Patho Exam 2 PDF

Patho Exam 2 Chapter 7 electrolytes Pg 133 chart for hypo and hypers Chapter 8 abg- pg 150 chart Chapter 41/42 Picture packet Chapter 9 - Inflammation and Wound Healing - The Steps of the Inflammatory Process: o The inflammatory process is the body’s response to tissue injury or...

Patho Exam 2 Chapter 7 electrolytes Pg 133 chart for hypo and hypers Chapter 8 abg- pg 150 chart Chapter 41/42 Picture packet Chapter 9 - Inflammation and Wound Healing - The Steps of the Inflammatory Process: o The inflammatory process is the body’s response to tissue injury or infection. It typically follows a multi-step process: ▪ Vasodilation: Blood vessels expand to allow increased blood flow to the affected area, which helps deliver immune cells and nutrients for repair. ▪ Increased Vascular Permeability: This allows proteins, immune cells (like neutrophils), and other factors to leak out into the tissue to begin the healing process. ▪ Chemotaxis: White blood cells, particularly neutrophils and macrophages, move toward the site of injury, guided by chemical signals (chemokines). ▪ Phagocytosis: The immune cells engulf pathogens, dead cells, and debris to help clear the infection or injury. ▪ Resolution or Repair: After pathogens or debris are cleared, the tissue begins healing through tissue regeneration or fibrosis (scar formation). - Wound Healing or Complications/Disruptions in Wound Healing: o Wound healing involves several stages: ▪ Hemostasis: The immediate response to stop bleeding by constricting blood vessels and forming a clot. Platelets secrete inflammatory mediators; serotonin, histamine, platelet derived growth factor. Vasoactive amines like epi cause short term vasoconstriction (limiting blood loss) ▪ Inflammatory Phase: The body cleans the wound with immune cells. Vasodialation, increased vascular permeability, chemotaxis happen. ▪ Proliferative Phase: New tissue (granulation tissue) and blood vessels form to begin repairing the tissue. Fibroblasts synthesizes collagen and provides the extracellular matrix for wound healing (key cell in  this process). 24-48 hours after the injury fibroblasts form the granulation tissue (foundation of scar tissue). Vascular endothelial cells create new blood vessels (angiogenesis). The granulation tissue secretes growth factors and cytokines like IL-1 and TGF (tell hypothalamus to reset temp= fever). Epithelial cells migrate and proliferate to fill in the gap. ▪ Maturation/Remodeling Phase: Collagen is reorganized to strengthen the wound. 3 weeks after the injury this begins. The scar tissue is refined and reshaped by fibroblasts and myofibroblasts. - Complications can include: o Infection: Delays healing and can lead to chronic wounds. o Excessive scarring: Keloids or hypertrophic scars. o Chronic inflammation: If the inflammatory phase doesn't resolve properly, it can result in chronic inflammation or even autoimmune responses. o Wound rupture; dehiscence, evisceration o Contractures- inflexible shrinkage can limit mobility o Stricture- narrowing of an open area like the esophagus because of scar tissue o Fistula- abnormal connection between 2 areas of tissues or organs (tracheoesophageal fistula) o Adhesions- abnormal bands of internal scar tissue that can limit mobility if in joint. Can also happen around internal organs. - Mast Cells: o Mast cells are critical for the initiation of the inflammatory response. They are located in connective tissues, near blood vessels, and release histamine, heparin, and other mediators upon activation. These substances contribute to vasodilation and increased permeability of blood vessels during inflammation, and are central to allergic reactions. o Mast cells are located in tissues adjacent to blood vessels. They are the richest source of histamine - Histamine: o Histamine is a potent vasodilator that increases the permeability of blood vessels, allowing white blood cells to enter tissues. It is released by mast cells and basophils and platelets during the early stages of inflammation and  is one of the key factors responsible for the redness, warmth, and swelling seen in inflamed areas. o Cause arteriolar vasodilation, large artery vasodilation and increased permeability of venules. o EX: sneezing, runny nose, pharyngeal irritation in upper respiratory tract. - Cytokines: o Cytokines are signaling molecules (such as interleukins, tumor necrosis factor [TNF], and interferons [IF]) released by immune cells (WBCs). They help regulate immune responses, inflammation, and tissue repair. Cytokines can attract other immune cells to the site of infection or injury and promote the healing process. o Modulate the inflammatory reaction by amplifying or deactivating the process, they simultaneously cause localized and systemic effects. - ESR (Erythrocyte Sedimentation Rate) and CRP (C-Reactive Protein): o ESR measures the rate at which red blood cells settle in a test tube; an elevated ESR suggests inflammation or infection. o CRP is a protein produced by the liver in response to inflammation. Elevated CRP levels are a sign of acute or chronic inflammation, and this test is often used to monitor the effectiveness of anti-inflammatory treatments. o CRP is a key acute phase protein important for marking foreign material for phagocytosis, activating the complement system, which augments immunity; and stimulating other inflammatory cytokines. Elevated CRP indicates active inflammation is occurring. o Elevated CRP, fibrinogen, and ESR alert that an active process of inflammation is occurring. - Neutrophils: o Neutrophils are the most abundant white blood cells and are key players in the early response to infection. They are the first to arrive at the site of infection or injury, where they perform phagocytosis to ingest and destroy pathogens. o Short lifespan 10 hours- a few days o Begin the process of phagocytosis of the foregin matter immediately. o Phagocytosis involves recognition and attachment of the leukocyte to the foreign matter, engulfment and deterioration or killing  - Systemic Responses in Inflammation: o Systemic responses to inflammation include: ▪ Fever: Often caused by pyrogens (fever-inducing substances) released during infection. ▪ Leukocytosis: An increase in white blood cell count, particularly neutrophils. ▪ Acute-phase reactants (e.g., CRP, fibrinogen) increase to help combat infection or injury. o Fever, pain, lymphadenopathy (swollen lymph nodes), anorexia, sleepiness, lethargy, anemia and weight loss are systemic responses. o Inflammatory mediators like prostaglandins (PGs), TNF and ILs are responsible. Chapter 10 - Infectious Diseases - WBC (White Blood Cells): o White blood cells are essential components of the immune system, responsible for fighting infections. The main types include: ▪ Neutrophils: First responders to bacterial infections. ▪ Lymphocytes: Involved in the adaptive immune response (e.g., T cells and B cells). ▪ Monocytes/Macrophages: Clear pathogens and debris, and coordinate immune responses. - Immunosuppression or Compromised Immunity: o immunosuppression refers to a reduced ability of the immune system to fight infections. It can result from: ▪ Diseases (e.g., HIV/AIDS, cancer). Medications (e.g., chemotherapy, immunosuppressive drugs for autoimmune diseases or organ transplants). Malnutrition: Lack of essential nutrients affects immune function. - Innate Immunity: o This is the body's first line of defense, involving non-specific responses: ▪ Physical barriers (e.g., skin). ▪ Immune cells (e.g., neutrophils, macrophages). ▪ Innate barriers also include natural killer T cells and cytokines ▪ Includes natural enzymes, bacterial and antiviral secretions that make the skin and mucous membranes inhospitable for pathogens  ▪ Inflammatory responses. Innate immunity responds immediately to a pathogen but does not have memory of past infections. ▪ If the innate defence mechanisms are inadequate the second line of defense; adaptive immunity is activated - Adaptive Immunity: ▪ Adaptive immunity involves a specific response to pathogens and has memory. The 2 major categories are: 1. B lymphocyte immunity: aka humoral immunity 2. T lymphocyte immunity: aka cell mediated immunity ▪ In both cases lymphocytes are the primary cell which originates from the bone marrow ▪ T-lymphocytes aka T cells mature in the thymus and after maturation they are found in the bloodstream and T-cell zones of lymph nodes ▪ B-lymphocytes aka B cells mature in the bone marrow, spleen, and lymph nodes ▪ During maturation T cells differentiate into CD4 cells (helper T cells) and CD8 cells (cytotoxic T cells) ▪ CD4 (helper T) influence all other cells of the immune system including other T cells they are involved in cell mediated immuniity and antibody mediated adaptive immunity ▪ CD8 cells attack the antigen ▪ This system is slower to respond than innate immunity but provides long-term protection after exposure to pathogens. - Respiratory Infection - Pertussis (Whooping Cough): o Pertussis is a highly contagious respiratory disease caused by Bordetella pertussis. Symptoms include: ▪ Severe coughing fits (hence "whooping" sound when inhaling). ▪ It primarily affects infants and can cause serious complications, including pneumonia and seizures. ▪ Early treatment with antibiotics, IV fluids and oxygen is necessary - CAP (Community-Acquired Pneumonia): o Mycoplasma pneumonia is a common cause of atypical pneumonia, often seen in younger adults. o Symptoms can be milder compared to bacterial pneumonia, with a dry cough, fever, and fatigue. o Treatment often involves antibiotics targeting Mycoplasma, such as azithromycin.  o S. pneumonaie is the most common cause of CAP o Classically its preceded by a viral illness that is followed by acute onset of high fever, rigors, productive cough, pleuratic chest pain, dyspnea, tachypnea, tachycardia, sweats and more o Crackles can be heard o Dx includes chest xray, sputum culture and a specific urine test can be used - Staph Infections - MRSA (Methicillin-Resistant Staphylococcus aureus): o MRSA is a resistant strain of Staphylococcus aureus. It causes skin and soft tissue infections and can lead to severe issues like sepsis or pneumonia. Treatment is challenging due to antibiotic resistance, so vancomycin or newer antibiotics are typically used. - Bacterial Meningitis: o Bacterial meningitis is a life-threatening infection of the meninges, the protective membranes covering the brain and spinal cord. Common pathogens include Neisseria meningitidis, Streptococcus pneumoniae, and Haemophilus influenzae. Symptoms include: ▪ Severe headache ▪ Stiff neck ▪ Fever ▪ Nausea/vomiting o Kernig’s and Brudzinski’s signs are commonly seen o Dx requires lumbar puncture o Bacterial- high dose antibiotics o Viral- resolves on its own so just supportive therapy - E. coli Infections: o Escherichia coli is a bacterium that normally resides in the intestines. However, some strains can cause foodborne illness and severe infections, such as: ▪ E. coli O157:H7, which can cause hemolytic uremic syndrome (HUS), leading to kidney failure particularly in children