Patho Test 1
Order by
118 terms
Terms | Definitions |
|---|---|
 allostasis | the ability to achieve stability through change, involving both the person's perception of the situation and the ability to mount an appropriate response |
| what serves as the control system for a person's perception of a situation? | previous experience and learning |
| when dooes instability occur? | whenever there is a discrepancy between what the person perceives the situation should be and what it is |
| what is allostasis termed? | Cognitive Activation Theory of Stress |
| how does allostasis differ from homeostasis? | homeostasis is based on physiologic responses, while allostasis involves both the perception of the situation and the ability to mount an appropriate response |
| homeostasis? | the ability or tendency of an organism or cell to maintain internal equilibrium by adjusting its physiological processes |
| what does homeostasis involve? | feedback control systems that regulate cellular function and integrate the function of the different body systems |
| stress? | a state manifested by a specific syndrome of he body developed in response to any stimuli that made an intense systemic demand on it |
| what is the perception of stress? | that one cannot adequately cope with demands made on a person or well being |
| what influences stress response? | perception and personal meaning of a potential stressor |
| what are the different types of stress? | physiologic and emotional/psychologic |
| what are factors that affect response to stressors? | internal (endogenous); external (exogenous); personal characteristics such as hardiness, sense of coherence, resilience, attitude |
| what are the 3 stages of GAS - General Adaptation Syndrome? | alarm reaction, stage of resistance, stage of exhaustion |
| describe alarm reaction (GAS Stage 1) | perception of a stressor physically or mentally; generalized stimulation of the SNS (fight or flight) response and the Hypothalamic-Pituitary-Adrenal (HPA) Axis; temporarily decreased resistance |
| describe stage of resistance (GAS stage 2) | body selects the most effective and economic channels of defense; increased levels of cortisol present during stage 1 drop because they are no longer needed; few overt physical signs and symptoms occur compared with the alarm stage; ideal transition from alarm to resistance is quick; adaptation occurs or person advances to exhaustion |
| describe stage of exhaustion (GAS stage 3) | occurs when all energy for adaptation has been exhausted; signs of wear and tear appear; physical symptoms of alarm reaction may briefly reappear in a final effort by the body to survive; this stage can be reversed by external sources (medication) |
| cerebral cortex | plans a course of action after evaluating a stressor in light of past experiences and future consequences |
| limbic system | mediator of emotions, feelings and behavior that ensure survival and self-preservation |
| reticular activating system | contained in the reticular formation; sends alertness impulses to the limbic and cerebral cortex; stress increases the frequency of alertness impulses and leads to wakefulness and sleep disturbances |
| pain | unpleasant sensory and emotional experience associated with actual or potential tissue damage; both protective and unpleasant physical and emotionally disturbing sensation |
| classification of pain | underlying pathology - nociceptive or neuropathic; duration - acute or chronic |
| context in which pain is viewed | nociception |
| nociception | the reception of painful stimuli from the physical or mechanical injury to body tissues by nociceptors |
| nociceptors | receptive nerve endings usually found in the skin or the walls of the viscera that respond to noxious stimuli |
| what do nociceptor neurons transmit? | impulses to the dorsal horn neurons using chemical neurotransmitters |
| what are the dimensions of pain? | physiologic, affective, cognitive, behavioral, sociocultural |
| what is the physiologic dimension of pain? | influences how stimuli are recognized or described - genetic, anatomic, physical determinants |
| what is the affective dimension of pain? | emotional response to pain experience (anger, fear, depression, anxiety); suffering |
| how is the affective dimension of pain eased? | pain relief, spirituality |
| what is the behavioral dimension of pain? | observable actions used to express or control pain - facial expressions, social withdrawal, less physical activity, relaxation techniques, medication |
| what is the cognitive dimension of pain? | beliefs, attitudes, memories and meaning attributed to pain; influence response to pain and must be incorporated into the comprehensive treatment plan |
| what is the sociocultural dimension of pain? | demographics, support systems, social roles and culture |
| what are the pathways for pain transmission (afferent nerve fibers)? | fast and slow pathways |
| what are the characteristics for fast pathway pain transmission? | sharply discriminated pain that moves directly from the receptor to the spinal cord using myelinated A fibers and from the spinal cord to the thalamus using neospinothalamic tract; fibers are larger; conduction velocities transmitting impulses at a rate of 6 to 30 m/sec |
| what are the characteristics for slow pathway pain transmission? | continuously conducted pain that is transmitted to the spinal cord using unmyelinated C fibers and from the spinal cord to the thalamus using the more circuitous and slower-conducting paleospinothalamic tract; smallest of all peripheral nerve fibers; transmit impulses at 0.5-2.5 m/sec |
| immunity? | the protection from disease, more specifically, infectious disease |
| immune response? | the collective, coordinated response of the cells and molecules of the immune system |
| innate immunity? | in place before infection and responds quickly to it; provides first line of defense against foreign bodies (infections, cancer cells, transplanted organs) |
| major components of innate immunity? | epithelial barriers that block entry; phagocytic cells (neutrophils and macrophages); natural killer cells; plasma proteins (complement) |
| what happens during innate immunity? | participating cells react to substances unique to cell walls of foreign bodies by activating complement and proteolytic cascades, producing antibacterial peptides, releasing interferons and phagocytosis; foreign cells are killed by osmotic lysis or apoptosis; cytokine release from participating cells activates slower but more specific acquired immune response |
| what is adaptive immunity? | recognizes and reacts to a large number of microbes and nonmicrobial substances, as well as the ability to distinguish among different and even closely related microbes and molecules |
| what are the components of adaptive immunity? | WBCs (lymphocytes) - T lymphocytes and B lymphocytes |
| what are the 2 types of adaptive immunity? | cell-mediated immunity; humoral immunity |
| what is cell-mediated immunity? | adaptive immunity in which T cells respond directly to antigens |
| what percentage of WBCs are T cells? | 36% |
| where are T cells thought to originate? | stem cells in bone marrow |
| what controls maturation of T cells? | thymus gland |
| what are the different types of T cells? | killer cells, helper cells, suppressor cells |
| what is the role of killer cells? | they bind to the surface of the invading cell, disrupt the membrane and destroy it by altering its internal environment |
| what is the role of helper cells? | they stimulate B cells to mature into plasma cells, which begin to synthesize and secrete immunoglobin |
| what is the role of suppressor cells? | they reduce the humoral response |
| what is humoral immunity? | immunoglobulin-mediated |
| which type of WBCs act in humoral immunity? | B cells |
| where do B cells originate? | in the bone marrow |
| what do B cells mature into? | plasma cells that produce antibodies |
| what do antibodies from B cells do? | destroy viruses and bacteria, preventing them from entring host cells |
| how do B and T cells communicate? | by secreting cytokines and activating the complement system |
| what is the purpose of B and T memory cells? | persist in small numbers as memory cells after invasion is prevented so that 2nd exposure to same antigen triggers a prompt, magnified immune response |
| what are antigens (immunogens)? | substances foreign to a host that can stimulate an immune response |
| how are antigens (immunogens) recognized? | by receptors on immune cells and by proteins (antibodies) or immunoglobulins, which are secreted in response to an antigen |
| what are examples of antigens? | microbes (bacteria, fungi, viruses, protozoa); nonmicrobial agents (plant pollens, poison ivy resin, insect venom) |
| what are the classes of immunoglobulins? | IgG, IgM, IgA, IgD, IgE |
| IgG | makes up 80% of plasma antibodies; appears in all body fluids; is the major antibacterial and antiviral antibody |
| IgM | first produced during an immune response; too large to easily cross membrane barriers in vessels |
| IgA | found mainly in body secretions (saliva, sweat, tears, etc); defends against pathogens on body surfaces (respiratory, GI) |
| IgD | present in plasma, easily broken down; predominant antibody on surface of B cells; mainly an antigen receptor |
| IgE | involved in immediate hypersensitivity/allergic reactions; stimulate the release of mast cells, which contain histamine and heparin |
| what happens during vascular response? | inflammatory changes occur in the microcirculation near the site of injury; blood vessel dilation; increased vascular permeability and leakage of fluid out of the vessel; WBC adherence to the inner walls of vessels and their migration through vessel walls to the site of injury |
| what is microcirculation? | areterioles, capillaries, venules |
| how fast after injury do inflammatory changes occur in microcirculation? | within seconds |
| what do vascular changes in vascular response deliver? | leukocytes |
| what do cells and chemicals that are associated with inflammation work together to accomplish once inside the tissue? | 1. limit and control inflammatory process; 2. prevent infection; 3. interact with components of the adaptive immune system; 4. prepare the area of injury for healing |
| how do cells and chemicals that are associated with inflammation limit and control the inflammatory process? | through the influx of plasma protein systems (clotting system), plasma enzymes, and cells (eosinophils) that prevent the inflammatory response from spreading to areas of healthy tissue |
| how do cells and chemicals that are associated with inflammation prevent infection and further damage? | by contaminating microorganisms through the influx of fluid to dilute toxins produced by bacteria and released from dying cells. |
| why do cells and chemicals that are associated with inflammation interact with components of the adaptive immune system? | to elicit a more specific response to contaminating pathogens through the influx of macrophages and lymphocytes |
| how do cells and chemicals that are associated with inflammation prepare the area of injry for healing? | through removal of bacterial products, dead cells and other products of inflammation (channels through epithelium or drainage by lymphatic vessels) and initiation of mechanisms of healing and repair |
| what does drainage by lymphatic vessels also facilitate? | development of acquired immunity because microbial antigens in lymphatic fluid pass through the lymph nodes, where they activate both B and T lymphocytes |
| what does the kinin system interact with? why? | the clotting system, to compartmentalize and trap invading pathogens |
| what is the primary role of the kinin system? | to activate and assist inflammatory cells |
| what is the primary kinin? | bradykinin |
| what does bradykinin do? | causes dilation of blood vessels; acts with prostaglandins to induce pain; causes smooth muscle cell contraction; increases vascular permeability; increases leukocyte chemotaxis |
| what is an autoimmune disorder? | caused by breakdown of tolerance in which the body's immune system begins to recognize self-antigens as foreign |
| what are proposed mechanisms of autoimmune disorders? | 1. exposure within the body of a previously sequestered antigen; 2. complications of an infectious disease; 3. development of a neoantigen; 4. forbidden clones of lymphocytes reactive agains self-antigen that did not mature nor proliferate later in life; 5. alteration of suppressor T cells |
| what is systemic lupus erythematosus? | a chronic progressive systemic inflammatory disease that can cause major organ systems to fail |
| what is deposited in blood vessels, collagen fibers and on organs in SLE patients? | connective tissue and fibrin deposits |
| what does SLE lead to? | necrosis and/or inflammation in blood vessels, lymph nodes, GI tract and pleura |
| what are predisposing factors of SLE? | stress, streptococcal or viral infections; exposure to sunlight or UV light; immunization, pregnancy, abnormal estrogen metabolism; some meds |
| what are the two forms of SLE? | discoid LE and systemic LE |
| what are discoid LE symptoms? | superficial lesions typically over cheeks and bridge of nose that scar after healing |
| what are systemic LE characteristics? | recurrent remissions and exacerbations |
| what are symptoms on skin of SLE patients? | skin eruption (rash); butterfly in 50%; patch alopecia |
| what are cardiopulmonary effects of SLE? | chest pain (including pleuritis), dyspnea, tachycardia, central cyanosis, hypotension |
| what are neurologic effects of SLE? | seizure disorders, confusion, emotional lability, psychosis, headaches, irritability, stroke, depression |
| what are urinary system effects of SLE? | infrequent urination; frequent urination, painful urination and bladder spasms (signs of UTI) |
| what is leading cause of death for SLE patients? | renal failure and UTIs |
| what are other effects of SLE? | often severe joint pain, anemia, positive antinuclear antibodies and LE prep, elevated sedimentation rate |
| what is scleroderma? | chronic connective tissue disease characterized by inflammation, fibrosis and sclerosis |
| what does scleroderma cause? | fibrotic changes involving the skin, synovial membranes, esophagus, heart, lungs, kidneys and GI tract |
| what is HIV/AIDS characterized by? | progressive immune system impairment and destruction of the cell-mediated response |
| what is HIV? | RNA-based retrovirus that requires a human host to replicate |
| what does HIV/AIDS destroy? | CD4+ cells (helper cells) that regulate the normal immune response |
| what does CD4+ antigen serve as in HIV patients? | receptor for HIV, allowing it it invade the cell and cause cell death |
| what cells can HIV infect? | any cell that has CD4+ antigen on its surface - monocytes, macrophages, bone marrow progenitors, glial, gut, epithelial |
| what can HIV cause? | dimentia, wasting syndrome, blood abnormalities |
| what are opportunistic diseases of AIDS? | bacterial infections, fungal infections, viral infections, neoplasms (Kaposi's sarcoma, malignant lymphomas) |
| how is HIV treated? | antiretrovirals, which are used to control the reproduction of the virus and slow the progressioin of HIV-related disease |
| how do non-nucleoside reverse transcriptase inhibitors work? | bind to and disable the protein that HIV needs to make more copies of itself |
| how do nucleoside reverse transcriptase inhibitors work? | causes a halt in production of faulty versions of building blocks that HIV requires to duplicate itself |
| how do fusion inhibitors work? | block HIV entry into cells |
| how do protease inhibitors work? | disable proteases (protein needed for HIV to duplicate itself) |
| hypotonic imbalance characteristics | less solute in relation to water; water gain or solute loss |
| what can cause hypotonic imbalance? | vomiting, diarrhea, burns, diuretics, excessive sweating, renal failure |
| what happens to cells with hypotonic fluids? | cells swell |
| hypertonic imbalance characteristics | more solute in relation to water; water loss or solute gain |
| what can cause hypertonic imbalance? | administration of hypertonic saline IV, hyperaldosteronism, cushing syndrome, diabetes, diarrhea, infufficient water intake |
| what happens to cells with hypertonic fluids? | cells shrink |
| signs and symptoms of fluid volume excess | cough and dyspnea, crackles in lungs, tachycardia and tachypnea, increased blood pressure and bounding pulse, neck and hand vein distention, pitting edema, weight gain, decreased HCT, confusion |
| treatment of fluid volume excess | monitor vital signs, semi-fowlers, diuretics, fluid restriction, strict I & O, daily weights, assessment to edema, Na+ restricted diet, monitor labs |
First Time Here?
Welcome to Quizlet, a fun, free place to study. Try these flashcards, find others to study, or make your own.