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all patho 1
| Question | Answer |
|---|---|
| Homeostasis | A dynamic, steady state within the normal range. Part of normal physiology |
| Example of homeostasis? | Electrolyte balance, temperature |
| Compensation | Making up for a defect, usually by moving some parameters outside their normal range. May be beneficial in short term, but often detrimental in long term |
| Example of compensation? | Enlarged left ventricle in response to increased blood pressure |
| What are 5 methods of cellular adaptation? | Atrophy, Hypertrophy, Metaplasia, Dysplasia |
| What is cell atrophy? | Cell shrivels due to loss of cell components |
| What causes cell atrophy? | Disuse, denervation, ischemia, nutrient starvation, interruption of endocrine signals, persistent cell injury, aging |
| How is atrophy adaptive? | Energy is directed to cells that need energy |
| The term atrophy can also apply to ____ | Organs. Decrease in organ size may involve some cell death, as well as cell atrophy. |
| What is hypertrophy? | Increase in cell size with increase in functional capacity |
| Hypertrophy is a response to | Increased demand for cell to meet increased workload |
| Examples of hypertrophy? | Increase in size of cells in heart ventricle from hypertension; Weight lifting. |
| How is hypertrophy adaptive? | Adapts to increased workload |
| What kinds of cells in the body hypertrophy? | Adipose (fat) and muscle cells |
| What is hyperplasia? | Increased division of cells (increased number of cells), in response to stressor or hormone stimulation |
| What causes hyperplasia? | Stressor or hormone stimulation |
| Examples of hyperplasia? | Increased number of RBC’s in response to high altitude. Prostate enlargement due to growth factors (hormone). Hyperplasia of the liver in response to drug use. Hyperplasia of endometrium, uterine stromal cells increase in number. |
| A callus is an example of _____ due to _____ | Hyperplasia; stress |
| How is hyperplasia adaptive? | Adapts to replace damaged cells, adds protection, allow cells to cope in different environment |
| What is metaplasia? | Replacement of one differentiated cell type that belongs there with another that is better able to withstand the injury |
| What causes metaplasia? | Injury, stress, change in environment |
| Examples of metaplasia? | GERD (Gastric Esophageal Reflux Disease), esophageal squamous epithelium are replaced by columnar epithelium that can better tolerate acidic conditions of gastric reflux |
| How is metaplasia adaptive? | Adapts to environment, stressors |
| When do metaplastic cells increase the risk of cancer? | When there are CHRONIC stressors |
| What is dysplasia? | Disorder growth of cells |
| What causes dysplasia? | Stressors |
| Dysplasia is marked by _____ cell growth that is also _____ | Abnormal, disordered |
| How is dysplasia adaptive? | Dysplasia does not appear to have positive adaptive benefit. |
| In _____ dysplasia, HPV infection if the stressor | Cervical |
| What is an example of cell injury or death due to lack of oxygen? | Hypoxia |
| What is an example of cell injury or death due to free radicals (e.g. reactive oxygen species)? | Ischemia leads to abnormal generation of reactive oxygen molecules (free radicals) |
| What effects do reactive oxygen species have on cells? | (Free radicals). They damage cell membranes, denature proteins, disrupt cell chromosomes. Also linked to initiation of inflammation cascade |
| What is an example of cell injury or death due to physical agents? | Physical/mechanical factors. Extreme temperatures, abrupt changes in atmospheric pressure, mechanical deformation, electricity, ionizing radiation. Ex. frostbite, burns, abrasions, lacerations |
| What is an example of cell injury or death due to chemical agents? | Toxic chemicals or poisons. Ex. Carbon tetrachloride, acetaminophen, heavy metals, toxic gases, corrosives, antimetabolites. Carbon monoxide, lead poisoning. |
| How do chemical agents cause cell injury? | Either directly, or when metabolized into reactive chemicals by the body |
| What is an example of cell injury or death due to biological agents? | Bacteria and viruses, as well as secondary effects of immune response. Ex. Polio virus is directly cytotopathic: can kill host cell directly without immune sys participation. |
| Cell injury by biological agent depends on... | Ability to gain access to cell and success in altering cell function |
| What is an example of cell injury or death due to radiation? | DNA or genetic damage due to radiation. Ex. acute radiation sickness w/ hematopoietic failure, destruction of epithelial layer of GI, neurologic dysfunction. |
| Radiation causes what 2 effects on cells? | Genetic damage and acute cell destruction |
| What is an example of cell injury or death due to nutritional imbalance? | Vitamin D deficiency affects bones, iron deficiency affects RBCs. Diabetes mellitis |
| Nutrition deficiencies can result from... | Poor intake, altered absorption, impaired distribution by circulatory system, inefficient cellular uptake |
| What are some common causes of cell injury due to nutritional balance? | Poverty, chronic alcoholism, acute and chronic illness, self-imposed dietary restrictions, malabsorption syndromes |
| Disuse of arm muscle can lead to _______ | Atrophy |
| Cell shrinkage due to disuse | Atrophy |
| Denervation to a group of cells | Atrophy |
| Lack of blood supply can lead to | Atrophy |
| Nutrient starvation can lead to | Atrophy |
| Interruption of endocrine signals can lead to | Atrophy |
| Persistent cell injury can lead to | Atrophy |
| Aging can lead to | Atrophy |
| What is the difference between ischemia and hypoxia? | Ischemia is the lack of blood supply, hypoxia is the lack of oxygen supply. |
| What is hypoxia? | Lack of oxygen that results in power failure within a cell, most often caused by ischemia |
| What can cause hypoxia? | Ischemia, heart failure, lung disease, RBC disorders |
| What is the most common cause of cell injury? | Ischemia. Injures cells faster than hypoxia alone |
| Why does ischemia cause faster/more injury than hypoxia alone? | Because ischemia not only disrupts oxygen supply, it also allows for metabolic wastes to accumulate and deprives the cell of nutrients for glycolysis |
| Ischemia leads to ____ deprivation, which is necessary for sodium-potassium and calcium pumps | ATP |
| Cell injury can result from what types of nutritional imbalance? | Nutrient deficiencies and excesses |
| What happens to an injured cell? (3) | 1. Intracellular accumulations (may or may not be reversible) 2. Reversible cell swelling 3. Irreversible cell injury |
| Examples of intracellular accumulations in an injured cell? | Fatty change, pathologic calcification |
| What is fatty change? | Reversible intracellular accumulation. Steatosis, accumulation of triglycerides in cell |
| What is an example of an intracellular accumulation of fat? | Fatty liver with alcohol abuse. Liver steatosis: ethanol interferes with lipid metabolism in hepatocytes. Lipids accumulate in vacuoles |
| What is pathologic calcification? | Irreversible. Calcium salts precipitate inside or outside of cells |
| What is an example of intracellular accumulation of calcium? | Hypercalcemia, calcium can precipitate in kidneys and cause kidney disease |
| Reversible cell swelling is also called _____ | Hydropic injury |
| What causes reversible cell swelling? | Failure of Na+/K+ pump. Increased Na+ inside cell pulls water into cell via osmosis |
| What can cause failure of Na+/K+ pump? | Insufficient ATP (due to ischemia, hypoxia) |
| Increased intracellular ______ can cause cell swelling | Concentration of Na+ |
| Irreversible cell injury causes cell _____ | DEATH |
| What 2 processes can cause cell death? | Necrosis and apoptosis |
| Cell death by necrosis is a _____ process | Pathological |
| How does cell death by necrosis occur after reversible swelling? | Continued swelling of organelles causes disruption of their membranes |
| What happens in cell necrosis? | Cell membrane ruptures, spilling cellular contents into interstitial fluid |
| Cell membrane rupture during necrosis causes _____ | Inflammation |
| What causes inflammation during necrosis? | Spilling of cellular contents into interstitial fluid |
| _________ enzymes inside the cell digest cell components | Lysosomal |
| What are biomarkers in relation to necrosis? | Intracellular components in the blood that can be used as markers of necrosis |
| Name one way necrosis can be detected | Biomarkers. Intracellular components in blood that can be used as markers of necrosis |
| What is an example of detectable necrosis of heart muscle? | Increased creatine kinase (CK) and/or cardiac troponin in the blood indicates myocardial damage |
| What is an example of a pancreatic necrosis marker? | Increased serum amylase indicates pancreatic damage |
| What are the terms used to describe necrotic tissue? | Coagulative, liquefactive; dry gangrene, wet gangrene |
| What is coagulative necrosis? | Area is composed of denatured proteins and is relatively solid. General tissue architecture is preserved for relatively long time (weeks) |
| Where can coagulative necrosis occur? | Heart, kidney, most other tissues |
| What is liquefactive necrosis? | Liquefied area of lysosomal enzymes and dissolved tissue may result and form an abscess or cyst |
| Where can liquefactive necrosis occur? | Brain is rich in degradative enzymes and has little supportive connective tissue |
| Liquefaction can also result from a ______ infection | Bacterial infection that triggers a localized collection of WBCs. |
| What is gangrene? | A large area of tissue that became necrotic from loss of blood supply and has been influenced by its environment to become wet/dry. |
| Gangrene is necrosis that results from _________ | Loss of blood supply |
| What is dry gangrene? | Coagulative necrosis |
| How is dry gangrene characterized? | Blackened, dry, wrinkled tissue that is separated from adjacent healthy tissue by an obvious line of demarcation. Generally only occurs in extremities. |
| What is wet gangrene? | Liquefactive necrosis |
| How is wet gangrene characterized? | Typically found in internal organs, appears cold and black, may be foul-smelling due to bacteria. May be life-threatening due to rapid spread of tissue damage and release of toxins into blood |
| What is apoptosis? | Programmed cell death, or cell suicide |
| Is apoptosis a normal or pathologic process? | Normal |
| What does apoptosis accomplish? | Normal process that has physiologic functions in removing unwanted, redundant or damaged cells |
| Certain types of ____ ______ may also trigger apoptosis. | Cell injury |
| “Abnormal” apoptosis? | Apoptosis may be triggered inappropriately in some disease processes and suppressed inappropriately by others |
| What triggers apoptosis? | Actions at cell membrane receptors or by intracellular factors |
| Apoptosis trigger _____ | CASPASES |
| What are the enzymes that, triggered by apoptosis, dismantle the cell? | Caspases. They become activated inside the cell and dismantle it in an orderly fashion. |
| What are apoptotic bodies? | Membrane-bound vesicles that package cell components |
| What are membrane-bound vesicles that package cell components in apoptosis? | Apoptotic bodies |
| Apoptotic bodes are disposed of by ______ | Phagocytic cells |
| True or false: Apoptosis triggers inflammation. | False. Cell contents are not released into the interstitial fluid, so inflammation does not occur |
| Does apoptosis trigger inflammation? Why? | No, because cell contents are not released into the interstitial fluid |
| Examples of apoptosis? | Embryonic webbing in utero, “pruning” of brain cells, neutrophils after immune response |
| Which cells undergo apoptosis? | WBCs |
| Do RBCs undergo apoptosis? | No, they are recycled |
| What is a telomere? | Cap at the end of chromosome. Shortens with each cell division |
| Cells undergo a finite number of replications. | |
| What is telomerase? | Enzyme that builds telomeres. Allows cancerous cells to keep dividing |
| What is algor mortis? | Postmortem reduction of body temperature |
| What is poikilothermia? | Body temperature equals environmental temperature after death |
| What is livor mortis? | Also called postmortem lividity. Purple discoloration of dependent areas of skin due to blood pooling |
| What is rigor mortis? | Stiff muscles after death |
| What is postmortem autolysis? | Dissolution of cells due to bacterial action after death |
| Put in order of occurrence: Rigor mortis, algor mortis, postmortem autolysis, livor mortis, poikilothermia | Algor mortis, poikilothermia, livor mortis, rigor mortis, postmortem autolysis |
| Where are mast cells located? | Connective tissue, especially around blood vessels and under mucosal surfaces |
| How do mature basophils become mast cells? | When stimulated by cytokines, mature basophils can migrate to connective tissue. Once in the tissue, they are called mast cells and can not reenter circulation |
| Structure of mast cells? | Have IgE receptors that allow them to bind and display IgE antibodies on cell surfaces. |
| What causes mast cells to release granules/degranulate? | When an appropriate stimulus occurs, such as antigen binding to IgE antibodies |
| What do the granule/degranulates released by mast cells contain? | Proinflammatory chemicals |
| What are the proinflammatory chemicals that mast cell granules contain? | Histamines, platelet activating factor and other vasoactive amines that are important mediators of immediate hypersensitivity responses (inflammation) |
| ____ cells are involved in wound healing and chronic inflammatory conditions | Mast cells |
| Phagocytosis begins when what 2 types of cells enter tissue? | Neutrophils and monocytes (macrophages) |
| Phagocytosis involved enzymes that digest _______. | Protein structures |
| What are some phagocytic enymes? | Lysozyme, neutral proteases, collagenase, elastase, acid hydrolases |
| What do neutrophils and macrophages do? | Specialize in collagen and extracellular matrix degradation |
| What is a phagosome? | When a microbe is small enough to be internalized, a phagocyte will endocytose it into a phagosome, which is then merged with a lysosome containing degradative enzymes |
| What is a lysosome? | Contains degradative enzymes |
| Large antigens may cause neutrophils to... | Release degradative enzymes extracellularly, causing damage to local tissues |
| What is interstitial fluid? | Fluid located between cells, but not in blood vessels |
| What are the events of the inflammatory process? (3) | 1. Increased vascular permeability 2. Recruitment and emigration of leukocytes 3. Phagocytosis of antigens and debris |
| During inflammation, what vasoactive chemicals are released? | Histamine, prostaglandins, leukotrienes |
| What do mast cells do in response to injury? | Mast cells in area of injury degranulate and release packets of histamine, prostaglandins and leukotrienes, initiating inflammation |
| True or false: Immediately after injury, there is a short period of vasoconstriction. | True. |
| What causes vasodilation in area of injury after short period of vasoconstriction? | Chemical mediators released by injured tissues |
| With vasodilation, round up of endothelial cells cause _____. | Increased capillary permeability |
| With vasodilation, the greater volume of blood increases ______. | Hydrostatic pressure. Amount of pressure within blood vessels |
| Increased _____ and increased _____ pushes fluid out of blood vessels into surrounding tissue. | Pressure; permeability |
| What contributes to local swelling after an injury? | Increased pressure and increased permeability pushes fluid into surrounding tissues |
| Because of dilated blood vessels and open capillaries, more blood is carried to injured area and causes.... (4) | Redness, pain, heat and swelling |
| What are the 4 classic manifestations of inflammation? | Redness, heat, pain and swelling (and loss of function) |
| Prostaglandins contribute to... (4) | Vasodilation, increased permeability. Also act as chemotactic factor and stimulates neutrophil emigration. Cause pain by enhancing sensitivity of pain receptors |
| What is hemostasis? | Stopping the bleeding |
| How is hemostasis achieved? | Platelets are activated and clotting cascade is activated |
| What initial vascular event helps to stop bleeding? | Initial transient vasoconstriction |
| What causes vasodilation? | Chemicals released by mast cells |
| Chemicals released by ____ causes vasodilation. | Mast cells |
| ______ brings increased blood flow to area of injury. | Vasodilation |
| Vasodilation and increased blood flow result in... (3) | 1. Brings more WBC to area, 2. Dilutes toxins (if present), 3. Causes edema |
| What does increased microvascular permeability cause? | Cause endothelial cells to retract, opening space between cells. Results in swelling |
| During inflammation, swelling is caused by _____ and _____. | Increased blood flow/pressure and increased permeability |
| What is endothelial activation? | Increase of adhesion molecules (selectins, etc). WBCs bind to receptors on endothelial cells |
| Through what processes do WBCs leave blood vessels and enter tissues (4)? | 1. Margination, rolling and adhesion 2. Diapedesis (transmigration) 3. Chemotaxis 4. Phagocytosis |
| What WBCs accumulate in tissues initially? | Neutrophils |
| What are some functions of neutrophils? | Early responders to acute bacterial infection. Have receptors on cell surfaces that enable them to bind to endothelial cells in areas of inflammation. Attracted to areas of inflammation via chemotaxis. Produce potent chemical mediators that destroy. |
| What are cytokines? | Chemotactic factors that attract neutrophils to area of inflammation |
| Where are neutrophils stored? | Bone marrow |
| Neutrophils are also called...? | Polymorphonuclear leukocytes (polys or PMNs) |
| Which circulating WBCs accumulate in tissues after neutrophils? | Macrophages |
| What circulating WBCs become macrophages after they enter the tissues? | Monocytes |
| What causes redness of inflammation? | Vasodilation, increased blood flow to site (in vessels) |
| What causes heat of inflammation? | Vasodilation, increased blood flow to site (in vessels) |
| What causes pain in inflammation? | 1. Swelling: Pressure onto pain neurons 2. Prostaglandins: sensitize pain receptors 3. Histamine activates pain receptors |
| What causes swelling of inflammation? | Vasodilation, increased capillary permeability |
| Is acute inflammation bad/abnormal? | No. Acute inflammation is beneficial |
| Can a person have inflammation without having an infection? | Yes. Injury. Endogenous danger signals can be released by uric acid, parts of cell membranes, r/a, cancer, CVA, chemotherapy |
| What are systemic manifestations of inflammation? (3) | 1. Fever 2. Fatigue and lethargy 3. Leukocytosis |
| What causes fever? | Pyrogens. Some cytokines are pyrogens, and some are produced by bacteria |
| What is the mechanism of pyrogens? | Pyrogens cause prostaglandin synthesis and release in hypothalamus. Signals hypothalamus to conserve and produce heat |
| What is the body’s “thermostat”? | Hypothalamus |
| In relation to fever, prostaglandins cause...? | Increased SNS output, resulting in vasoconstriction to decrease heat loss. Other brain signaling results in shivering to generate heat |
| Fever and lethargy are caused by circulating _____. | Cytokines |
| What is leukocytosis? | Elevated WBC number due to inflammation |
| What happens to WBCs after they fight infection? | They die from apoptosis |
| What is acute inflammation? | Less than 2 weeks. First step of tissue healing. |
| If acute inflammation persists for longer than ____, can become ____ inflammation | Chronic |
| Chronic inflammation _____ with healing. | Interferes |
| What is regeneration in tissue healing? | Replaces injured tissue with parenchymal (functioning) cells of same type |
| What is an example of connective tissue repair/regeneration? | Scar tissue. Repair of cells that can not divide (enough) |
| What is scar tissue formation? | Replaces cells that cannot regenerate or cells that regenerate minimally, with connective tissue (scar formation). Also called wound healing, or simply, repair. |
| Compare scar tissue with surrounding tissue? | Scar tissue lacks properties of surrounding tissue. |
| What is an example of connective tissue repair/regeneration? | Scar tissue formed in cardiac muscle |
| What happens with healing in the liver? | Hepatocytes in the liver regenerate. Connective tissue repair with scar formation may also occur in the liver. |
| When can liver function be restored by regenerating hepatocytes? | If supporting framework is present |
| What is an example of restored liver function, with supporting framework still intact? - Some types of acute hepatitis | |
| What do nodules of regenerating cells in the liver cause? | Nodules can distort liver architecture and cause loss of function if supporting framework is damaged by scar formation |
| What is an example of liver damage to scar formation? | Cirrhosis |
| What are 2 terms used to describe healing of surface wounds? | First and second intention |
| What are the characteristics of a wound that heals by primary intention? | One that has its edges approximated/touching. Bc edges are together, tissue will heal relatively quickly following the processes of CT repair |
| What interferes with primary intention would healing? | Infection, other factors that impair healing |
| What are some examples of wounds that heal by primary intention? | Surgical incision |
| How long does is usually take for epithelial cells to grow over a wound? | 48 hrs |
| What should a nurse recommend to a patient with a wound healing by primary intention? | No soaking/swimming/immersion in water bc it loosens up the healing matrix |
| What are the characteristics of a wound healing by secondary intention? | One that is open or gaping, in which a lot of tissue has been damaged. Heals from bottom upward. Same processes of CT repair occur, but take longer, even without infection, etc. |
| What are some examples of wounds that heal by secondary intention? | Pressure ulcers, burns |
| What are the phases of tissue healing/connective tissue repair? | 1. Inflammation 2. Reconstruction (Proliferation) 3. Maturation (Remodeling) |
| How long does the inflammation phase last for primary intention wounds? | 1-2 days |
| When does the reconstruction/proliferation phase occur? | 2-3 days, up to 3 weeks after wound occurrence (for primary intention healing) |
| What is the reconstruction/proliferation phase? | Epithelial migration in response to growth factors released by macrophages in area |
| What triggers the epithelial migration involved in wound proliferation? | Growth factors released by macrophages |
| Which stage of wound healing is characterized by angiogenesis, epithelial migration, fibroblast migration and building of collage and extracellular matrix? | Reconstruction/proliferation phase |
| How long after a wound occurs does maturation/remodeling happen? | 3 wks to 2 yers (in primary intention) |
| What is maturation/remodeling? | Reorganization of collagen that increases tensile strength. New scar is formed that is not as strong as mature scar. |
| What happens during the maturation/remodeling phase of wound healing? | Collagen is taken down and put back neatly. There is increased tensile strength, as well as change in color (becomes whiter) |
| What are some local factors that can impair tissue healing? | Factors that cause excessive or prolonged inflammation, or factors that interfere with reconstruction and maturation |
| What are examples of factors that cause excessive or prolonged inflammation? | Wound infection, mechanical stress, repeated injury |
| What are some examples of local factors that interfere with reconstruction and maturation? | Foreign body, large hematoma (collection of blood), wound separation/ dehiscence, poor blood supply to injured area Local factors that interfere with reconstruction/maturation: poor blood supply to injured area: examples? |
| What are systemic factors that can impair tissue healing? | Like local factors, those that suppress inflammation and interfere with reconstruction and maturation |
| What are some examples of systemic factors that suppress inflammation? | High levels of glucocorticoids (corticosteroids) from medication or in response to chronic stressors; immunosuppressants, AIDs, diabetes, malnutrition, alcohol abuse, old age, poor oxygen supply |
| What are some examples of systemic factors that interfere with reconstruction and maturation? | Poor oxygen/nutrient supply, impaired fibroblast (and other reconstructive cells) function |
| What systemic factors of reconstruction and maturation interference cause poor oxygen supply? | Chronic ischemia, hypoxia. Anemia, cigarettes, diabetes |
| What contributes to poor nutrient supply that interferes with reconstruction/maturation in wound healing? | Poor nutrition or malnutrition, vitamin C deficiency |
| What is fibrosis? | Excessive secretion of collagen with scar formation. Interferes with normal organ function |
| What is an example of a condition that causes fibrosis? | Hepatitis C |
| What are the steps in bone healing? | HFCOC. 1. Hematoma formation 2. Fibrocartilage formation 3. Callus formation 4. Ossification 5. Consolidation and remodeling |
| What are some factors that impair bone healing? | Nutrition, immunosuppression, age, gender, alcohol, vitamins, stress/use |
| What is increased capillary hydrostatic pressure? | Pushes fluid out of capillary |
| Examples of increased capillary hydrostatic pressure? | Inflammation, venous congestion |
| Congestive heart failure increases capillary _____ pressure, and leads to ____. | Hydrostatic, edema |
| What causes decreased blood colloid osmotic pressure? | Decreased plasma albumin |
| Decreased blood colloid osmotic pressure can be due to ____ and _____ of albumin. | Loss of albumin, decreased albumin synthesis. |
| What is increased microvascular permeability? | Allows plasma proteins to leak into interstitial space, causing increased interstitial osmotic pressure |
| What is interstitial osmotic pressure? | Pull of fluid into interstitial space |
| What can cause increased interstitial osmotic pressure? | Increased capillary permeability. (inflammation) |
| What can impaired lymphatic drainage cause? | Edema, due to increased interstitial fluid |
| What are 4 factors that can cause edema? | 1. Increased capillary hydrostatic pressure 2. Decreased blood colloid osmotic pressure 3. Increased capillary permeability 4. Impaired lymphatic drainage |
| What are 5 ways to assess edema? | 1. Visual inspection 2. Palpation (pitting edema) 3. Measurement of girth of parts 4. Daily weight 5. Intake/output |
| Proteinuria indicates loss of _____ function | Kidney function |
| Liver disease indicates lack of _____ production | Protein |
| Do not take BP where _____ are removed | Lymph nodes |
| Chronic inflammation is marked by ______ tissue ____. | Continued tissue damage |
| What is cachexia? | Muscle wasting |
| What is a benefit of edema? | Can flush toxins by increasing blood flow |
| Lack of protein synthesis in liver disease causes low protein in the blood resulting in increased _____. | Interstitial fluid, edema |
| Who has more extracellular fluid than intracellular fluid? | Infants |
| Who has more intracellular fluid than extracellular fluid? | Adults |
| Who has the most water of body mass? | Males. Females typically less bc of more body fat |
| Who has the lowest amount of water in body mass? | Older adults |
| Which group is most vulnerable to fluid imbalances? | Neonates and infants and older adults |
| Liver produces_______ | Angiotensinogen |
| Angiotensinogen is converted to angiotensin I by ______ | Renin |
| Renin is released by kidney in response to... | Low BP, or low fluid volume |
| Angiotensin I gets converted to angiotensin II by _____ | ACE |
| ACE is | angiotensin-converting enzyme, produced in the lungs |
| Angiotensin II acts on __________, causing it to release ______ | Adrenal gland; aldosterone |
| Aldosterone acts on __________ | collecting ducts of kidney |
| What does aldosterone do? | Make nephrons reabsorb water (retention of Na+Cl-) |
| What does aldosterone induced retention of water do to BP? | Increases BP |
| Fluid homeostasis involves what 4 factors? | Fluid intake, distribution, excretion and loss |
| How can one intake fluid? | Orally, rectally |
| How is fluid distributed? | Between vascular and interstitial fluid, or between interstitial and intracellular |
| How does fluid move between vascular and interstitial fluid? | Via capillary filtration, hydrostatic and oncotic forces |
| How does fluid move between interstitial and intracellular? | Osmosis |
| What is the hormone that increases fluid into the vascular system, as well as produces less, more concentrated urine? | ADH. Anti-diuretic hormone |
| What triggers ADH release? | Increased plasma osmolality activates osmoreceptors, in the hypothalamus. Stimulates ADH release from posterior pituitary |
| ADH is released from the ______. | Posterior pituitary gland |
| ADH acts on the _____ to do what? | Kidney tubules to reabsorb water. Water moves from kidney tubules back into blood |
| Osmoreceptors in the hypothalamus that trigger release of ADH, also triggers _____. | Thirst, to increase fluid intake and reduce blood osmolarity to set point |
| What does aldosterone do? | Think “volume”. Increases fluid volume |
| What triggers aldosterone? | Decreased volume to renal artery |
| Aldosterone is released by _____ | Adrenal cortex |
| How does aldosterone work? | Acts on kidney by increasing Na+ reabsorption from distal tubule into plasma. Where sodium goes, water follows |
| Where sodium goes, ______ follows | Water |
| Elevated serum levels of what electrolyte directly triggers aldosterone? | K+. To maintain ion balance, potassium is moved from plasma and excreted |
| BP and volume are also regulated by _____ which inhibits ADH release. | Atrial Naturetic Peptide |
| What kind of IV fluid goes to extracellular fluid only? | Isotonic!! |
| What does NS in isotonic IV solutions mean? | Normal saline: 0.9% NaCl |
| Which type of IV solution is used to make up for loss of water? | Hypotonic |
| Which type of IV solution should you give with low BP, or volume issue? | Isotonic solution |
| What type of IV solution should you give with longer term IV fluid with no other input? | Hypotonic solution, NS is not enough water. |
| Which type of IV solution allows movement of fluid into cells? | Hypotonic |
| What is ECV excess? | Normal concentration, too much volume |
| What is ECV deficit? | Normal concentration, not enough volume |
| What is hypernatremia? | Too high of concentration |
| What is hyponatremia? | Too low of concentration |
| What is clinical dehydration? | ECV deficit, plus hypernatremia |
| What is lost during insensible perspiration? | Just water |
| What is lost during respiratory loss? | Just water |
| What is lost during sweating? | Salt and water |
| What is lost during diarrhea? | Lots of salt and water |
| What is lost during urination? | Dilute salt and water |
| Normal saline (NS) IV moves 1/3 into vascular, which ______ hydrostatic pressure | Increases |
| Which fluid imbalance has normal serum sodium, and extracellular fluid overload? | ECV excess |
| What are some risk factors in ECV excess? | Risk factors such as excessive intake of sodium and water, renal retention of saline due to excessive aldosterone |
| What can cause renal retention of saline (ECV excess)? | Oliguria due to acute kidney failure; end-stage renal disease (ESRD), CHF (excessive aldosterone), cirrhosis, hyperaldosteronism, excessive ingestion of black licorice, Cushing’s syndrome, medications that cause renal retention of saline |
| Renal retention of saline causes which fluid imbalance? | ECV excess |
| What 3 conditions cause excessive aldosterone? | Hyperaldosteronism, CHF, cirrhosis |
| Excessive ingestion of black licorice can cause ____ | ECV excess. Black licorice has aldosterone-like effect |
| What are some clinical assessments of ECV excess? | Rapid weight gain, edema in dependent areas, bounding pulse, distended neck veins when partially upright, bulgin fontanel in infants, crackles/rales in lungs, dyspnea, orthopnea, short of breath lying down |
| Crackles/rales can be a sign of which fluid imbalance? | ECV excess |
| Bounding pulse can be a sign of which fluid imbalance? | ECV excess |
| Distended neck veins when partially upright can be a sign of which fluid imbalance? | ECV excess |
| Edema in dependent areas can be a sign of which fluid imbalance? | ECV excess |
| A bulging fontanel in infants can be a sign of which fluid imbalance? | ECV excess |
| Dyspnea, orthopnea and shortness of breath while lying down can be a sign of which fluid imbalance? | ECV excess |
| Excess fluid retention results from excessive salt intake because... | Water follows salt |
| What are important teachings for patients with ECV excess? | Sodium restriction, taking daily weight, non-food sources of sodium, indications of ECV excess if sleeping upright |
| What is ECV deficit? | Loss of sodium-containing fluid |
| What are some causes of ECV? | Adrenal cortex is not secreting aldosterone, 4+ days of bed rest, emesis, diarrhea, burns, rapid 3rd space accumulation (acites), fistula drainage, nasogastric suction, intestinal decompression, blood loss |
| What is third space accumulation? | Accumulation of fluid that is not part of normal fluid distribution |
| What are ascites? | Fluid accumulation in the peritoneal cavity. Rapid ascites fluid accumulation can cause ECV to decrease/cause deficit |
| Liver issues and lack of protein in the blood can cause | 3rd space accumulation |
| An acute GI obstruction can cause _____ | ECV deficit, due to fluid collection in the GI. So much fluid can be moved rapidly into the GI that ECV is decreased |
| Why might excessive bed rest cause ECV deficit? | Because lying down causes more blood to pool centrally due to gravity. Kidneys are well-perfused, and excrete fluid |
| Not enough aldosterone secretion may cause which fluid imbalance? | ECV deficit |
| Diarrhea, burns, emesis may cause which fluid imbalance? | ECV deficit |
| What are some clinical sign of ECV deficit? | Hypotension, weak, rapid pulse, dizziness with change in position, oliguria, prolonged capillary refill time, poor skin turgor, dry mucous membranes, absence of tears and sweat, longitudinal furrows in tongue |
| ECV deficit can lead to ____ | Hypovolemic shock |
| Low blood pressure can be a sign of which fluid imbalance? | ECV deficit |
| A weak, rapid pulse can be a sign of which fluid imbalance? | ECV deficit |
| Oliguria can be a sign of which fluid imbalance? | ECV deficit |
| Poor skin turgor can be a sign of which fluid imbalance? | ECV deficit |
| Absence of tears and sweat can be a sign of which fluid imbalance? | ECV deficit |
| Soft sunken eyeballs can be a sign of which fluid imbalance? | ECV deficit |
| Longitudinal furrows in the tongue can be a sign of which fluid imbalance? | ECV deficit |
| Prolonged capillary time can be a sign of which fluid imbalance? | ECV deficit |
| Important teachings for patients with ECV deficit? | Replace body fluid losses with both salt and water |
| What IV solution is used to treat ECV deficit? | Normal saline/ isotonic colution |
| What is clinical dehydration? | Combination of ECV deficit and hypernatremia |
| What is important to teach a patient with diarrhea, excessive sweating, or emesis? | To replace with fluids containing both salt and water. Electrolyte containing fluids |
| What is hypernatremia? | Excess salt relative to water in the blood |
| What can cause hypernatremia? | Loss of more water than salt; gain of more salt than water |
| Hypernatremia: loss of more water than salt can be caused by...? (2) | Diabetes insipidus: not enough ADH; diarrhea without fluid replacement (clinical dehydration); excessive sweating without fluid replacement |
| Gain of relatively more salt than water (hypernatremia) can be caused by... | Decreased thirst sensation with aging; inability to respond to thirst; limited or no access to water, difficulty swallowing, self-limited water intake, high solute intake without adequate water (tube feedings), hypertonic saline |
| What is diabetes insipidus? | Not enough ADH is produced, causing excessive dilute urine. Salt remains in the body. |
| What can cause diabetes insipidus? | Brain surgery, brain trauma, infection, tumor |
| Craving for cold/ice water is common in ____ | Diabetes insipidus |
| In diabetes insipidus, an alert patient can drink enough to remain safe. If the patient is not alert, ____ is given. | vasopressin (desmopressin) (ADH) |
| How is DI monitored? | Serum sodium checks every 4 hrs, urine specific gravity every 6 hr, record intakes and outputs, monitor LOC for any confusion |
| What is hyponatremia? | Blood contains excess water relative to salt |
| What can cause hyponatremia? | Excessive ADH release stimulated with stressors, nausea, anesthesia, pain and increased osmolarity |
| What are some clinical signs of hyponatremia? | Nausea, emesis, malaise/lethargy, confusion, serum sodium of < 130 mEq/L |
| Why could hyponatremia cause confusion? | Because of the low osmolarity of the blood, water moves into cells (water moves toward higher concentrations). Water moving into the cells can cause neuronal cell swelling, resulting in confusion. Can progress to seizure or coma |
| In hyponatremia, what can cause gain of relatively more water than salt? | Excessive D5W, excessive tap water enemas, rapid/excessive/forced water drinking, excessive ADH (SIADH), ibuprofen/other nonselective NSAIDs |
| In hyponatremia, what can cause loss of relatively more salt than water? | Diuretics, sweating/emesis/diarrhea with excessive replacement of water but not electrolytes |
| What is important to teach to patients with hyponatremia? | Alternatives to tap water enemas, replace body fluids losses with fruit juices or boullion instead of tap water, why prescribed fluid retention is used to treat hyponatremia |
| What is SIADH? | Syndrome of inappropriate (excessive) ADH. ADH acts on kidneys to pull water back into blood, causing hyponatremia, or ECV excess |
| What can cause SIDH? | Meningitis/other infections, head injury, pituitary tumor or surgery, cancers (small-cell lung cancer) can secrete ADH, ecstasy |
| What are some SIDH interventions? | Prescribed fluid restriction (may need to shut off water in room), monitoring for confusion, salt tablets may be prescribed, soft moist foods may help tolerate fluid restriction |
| What 2 hormones aid in retention of fluid? | ADH, aldosterone |
| What type of IV solution has fluid distribution that is 1/2 saline (extracellular), and 1/2 water (1/3 extracellular, 2/3 into cells)? | Hypotonic fluid that contains sodium |
| Which IV solution has fluid distribution that is aprox. 1/3 extracellular (vascular and interstitial) and 2/3 intracellular? | Hypotonic fluid with no sodium |
| Which hormone affects volume? | Aldosterone |
| Which hormone affects concentration? | ADH |
| Which should you treat first: ECV deficit or hyponatremia? | Volume deficit with isotonic IV solution |
| Week 4 | |
| What is an ion? | Charged molecule |
| What is the chemical symbol for potassium? | K+ |
| What is the chemical symbol for calcium? | Ca+ |
| What is the chemical symbol for magnesium? | Mg+ |
| What are the principles of electrolyte homeostasis and imbalances? (4) | 1. Intake and absorption 2. Distribution 3. Excretion 4. Loss through abnormal routes |
| To maintain homeostasis, ___ + ____ must equal ____ + ____ | Intake, absorption; excretion, loss |
| Which electrolyte imbalances are “floppy”? | Hyperkalemia, hypokalemia, hypercalce,ia, hypermagnesemia |
| Which electrolyte imbalances are “twitchy”? | Hypocalcemia, hypomagnesemia |
| Potassium ions are necessary for normal function of all cells, especially ___ and ____ cells | Neurons, muscle cells |
| The ratio of potassium inside/outside of the cell determines its ____ potential. | RMP: resting membrane potential |
| Most of the potassium ions in the body are _____ the cells | Inside |
| The sodium-potassium pump used ____ to maintain cell homeostasis | ATP |
| Normal muscle cells have a very small electrical charge across their membranes, called the ______. | Resting membrane potential |
| If potassium ratio is altered, _______ will be different and muscle can have abnormal function. | Resting membrane potential |
| Potassium imbalances can affect... | Function of skeletal muscle, smooth muscle and/or heart muscle |
| The word ‘potassium’ comes from the word ____ | Potash, meaning plant residue |
| How do we take in potassium? | Through diet, or potassium-containing medication |
| What foods contain potassium? | Fruits- bananas, oranges, raisins, cantaloupe, apricots. Vegetables- Asparagus, bok choy, broccoli, carrots, celery. Other- nuts, molasses, sunflower seeds |
| What mechanism pumps K+ ions into cell to keep intracellular K+ level high? | Sodium-potassium pump |
| What causes K+ to move from plasma into cells? | Alkalosis, insulin, and beta-adrenergic stimulation |
| What causes K+ to move from cells into plasma? | Acidosis due to mineral acids (caused by bicarbonate loss in diarrhea) |
| Potassium is normally excreted in... | Urine, feces, sweat |
| More potassium is excreted than normal in ____ | Diarrhea |
| Potassium excretion by the kidneys is ____ dependent | Flow dependent |
| Flow-dependent excretion of K+ in kidneys means... | The larger the urine volume, the more potassium is excreted |
| What hormones increase potassium excretion in the urine? | Aldosterone, glucocorticoid hormones (cortisol) Aldosterone pulls in ___ from the urine, and pushes ___ out |
| Potassium may be lost through abnormal routes via.... | emesis, drainage from tubes inserted into the GI tract (nasogastric tubes), or other losses of body fluids |
| What is hypokalemia? | Serum potassium concentration that is below normal (< 3.5 mEq/L). Plasma deficit of K+, whole body K+ may be decreased, normal, or increased |
| With hypokalemia, whole body potassium levels may be... | Decreased, normal or increased |
| What are the 4 general risk factors for hypokalemia? | 1. Decreased K+ intake 2. Shift of K+ from plasma into cells 3. Increased K+ secretion 4. Loss of K+ through abnormal route |
| What are risk factors for decreased potassium intake? | Anorexia; unusual weigh-loss diets that do not contain K+; NPO orders; prolonged IV therapy without K+ |
| What are risk factors that shift K+ from plasma into cells? | Alkalosis; hypersecretion of insulin (response to TPN- total parenteral nutrition); insulin overdose; excessive beta-adrenergic stimulation (epinephrine, albuterol); hypothermia |
| What does insulin do to K+ in the plasma? | Moves K+ into cells |
| What are risk factors for increased K+ excretion? | medications that cause increased K+ excretion in urine); increased effect of aldosterone (hyperaldosteronism, CHF, cirrhosis); hypomagnesemia; black licorice; diarrhea, laxative overuse, colon cleansing/irrigation |
| What causes loss of K+ through abnormal routes? | Emesis, nasogastric suction, intestinal decompression |
| What are some clinical signs of hypokalemia? | Abdominal distention, decreased bowel sounds, constipation, paralytic ileus (GI not moving); polyuria; orthostatic hypotension; flaccid skeletal muscle weakness; flaccid paralysis; cardiac dysrhythmias; quadriceps weakness |
| Cardiac dysrhythmias can be caused by | Both hypokalemia and hyperkalemia |
| Quadricep weakness is a sign of ____ | Hypokalemia |
| Why is hypokalemia a “floppy” disorder? | Hyperpolarization makes it harder to reach action potential (more negative) |
| What are important teachings for a patient with hypokalemia? | Safe weight loss diet, bowel management to prevent diarrhea from laxative overuse. need for increased K+ intake to offset loss in diarrhea; K+ rich foods |
| What is hyperkalemia? | Serum potassium concentration that is above normal (>5.0 mEq/L). Indicates a plsma excess of K+ |
| In hyperkalemia , the whole body K+ level may be... | Increased, normal or decreaed |
| What are the 3 general risk factors fro hyperkalemia? | Increased K+ intake, shift of K+ from cells to plasma, decreased K+ excretion |
| What are risk factors for increased K+ intake? | Oral intake is rarely a problem unless combined with decreased urine output. Too much/rapid KCl; insufficient mixing of KCl in IV bag; stored blood (K+ leaks out of cells into plasma in old blood); large does of penicillin G |
| When is use of stored blood an issue? | When using large amounts ≥ 8 unitsl blood older than 3 days |
| What risk factors shift K+ from cells into plasma? | Acidosis due to mineral acids (loss of bicarbonate in diarrhea); crushing injury or massive cell death; insulin deficiency |
| What risk factors cause decreased K+ excretion? | Mediations, oliguric renal disease, severe hypovolemia , decreased aldosterone effect |
| How does severe hypovolemia cause decreased K+ excretion? | Decreased ECV causes decreased kidney perfusion, producing less urine and excreting less K+ |
| What are some clinical signs of hyperkalemia? | Intestinal cramping and diarrhea; flaccid skeletal muscle weakness; flaccid paralysis; cardiac dysrhythmias |
| Which electrolyte imbalance causes most potentially dangerous dysrhythmias? | Hyperkalemia |
| What are some important teachings for patients with hyperkalemia? | Stop K+ containing preparations (KCl based salt substitutes), if urine volume decreases; reduce intake of K+ rich foods) |
| What normal ranges for serum calcium? | 9-11 mg%; 4.5-5.5 mEq/L |
| Lab reports measure ____ calcium | Total calcium |
| True or false: ionized calcium can be measured with low/high total calcium. | True |
| What is the physiologically active form of calcium? | Free, ionized calcium |
| Are calcium ions bound to albumin physiologically active? | No. Physiologically inactive while bound |
| Are calcium ions bound to small organic anions like citrate physiologically active? | No. |
| Plasma calcium and plasma ____ vary inversely | Plasma phosphate |
| What decreases the amount of physiologically available Ca++? | Alkalosis. Bicarbonate binds to Ca++ |
| Which hormone regulates plasma Ca++ concentration? | Parathyroid hormone (PTH) |
| What does PTH do? | Increases plasma Ca++: takes it from bones and improves absorption of vitamin D needed for Ca++ absorption. |
| Where is calcium absorbed? | Duodenum (more acidic) |
| What is hypocalcemia? | Plasma deficit of Ca++l serum levels may not reflect body stores |
| What are the 4 general risk factors for hypocalcemia? | Decreases Ca++ intake or absorption; decreased physiological availability of Ca++; Increased Ca++ excretion; loss of Ca++ by abnormal route |
| What risk factors cause decreased Ca++ intake or absorption? | Chronic malnutrition or poor calcium intake, vitamin D deficiency (lack of sunlight); antacid overuse (non-calcium); chronic diarrhea (includes laxative overuse); steatorrhea |
| Why does antacid overuse cause decreased calcium absorption? | Because the bicarbonate in antacids makes GI less acidic |
| What is steatorrhea? | Floating fats in stools (such as in pancreatitis) bind and excrete Ca++ |
| What risk factors cause decreased physiological availability of Ca++? | Massive transfusion with citrated blood; hypoparathyroidism (that includes removal of parathyroid glands); alkalosis (decreased acidity); overuse of phosphate-containing laxatives and enemas |
| What are clinical signs of hypocalcemia? | Positive Chvostek sign, positive Trousseau sign; muscle twitching, cramping; carpopedal spasm, tetany; laryngospasm; seizures, cardiac dysrhythmias |
| Why is hypocalcemia a twtitchy disorder? | Depolarization makes it easier to reach action potential |
| What are important teachings patients with hypocalcemia? | Bowel management to prevent laxative overuse; calcium rich foods; alternate Ca++ sources for those who do not eat dairy; need or increased Ca++ for those with chronic diarrhea or malabsorption |
| What are some calcium rich foods? | Milk, dairy products; almonds, cream of wheat and farina cereal; chocolate, canned fish (with bones); oranges; oysters, tofu, dark leafy greens, corn tortillas |
| What is hypercalcemia? | excessive plasma Ca++ |
| What are some general risk factors of hypercalcemia? | Increased Ca++ intake/absorption; shift of Ca++ from bones to plasma; decreased Ca++ excretion |
| What risk factors cause shift of Ca++ from bones to plasma? | prolonged immobilization, cancers, bone tumors, hyperparathyroidism, ectopic release of parathyroid- hormone related peptide |
| Is hypercalcemia floppy or twitchy ? | floppy |
| What are some clinical signs of hypercalcemia? | Anorexia, constipation, nausea and emesis, muscle weakness, fatigue, confusion and lethargy, personality and mood changes; polyuria |
| What are important teachings for a patient with hypercalcemia? | Avoid massive vitamin D supplementation; need for adequate hydration to prevent renal damage with hypercalcemia |
| What are normal ranges for serum magnesium? | 1.5-2.5 mEq/L |
| What are parts of total body magnesium? | Ionized magnesium (physiologically active form), Mg++ bound to albumin (physiologically inactive); Mg++ bound to small organic anions like citrate (physiologically inactive) |
| Magnesium is absorbed primarily from the ____ | Terminal ileum |
| What is hypomagnesemia? | Plasma Mg++ deficit |
| More Mg++ mean less ____ | Ach |
| Hypomagnesemia means less magnesium, more Ach released from motor nerve | Twitchy |
| What are the general risk factors for hypomagnesemia? | Decreased Mg++ intake or absorption; decreased physiologically availability of Mg++; increased Mg++ excretion; loss of Mg++ by abnormal route |
| What risk factors cause decreased Mg++ intake? | Malabsorption syndromes, chronic diarrhea, steatorrhea, chronic malnutrition, chronic alcoholism, ileal resection |
| What risk factors cause increased Mg++ excretion? | Diuretic therapy, diabetic ketoacidosis, hyperaldosteronism, chronic alcoholism, steatorrhea |
| What risk factors cause loss of Mg++ through abnormal route? | Acute pancreatitis |
| What are some clinical signs of hypomagnesemia? | Insomnia, hyperreflexia, positive Chvostek sign, positive Trousseau sign, skeletal muscle cramps, twitching, tremors, tetany, nystagmus, seizures, extreme confusion, cardiac dysrhythmias |
| Is hypomagnesemia floppy or twitchy? | Twitchy. Less Mg++ mean MORE ACH |
| What are important teachings for a patient with hypomagnesemia? | Information about alcoholism treatment, if applicable. Mg++ rich foods |
| What foods are rich in Mg++ | Dark chocolate, nuts, dark green vegetables, legumes |
| What is hypermagnesemia? | Plasma Mg++ excess |
| What are the general risk factors for hypermagnesemia? | Increased Mg++ absorption, decreased Mg++ excretion |
| What risk factors cause increased Mg++ absorption? | Excessive use of Mg++ (antacids) |
| What risk factors cause decreased Mg++ excretion? | oliguric renal disease, adrenal insufficiency |
| What are some clinical signs of hypermagnesemia? | Hypotension, drowsiness, lethargy, weak or absent deep tendon reflexes, flaccid muscle paralysis, respiratory depression, cardiac dysrhythmias |
| What are some important teachings for a patient who has hypermagnesemia? | Replace chronic Mg++ laxative use with alternative methods of bowel management for older adults; avoid Mg++ containing antacids and laxatives if urine volume decreases |
| Which electrolyte imbalances cause cardiac dysrhythmias? | All except hypercalcemia |
| What is the order of cellular events in inflammation? | a.)endothelial cell activation (increase in adhesion molecules) b.) WBCs leave vessels into tissues 1.) Margination 2.) Diapedesis 3.) Chemotaxis- action at site: phagocytes and neutrophils, collagenase 4.) Phagocytosis (macrophage) |
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