NURS548 Advanced Pathophysiology Midterm Review 2022/2023

Apoptosis A form of programmed cell death that eliminates senescent cells, DNA,, and damage or unwanted cells. Neoplastic cells do not die off (apoptosis) to keep the number of total cells constant. ... Labile Cell Continuously dividing tissues are those in which cells continue to divide and replicate throughout our life, replacing cells that are continually being destroyed. They include the surface epithelial cells of the skin, oral cavity, vagina, and cervix; the columnar epithelium of the gi tract, uterus, and fallopian tubes; the transitional epithelium of the urinary tract; and bone marrow cells. These tissues can easily regenerate after injury as long as a pool of stem cells is preserved. Stable cells Cells that normally stop dividing when growth stops. cells in these tissues remain dormant in the G0 stage of the cell cycle. They are, however, capable of undergoing regeneration when confronted with an appropriate stimulus. Stable cells constitute the parenchyma of solid organs such as the liver and kidney. They also include smooth muscle cells, vascular endothelial cells, and fibroblasts, the proliferation is particularly important to wound healing. Permanent Cell Cells in the permanent tissues to not proliferate. they are considered to be terminally differentiated and do not undergo mitotic division in postnatal cells. They include nerve cells, skeletal muscle cells, and cardiac muscle cells. These cells do not normally regenerate; once destroyed they are replaced with fibrous scar tissue that lacks the functional characteristics of the destroyed tissue. Cell Cycle Page 72 of textbook Proto-Oncogene Normal genes that become cancer-causing genes if mutated. They encode for normal cell proteins such as growth factors, growth factor receptors, transcription factors that promote cell growth, cell cycle proteins and inhibitors of apoptosis. Proto-oncogenes are associated with gene overactivity. Oncogenesis 3 stages: Initiation; Promotion; Progression Initiation Initial mutations occur by a carcinogenic agent such as chemicals, radiation, or viruses causing DNA damage and cell mutation Promotion mutated cells are stimulated to divide- activation of oncogenes by promoter agent Progression tumor cells compete with one another and develop more mutations which make them more aggressive Sequence of events in cellular response to inflammation includes leukocyte 1. margination and adhesion 2. transmigration 3. Chemotaxis 4. activation and phagocytosis non-osseous, malignant neoplasm of tissues derived from mesoderm Sarcoma Benign tumor of adipose tissue lipoma Benign neoplasm arising in glandular tissue adenoma malignant tumor of bone osteosarcoma benign tumors tissue name + "oma" Malignant tumor-epithielial tissue tissue name + "Carcinoma" malignant tumor- mesenchymal tissue tissue name + "sarcoma" What happens during the vascular stage of acute inflammation Prostaglandins and leukotrienes affect blood vessels. arterioles & venules dilate increased blood flow to the injured area redness and warmth result capillaries become more permeable allows exudate to escape into tissues swelling and pain result Serous exudate watery fluid low in protein content that result from plasma entering the inflammatory site Hemorrhagic exudate Occurs with severe tissue injury that causes damage to blood vessels or when there is significant leakage of red cells from capillaries fibrinous exudate contains large amounts of fibrinogen and form a thick and sticky meshwork, much like fibers of a blood clot. Membranous exudate develops on mucous membrane surfaces and are composed of necrotic cells enmeshed in fibro-purulent exudate. Purulent exudate contains pus, which is composed of degraded white cells, proteins and tissue debris. Process that occurs when there is injury to tissue leukocytes mobilize to the area via the bloodstream. Once they reach the compromised area, the 1st process is "pavementing", whereby the leukocytes collect along the endothelial lining of the blood vessel. This allows them to "get out of the flow of traffic", in preparation of making a "left hand turn" out of the blood vessel. Once they make this left hand turn and leave the blood vessel (emigration), they are directed to the site of injury (it is very dark inside) by way of chemical signals (chemotaxis). Now they can "clean up" the area and remove unwanted debris via the process of phagocytosis. Histamine Produces dilation of arterioles and increases the permeability of venules. Serotonin is a vasoactive dilator. Found primarily with platelet granules and is released during platelet aggregation. granulomatous chronic inflammation a distinctive form of chronic inflammation where macrophages mass together around foreign bodies Connective tissue surrounds and isolates the mass Associated with foreign bodies (splinters, sutures, silica, asbestos) and with microorganisms that cause TB, syphilis, sarcoidosis, deep fungal infections and brucellosis Mechanisms of fever ens release causing non-specific complaints 2. resetting of the thermostatic set point 3. temperature raising responses: vasoconstriction, shivering, piloerection, increased metabolism 4. Core body temperature reaches new set point 5. temperature-reducing responses: vasodilation, sweating, increased ventilation Manifestations of fevers 1 Predromal period 2 chill stage 3 flush stage 4 defervescence stage Predromal period Characterized by nonspecific complaints Chill stage (during which temperature is rising) Characterized by sensation of being chilled, with generalized shaking Flush stage Characterized by cutaneous vasodilation and warm and flushed skin Deferevescence stage Sweating Common manifestations of fever anorexia, myalgia, arthralgia, and fatigue Increased respirations and HR dehydration may occur d/t sweating and increased RR Type I Immediate Hypersensitivity response IgG-mediated- mast cell degranulation Ex. hay fever, anaphylaxis Type II Antibody-mediated hypersensitivity Formation of antibodies (IgG, IgM) against cell surface antigens. Complement is usually involved Ex. hemolytic anemia, hemolytic disease of newborn, Goodpasture disease Type III Immune-complex-mediated hypersensitivity Formation of antibodies (IgG, IgM) that interact with exogenous or endogenous antigens to form antigen-antibody complexes that cause vessel or tissue injury Ex. Arthus reaction, autoimmune diseases (lupus, rheumatoid arthritis), Type IV Cell-mediated hypersensitivity Sensitized T lymphocytes release cytokines that cause direct cell-mediated cytotoxicity or delayed hypersensitivity disorders Ex. TB, contact dermatitis, transplant rejection Anaphylaxsis systemic response to the inflammatory mediators released in Type I hypersensitivity. It is a life-threatening hypersensitivity reaction characterized by widespread edema, difficulty breathing and vascular shock secondary to vasodilation. histamines, acetylcholine, kinins, leukkotrienes, and prostaglandins asll cause vasodialtion Acetylcholine, kinins, leukotrienes and prostaglandins all can cause bronchoconstriction Mechanisms of autoimmune diseases occur more commonly in women familial clustering environmental factors- breakdown in T-cell anergy, release of sequestered antigens, molecular mimicry, superantigens Course of HIV infection Primary Latent Overt AIDS PRIMARY INFECTION PHASE signs of systemic infection- fever, fatigue, myalgias, sore throat, night sweats, GI issues, rash, headache Seroconversion: immune system responds and antibodies against HIV appear (1-6months) Latent Period No signs/symptoms Virus is replicating, Th cell count gradually falls May last 10 years or longer Overt AIDS Th cell count 200, or AIDS-defining illness death within 2-3 years if no treatment Lymphocytes B-Cells Create antibodies Lymphocytes T cells Control immune response; cell mediated immunity Lymphocytes Natural Killer Cells (NKC) kill antigenic cells Clinical manifestations of acute leukemia Bone marrow depression;malaise, easy fatiguability; fever;bleeding, petechaie, ecchymosis, ginival bleeding, epitaxis; bone pain and tenderness on palp; headache; nausea; vomiting; papilledema; cranial nerve palsies; seizure; coma; abdominal discomfort; increased vulnerability to infections; hematologic abnormalities; anemia; thrombocytpenia; metabolic disorders Acute Lymphocytic Leukemia (ALL) Most common leukemia in childhood, peak incidence 2-4 years of age Acute Myelogenous Leukemia (AML) Chiefly an adult disease, but also seen in children and adolescents Type of leukemia associated with Down's Symdrome Chronic Lymphocytic Leukemia (CLL) Mainly a disorder of older persons men are affected twice as much as women Chronic Myelongenous Leukemia (CML) Predominantly a disorder of adults between 30 and 50 years of age Incidence is slightly higher in men than women Associated with the presence of the Philadelphia chromosome Hodgkins Lymphoma Found in a single node or chain of nodes and spreads to the first anatomically contiguous lymphoid tissue. Staging extremely important in guiding therapy Characterized by Reed-Sternberg cells. Malignant B cells invade lymphoid organs Non-Hodgkins Lymphoma Originate from malignant transformation of either B cell or T cell Spreads in an unpredictable fashion Thrombopoietin Made in liver, kidney, smooth muscle, bone marrow Megakaryocytes Formed in bone marrow Break apart for form many platelets Platelets Live 8-9 days in circulation Many are stored in spleen