedomonas Current outbreaks of measles and whooping Clostridium cough (Fort Bend County) Salmonella Shigella Vaccines stimulate the immune system to Escherichia coli make antibodies against pathogen Where would you normally find these pathogens?  Staphylococcus Streptococcus Found on skin, vagina, nares, oropharynx Release endotoxin causing rash and fever Most common cause of nosocomial infections/surgical site Have capsules that prevent phagocytosis by WBC’s infections Causes: streptococcal pharyngitis Result in cellulitis scarlet fever Can cause endocarditis in IV drug users rheumatic fever Resistant to antibiotics: glomerulonephritis necrotizing fasciitis MRSA – Methicillin resistant staphylococcus aureus toxic shock syndrome VRSA – Vancomycin resistant staphylococcus aureus S. pneumonia – common community acquired Some bacteria develop ability to secrete beta pneumonia  can cause meningitis lactamase enzyme S. faecalis- source of UTI, nosocomial and endocarditis Diphtheria, Adults should receive Tdap vaccination every 10 years because it offers the best prevention against pertussis, Pertussis, and tetanus, and diphtheria. Meningitis Tetanus (DPT) Inflammation of meningeal layers that surround brain and spinal cord Can be bacterial or viral: S. pneumoniae/N. meningitides/H. influenza (bacterial worse than viral) Signs & Symptoms: nuchal rigidity, fever, headache Kernig’s sign (attempt to extend the leg at the knee  pain in neck and leg Brudzinski sign (patient flexes knees and hip when you flex the neck) Lumbar puncture (LP) is diagnostic tool Complications: seizures, brain damage, ischemia of extremities, visual or hearing loss Vaccines: H. influenzae, meningococcal and pneumococcal Clostridium difficile Viral Infections C. difficile is a spore-forming, toxin-secreting anaerobic bacteria. Emits toxins that disrupt the intestinal mucosa and erode the intestinal epithelial cells Viral infections CANNOT be treated with Forms pseudomembranes that contain necrotic tissue, antibiotic therapy white blood cells (WBCs), and mucus. Most treatment regimens include supportive Symptoms: therapy: Watery diarrhea (10-15 per day) Antipyretics Abdominal pain/cramping Analgesics Dehydration Fever IV Hydration Weight loss Antivirals* not available for all viral infections Predisposing factor is long-term antibiotic use IV steroid therapy Contagion between patients is possible; this is a source of nosocomial infection. Rest Alcohol based sanitizer is not effective against C. diff spores. Epstein Barr Virus (EBV) Influenza Known as infectious mononucleosis or “the kissing disease” Infects the cells of the oropharynx  it invades the bloodstream  Major strains: A (most severe), B, and C incites an immune response that causes proliferation of B Invades upper then lower respiratory tract lymphocytes within lymphoid tissue, resulting in lymphadenopathy. Occurs through droplet infection and aerosols generated Clinical manifestations: by coughs and sneezes of individuals. Pharyngitis, fatigue, headache, fever, chills, abdominal pain, Clinical manifestations: nausea, and vomiting are usually presenting symptoms. fever, chills, headaches, myalgias, cough, sore throat Pharyngitis is often the most prominent sign with tonsillar enlargement and exudate. Treatment: supportive care Diagnostics: Amantadine, Rimantadine, Zanamivir, and Oseltamivir are antiviral medications that can be Test for antibodies against the virus used to shorten the course of the disease Potential complication: Splenomegaly Typically resolves in 7 days Avoid strenuous activities or contact sports for at least 3 Prevention: Influenza vaccine is recommended annually weeks or until the spleen returns to its normal size. for all persons older than age 6 months. Measles Mumps Transmission: respiratory droplets Transmission: direction contact and/or Incubation period: 7-14 days respiratory droplets Prodromal stage: 4-7 days Incubation period of 14 - 25 days Prodromal symptoms 3- 5 days Clinical manifestations: High fever, cough, upper respiratory illness, conjunctivitis with periorbital edema, and photophobia. Symptoms: Hallmark sign: Unique white areas in the oral buccal mucosa called Inflammation of the parotid salivary Koplik spots that appear in the prodromal stage. gland, sore throat, fever, joint pain After the appearance of Koplik spots, the characteristic tiny Males can develop orchitis, can lead to maculopapular, mildly pruritic rash appears on the body. sterility. The rash develops from head to toe and then fades after 5 to 7 days. Diagnostics: mump specific IgG and PCR testing of virus Diagnostics: Specific measles IgM and IgG immunoglobulins can be Typically lasts 5 days; supportive care found in the blood. Vaccination administered at 12-15 months Treatments: supportive measures such as rest, fluids, isolating from and 4-6 years old others. Rubella Varicella Zoster (Chickenpox) Mostly impacts children Transmission: droplet inhalation or contact Incubation: 10-21 days Transmission: respiratory droplets The triad of rash, malaise, and low-grade fever are typical signs. Incubation period:14 to 19 days The characteristic chickenpox vesicle is described as a “dewdrop on a rose petal.” Most contagious when the rash is erupting and are noncontagious after 7 days of rash. First appear on the scalp, face, trunk, and proximal limbs Rapid progression over 12 to 14 hours to papules, clear vesicles, and Symptoms: fever, sore throat, and rhinitis, Forchheimer pustules, with subsequent central umbilication and crust and scab spots, which are pinpoint red macules, and petechiae over formation. the soft palate and the uvula Diagnostics: PCR testing of skin lesions Hallmark sign: generalized, tender lymphadenopathy that Treatment: supportive measures, antipyretics, hydration, oatmeal involves all nodes, but particularly the cervical nodes. baths, and antihistamines Diagnostics: specific IgM and IgG immunoglobulins and PCR Vaccination is recommended testing Treatment: supportive care Herpes Zoster (Shingles) Herpes Simplex Viruses (HSV), HSV-1 and HSV-2 A reactivation of the varicella zoster virus that The two viruses are distinctly categorized because they usually infect different parts of the body. remains dormant in the sensory spinal neurons HSV-1 is the common cold sore virus. HSV-2 is the genital herpes infection. Can remerge due to immunosuppression/cancer or Can cause acute and latent infection. stress Acute infection: abrupt onset of vesicular lesions within the epidermis and mucous membranes. The fluid-filled vesicles Usually along a dermatome (one side) contain active viral particles. The acute phase ceases and is followed by a period of dormancy Symptoms: when the virus is inactive. painful fluid filled vesicles, skin sensitivity, Herpes viral DNA remains dormant within the neurons and evades immune destruction. tingling, burning, itching Reactivation of HSV occurs during periods of stress, illness, or immunosuppression. Treatment: Acyclovir (medication) can lessen severity Acyclovir (medication) can help lessen severity Prevention: Immunization 50 years and older Fungal Infections Candida albicans Plant-like organisms that live in air, soil, plants, water, and even the human body Part of normal flora of the gastrointestinal and vaginal tracts. Fungi reproduce through spores in the air Becomes pathogenic when an overgrowth occurs Affect those with weakened immune systems (HIV/AIDS patients) A person with weakened immune system can develop widespread dissemination of Candida within the body, which can then progress to Can affect: overwhelming sepsis. Skin Risk factors: antibiotic use, diabetes, HIV, steroids, oral contraceptives Nails Treatment: antifungal medications (Ex. Nystatin) Lungs Presents as: GI tract Thrush GU and vaginal tract Esophageal infection Hard to treat* Vulvovaginitis Balanitis Parasitic Infection: Malaria Caused by Plasmodium = parasite that lives in the Anopheles mosquito THANK YOU Mosquito bites human  Plasmodium enters the red blood cells (RBCs)  degrades the blood cell constituents, particularly hemoglobin. RBCs become deformed, obstruct small blood vessels, and accumulate within the spleen. Accumulation of bilirubin from hemoglobin breakdown results in jaundice. Clinical manifestations: fever, chills, headache, myalgia, nausea, vomiting, and orthostatic hypotension are common. Treatment: Chloroquine is the medication used to treat malaria; there is some resistance Prevention: Mefloquine is a prophylactic med that can be taken if travel is planned.  Human Immunodeficiency Virus (HIV) Retrovirus Slowly progressive disease 2 major strains: HIV-1 – most commonly seen in US HIV-2 – limited to West Africa Transmission routes: Human Blood Semen Immunodeficiency Virus Vaginal fluids Transplacenta Shermel Edwards-Maddox, PhD, RN,(HIV) Breast milk CNE, RN-BC Saliva (into open mouth wounds) HIV Pathophysiology HIV Pathophysiology HIV attacks CD4 cells and macrophages Enzyme driven illness CD4 cells are involved in both humoral and cell-mediated HIV attaches to the CD4 receptor cell immune reactions. Reverse transcriptase changes viral RNA into viral DNA HIV slowly debilitates body immune systems, both T cell Integrase allows viral DNA to be in integrated into host and B cell immunity. DNA Macrophages serve as reservoir for the virus Protease helps assemble protein component to build Allows virus to go undetected new viruses Also help disseminate/spread the virus Host becomes a “factory” for manufacturing more viruses Macrophages are found at mucous membranes After using the host cell, the virus destroys the CD4 cell causing a weakened immune response. Risk Factors for Stages of HIV Infection Contracting HIV Acute infection Unprotected sexual activity Heterosexual females at higher risk than heterosexual males MSM (men who have sex with men) Chronic infection Receptive partner is at higher risk than the insertive partner IV drug abusers African American males AIDS Hispanic male History of sexually transmitted diseases (STD) Frequent blood transfusions Offspring of infected mothers Clinical Manifestations: Clinical Manifestations: Acute Phase Chronic Phase Presents like a flu-like virus Known as the latent stage similar to mononucleosis Can last from 6 months to 10 years Fever, headache, fatigue, pharyngitis, Symptoms can range from mild to severe: lymphadenopathy, myalgia Cough Shortness of breath Occurs within 28 days of contracting the virus Weight loss Diarrhea Lasts a couple of weeks and then resolves Fatigue Symptoms are often disregarded Viral load is slowly increasing After this stage resolves the patient CD4 count is decreasing becomes asymptomatic Clinical Manifestations: AIDS Laboratory Studies & Diagnostics Screening for HIV is highly recommended AIDS= acquired immune deficiency syndrome Presence of HIV virus in the bloodstream CD4 count diminishes to 200 or less HIV RNA blood test Symptoms: Virus is detectable between 4 – 11 days after infection Rapid weight loss Presence of HIV antibodies: Recurring fever or profuse night sweats It can take between 2 weeks and 6 months for immune A red rash that doesn't itch, usually on your torso. system to make antibodies Prolonged swelling of the lymph glands in the armpits, groin, or neck CD4 count is used to monitor the course of the disease Complications: Normal CD4 count: 800- 1,200 cells/mm3 Kaposi sarcoma Impaired immunity: below 500 cells /mm3 Pneumocystis jirovecii Pneumonia (PJP) If CD4 count drops below 200 cells/mm3 AND there is an Other opportunistic infections opportunistic infection, then the diagnosis of AIDS is made. Treatment and Management of HIV Complications of HIV/AIDS Treatment can be challenging: Antiretroviral therapy (ART) is the only long- Latency of disease term successful treatment Opportunistic Infections Medications work by attacking the virus Tuberculosis Immunocompromise Candida (thrush) at various stages Highly mutable virus Pneumocystis jiroveci pneumonia (PJP) Candida Infection Histoplasmosis Examples: protease inhibitors, transcriptase inhibitors, integrase Toxoplasmosis inhibitors, fusion inhibitors Histoplasmosis Hepatitis A, B, C Treatment be started as soon as possible Can live a long life if compliant with Malignancies medications Kaposi sarcoma Non-Hodgkin’s lymphoma Cervical cancer Anal cancer Kaposi sarcoma lesions Lymphadenopathy from lymphoma Preventative Treatment of HIV Practice Question #1 PREP- pre-exposure prophylaxis PEP- post exposure prophylaxis In each of the following situations, identify which option has the highest Uses antiviral medications in highly Uses antiviral medications after a single risk for human immunodeficiency virus (HIV) transmission? susceptible, uninfected individuals high-risk event to prevent contraction of Examples: Truvada, Descovy HIV Must be started within 72 hours to be A. Transmission to women OR to men during sexual intercourse Strategy used when one partner is HIV positive, and the other is HIV negative effective B. First 2 to 6 months of infection OR 1 year after infection Must take the medication every single day Includes a 28-day course of triple ART C. Perinatal transmission from HIV-infected mothers taking antiretroviral Continue to use condoms Only to be used in emergency situations therapy OR HIV-infected mothers using no therapy Follow up with their health care provider D. A splash exposure of HIV-infected blood on skin with an open lesion every 3 months OR a needle-stick exposure to HIV-infected blood Answer to Practice Question #1 Practice Question #2 In each of the following situations, identify which option has the highest risk for human immunodeficiency virus (HIV) transmission? What is a primary reason that the normal immune response fails to contain the HIV infection? A. Transmission to women OR to men during sexual intercourse B. First 2 to 6 months of infection OR 1 year after infection A. CD4+ T cells become infected with HIV and are destroyed. C. Perinatal transmission from HIV-infected mothers taking antiretroviral B. The virus inactivates B cells, preventing the production of HIV antibodies. therapy OR HIV-infected mothers using no therapy C. Natural killer cells are destroyed by the virus before the immune system can D. A splash exposure of HIV-infected blood on skin with an open lesion be activated OR a needle-stick exposure to HIV-infected blood D. Monocytes ingest infected cells, differentiate into macrophages, and shed viruses in body tissues Answer to Practice Question #2 What is a primary reason that the normal immune response fails to contain the HIV infection? A. CD4+ T cells become infected with HIV and are destroyed. B. The virus inactivates B cells, preventing the production of HIV antibodies. C. Natural killer cells are destroyed by the virus before the immune system can be activated D. Monocytes ingest infected cells, differentiate into macrophages, and shed viruses in body tissues Rationale: Activated CD4+ T cells are an ideal target for HIV because these cells are attracted to the site of concentrated HIV in the lymph nodes, where they become infected through viral contact with CD4 receptors. CD4+ T cells normally are a major component of the immune system and their infection renders the immune system ineffective against HIV and other agents. The virus does not affect natural killer cells and B lymphocytes are functional early in the disease, as evidenced by positive antibody titers against HIV. Monocytes do ingest infected cells and may become sites of HIV replication and spread the virus to other tissue but this does not make the immune response ineffective.  The Immune System Complex defense mechanism that protects from injurious agents Can decipher which substances are “self” vs. “non-self” Immune System Function Non-self = antigens In a normally functioning immune system Rapid identification of an antigen and subjects it to barriers and protective cellular forces that destroy the threat Professor Shermel Edwards-Maddox, PhD, RN, RN-BC 0 Innate vs. Adaptive Immunity Adaptive Immunity Goals: recognize self from non-self (antigen) recognize and target a specific antigen Innate Adaptive limit its response 1st line of defense Occurs after innate development memory for future exposures (specificity) Natural mechanism More specific Barriers defense Memory response allows for quicker response upon 2 nd Normal flora Exposure to exposure WBC’s antigen Enzymes Use memory for Driven by lymphocytes that originate in bone marrow in Chemicals specific antigens immature form cannot initiate immunity until mature. 2 Types of Adaptive Immunity Humoral Cell-mediated  2 Categories of Adaptive Immunity Humoral- B Cell Immunity Immunity is developed by B lymphocytes producing Humoral Immunity Cell Mediated Immunity antibodies Known as B cell immunity Known as T cell immunity They are naïve or immature until they encounter antigens. Mature in the bone marrow, spleen, and Mature in the thymus gland  found in lymph nodes bloodstream and lymph nodes After exposure to an antigen, B cells mature into plasma Protects against extracellular pathogens Protects against intracellular pathogens cells. Plasma cells have the ability to produce specific proteins called immunoglobulins (Igs), also called antibodies. Ex: IgG, IgA, IgE, IgM, IgD Specifically recognize and bind to particular antigens Support is provided by helper T cells to help promote/escalation of immune response Cell Mediated Immunity Cell Mediated- T Cell Immunity Adaptive Immunity: Passive or Active Immune response without the use of antibodies Active Acquired Passive Acquired Uses macrophages, T-lymphocytes, and cytotoxic cells Obtained through exposure to an Premanufactured immunoglobulins are for a direct approach at pathogen destruction antigen or through immunization given or passed down. Antigen provokes antigen presenting cell (APC) which (vaccine). The body passively accepts processes antigen The patient’s body has to synthesize immunoglobulins and the body DOES specific immunoglobulins against an NOT have to manufacture them. Stimulates T-helper cells and activates macrophages antigen. This is short-term immunity. Antigen fragments are put on the surface of the APC, Either the patient contracts a disease Administered when the patient needs triggering CD8 cells known as cytotoxic cells IMMUNITY NOW because of being with and develops Igs and then recovers or CD8 cells destroy cell via apoptosis the patient is given a vaccine. close contacts or a family member who has the virus. Both endow long-term immunity. Example: hepatitis B immunoglobulin (Hbig) and immunoglobulins in breast milk Immunizations and Boosters Antibody Titer A vaccine is a weakened or inactivated virus Antibody screening tests, referred to as antibody titers, confirm adequate immune protection It cannot cause disease; it has the genes for disease removed. by measuring IgM and IgG immunoglobulins. A vaccine is administered to the body and the body “thinks” it is an antigen. If a patient has a negative titer: The body then builds specific Igs against it. They have not been exposed to disease Sometimes more than one dose is needed. Never developed immunity Example: hepatitis B vaccine (three doses) Need vaccination/booster Booster: This is a repeated vaccine administered some time after the initial vaccine in order to “remind” the body to make immunoglobulins. Examples: MMR booster is recommended before college Tdap every 10 years Influenza vaccine COVID-19 Copyright © 2016 F.A. Davis Company  Structure and Function of the Head Cranium encases and protects brain and brainstem Consists of 22 cranial and facial bones Movements of these bones allows for facial expressions, eating, speech, and head movement Information processing center Head and Neck Disorders Aids in sensory functions Shermel Edwards-Maddox, PhD, RN, CNE, CHSE, RN-BC Disorders of the Head Headaches Most commonly treated disorder Interferes with functions needed for daily living: Concentration ability Vision and hearing Appetite Exercise ability Can be benign or a warning sign of a serious condition: Ex: brain tumor or subarachnoid hemorrhage 3 Types of Headaches Headaches Traumatic Brain Injury (TBI) Tension Cluster Migraine Assessment of Headaches Tension Headaches Medical and social history Occurring episodically because of stress Neurological exam The pain is dull, aching with gradual in onset and presents as a pressure or “bandlike” sensation in the Headache Impact Test (HIT-6) head. Headache diary Pain is often bifrontal or occipitofrontal. CT scan Often associated with muscular tightness in the neck, shoulders, and occipital area MRI Vital signs and neurological examination are normal. EEG Nonopioid medications provide relief Cluster Headaches Migraine Headaches A neurovascular disorder characterized by severe, unilateral, periorbital Etiology: genetic, environmental and neurological factors pain. 75% of the sufferers being women Involves the activation of the hypothalamus and the trigeminal nerve Neurogenic process with secondary changes in cerebral perfusion, causing recurrent Commonly occurs in early morning hours or during sleep. headaches Pain is described as sharp, stabbing, and unilateral with radiation to the Low serotonin levels lead to constriction/dilation of blood vessels cheek, jaw, occipital region, or neck. The hallmark signs include: Without treatment, a migraine headache can last 4 to 72 hours. tearing of the eyes Unilateral, vascular, throbbing headache conjunctival injection Associated symptoms of nausea, vomiting, and sensitivity to light and sound. rhinorrhea eyelid edema Often preceded by an aura, a visual or sensory experience that occurs before the ptosis headache. Triggers: Alcohol, tobacco, stress, allergy, and weather changes Commonly precipitated by stress, hormones, smoking, weather changes, food additives, Vital signs and neurological examination are normal. caffeine, alcohol, or excessive fatigue. Nonopioid medications provide relief Treatment of migraine is focused on alleviating pain: Acute headache Preventative treatment Traumatic Brain Injury (TBI) Structure and Function of the Neck Injury to the brain that causes temporary, short-term or long-term problems with brain function Made of vertebrate and muscles Extent and location of injury determine level of disability Etiology: Supports the head and that it houses arteries Accidents involving automobiles, motorcycles, bicycles that supply blood to the brain from the heart. Falling Excessive alcohol ingestion Carotid arteries Abuse of infants and elderly being cared for by caregivers Jugular veins Symptoms: Headache and fatigue Assists in movement Blurred vision Vomiting Contains: Confusion Memory problems Larynx Loss of consciousness Thyroid gland Seizures Changes in speech Lymphatic tissue Treatment: Varies based on extent of injury Lymphatic Tissue of the Neck Multiple Myeloma Function to transport lymph, a fluid containing WBCs, Cancer of the lymphatic system throughout the body. Arises from B-lymphocytes that are neoplastic and Lymph nodes: serve as centers for proliferation and invade bone marrow response of immune cells Pathophysiology: proliferation of malignant plasma 100’s of them throughout the body (neck, groin, cells in bone marrow and osteolytic bone lesions throughout the skeletal system chest, axilla) Overproduction of monoclonal antibody Examples: tonsils, adenoids, spleen and thymus Disrupts normal antibody production Lymph nodes filter the debris that has been collected Weakens immune system through the use of macrophages. Incurable Become enlarged when pathogens have invaded the More common in men; African-Americans body Risk factors: exposure to chemicals, Agent Orange, Known as lymphadenopathy radiation, genetic factors  Multiple Myeloma Thyroid Disorders Clinical Manifestations: Diagnostics: Butterfly shaped gland on front of the neck Severe bone pain Bone marrow biopsy Pathologic fractures X-rays Functions: metabolism, growth and development of the human Hypercalcemia (high blood CBC body calcium levels) Urine – Bence Jones proteins In response to TSH, produces two hormones Anemia Management: T3- trioodothronine Recurrent infection Steroids Weight loss Chemotherapy T4- thyroxine Fatigue Stem cell transplant Hyperthyroidism: gland is overly reactive Renal insufficiency Complications Hypothyroidism: gland is under active Fractures Leads to bone destruction, bone marrow failure, renal failure, and neurological Assessment and Diagnostics: complications Palpate thyroid gland Example of Osteolytic Lesions T3/T3/TSH levels Altered Thyroid Function Practice Question Hyperthyroidism: Hypothyroidism: When a patient is experiencing a cluster headache, the nurse will plan to Sudden weight loss, without changes in Increased sensitivity to cold assess for appetite Unintentional weight gain Tachycardia, irregular heartbeat or A. nuchal rigidity Pale, dry skin palpitations Thin, brittle hair or nails B. projectile vomiting Nervousness, anxiety, and irritability Tremor in the hands and fingers Constipation C. unilateral eyelid swelling Depression D. throbbing, bilateral facial pain Sweating Fatigue Changes in bowel patterns, more frequent bowel movements Weakness Fatigue, insomnia, muscle weakness Practice Question A 39-year-old female presents to the clinic with complaints of difficulty swallowing, hoarseness, and a noticeable swelling in her neck. On physical examination, the nurse palpates a firm, non-tender mass in the region of the thyroid. The patient also reports feeling more fatigued than usual and has QUESTIONS? gained weight over the past few months. Based on these findings, which of the following actions should the nurse take next? A) Perform a thorough neck assessment and document the size, shape, and consistency of mass B) Instruct the patient to rest and drink warm fluids to soothe the throat C) Recommend an over-the-counter thyroid supplement to improve symptoms D) Refer the patient for immediate surgery to remove the thyroid mass  Focus on the following: ► Normal physiological mechanisms of integumentary Hair, Skin and Nail ► Selected skin/dermatological disorders ► Risk factors, clinical manifestations, Disorders diagnostics, treatment and complications ► Conditions that lead to death* ► ABCDE skin evaluation ► Health promotion regarding skin Shermel Edwards-Maddox PhD, RN, CNE, CHSE, RN-BC disorders Module Terminology The Integumentary System- Structure and Function ◆ The skin is the largest organ of the Pruritus body. Cyanosis ◆ Physical barrier that protects the Jaundice underlying tissues and structures from microorganisms, physical Erythema trauma, ultraviolet radiation, and dehydration. Excoriation ◆ Vital role in temperature Alopecia maintenance, fluid and electrolyte balance, absorption, excretion, Uticaria sensation, immunity, and vitamin D synthesis. Nevi Think-Pair-Share Nail- Structure and Function How does the skin do the following? ◆ Protect fingers and toes Give an example of each: ◆ Enhance dexterity ◆ Made up of dead matrix cells Control and regulate temperature ◆ Grow continuously Barrier protection Excretion and absorption ◆ Can inform about systemic Immunity disorders Vitamin D production Hair- Structure and Function Sweat Glands ◆ Filamentous, keratinized ◆ Eccrine- originate in the dermis and structure that originates from open to the skin surface hair follicles in the dermis ◆ Transport sweat to the outer skin surface to regulate body temperature ◆ Associated with sebaceous glands ◆ Several million located all over the body ◆ Arrector pili- muscle that contracts to “goose bumps” as ◆ Apocrine- located deep in the dermis, part of thermoregulation. open through a hair follicle ◆ Can reflect metabolic changes ◆ Found in axilla and groin ◆ Has growing and resting cycles ◆ Secrete oily substance that mixes with bacteria body odor  Diagnostic Tools to Assess the The Integumentary System as a Mirror Integumentary System ► The skin is the most visible organ ► Medical conditions in other body systems can manifest in ► Skin scraping the integumentary system ► Patch testing ► Example: Immunological ► Biopsy ► Changes in color or texture ► Wood’s UV Light ► Can help in diagnosing other disorders Common Changes Associated with Aging How does the integumentary system change with age? ◆ Skin ◆ Insert text here…. ◆ Pale ◆ Skin lesions ◆ Dry ◆ Loses turgor ◆ Hair: Thinner ◆ Nails: Thickened, yellow, brittle Skin Lesions Skin, Hair, and Nail Disorders Primary Secondary ◆ Macule and patch Erosion Skin Disorders Nail Disorders ◆ Hair Disorders ◆ Papule and plaque Ulcer ► Vitiligo Paronychia ◆ Pattern Baldness ◆ Nodule and tumor ◆ Scar ► Albinism Alopecia Onychomycosis ◆ Vesicle and bulla ◆ Fissure ► Melasma Ingrown Nails ◆ Wheal ► Cellulitis ◆ Pustule ► Pressure Ulcers ◆ Cyst ► Psoriasis ► Skin Cancers Be familiar with Box 41-1 on page 1100 Consider making mini concept maps on these integumentary orders ► Shingles* *Addressed in Module 1 Cellulitis and MRSA Skin Infections Disorders of Skin Color ► Often the source of cellulitis infections Albinism Vitiligo Melasma ► Spread through direct contact Genetic disorder Abnormal production Known as chloasma ► Risk factors: Skin, hair, and eyes of melanin ► Recent hospitalization/long term care facility Dark macules on the face lack pigment Unknown cause ► Having invasive medical device Related to pregnancy and ► Contact sports/sharing personal items Results in Discolored patches on sun damage photosensitivity the skin ► Appear as a bump or infected area that may be: ► Red, swollen or painful, warm to the touch ► Full of pus or other drainage ► Perform culture for identification of pathogen ► Treatment: ► Antibiotics/Ointments ► Dressing changes/surgical debridement ► Patient teaching  Measures to Reduce Risk Factors for MRSA Skin Injury / Pressure Ulcer Stages ► Referred to now as “pressure injury” ► Keep wounds covered. ► Also known as decubitus ulcers or ► Do not share personal items. bedsores ► Avoid unsanitary or unsafe nail care practices. ► Found on bony prominences ► If treatment has been started, do not stop until recovery ► Pressure decreases blood flow to the skin is complete. ► Sustained pressure produces blisters  skin ► Use universal precautions when touching others to avoid breakdown and tissue ulceration. contact with contaminated body fluids. Wash your ► Classified by: hands. ► Stage I ► Clean sports equipment between uses to avoid spread of ► Stage II infection. ► Stage III ► Wash clothes, sheets, towels, razors, and other personal ► Stage IV items before and after use. ► Unstageable ► Clean hands often. Treatment of Pressure Ulcers/Injuries ► Prevention is the best option ► Wound care Risk Factors ► Dressing changes ► Cleaning the wound for Skin Injury ► Medications / Pressure ► Topical creams ► Antibiotics Ulcer ► Antifungals ► Surgical intervention ► Wound Vacuum Therapy ► Hyperbaric chambers Hyperbaric Oxygen Chamber Vascular Skin Lesions Psoriasis Match the pictures with the correct term. A B ► Chronic thickening of epidermis T-cell-mediated autoimmune response to antigen Petechiae ► ► ► Presents with silver-white scales covering red, ► Ecchymosis circumscribed, thickened plaques D ► Auspitz Sign ► Hematoma C ► Frequently found on elbows, knees, and scalp ► Cherry angioma ► Common in colder climates Increases with age ► Spider angioma ► ► Treatments: ► Telangiectasis E F ► Topical agents ► Steroid medications ► Emollients to soften and hydrate area Nevi Eczema- Atopic Dermatitis ► Known as moles ► Most common benign skin tumor ► Type of hypersensitivity that can be ► Can be pigmented or depigmented triggered by environment and/or allergens. ► Develop during childhood (3 to 5 years of age) ► Causes dry, lichenified lesions ► Present as papules and nodules ► Can be hypo or hyperpigmented ► Vary in size ► Seen in the antecubital, popliteal, ► Atypical = irregular in shape, vary in color neck, hands, feet, eyelids and ears. ► High susceptibility to cancerous changes ► Treatment: allergen control, topical steroid creams and immune ► Require biopsy to rule out cancer modulating medications.  Malignant Melanoma Risk ◆ Sun exposure Nonsolar sources of UV ◆ Male gender Chemical exposure Factors for ◆ ◆ radiation ◆ Human papillomavirus Medical therapies (HPV) Basal Cell Carcinoma Skin ◆ ◆ Family and genetic history ◆ Long-term skin Make sure to know the major differences between these types of Cancers ◆ Moles inflammation or injury skin cancers! ◆ Pigmentation ◆ Alcohol intake; smoking irregularities ◆ Inadequate niacin in Squamous Cell ◆ Fair skin that burns and diet Skin Cancer Carcinoma ◆ freckles easily; light hair and eye color Age ◆ Depressed immune system Risk Reduction Strategies to Prevent Skin Cancers ► Reduce skin exposure ABCDE’s For Skin Cancer ► Always use sunscreen when sun exposure is anticipated. ► Reapply every 2 hours or more often if sweating or swimming ► Minimum SPF 15 everyday; SPF 30 or higher if outside ► Wear long-sleeve shirts and wide-brimmed hats. ► Avoid sunburns. ► Wear sunglasses that wrap around. ► Have annual skin cancer screenings ► 2-3 times a year if at high risk or have a history of skin cancer ► Avoid sun exposure between 10am-4pm ► Layer clothing  Basal Cell Carcinoma Cultural Most common form of skin cancer Variations ► ► Begins in the basal cells (produce new skin cells) in Skin ► Cause: exposure to ultraviolet (UV) rays Cancer ► Slow-growing ► Often appearing on the face (nose), head, and neck ► Are not painful or itchy Melanoma Squamous Cell ► Arise because of malignant degeneration of melanocytes located either along the basal layer of the epidermis or Carcinoma ► in a nevus. Most lethal of the skin cancers; 70% of malignant melanomas arise from a preexisting nevus. ► Originates in upper portion of Squamous cell on the back of the hand ► Initially the cells grow radially through the epidermis; the dermis ► Spread vertically through the dermis, which allows for metastasis. ► Spreads through the lymphatic (lymph nodes) and ► Commonly on sun-exposed areas: vascular systems (liver, lungs, and central nervous system) face, ears, neck, lips, and backs Risk Factors: of the hands. ► ► Fair, sun-sensitive skin, burn easily, tans poorly, Scandinavian descent ► Appears red, scaly, patch-like, ► Red or blond hair with blue or green eyes thickened wart-like, and may ► 50-100 nevi ► Unusual or irregular nevi crust over ► Hx of sunburns or indoor tanning use ► Positive family hx ► Bleeds occasionally ► Age: 50 years or older Melanoma – Symptoms and Treatment Hair ► Atypical lesions that are asymmetric, with border irregularity; ► Can reflect metabolic changes ► dark black, blue or varied color ► Texture ► greater than 6 mm in diameter ► elevated above skin’s surface ► Growth ► Areas: ankles, back, legs, arms, face, back of ► Pattern knee Brittle Hair ► Loss ► Treatment Options: ► Examples: ► Surgery ► Hypothyroidism ► Local ablation therapy ► Surgical resection to remove tumor and 3 to ► Infections 5-cm margin ► Psoriasis ► Regional lymphadenectomy ► Pregnancy ► Medications ► Liver and kidney disease ► Chemotherapy ► Nutritional deficits/anemia ► Radiation therapy for metastasis Hair Loss