Download Immune System Processes and Autoimmune Disorders and more Exams Nursing in PDF only on Docsity!
Patho Exam 2 (Xavier ABSN) Questions With Complete Solutions hypertrophy an increase in individual cell size that results in enlargement of functioning tissue mass hyperplasia increase in number of cells atrophy cellular adaptation in which cells revert to a smaller size in response to changes in metabolic requirements/ environment metaplasia the replacement of one cell type by another cell type dysplasia deranged cellular growth within a specific tissue cause of hypertrophy either physiological or pathological process; increases cell size in order to manage workload asked of cells cause of hyperplasia stimulated by hormonal or compensatory cellular mechanisms
cause of atrophy a cell's environment can not sustain its metabolic requirements; allows for less metabolic demand and more efficient functioning cause of metaplasia a result of the cell's genetic programming in response to a change in environmental conditions cause of dysplasia chronic inflammation, precancerous condition physiological hypertrophy cells become bigger in response to demands from the body pathological hypertrophy the enlargement of cells without the necessary support network hypoxia deficiency in the amount of oxygen reaching the tissues pathway of hypoxia the cell enters anaerobic metabolism, during which it generates 2 ATP; a low amount of energy and pyruvic acid; pyruvic acid changes to lactic acid effect of hypoxia inadequate cell energy slows down all metabolic functions of the cell and lactic acid alters cellular biochemical activity
result of damage to __________________ leads to: -injurious agents can affect any of the organelles -water can enter ICF=swelling -damaged mitochondria= unable to produce energy -nucleus vulnerable=unable to reproduce examples of intracellular accumulations -hepatocytes that become injured via alcohol abuse and accumulate fat cells -familial hypercholesterolism= leads to excess cholesterol in epithelial cells inadequate alveoli diffusion (pneumonia) example of dysfunction of the Na /K⁺ ⁺pump ischemic-reperfusion injury example of free radical injury HIV example of infectious agents allergies example of immunological reactions starvation (marasmus) example of nutrition imbalance diabetes mellitus
example of chemical injury hypertension exerts shearing force against endothelial cell membranes, creating injury on interior of arteries diabetic hyperglycemia high blood glucose levels chemically injure membrane of endothelial cells free radicals ______________ react w/ constituents of cell membrane and organelle membrane-->oxidative degeneration--->disrupts internal organelles, damages nucleus/DNA angiotensin 2 acts as potent vasoconstrictor, raises blood pressure aneurysm a weakened area in an arterial wall because of hypertension apoptosis cells degenerate at a specific time period with no adverse effects on the body necrosis cell death cause by injury and may adversely effect organ as a whole
inflammatory mediators such as histamine and bradykinin enable the blood vessels to dilate and become more permeable--
permits fluids, WBCs and platelets to travel out of the site of injury or infection second step of vascular permeability fluid that leaves the capillaries is rich in protein and WBCs begin process of phagocytosis purulent fluid rich in WBCs transudate fluid w/ little protein first step in cellular chemotaxis a chemical signal from microbial agents, endothelial cells and WBCs attract platelets and other WBCs to the site of injury margination second step in cellular chemotaxis; WBCs line up along endothelium in this process cytokines and acute phase proteins modulate inflammatory reaction by amplifying or deactivating the process CRP
a key acute-phase protein secreted by the liver that is both pro- inflammatory and anti-flammatory; integral to identifying foreign material in immune system, activates complement system, stimulates other cytokines and prevents WBC adhesion to endothelium elevated CRP level indicates acute inflammation systemic effect of cytokines stimulation of liver to produce acute phase proteins which also stimulate, modulate or deactivate the reaction leukocytosis an elevated numbed of WBCs in the bloodstream; increase also occurs during cellular phase leukopenia deficiency of white blood cells three main stages of inflammation -vascular permeability -cellular chemotaxis -systemic responses neutrophils first responders, involved in phagocytosis; their action causes a respiratory burst in mitochondria which can lead to release of
dilates blood vessels and induce inflammation through release of histamines and heparin; recruits macrophages and neutrophils; used in wound healing/allergic reactions macrophage phagocytic cell that consumes foreign pathogens and cancer cells; stimulates response of other immune cells natural killer cell kills tumor cells and virus infected cells dendritic cell presents antigens on its surface, thereby triggering adaptive immunity monocyte differentiates into a macrophage or dendritic cell in response to inflammation neutrophil first responders at the site of infection or trauma; this abundant phagocytic cell represents majority of WBCs; releases toxins that kill/inhibit bacteria/fungi and recruits other immune cells to site of infection basophil
responsible for defense against parasites; releases histamines that cause inflammation and may be responsible for allergic reactions eosinophil releases toxins that kill bacteria and parasites but also cause tissue damage clinical manifestation of fever elevated body temperature effect of fever increases efficiency of WBCs in their defense of the body against foreign invaders clinical manifestation of histamine release sneezing, rhinorrhea, eye tearing, sinus inflammation, pharyngeal irritation effect of histamine release arteriolar vasodilation, large artery vasoconstriction, increased permeability of venules prostaglandin and leukotriene production inflammation/injury--> phospholipids of WBC membrane--> broken down via phospholipidase--> produces arachidonic acid-->broken down further by 1)cyclooxyegenase 1/2)cyclooxygenase 2/3)lipooxygenase
provokes hypotension, tachycardia, and acidosis lymphadenopathy enlarged lymph nodes effect of lymphadenopathy injurious agents invade lymph, which spreads to other nodes 3 outcomes of acute inflammation -resolution -fibrosis -chronic inflammation effect of chronic inflammation destructive macrophage products (free radicals, proteases, cytokines, angiogenesis growth factors, fibroblasts) repeatedly damage tissue --> cell death autoimmune disease an antigen incites the inflammatory reaction that initiates production of antibodies that attack bodies' own tissues; antibodies produce a persistent inflammatory reaction that causes chronic tissue damage granuloma an area where macrophages have aggregated and are transformed into epithelial-like or epithelioid cells
labile cells cells that continuously proceed through the cell cycle G0 phase a resting stage of the cell cycle in which DNA replication and cell division stop G1 phase cells enter cell cycle to prepare for mitosis G2 phase cells continue to prepare for mitosis S phase cells undergo chromosomal duplication M phase cell undergoes mitosis skin cells example of labile cells stable cells cells that are in a resting stage until stimulated, when they enter the cell cycle hepatocyte example of stable cell
wounds that heal under conditions of minimal tissue loss secondary intention wound closure in which the edges are separated; granulation tissue develops to fill the gap; and, finally, epithelium grows in over the granulation, producing a larger scar than results with primary intention tertiary intention wound that heals by drainage, granulation, and then late suturing factors affecting wound healing -nutrition -oxygenation -circulation -immune strength -contamination -obesity -age complications of wound healing -keloid -contractures -dehiscence -evisceration -stricture
-fistula -adhesion innate immune system composed of the body's natural anatomic barriers, normal flora, WBCs and protective enzymes/chemicals. macrophages phagocytize foreign substances; provide constant surveillance of different organ systems; stimulate inflammatory reaction role of cytokines -promote leukocyte recruitment and acute inflammation reactions -regulate lymphocyte growth, activation, and differentiation -activate macrophages -stimulate growth/production of new blood cells humoral immune response exposure to antigen-->intact antigens activate B cells-->B cells give rise to plasma and memory B cells--> secrete antibodies that defend against pathogens and toxins in ECF humoral AND cell-mediated immune response exposure to antigen--> antigens engulfed and displayed by dendritic cells-->activate helper T cells (which also activate B cells and secrete cytokines that activate cytotoxic T cells)-->give rise to active/memory helper T cells
clinical manifestations of IgE-mediated hypersensitivity localized/systemic anaphylaxis, seasonal allergies, food allergies, hives and eczema IgG mediated cytotoxic hypersensitivity cells are destroyed by bound antibody, either by activation of complement or by a cytotoxic T cell with an Fc receptor for the antibody clinical manifestations of IgG mediated cytotoxic hypersensitivity RBCs destroyed by complement and antibody during a transfusion of mismatched blood types or during erythroblastosis fetalis immune complex mediated hypersensitivity antigen-antibody complexes are deposited in tissues, causing activating of complement, which attracts neutrophils to the site clinical manifestations of immune complex mediated hypersensitivity glomerulonephritis, RA, systemic lupus erythematosus cell-mediated hypersensitivity Th1 cells secrete cytokines, which activate macrophages and cytotoxic T cells and can cause macrophage accumulation at the site
clinical manifestations of cell mediated hypersensitivity contact dermatitis, tuberculin reaction, type 1 diabetes, MS, and RA pathophysiology of autoimmunity T cells or Igs cannot make a distinction between non-antigenic cell surface markers and antigenic foreign cell surface markers molecular mimicry when an infectious agent is composed of antigens that have the same amino acid sequence as some self antigens primary immunodeficiency congenital; usually genetic errors secondary immunodeficiency loss of immune functioning as a result of an illness or treatment pathophysiology of systemic lupus erythematosus Anti-double stranded DNA antibodies form immune complexes deposited on organs and tissues; triggers inflammation that damages organ membranes clinical manifestations of systemic lupus erythematosus fever, skin rash, joint inflammation, and kidney/serosal membrane damage pathophysiology of rheumatoid arthritis
