Nursing pathophysiology – Flashcards

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Hypertrophy
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-increased size and functional capacity of cells -increased workload causes increase in size -will revert to normal if the cause is removed -ex: body buider--muscle mass
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Atrophy
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-decreased size and functional capacity -decrease use causes decreased size of cells examples: occurs in muscles, brain, and kidneys physiologic-uterus shrinkage post partum
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Hyperplasia
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increase in number of cells...leads to increase in size of the organ physiologic-breasts and uterus during pregnancy; scar tissue in wound healing nonphysiologic-due to excessive hormonal stimulation-thyroid/endometrial, benign prostatic; skin warts and calluses
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metaplasia
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A reversible change of type of cell or replacement of one cell type to another cell type -reprogramming of undifferentiated stem cells-substitution of cells better equipped to survive -may be due to chronic irritation and inflammation may precede the development of cancer Ex: lungs, cervix
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Dysplasia
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-deranged or disorderly overgrowth of cells -results in cells that vary in size, shape and appearance -minor degrees associated with chronic inflammation/irritation -pre-malignant reversible examples: squamous epithelium of respiratory tract or uterus (pap smear)
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Role of cortisol in the stress response
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Antagonizes the effects of insulin to maintain BS level; enhances the effects of catecholamines; suppresses osteoblast activity; suppresses the immune response. -Raises your glucose levels because it is thinking fight or flight. -Too much-constant high level of sugar. Risk for diabetes with chronic stress -Released by adrenal cortex
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Regulation of the neuroendocrine response to stress
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-Regulated by the HPA axis which consists of the hypothalamus, pituitary gland, and the adrenal cortex. The axis is stimulated during the generalized stress response.
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Physiological response of catecholamines in response to stress
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Epinephrine and norepinephrine are released with the activation of the sympathetic nervous system. Effects include increased BP/HR/RR, pupils dilate, contractility increases, selective bloodflow to vital organs (Heart, brain, muscles). Decreased blood flow to the rest (GI, GU, Skin)
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Stage 1 of GAS-Alarm stage
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Recognition of danger and preparation to deal with the threat (Aka fight or flight) Short term response to stress or trauma If this energy is repeatedly not used by physical activity, it can become harmful Also called the generalized stress response Stimulation of the HPA axis (hypothalamus, pituitary gland, and adrenal cortex) -Sympathetic nervous system stimulates catecholamines -Corticotropin releasing hormone production(cortisol)
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Stage 2 of GAS-Resistance stage
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-the source of stress begins to resolve. Homeostasis begins restoring balance and period of recovery for repair and renewal takes place -Stress hormone levels may return to normal but there are still some present. The body adapts by a continued effort in resistance and remains in a state of arousal
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Stage 3 of GAS-Exhaustion stage
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-At this stage, the stress has continued for some time. The body's ability to resist is lost because its adaption energy supply is gone (often referred to as overload, burnout, adrenal fatigue, maladaptation, or dysfunction)
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Cellular response to stressors
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When confronted with stresses that endanger a cells normal structure and function, it undergoes an adaptive changes in an attempt to permit survival and maintenance of function. Cells adapt by altering their pattern of growth. The adaption ceases once the need for adaptation has ceased.
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Punnet Square
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A genetic tool that is utilized to predict possible combinations of alleles that can occur with transmission of a single gene; recognizes dominant and recessive traits
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Autosomal dominant disorders
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Single mutant allele is transmitted from affected parent to offspring. It may manifest as a new mutation. Male or female can carry as they are not sex linked. Each child has a 50% chance of getting the disease Ex: Marfan's syndrome, neurofibromatosis, Huntington's Choria, and Retinoblastoma
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Autosomal recessive disorders
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Both members of the gene pair are affected. Parents may be unaffected, but are carriers of the defective gene. It affects both sexes. 25% will be affected or have the disease. 50% will be carriers, but not have the disease. 25% will not be affected Ex: Phenylketonuria (PKU), Sickle cell anemia, cystic fibrosis, Tay Sachs
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Structural chromosomal alteration of deletion disorders
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Inversion and translocation: abnormality might not affect the individual, but can cause serious problems for the offspring ex; Cri du Chat syndrome
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Multifactorial inheritance disorder
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-Multiple genes control the trait and can be influenced by environmental factors -ex: cleft lip, club foot, pyloric stenosis, coronary artery disease, diabetes mellitus, hypertension, Schizophrenia, manic depressive disorder
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Radiation exposure
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Heavy doses of ionizing radiation have been shown to cause microcephaly, skeletal malformations, and mental retardation. There is no evidence that diagnostic levels cause congenital abnormalities
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Allele
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Alternate forms of a gene (one from each parent). Can carry dominant or recessive traits. Determine if the trait is expressed in an individual
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DNA
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chemical basis for hereditary traits, an individual's blueprint found with chromosomes in cell nucleus and the mitochondria contains genes double helix polymer found in the nucleus of each cell composition: nucleotides Deoxyribose Phosphoric Acid 4 nitrogenous bases (purines: guanine and adenine, pyrimidines: cytosine and thymine)
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RNA
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Single strand contains ribose instead of deoxyribose Uracil replaces thymine as a nitrogenous base Uses the code from DNA to make proteins DNA opens, transcribes, then translates the DNA to make proteins needed by the body
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mRNA (messenger)
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-encodes as a chemical blueprint for protein production. It is transcribed from a DNA template, and carries coding information to the sites of protein synthesis, the ribosomes. It is translated into a polymer of amino acids: a protein.
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rRNA (ribosomal)
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the RNA component of the ribosome, the cell structure that is the site of protein synthesis in all living cells. Provides a mechanism for decoding mRNA into amino acids and interacts with tRNAs during translation
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tRNA (transfer)
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Specify which sequence from the genetic code corresponds to which amino acid
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Early response of the inflammatory response
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This is the acute response that happens almost immediately. Its main aim is to remove the injurious agent and limit the extent of the tissue damage. Divided into vascular and cellular stages.
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Vascular response of the inflammatory response
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Begins immediately with brief arteriolar vasoconstriction followed by vasodilation of the arterioles and venules that supply the area. Area becomes red (erythema) and warm. There is an increase capillary permeability which localizes the infection. The increased exudation of the plasma and blood into the tissue causes edema. At the same time a biochemical mediator stimulates the endothelial cells to contract and become sticky and spaces are created for leukocytes to get through.
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Cellular response of the inflammatory response
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Leukocytes move to the area of injury. They leave vessels routinely through: Margination: rolling along the wall of the now sticky blood vessel Adhesion and transmigration: endothelial cells and leukocytes have complementary adhesion molecules. The leukocytes briefly stick and release and roll along the endothelium like a tumbleweed. It becomes stickier and stickier until it stops and squeezes through the gaps between the endothelial cells into the area of infection Chemotaxis and activation: the leukocytes are going to follow the chemokines to the pathogens. They are activated and then phagocytize or degranulate the pathogen
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Neutrophils
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These granulocytes are the first to arrive on the scene. They have a short lifespan (about 10 hours). They have enzymes and other antibacterial agents used to destroy and degrade pathogens. Immature ones are released from the bone marrow and are also found at the site due to excessive demand for phagocytes. The babies are shaped like bands
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Phagocytes
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These are the neutrophils, monocytes, and macrophages. Monocytes mature into macrophages that engulf more foreign material than neutrophils can. Differ by their speed of arrival, length of time they remain active, what atracts them, and what enzymes they release and utilize.
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Eosinophils
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This granulocyte is not a phagocyte. They regulate inflammation and allergic reactions by controlling the release of specific chemical mediators in those processes. Contain a protein that is highly toxic to parasites.
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Mast cells
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This cell is stimulated by injury or agents of immune response (like with allergies). These cells degranulate and release mediators.
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Basophil
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granulocyte, similar to mast cell. Release histamine (causes dilation and increased permiability of capillaries), bradykinin (causes increased capillary permeability and pain), and serotonin
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Acute inflammation
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lasts less than two weeks. Usually self limiting and rapidly controlled by host's defenses. The early reaction of local tissues and their blood vessels to injury; characterized by exudation of fluid and plasma proteins and the emigration of leukocytes-mainly neutrophils.
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Chronic inflammation
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Lasts greater than 2 weeks. Self perpetuating and may last for weeks to years. Associated with proliferation of blood vessels, tissue necrosis, and fibrosis (Scarring) Causes:unsuccessful acute response, the result of a microorganism with a thick waxy cell, or prolonged exposure to irritants Cellular characteristics: increased macrophages, lymphocytes instead of neutrophils, and fibroblasts
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Cause of an allergic reaction
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immune response to exogenous and endogenous antigens that produce inflammation and cause tissue damage
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Type I Immediate Hypersensitivity
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Reactions begin rapidly, often within minutes after contact with the allergen; exposure by inhalation, ingestion, injection, or skin contact. Reactions can range from atopic (local) to anaphylactic (systemic) depending on portal of entry. IgE mediated response to mast cells degranulate and release inflammatory mediators.
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Type II Antibody Mediated Hypersensitivity
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Reaction mediated by IgG and IgM antibodies binding to normal or altered antigens on cell surface and connective tissue. Injury to self can result from destruction, inflammation, and cell dysfunction -ex: mismatched blood transfusion, hemolytic disease in newborn, and certain drug reaction
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Type III antibody Immune complex mediated hypersensitivity
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Antigen-antibody complexes are formed in the blood and get deposited in vessel lining or tissues which attracts complements (IgG or IgM) and cause an inflammatory response. Ex: autoimmune disease, vasculitis, SLE, glomerulonephritis. Reactions range from atopic to anaphylactic
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Type IV T cell mediated Hypersensitivity
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Cytotoxic T cell kills antigen presenting target cell. Helper T cells secrete cytokines who recruit tissue damaging inflammatory cells Ex: viral hepatitis TB test
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Opportunist infectious agents
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secondary invaders; an immune deficiency provides the portal ex. IV hyperailmentation, foley catheter (ecoli, UTI)
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Prions
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proteins transmitted by injection, transplant, food-Mad Cow disease
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Virion
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the infectious particle; viruses are the most frequent cause of human illness. Capsid-protein based coating
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Bacteria
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spirochetes and mycoplasmas
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Fungal/yeast
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live in soil, skin (ringworm), or GI tract
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Rickettstiae
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transmitted to humans through the bite of the vector. Rocky mountain spotted fever
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Chlamydiae
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An elementary body attaches to and enters the host cells and undergoes replication
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Parasites
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burrow into skin or mucous membranes, produce an allergic inflammatory response, release histamine and eosinophilia-kill parasites
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Incubation period
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the phase during which the pathogen begins active replication without producing recognizable symptoms in the host
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Prodromal stage
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Most contagious stage. The initial appearance of symptoms in the host although the clinical presentation during this time may only be a vague sense of malaise. May experience mild fever, headache, and fatigue.
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Acute stage
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Period during which the host experience the max impact of the infectious process corresponding to rapid proliferation and dissemination of the pathogen. During this phase, toxic byproducts of microbial metabolism, cell lysis, and the immune response mounted by the host combines to produce tissue damage and inflammation
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Convalescent period
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Characterized by containment of infection, progressive elimination of the pathogen, repair of damaged tissue and resolution of associated symptoms
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Complement system
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Proteins floating in the bloodstream aid the phagocytes and antibodies in destroying the pathogens during inflammation. It causes vasodilation and increased vascular permeability. It promotes leukocyte activation, adhesion, chemotaxis, and enhances phagocytosis.
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Clotting system
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Coagulation cascade; forms fibrous exudates and meshwork to prevent the spread of infection, stops the bleeding by forming a clot, and increased vascular permeability
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Kinin system
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Produces pain; linked to the clotting system and releases bradykinin
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Innate immunity (non-specific)
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-major components are the skin and mucous membranes, phagocytic leukocytes (neutrophils and macrophages), specialized lymphocytes (NK cells). and several plasma proteins -Distinguish self from non-self -Response w/i minutes to hours
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Adaptive immunity
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-specificity and selectivity -memory: recalls encounters with the same agent Diversity- able to respond to wide variety of antigens, makes antibodies to mount an effective response against the agent
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Humoral immunity
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-part of adaptive immunity -mediated by molecules called antibodies that are produced by cells called B lymphocytes
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Cell mediated adaptive immunity
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Involve cytotoxic T cells, NK cells, and macrophages
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Antibodies
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Receptors on immune cells that recognize antigens
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Antigen
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substances foreign to the host cell that stimulates an immune response
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HIV transmission
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blood to blood contact, sexual contact, blood, semen, vaginal fluids, dirty needles, breast milk
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HIV course of infecton
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Acute phase: lasts 6-8 weeks after initial introduction of virus. The host hasn't formed antibodies yet, so diagnosis are falsely negative Chronic phase: Levels of antibodes become measurable. Flu like symptoms occur Clinical AIDS: usually occur when CD4 cound <200 cells/mm3
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Autoimmune disorder
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group of disorders caused by a breakdown of the immune system to differentiate between self and non self antigens. Ability of immune system to differentiate is called self tolerance
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B lymphocytes
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Mature in bone marrow and move to peripheral lymphoid tissue. When exposed to antigen, differentiate into plasma cells that produce antibodies. Activated by CD4 helper T cells. Mediates humoral immunity. Can transform into memory cell
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T lymphocytes
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Activate other T and B cells. Role in cell mediated immunity. Arise from bone marrow then mature in thymus
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Helper T cells
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CD4 are activated by specific antigens in Class II MHC molecules. Secrete cytokines and can trigger B cells to proliferate and differentiate into a clone of plasma cells that produce antibodies
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Cytotoxic T cells
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CD8 recognise class I MHC antigen complexes on target cell surfaces. Performs its killing function by injecting cytotoxic proteins into target cell
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IgG
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most abundant of the circulating immunoglobulins. Only one that crosses the placenta. Activates complement and has antiviral, antibacterial, and antitoxin properties
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IgA
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found in saliva/tears/breast milk. Protects mucous membranes
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IgM
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Cannot cross placenta. First circulating antibody to appear in response to an antigen
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IgD
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Found on B lymphocytes and is needed for maturation of B cells
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IgE
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involved in inflammation and allergic response.
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Extracellular electrolytes
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sodium, chloride, bicarbonate
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Intracellular
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potassium, sodium, bicarbonate
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Calcium
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Mostly found in bone. the rest is in intracellular fluid
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Main system for fluid and electrolyte balance
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renal and respiratory
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Diffusion
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movement of uncharged particles along a concentration gradient
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Osmosis
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movement of water across a semipermeable membrane. Diffuses down a concentration
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Serum osmolarity
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concentration of solutes in blood serum
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Isotonic fluid
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2 solutions have the same solute concentration. No effect on cell size.
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Hypertonic fluid
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one of 2 solutions with a higher concentration of solutes causing cells to shrink
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Hypotonic fluid
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one of 2 solutions with a lower concentration of solutes causing increased cell size
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Crystalloid IV fluids
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Normal saline, ringers lactate, d5w
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Colloid IV fluids
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Hypertonic solutions like 3% normal saline, albumin
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Trans cellular fluid
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portions of bodys total water contained within epithelial spaces. CSF and synovial fluid
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Capillary Filtration pressure (hydrostatic)
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pushing pressure that the fluid places on the walls of the capillary. Water is pushed out of the capillary into interstitial spaces. Determined by arterial/venous pressure and influenced by volume
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Capillary osmotic (oncotic) pressure
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Pulls water back into the capillary. Gradient generated by the plasma proteins (mainly albumin) that are too large to pass through the capillary wall pores. Keeps fluid in vascular space like a magnet
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Hydrostatic pressure
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promotes movement of water into the capillary.
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Osmotic or oncotic
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Promotes movement of water out of the capillary into tissue space
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Lymphatics role in fluid balance
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represents an acessory route where fluid and plasma proteins from interstitial spaces return to circulation via this system
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Third spacing
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represents the loss or trapping of extracellular fluid into the transcellular space. Does not contribute to balance of ECF and ICF. Leads to intravascular volume deficit. EX ascites, burns, peritonitis, bowel obstruction
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Localized edema
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allergic or inflammatory conditions results from the release of histamine and other inflammatory mediators that cause dilation
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Generalized Edema
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generally the result of increased vascular volume. Hands and feet swell in hot weather or pregnant women
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Causes of Edema
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decreased capillary colloid osmotic pressure increased capillary filtration hydrostatic pressure increased capillary permeability obstruction of lymph flow
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Assessment of Edema
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Assessed visually (localized or general), palpation for pitting (1-4+), and measurement of affected parts
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Intake/Output measurement
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I: water through GI, IV O: Urine, wound drainage, ostomies, gastric suction
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ADH
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regulates water output and helps conserve body water
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Potassium
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3.5-5 mEq/L inc: severe tissue trauma, untreated addisons disease, acute acidosis, misuse of K+ sparing diuretics, overdose, renal failure dec: diuretics, insufficient intake, hyperinsulinemia, vomitting, diarrhea, laxative abuse
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Sodium
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135-145 mEq/L inc-loss of water, too much intake, thirst deficit, watery diarrhea, strenuous exercise, renal failure dec-excessive water retention, elevated blood glucose, Na loss, replacement of only water, too much ADH-SIADH, drugs
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Magnesium
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1.8-3 mg/dL inc-renal insufficiency, excessive use of mg antacids dec-diarrhea, hemodialysis,kidney disease, chronic alcoholism, often associated with hypokalemia
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Calcium
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8.5-10.5 mg/dL Inc-cancer, hyperparathyroidism, Vitamin D intoxication Dec- renal failure, parathyroid hormone deficiency, vitamin d or dietary calcium deficiency
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serum sodium
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regulates extracellular fluid volume, acid base balance, and function of the nervous system. Brain and nervous system most affected. Most abundant cation
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Hyponatremia
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skeletal muscle cramps, weakness, fatigue, nausea, vomitting, lethargy, headache, seizures, muscle twitching, coma, brain swelling
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Hypernatremia
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thirst, decreased urine output, tachycardia, BP drops, dry mucous membranes, restlessness, coma, seizures
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Serum potassium
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major intracellular cation, critical to many body functions such as maintenance of the osmotic integrity of cells, acid base balance, and the kidneys ability to concentrate urine. Critical in conducting nerve impulses
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Hypokalemia
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causes diuretics, insufficient intake, alkalosis, hyperinsulinemia weakness, skeletal muscle paralysis, dysrhythmias, intestinal ilus treatment: replace oral, IV
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Hyperkalemia
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severe tissue trauma, untreated addisons disease, acute acidosis, misuse of potassium confusion, anxiety, dyspnea, weakness/heaviness in legs most severe disrupts electrical activity of the heart which can lead to ventricular tachycardia or fibrillation which leads to death
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Relationship of calcium to phosphorus
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inverse relationship
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Hormone responsible for calcium regulation
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parathyroid hormone
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Clinical example of condition with low protein
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nephrotic syndrome
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Clinical signs of hypervolemia
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weight gain/edema/jugular vein distintion/full bounding pulse/shortness of breath/crackles in lungs
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Clinical signs of hypovolemia
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dark urine with strong odor/urine amount less than 30ml/hr/poor skin turgor/dry mucous membrane/weight loss/weakness/fatigue/dizziness/postural hypotension/tachycardia/delayed capillary refill/sunken eyes/thirst (later sign)
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Outcome of RAA mechanism stimulation
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increased aldosterone which causes increased blood pressure
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Best laboratory indicator of renal function
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Creatinine and Blood urea nitrogen
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Respiratory acidosis
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hypercapnia typically occurs when the lungs cannot remove all of the CO2, resulting in decreased pH. caused by impaired ventilation which can stem from decreased respiratory drive, lung disease, airway obstruction, increased CO2 production. Can be acute or chronic (most likely from COPD)
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Respiratory alkalosis
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hyocapnia occurs when lungs get rid of CO2 faster than oxygen being produced, increased pH. Caused by hyperventilation or RR in excess
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Metabolic alkalosis
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inc serum pH due to a primary excess in HCO3-. Causes include gaining bases in excess by excess ingestion of bicarbonate containing antacids or excess IV infusion of a base equivlent, and the loss of fixed acids
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Relationship of water, sodium, and BP
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water always follow sodium. If body retains sodium, increased water, increased BP.
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pH normal values
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7.35-7.45
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paCO2 normal values
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35-45
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HCO3 normal values
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22-26
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