Chapter 2 & 3 Notes PDF

**Chapter 2 Immunity** **[Physiological Response to Stress]** - Fight-or-flight response - Results from activation of the sympathetic and endocrine systems - Includes increased heart rate, increased respirations, diaphoresis, increased blood flow to muscles, increased muscle strength,...

**Chapter 2 Immunity** **[Physiological Response to Stress]** - Fight-or-flight response - Results from activation of the sympathetic and endocrine systems - Includes increased heart rate, increased respirations, diaphoresis, increased blood flow to muscles, increased muscle strength, increased mental alertness, increased fat and protein mobilization, increased glucose availability, and decreased inflammation 9781284121131\_CH02\_FIG01.jpg Hypothalamus and pituitary gland releases hormones\* Adrenal gland helps us with stress\* Figure 02.F01: Physiological response to stress Figure 02.F03: Effects of stress **[Question Time]** - During sympathetic facilitation (stimulation) the body is in fight or flight. - **True** or false **True**. During **sympathetic facilitation** or stimulation, the body is in a state of **\"fight or flight\"**. This is part of the **sympathetic nervous system**, which is responsible for preparing the body to respond to stress or perceived threats. When activated, the sympathetic nervous system triggers various physiological changes, including: - Increased heart rate - Dilated pupils - Increased blood flow to muscles - Release of adrenaline (epinephrine) and other stress hormones - Increased respiration rate - Inhibition of non-essential functions like digestion These changes are designed to help the body respond to danger by either fighting or fleeing from the threat. Top of Form Bottom of Form **[Immune system ]** **[\*Autoimmune dysfunction = something went wrong with their immune system that doesn't allow them to recognize their tissues as their own so they start attacking their own tissues\*]** - Self-regulated - Self-limiting - Must be able to distinguish self from non-self - Antigens from the environment - Innate - general immediate nonspecific protection against all invaders - Adaptive (acquired) -- is slower (7-10 days) and provides protection (form antibodies) specific to an antigen **[Innate Defense Barriers]** (1 of 2) (skin release of melanin helps to protect skin from sun) - Nonspecific - Immediate response - Distinguish self from nonself - Do *not* distinguish between pathogens - Include - Skin and mucous membranes - Chemicals - Physical and chemical barriers not completely impenetrable - Additional bloodborne innate defenses include - Inflammatory response - Pyrogens - Interferons - Complement proteins **[Question time]** - The skin contributes to our immune system. - **True** or false? **True**. The skin plays a crucial role in the **immune system**. It serves as the body's **first line of defense** against harmful pathogens, like bacteria, viruses, and fungi. Here\'s how: 1. **Physical Barrier**: The outermost layer of the skin, the **epidermis**, particularly the **stratum corneum** (dead skin cells), acts as a tough barrier that prevents pathogens from entering the body. 2. **Acid Mantle**: The skin secretes oils and sweat that form an **acidic mantle** on the surface, which inhibits the growth of many harmful microorganisms. 3. **Immune Cells**: The skin contains specialized immune cells such as **Langerhans cells**, which are a type of dendritic cell that detect and capture pathogens, then alert other immune cells to initiate a response. 4. **Inflammatory Response**: If pathogens break through the skin barrier, the immune system can trigger an inflammatory response, leading to increased blood flow and the recruitment of white blood cells (such as macrophages and neutrophils) to fight the infection. So, the skin is not just a protective shield but also an active participant in immune defense. **[Inflammatory Response]** - Vascular reaction. - Triggered by mast cells (variation of basophil (WBC) that releases histamine-potent dilatator) - Manifestations include erythema, edema, warmth, heat, and pain. 9781284121131\_CH02\_FIG04.jpg Figure 02.F04: Inflammatory Response Phagocytic- Macrophages eats dead tissues, bacteria and viruses in the body **[Pyrogens]** - Fever-producing molecules released by macrophases - Produced by macrophages and sent to hypothalamus - They cause the temperature to rise - This increases metabolism to increase healing and increase phagocytosis - Macrophages eat bacteria and dead tissues to regulate temperature - Severe fever---life-threatening -\> can start to destroy enzymes in our body - 105 in adults - 103 infants (03 months 100. 3-6 months 101. 6 months and older 103) **[Interferons]** - Proteins released from virus-infected cells. - Bind to nearby uninfected cells. - The uninfected cells release an enzyme that prevents viral replication. - When the virus infects these cells, they are unable to replicate. **[Complement Proteins]** - Several Plasma proteins that enhance antibodies - Activated by antigens - Play multiple roles in the immune and inflammatory response - Attack bacteria itself and macrophages will come eat it up - Vasodilation to the infected area - Chemotaxis (complement proteins will send proteins out into bloodstream and tell immune system to draw wbcs to the area) **[Question time]** - Innate defenses Do not!!! provide which of the following functions? - A. Antibody creation - B. Increase in body temperature - C. Vasodilation to allow immune cells to get to the infection - D. Chemicals to draw immune cells to the infection - E. All of the above The correct answer is **A. Antibody creation**. Here\'s why: **Innate defenses** are the body\'s first line of defense against pathogens, and they include things like physical barriers (skin, mucous membranes), inflammation, fever, and the action of immune cells like neutrophils and macrophages. However, **antibody creation** is a function of the **adaptive immune system**, not the innate immune system. Here's a breakdown of the options: - **A. Antibody creation**: **False**. Antibody creation is a characteristic of the **adaptive immune response**, specifically carried out by **B cells** after exposure to an antigen. - **B. Increase in body temperature**: **True**. Fever is a common innate defense mechanism that helps slow the growth of pathogens and enhances immune function. - **C. Vasodilation to allow immune cells to get to the infection**: **True**. This is part of the **inflammatory response**, a key component of innate immunity, which helps immune cells reach the site of infection more easily. - **D. Chemicals to draw immune cells to the infection**: **True**. Chemicals like **cytokines** and **chemokines** are released during the inflammatory response to recruit immune cells to the site of infection. - **E. All of the above**: **False**, because antibody creation (A) is not part of the innate immune response. So, the only function not provided by innate defenses is **antibody creation**. Chap 2 part 2 https://www.youtube.com/watch?v=o99Pri0OlNQ **[Adaptive (acquired) Defenses]** - Specific - Develop over time - Use memory system - Distinguish self from non-self *and* between pathogens - Include different lymphocytes that travel in lymph tissues. They mature into: - T cells: cell-mediated immunity - B cells: humoral immunity -- where we get antibodies **[Cellular Immunity (T CELLS)]** - Mediated by T cells on recognition of antigen. - T cells are produced in bone marrow and mature in the thymus. - Types of T cells - T helper which activates B cells to produce antibodies(immunoglobulins) - T suppressors turn off antibody production - Killer cells or cytotoxic cells destroy infected cells by destroying cell walls - T cells protect against viruses and cancer. T cells will poke cells into the bacterial, viral or fungal, cancerous wall and it induces apoptosis, and the cell will let in too much fluid and electrolyte it won't be balanced anymore and break down. **[Humoral Immunity (inside humor)]** - Mediated by B cells on encountering antigen. - B cells made and mature in bone marrow. (spleen and lymph nodes) - B cells differentiate into two types - Memory cells (memory cells will take that memory of the antigen or infectious agent and then step aside and keep the memory to help if were ever infected again to create antibodies to fight against it.) - Immunoglobulin-secreting cells (plasma cells or effector cells) - Antibodies are produced 72 hours after initial antigen exposure. - They protect against bacteria, viral reinfection and immediate inflammatory response - Each b cell has receptor for specific antigen - Subsequent exposure to same antigen leads to quicker response (memory cells).  Figure 02.F06: Development of cellular and humoral immunity9781284121131\_CH02\_TABLE02.jpg Table 2.02: Immunoglobulins and Their Functions **[Acquired Immunity]** - Active immunity - Acquired by having the disease (i.e., prior antigen exposure) and by vaccinations - Long lasting but takes a few days to become effective - Passive immunity - Receiving antibodies from external sources: maternal--fetal transfer of immunoglobumins and breastfeeding - Short lasting **[Question time]** - Which of the following are paired correctly? - **A. Physical barriers are part of the innate defenses** - B. B cells are part of the innate defenses - C. T cells are part of the innate defenses - D. Cytotoxic cells are part of the innate defenses The correct answer is **A. Physical barriers are part of the innate defenses**. Here's a breakdown of each option: - **A. Physical barriers are part of the innate defenses**: **True**. Physical barriers like the **skin**, **mucous membranes**, and **cilia in the respiratory tract** are part of the **innate immune system**. They provide the first line of defense against pathogens by physically blocking their entry into the body. - **B. B cells are part of the innate defenses**: **False**. **B cells** are part of the **adaptive immune system**, not the innate immune system. They are responsible for producing **antibodies** that target specific pathogens once the body has been exposed to them. - **C. T cells are part of the innate defenses**: **False**. **T cells** are also part of the **adaptive immune system**. Specifically, **cytotoxic T cells** (CD8+ T cells) play a role in identifying and killing infected cells, while **helper T cells** (CD4+ T cells) help activate other immune cells. - **D. Cytotoxic cells are part of the innate defenses**: **False**. **Cytotoxic cells** (often referring to **cytotoxic T cells** or **NK cells**) are not exclusively part of the innate immune system. While **Natural Killer (NK) cells** are part of the innate system, **cytotoxic T cells** are part of the adaptive immune response. So, **physical barriers** like skin and mucous membranes are the only option listed that are correctly paired with the **innate defenses**. **[Alterations in immunity -When something good goes bad]** - Hypersensitivity - Exaggerated immune response to a foreign substance - Autoimmune - Mistakes self as nonself - Immunodeficiency - Inadequate immune reaction **[Hypersensitivity]** - Inflated response to antigen - Leads to inflammation, which destroys healthy tissue - Can be immediate or delayed - Four types: - Type I: Immunoglobulin E mediated - Type II: cytotoxic hypersensitivity reaction -- tissue specific - Type III: immune complex--mediated - Type IV: delayed hypersensitivity reaction -- cell mediated Types of Hypersensitivity\ (1 of 6) - Type I, IgE mediated - Produces an immediate response. Immunoglobulin E is known to trigger allergic responses - Local or systemic. - Allergen activates T-helper cells that stimulate B cells to produce IgE. - IgE coats mast cells and basophils, sensitizing them to the allergen. These cells release histamine, cytokines and prostaglandins which all cause the allergic response - At next exposure, the antigen binds with the surface IgE, releasing mediators and triggering the complement system. - Type I, IgE mediated - Examples: - Hay fever, food allergies, and anaphylaxis - Causes inflammation and pruritus - Treatment includes epinephrine, antihistamines, corticosteroids, and desensitizing injections. - Type II, cytotoxic hypersensitivity reaction - IgG or IgM type antibodies bind to antigen on individual's own cells. - Antigen may be intrinsic or extrinsic. - Recognition of these cells by macrophages triggers antibody production. - Lysis of cells occurs because of the activation of the complement and by phagocytosis. - Usually immediate responses. - Type III, immune complex--mediated hypersensitivity reaction - Circulating antigen--antibody complexes accumulate and are deposited in the tissue. - Tissues involved are usually kidneys, joints, skin and blood vessels - Triggers the complement system, causing inflammation. - Example: - Autoimmune conditions (e.g., systemic lupus erythematosus) - Treatment is disease specific. - Type IV, delayed hypersensitivity reaction - Cell-mediated rather than antibody-mediated involving the T cells. - Antigen presentation results a delayed response of macrophages and T cells - Causes severe tissue injury and fibrosis - Examples: - Tuberculin skin testing, transplant reactions, and contact dermatitis - Treatment is disease specific.  Table 2.04: Overview of the Hypersensitivity Reactions **[\ ]** **[Question time]** - Which hypersensitivity reaction is paired correctly? - A. Type I -- takes 1-3 days to present - B. Type ii -- affects kidneys and joints - C. Type iii -- deposits antigen-antibody complexes into tissues - D. Type iv -- releases immunoglobulin e in the involved tissues The correct answer is **C. Type III -- deposits antigen-antibody complexes into tissues**. Here's a breakdown of each option: - **A. Type I -- takes 1-3 days to present**: **False**. Type I hypersensitivity reactions, also known as **immediate-type** reactions (e.g., allergies), occur **within minutes to hours** after exposure to an allergen. They are mediated by **IgE** and involve mast cell degranulation. - **B. Type II -- affects kidneys and joints**: **False**. Type II hypersensitivity reactions are **cytotoxic** reactions where **IgG or IgM antibodies** bind to antigens on the surface of cells, leading to cell destruction. While these reactions can affect various organs, **kidneys and joints** are not specific to Type II. A more common example is **hemolytic anemia**. - **C. Type III -- deposits antigen-antibody complexes into tissues**: **True**. Type III hypersensitivity reactions involve the formation of **antigen-antibody complexes** (typically involving **IgG**), which can deposit in various tissues, leading to inflammation and damage. Examples include **systemic lupus erythematosus (SLE)** and **rheumatoid arthritis**. - **D. Type IV -- releases immunoglobulin E in the involved tissues**: **False**. Type IV hypersensitivity reactions are **delayed-type** reactions and do not involve **IgE**. Instead, they are mediated by **T cells**, particularly **CD4+ helper T cells** and **CD8+ cytotoxic T cells**, leading to tissue inflammation. Examples include **contact dermatitis** and **tuberculin skin test responses**. So, **C** is the correct pairing! Type III hypersensitivity is indeed characterized by the deposition of antigen-antibody complexes in tissues. Top of Form Bottom of Form Ch 2 part 3 https://www.youtube.com/watch?v=G38XqDwpJgg **[Transplants]** - Making the best match of tissue antigens is key for success. - Donor sources may be living or a cadaver. - Four categories - Allogenic: donor and recipient are related or unrelated, but share similar tissue types - Syngenic: donor and recipient are identical twins - Autologous: donor and recipient are the same person; most successful (storing your own blood) - Xenogenic: use of tissue from another species (pig heart valve) - Autologuous is when donor recipient are the same person ex: when you store your own blood and use it later **[Patterns of Transplant Reactions (1 of 2)]** - Hyperacute tissue rejection - Immediate or three days after transplant - Due to the complement system -- antibodies are made - Tissue becomes permanently necrotic due to lack of vascularity because it is so new - Acute tissue rejection - Most common - Treatable - Occurs between four days and three months after transplant: cell mediated response - Manifestations: fever, erythema, edema, site tenderness, and impaired function of transplanted organ - Chronic tissue rejection (Ex; hardening of blood tissues) - Occurs four months to years after transplant. - Likely antibody-mediated response. - Antibodies and complements deposit in vessel walls of transplanted tissue, resulting in ischemia. **[Human leukocyte antigen (HLA TYPING) OR Major histocompatibililty complex]** - Genes code for proteins (GLYCOPROTEINS) on cell surfaces (many alleles or variations) - Since there are many variations of these proteins it is difficult to find two people with the same or similar tissue type - Receptors on macrophages that have ingested foreign particles signal to t cells who either recognize our own tissue or similar tissue and ignore or attack it if we see it is foreign - https://www.britannica.com/science/major-histocompatibility-complex **[Transplant Reaction Classifications (1 of 2)]** - Host vs. graft disease - Host fights the graft. - The recipient's immune system attempts to eliminate the donor cells. - Graft vs. host disease - Graft fights the host. - Frequent and potentially fatal complication of bone marrow transplants. - Occurs when immunocompetent fatal cells recognize host tissue as foreign and mount a cell-mediated immune response. - The host is usually immunocompromised and unable to fight graft cells; the host's cells are destroyed - Treatment: Immunosuppressive therapy **[Question time]** - The best type of transplant to prevent rejection would be: - A. Allogeneic - B. Xenogenic - C. Autologous - D. syngenic The correct answer is **C. Autologous**. Here's why: - **A. Allogeneic**: **False**. An **allogeneic transplant** involves the transplantation of organs or tissues between **genetically different individuals** of the same species. Rejection is a concern here because the recipient's immune system may recognize the transplanted tissue as foreign and attack it. - **B. Xenogenic**: **False**. A **xenogenic transplant** involves transplanting organs or tissues between **different species** (e.g., a pig heart into a human). This carries a very high risk of rejection because of the significant genetic differences, and it often requires heavy immunosuppressive therapy. - **C. Autologous**: **True**. An **autologous transplant** involves using the **recipient's own cells, tissues, or organs** for transplantation. Since the tissue is from the same individual, there is no risk of immune rejection. This is the best option for preventing rejection because the immune system recognizes the transplanted tissue as \"self.\" - **D. Syngeneic**: **False**. A **syngeneic transplant** involves transplanting organs or tissues between **genetically identical individuals**, such as identical twins. While this minimizes the risk of rejection compared to allogeneic transplants, it is still not as ideal as an autologous transplant, where there is no foreign tissue involved. In summary, **autologous transplants** are the best for preventing rejection because the body's immune system recognizes the transplanted tissue as its own. **[Autoimmune disorders]** - Immune system loses the ability to recognize self tissue. - Defenses are directed against host. - Can affect any tissue. - The mechanism that triggers this response is not clear. - Known characteristics - Genetics plays a role. - More prevalent in females. - Onset is frequently associated with an abnormal stressor, physical or psychological. - Are frequently progressive relapsing-remitting disorders characterized by periods of exacerbation and remission. **[Example: Systemic Lupus Erythematosus wolf (1 of 4) =LUPUS MEANS WOLF]** - Chronic inflammatory autoimmune condition. - May affect connective tissue of anybody organ. - discoid only affects skin - Remission and exacerbations---stressors tend to trigger. - Disease progression varies from mild to severe. - More common in women, Asians, and African Americans. - Cause is unclear, but it's thought that B cells are activated to produce autoantibodies and autoantigens that combine to form immune complexes, which attack the body's own tissues. - Also, hyperactive t helper cells and repressed T suppressor cells - Triple threat! - **[Diagnostic criteria (four or more of the following) = SOAPBRAINMD]** - **S**erositis- serous membrane can get inflamed, lining around heart abdominal and thoracity cavities, mucous lining, - **O**ral ulcers - **A**rthritis- polyarthiritis : multiply joints are swollen, sensitivity and swollen. - **P**hotosensitivity - **B**lood disorders (decreased count) - **R**enal involvement - **I**mmunological phenomena- decrease WBC - **A**ntinuclear antibody -- Positive antibody testing. - **N**eurological disorders (seizures/psychosis) - **M**alar rash (butterfly rash over cheeks) - **D**iscoid rash (patchy redness that can cause scarring) - Diagnosis - 11 criteria, X-rays, elevated sedimentation rate,\ C-reactive protein, urinalysis, echocardiogram, and blood test for complications - Treatment - No cure---only symptom management - Stress management and health promotion behaviors - Pharmacological - NSAIDs, antimalarials, corticosteroids, immunosuppressants, and DMARDs - Plasmapheresis - Prognosis improves with early diagnosis and treatment. 9781284121131\_CH02\_TABLE05.jpg Table 2.05: Common Manifestations of Systemic Lupus Erythematosus Question time - In SLE some positive signs include all of the following excluding: - A. Malar rash - B. Decreased wbc with testing - **C. Proper platelet count with testing** - D. Joint inflammation In systemic lupus erythematosus (SLE), the positive signs typically include: - **A. Malar rash**: This is a classic feature of SLE, often referred to as the \"butterfly rash\" across the cheeks and nose. - **B. Decreased WBC with testing**: Leukopenia (a low white blood cell count) is common in SLE. - **D. Joint inflammation**: Arthritis or joint pain/inflammation is a common symptom of SLE. However, the correct answer to the question is: - **C. Proper platelet count with testing**: In SLE, thrombocytopenia (low platelet count) is more commonly seen rather than a normal or \"proper\" platelet count. So, the option \"C\" does not typically indicate a positive sign of SLE. Top of Form Bottom of Form Chap 2 part 4 https://www.youtube.com/watch?v=T3MVhHwgA-g **[Immunodeficiency = ex: HIV or AIDS, or primary or secondary cause meaning genetic, congenital, drug issue, infection..etc]** - Diminished or absent immune response - Renders the person susceptible to disease normally prevented - Opportunistic infections -- pathogens normally fought cause disease in people with decreased immune function - Usually due to decreased normal flora (probiotics help these as a side note) - May be acute or chronic ; ex: drug therapy -- acute , chronic; hiv or aids. - Classifications - Primary -- genetic or congenital - Secondary -- specific cause (drug therapy, infection etc) AIDS- **[human immunodeficiency virus]** - HIV = needs cells infect, cells will affect RNA,and cells and rna will go back to infect dna. - Parasitic retrovirus that infects CD4 and macrophages upon entry - Cd 4 is the protein on t helper cell surfaces, that if affected with aids or HIVS - Retrovirus goes back through rna to dna, permanently changing dna - Two primary types - Type 1 is the most common strain in usa. - Type 2 is more common in West Africa; progresses to disease more slowly. - In the US, rates rising among women and African Americans - Transmission - Blood and bodily fluids, sharing needles, use medication for preventative... **[AIDS Progression (1 of 2)]** - Asymptomatic phase. - Virus is reproducing, usually for several years. - Acute retroviral syndrome: May have flu like symptoms - Antiretroviral therapy used to treat early - Highly active antiretroviral therapy is recommended early. 3 or more antiretroviral medications - Infections begin as the viral number rises, destroying the CD4 cells - May begin to have symptoms such as swollen nodes, diarrhea, weight loss, fever cough - Progression takes three forms. - Immunodeficiency -- opportunistic deficiencies - Autoimmunity -- arthritis, pneumonitis - Neurological dysfunction -- aids dementia - Diagnostic test (used for diagnosis and for determining progression) - antibody testing or antibody/antigen testing - Cd4 testing will be used with viral load to watch progression and response to treatment - HIV antibody - Rapid test - Home test - Then should follow up with blood test **[AIDS Classification System]** - Two systems, one based on lab findings and the other based on clinical manifestations - Laboratory findings---CD4 cell count - Category 1: \> 500 cells/μL - Category 2: 200--499 cells/μL - Category 3: \< 200 cells/μL - Clinical presentation - Category A: asymptomatic - Category B: some less serious manifestations of immune deficiency - Category C: AIDS-defining illnesses present **[Aids treatment]** - No cure. - Combination therapy works best. - Highly active antiretroviral therapy - May have to change regimen due to viral adaptation. - Other medicines and vaccines will be used to prevent opportunistic infections as needed. - Vaccinations. - Transmission prevention.  Table 2.06: HIV/AIDS Classification Systems **[Question time]** - Hiv is a retrovirus which means it damages the outer protein covering of the cell. - True or false **[Individuals at Risk for Immune Dysfunction]** - Very young and very old - Poor nutrition - Impaired skin integrity - Circulatory issues - Alterations in normal flora due to antibiotic therapy - Chronic diseases, especially diabetes mellitus - Corticosteroid therapy - Chemotherapy - Smoking - Alcohol consumption - Immunodeficiency states **[Immune-Building Strategies]** - Increasing fluid intake - Eating a well-balanced diet - Increasing antioxidants and protein intake - Getting adequate sleep - Avoiding caffeine and refined sugar - Spending time outdoors - Reducing stress **[Question time]** - I should go home and meditate. It is good for my immune system. - True or false **Chapter 3 -Hematopoietic Function** **[Normal hematopoietic function = blood is a solution and in a solution will have a solvent which is plasma/water, and solutue will be wbc. Rbc, platelets, macro and micro nutrients, hormones, gers rids of waste, acts a buffer, our PH scale normal 7.35-7.45... etc]** **[Hematopoiesis]** - Process of forming blood - Plasma: liquid protein - Leukocytes: white blood cells - Erythrocytes: red blood cells - Hemoglobin: oxygen-carrying component - Hematocrit (spin it!): amount of blood volume occupied by erythrocytes - Thrombocytes: platelets **[Hemostasis]** - Stoppage of blood flow - Normal when it seals a blood vessel to prevent blood loss and hemorrhage -- cut or damage! - Abnormal when it causes inappropriate clotting or when clotting is insufficient to stop blood flow -- stroke! **[Stages of Hemostasis with a cut]** 1\. Vessel spasm 2\. Formation of platelet plug (see blood vessel picture for steps) 3\. Blood coagulation 4\. Clot retraction 5\. Clot dissolution (macrophages eat debris and fibroblasts form new fibers) 9781284121131\_CH03\_FIG01.jpg Figure 03.F01: Blood clotting  Figure 03.F03: Clotting cascades 1. Prothrombin 2. Thrombin 3. Fibrinogen 4. Fibrin 5. Platelets **Question time** - The correct (short) order of the creation of platelet plug is: - A. Thrombin -- prothrombin -- fibrin -- fibrinogen - B. Thrombin -- fibrinogen - prothrombin -- fibrin - C. Thrombin -- prothrombin - fibrinogen - fibrin - D. prothrombin - Thrombin -- fibrinogen - fibrin **[White blood cell disorders]** **Disorders of the WBCs** - Leukocytes: key players in the inflammatory response and in fighting infections - Normal range = 5,000 to 10,000 cells/mL^3^ blood - Leukopenia: decreased levels (penia- means thin or lower) - Leukocytosis: increased levels 9781284121131\_CH03\_TABLE01.jpg -REMEMBER MOST TO LEAST! Never- Neutrophils 70% WBC in our blood stream, helps to fight of bacteria cells!! Let -- Lymphocyte 30 % - help to fight viral infection, Monkeys- Monocytes 7% , turns into macrophages, those help to phagocytize bacteria, dead cells, and cellular debris in the body Eat- eosinophils 3%, will see them with antigens antibody complexes and parasitic infections Bananas- basophil1%, closely related with mast cells that releases histamine, and histamine happens during a immune response where we basil dilate blood vessel Figure 03.F04: Leukocyte movement **[Neutrophils]** - One type of leukocytes - Usually the first to arrive at the site of infection - Normal range is 2,000--7,500 cells/mL Neutropenia\ (1 of 2) - Neutrophils \< 1500 cells/mL - Causes - Increased usage - Drug suppression - Radiation therapy - Congenital conditions - Bone marrow cancers - Spleen destruction - Vitamin deficiency - Manifestations - Depends on severity and cause - Infections and ulcerations, especially of the respiratory tract, skin, vagina, and gastrointestinal tract - Signs and symptoms of infection (e.g., fever, malaise, and chills) - Diagnosis: neutrophil levels and bone marrow biopsy - Treatment: antibiotic therapy and hematopoietic growth factors 9781284121131\_CH03\_FIG05.jpg Figure 03.F05: The role of neutrophils **[Question time]** - Neutrophils best help to fight which type of infection? - A. Viral - **B. Bacterial** - C. Dead cells - D. transplants **[Infectious Mononucleosis]**(1 of 2) - "Kissing disease"---oral transmission. Really 'spit disease' as it can live outside the body - Self-limiting. - Most prevalent in adolescents and young adults. - Caused by Epstein-Barr virus in the herpes family. - EBV infects the B cells by killing the cell or being incorporated into its genome. - Those B cells incorporated with EBV produce heterophile antibodies. - Once the disease is eliminated, a few B cells remain altered, giving the individual an asymptomatic infection for life and the potential to occasionally spread the EBV to others. - Manifestations - Insidious onset. - Incubation = 4--8 weeks. - Initially see anorexia, malaise, and chills. - Manifestations intensify to include leukocytosis, fever, chills, sore throat, and lymphopathy. - Acute illness usually lasts 2--3 weeks; may not fully recover for 2--3 months. - Treatment: symptomatic and supportive **[Question time!]** - Infectious mononucleosis: - A. Is only communicable with kissing - B. Is a rare virus - C. Is a quick moving infection - **D. Is found to affect b cells** **D. Is found to affect B cells**. Infectious mononucleosis (commonly caused by Epstein-Barr virus, or EBV) primarily infects **B lymphocytes** (a type of white blood cell), which are involved in the body's immune response. Here's why the other options are not correct: - **A. Is only communicable with kissing**: While kissing (due to the exchange of saliva) is a common way to spread the virus, **EBV can also be spread through other bodily fluids**, such as blood, semen, and organ transplants, or through shared items like utensils and toothbrushes. - **B. Is a rare virus**: Epstein-Barr virus is actually quite common and is found in a large percentage of the population worldwide. - **C. Is a quick-moving infection**: Infectious mononucleosis typically has a more gradual onset and lasts longer (several weeks), with symptoms like fever, sore throat, and swollen lymph nodes, rather than being a \"quick-moving\" infection. So, the most accurate statement about infectious mononucleosis is that it **affects B cells**. Top of Form Bottom of Form **[Lymphomas]** - Cancers affect lymphatic system - Most common hematologic cancer in the US - Two main types - Hodgkin's - Non-Hodgkin's **[Hodgkin's Lymphoma (1 of 4)]** - Least common of the two - Solid tumors with the presence **of Reed-Sternberg cells**. Which are Abnormal b lymphocytes which are much larger - Typically originate in the lymph nodes of the upper body - Several subtypes - Very curable with treatment - Manifestations: painless enlarged nodes, weight loss, fever, night sweats, pruritus, coughing, difficulty breathing, chest pain, recurrent infections, and splenomegaly - Staging - Stage I: The lymphoma cells are in one lymph node group or one part of a tissue or an organ. - Stage II: The lymphoma cells are in at least two lymph node groups on the same side of the diaphragm, or the lymphoma cells are in one part of a tissue or an organ and the lymph nodes near that organ. - Staging - Stage III: The lymphoma cells are in lymph nodes above and below the diaphragm. Lymphoma cells may be found in one part of a tissue or an organ near these lymph node groups. Cells may also be found in the spleen. - Stage IV: Lymphoma cells are found in several parts of one or more organs or tissues, or the lymphoma cells are in an organ and in distant lymph nodes. - Recurrent: The disease returns after treatment. - Diagnosis: physical examination, presence of Reed-Sternberg cells in a lymph node biopsy, complete blood count, chest X-rays, computed tomography scan, magnetic resonance imaging, positron emission tomography scan, and bone marrow biopsy - Treatment: chemotherapy, radiation, and surgery **[Question time!]**\ **[Which letter represents stage iii Hodgkin's lymphoma?]**  **[Non-Hodgkin's Lymphoma]** - More common - Poor prognosis - Many different types - Similar to Hodgkin's manifestations, staging, and treatment - Different in the spread and diagnosis - Can originate in the T or B cells - No Reed-Sternberg cells Blood cell review!\ http://www.allthingsstemcell.com/wp-content/uploads/2009/02/hematopoiesis\_simple1.png **[Leukemia (1 of 4)]** - Second most common blood cancer - Cancer of the leukocytes - Leukemia cells abnormally proliferate, crowding normal blood cells - Risk factors: exposure to chemical, viral, and radiation mutagens; smoking; use of chemotherapies; Down syndrome; and immunodeficiency disorder - Types - Acute lymphoblastic leukemia (how to remember: a kid pointing at A L L detergent) - Affects primarily children - Responds well to therapy - Good prognosis - Acute myeloid leukemia - Affects primarily adults - Responds fairly well to treatment - Prognosis somewhat worse than that of acute lymphoblastic leukemia - Types - Chronic lymphoid leukemia - Affects primarily adults - Responds poorly to therapy, yet most patients live many years after diagnosis - Chronic myeloid leukemia - Affects primarily adults - Responds poorly to chemotherapy, but the prognosis is improved with allogeneic bone marrow transplant - Manifestations: leukopenia, anemia, thrombocytopenia, lymphadenopathy, joint swelling, bone pain, weight loss, anorexia, hepatomegaly, splenomegaly, and central nervous system dysfunction - Diagnosis: a history, physical examination, peripheral blood smears, complete blood count, and bone marrow biopsy - Treatment: chemotherapy and bone marrow transplant **[Multiple Myeloma (1 of 2)]** - Plasma cell cancer (third most common) - Excessive numbers of abnormal plasma cells in the bone marrow, crowding the blood-forming cells and causing Bence Jones proteins to be excreted in the urine\* - Bone destruction leads to hypercalcemia and pathologic fractures - Often well advanced upon diagnosis - Manifestations - Insidious onset\* - Include: anemia, thrombocytopenia, leukopenia, decreased bone density, bone pain, hypercalcemia, and renal impairment - Diagnosis: serum and urine protein, calcium, renal function tests, complete blood count, biopsy, X-rays, computed tomography, and magnetic resonance imaging - Treatment: chemotherapy and complication management Symptoms nunomic hyperCalcemia Renal dysfunction Anemia Bone pain **[Question time!]**\ - What disease is this?  - A. Infectious mono - B. Lymphoma - C. non-hodgkins - D. Multiple myeloma **[Chap 3 part 3 https://www.youtube.com/watch?v=OAzyWOSf3FI]** **[Red blood cells- "I'm so tired"]** **Disorders of the RBCs** - Erythropoiesis - Production of erythrocytes - Regulated by erythropoietin from kidneys - You can take it as a drug erythropoietin stimulating agents - Occurs in bone marrow - Disorders typically result from a deficit or defect in the erythrocytes. **[Anemia]** - Results from a decreased number of erythrocytes, reduction of hemoglobin, or presence of abnormal hemoglobin (see hemoglobin video) - Decreases O~2~-carrying capacity, leading to tissue hypoxia - Several types with varying etiology - General manifestations: weakness, fatigue, pallor, syncope, dyspnea, and tachycardia **[Iron-Deficiency Anemia (1 of 2)]** - Very common - Iron is necessary for hemoglobin production - Causes: decreased iron consumption, decreased iron absorption, or increased bleeding - Additional manifestations: cyanosis to sclera, brittle nails, decreased appetite, headache, irritability, stomatitis, pica=weird tendency to eat things, and delayed healing - Test before supplement! - Diagnosis: complete blood count (low hemoglobin, hematocrit, MCV, and MCHC), serum ferritin, serum iron, and transferrin saturation - Treatment: identify and treat cause, increase dietary intake, and administer iron supplements **[Pernicious Anemia]** (1 of 2) - Vitamin B~12~ deficiency usually caused by a lack of intrinsic factor. - Cause: autoimmune damaging parietal cells that release intrinsic factor in the stomach - Vitamin B~12~ is required for DNA synthesis. - Leads to decreased maturation and cell division. - May see myelin breakdown and neurological complications. - Manifestations: bleeding gums, diarrhea, impaired sense of smell, loss of deep tendon reflexes, anorexia, personality or memory changes, positive Babinski's sign, stomatitis, paresthesia, and unsteady gait, difficulty of energy, numbness and tingling. - Diagnosis: serum B~12~ levels - Treatment: injectable B~12~ **[Aplastic Anemia (1 of 2)]** - Bone marrow depression of all blood cells (pancytopenia).= wbc , rbc and platelets - Causes: idiopathic, autoimmune, medications, medical treatments, viruses, and genetic abnormalities. - Onset may be insidious, sudden, and severe. May be temporary or permanent - Manifestations: - Anemia (e.g., weakness, pallor, dyspnea) - Leukocytopenia (e.g., recurrent infections) - Thrombocytopenia (e.g., bleeding) - Diagnosis: complete blood count and bone marrow biopsy - Treatment: identify and manage underlying cause, oxygen therapy, infection control, infection treatment, bleeding precautions, blood transfusions, and bone marrow transplants **[Question time!]** - Pernicious anemia is seen with patients who have a vitamin B6 deficiency due to dysfunction of intrinsic factor. - True or **false , B12** **[Hemolytic Anemia]** - Excessive erythrocyte destruction - Causes: idiopathic, autoimmune, genetics, infections, blood transfusion reactions, and blood incompatibility in the neonate - Several types including sickle cell anemia, thalassemia, and erythroblastosis fetalis **[Sickle Cell Anemia (1 of 5) = Crescent shape]** - Neither recessive nor dominant---co-dominant. - Hemoglobin S causes erythrocytes to be abnormally shaped. - Abnormal erythrocytes carry less oxygen and clog vessels, causing hypoxia and tissue ischemia. - More common in people of African and Mediterranean descent. - Also seen in people from South and Central America, the Caribbean, and the Middle East - Forms of sickle cell anemia (heterozygous) - Sickle cell trait. (got one normal one sickcell trait from one parent) - Heterozygous. - Less than half of erythrocytes are sickled. - Sickle cell disease (got it from both parents homozygous) - Homozygous. - Most severe. - Almost all erythrocytes are sickled. - Manifestations - Typically appear around 4 months of age - Sickle cell crisis - Painful episodes that can last for hours to days - Pain caused by tissue ischemia and necrosis - Triggered by dehydration, stress, high altitudes, and fever - Diagnosis: hemoglobin electrophoresis, complete blood count, and bilirubin test - Life expectancy improving with better management - Treatment - No cure, palliative - Stem cell research showing promise - Medications (e.g., Hydrea \[hydroxyurea\]) - Avoid sickling triggers - Other strategies: oxygen therapy, hydration, pain management, infection control, vaccinations, blood transfusions, bone marrow transplants, genetic counseling 9781284121131\_CH03\_TABLE02.jpg Table 3.02: Complications of Blood Vessel Occlusions in Sickle Cell Anemia **[Thalassemia (1 of 2)]** - Autosomal dominant inheritance (and its genetic issue) - Abnormal hemoglobin from a lack of one of two proteins that make up hemoglobin (alpha and beta globin) - Most common in people of Mediterranean descent - Also seen in those of Asian, Indian, and African descent - Manifestations: delayed growth and development, fatigue, dyspnea, heart failure, hepatomegaly, splenomegaly, bone deformities, jaundice - Severe cases can lead to death in childhood. - Life expectancy can improve with effective management. - Diagnosis: complete blood count (low MCV, MCHC) and iron levels. - Treatment: blood transfusion, chelation therapy, and splenectomy. Let's practice!  Iron deficiency Anemia where RBC looks paler http://slideplayer.com/8418640/26/images/25/Normal+and+Anemic+Blood+Cells.jpg  = SICKLE CELL ANEMIA **[Polycythemia (1 of 2)]** - Abnormally high erythrocytes (high RBC) - Rare - Considered a neoplastic disease - Increased blood volume and viscosity, leading to tissue ischemia and necrosis - Complications: thrombosis, hypertension, heart failure, hemorrhage, splenomegaly, hepatomegaly, and acute myeloblastic leukemia - Manifestations: cyanotic or plethoric skin, high blood pressure, tachycardia, dyspnea, headaches, visual abnormalities - Diagnosis: complete blood counts, bone marrow biopsy, and uric acid levels - Treatment: chemotherapy, radiation, phlebotomy, and managing clotting disorders **Chapter 3 part 4 https://www.youtube.com/watch?v=gxEF3oEosR4** **[Platelet disorders]** **[Disorders of Platelets]** - Normal platelet levels range from 150,000 to 350,000 cells/mL^3^ - Include issues in quantity and quality of platelets - Thrombocytosis: increased levels - Thrombocytopenia: decreased levels of platelets **[Hemophilia A (genetic disorder) ]** - X-linked recessive bleeding disorder - Deficiency or abnormality of clotting factor VIII - Varies in severity - Manifestations: bleeding or indications of bleeding (e.g., bruising, petechia, etc.) - Diagnosis: clotting studies and serum factor VIII levels - Treatment: clotting factor transfusions, recombinant clotting factors, and bleed precautions **[Von Willebrand's Disease (1 of 5)]** - Most common hereditary bleeding disorder - Decreased platelet adhesion and aggregation - Manifestations: bleeding or indications of bleeding (e.g., bruising, petechia, etc.) - Forms of von Willebrand's disease (has genetic linked) - Type 1 - Most common and mildest form - Follows autosomal dominant - Reduced von Willebrand's factor levels - Can cause significant bleeding with trauma or surgery but is milder than the other types so no spontaneous bleeding - Forms of von Willebrand's disease - Type 2 - Either autosomal dominant or recessive. - Five subtypes. - von Willebrand's factor building blocks are smaller than usual or break down easily. - Forms of von Willebrand's disease - Type 3 - Follows autosomal recessive - No measurable von Willebrand's factor or factor VIII - Causes severe bleeding problems - Acquired type - Occurs with Wilms' tumor, congenital heart disease, systemic lupus erythematosus, and hypothyroidism - Diagnosis: bleeding studies and factor VIII levels - Treatment - Mild cases usually do not require treatment - infusions - Bleeding precautions - Measures to control bleeding  **[Question time]** - Which is the best match for the types of von Willebrand's disease? - A. Type I is the least common and most aggressive form - **B. Type 2 is when the building blocks that make up the von Willebrand factor are too small** - C. Type 3 is mild and barely diagnosable - D. Acquired occurs due to inherited genes - **Type 1**: This is the **mildest form** and the **most common**, characterized by a partial deficiency of von Willebrand factor (vWF). It is not the least common or most aggressive. - **Type 2**: This type involves **qualitative defects** in von Willebrand factor, meaning that the vWF does not function properly. One of the subtypes of Type 2 (e.g., Type 2A) involves the production of vWF that is too small or defective, leading to a bleeding tendency. - **Type 3**: This is the **most severe form**, where there is an **almost complete absence** of von Willebrand factor, leading to more severe bleeding. It is not mild. - **Acquired von Willebrand disease** is **not inherited**, but can develop secondary to other conditions like heart disease, certain cancers, or autoimmune disorders. **[Disseminated Intravascular Coagulation (1 of 2)]** - Life-threatening complication of many conditions - Results from an inappropriate immune response in response to acute infection - Widespread coagulation followed by massive bleeding because of the depletion of clotting factors (clot clot clot then bleed bleed bleed) - Manifestations: tissue ischemia and abnormal bleeding - Complications: shock and multisystem organ failure - Diagnosis: complete blood count and bleeding studies - Treatment: identify and treat underlying cause **[Idiopathic Thrombocytopenia Purpura (1 of 5)]** - HypOcoagulation resulting from an autoimmune destruction of platelets - Acute form - More common in children - Sudden onset - Self-limiting - Chronic form - More common in adults age 20--50 - More common in women - Causes: idiopathic, autoimmune diseases, immunizations with a live vaccine, immunodeficiency disorders, and viral infections - Manifestations: bleeding or indications of bleeding (e.g., bruising, petechia, etc.) - Deficiency of enzyme necessary for cleaving von Willebrand's factor, leading to hypercoagulation. - Hypercoagulation depletes platelet levels. - Characterized by thromboses, thrombocytopenia, and bleeding. - Causes: idiopathic causes, heredity, bone marrow transplants, cancer, medications, pregnancy, and HIV. - Idiopathic thrombocytopenic purpura causes hyper coagulation due to destruction of the patient's platelets. - True or false. The statement is **false**. Idiopathic thrombocytopenic purpura (ITP) does **not** cause hypercoagulation. Instead, it leads to a **reduced platelet count** due to the **destruction of platelets**. ITP is an autoimmune disorder where the body mistakenly attacks and destroys its own platelets, which are essential for blood clotting. This results in a **low platelet count (thrombocytopenia)**, which impairs the blood's ability to clot effectively, increasing the risk of bleeding and bruising, not clotting. **Why it's False:** Hypercoagulation refers to an increased tendency of the blood to clot, which leads to a higher risk of conditions like deep vein thrombosis (DVT), pulmonary embolism, or stroke. However, in ITP, the opposite occurs---because there are fewer platelets available, the primary concern is bleeding, not clotting. The body cannot form normal blood clots due to the lack of platelets, which are crucial for the clotting process. **More on ITP:** - **Pathophysiology**: ITP occurs when the immune system produces antibodies that target and destroy platelets, often after an infection or sometimes with no obvious trigger. Platelet destruction takes place mainly in the spleen, and because of this, the platelet count decreases significantly. - **Symptoms of ITP**: These may include easy bruising (purpura), spontaneous nosebleeds, bleeding gums, or even internal bleeding in severe cases. Since the platelet count is low, the body\'s ability to stop bleeding is compromised, leading to these symptoms. - **Treatment**: Treatment for ITP often involves medications such as corticosteroids (which suppress the immune system), immune globulin, or in some cases, treatments like platelet transfusions or spleen removal (splenectomy) if the condition is severe and unresponsive to medication. In summary, ITP is associated with **bleeding tendencies** due to reduced platelet levels, not with hypercoagulation. Thus, the statement is incorrect.