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63 Cards in this Set

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1. Describe the cellular adaptations occurring in atrophy, hypertrophy, hyperplasia, dysplasia, and metaplasia. Identify conditions under which each can occur
(pages 66-69)
Atrophy-is a decrease or shrinkage in cellular size. Example:decrease in workload, pressure, use, blood supply, nutrition, hormonal stimulation, and nervous stimulation.
Hypertrophy-is an increase in the size of cells and consequently in the size of the affected organ. Example: A pathologic example is pathophysiologic hypertrophy in the heart secondary to hypertension or problem valves.
Hyperplasia-is an increase in the number of cells resulting from an increased rate of cellular division. Example: Compensatory hyperplasia is an adaptive mechanism that enables certain organs to regenerate. i.e. liver regeneration after two weeks of 70% percent removal.
Dysplasia-refers to abnormal changes in the size, shape, and organization of mature cells. Example: “…are encountered in epithelial tissue of the cervix and respiratory tract, where they are strongly associated with common neoplastic growths and often are found adjacent to cancerous cells.
Metaplasia-is the reversible replacement of one mature cell type by another, sometimes less differentiated, cell type. Example: “The best example of metaplasia is replacement of normal columnar ciliated epithelial cells of the bronchial (airway) lining by stratified squamous epithelial cells.
2. Identify the mechanism of cellular injury from hypoxia
(page 70) “Hypoxia, or lack of sufficient oxygen, is the single most common cause of cellular injury…The most common cause of hypoxia is ischemia (reduced blood supply).”
3. Identify the major types of cellular necrosis and site examples of the tissues involved in each type
(page 90-92) Coagulative necrosis. Occurs primarily in the kidneys, heart, and adrenal glands; commonly results from hypoxia.
Liquefactive necrosis. Commonly results from ischemic injury to neurons and glial cells in the brain.
Caseous necrosis. Usually results from tuberculous pulmonary infection, especially by Mycobacterium tuberculosis.
Fat necrosis. Occurs in the breast, pancreas, and other abdominal structures.
Gangrenous necrosis. Refers to death of tissue and results from sever hypoxic injury, commonly occurring because of arteriosclerosis, or blockage, or major arteries, particularly those in the lower leg.
Gas gangrene. A special type of gangrene caused by infection of injured tissue by one of many species of Clostridium.
4. Define apoptosis
(page 92) Apoptosis (“dropping off”) is an important, distinct type of prelethal injury leading to cell death.
5. Characterize somatic death and its manifestations
(page 99) Rigor mortis-“detachment of myosin from actin” and muscle stiffening. Usually with 12 to 14 hours rigor mortis affects the entire body. (starts within 6 hours)
Algor mortis-Postmortem reduction of body temperature.
Livor mortis-Gravity causes blood to settle in the most dependent, or lowest, tissues, which develop a purple discoloration.
6. Describe the vascular effects of inflammation
(page 154) “First, arterioles near the site of injury constrict briefly. Then they dilate, which increases blood flow to the inflamed site, increases pressure in the microcirculation, and increases the exudation of plasma and blood cells into the tissues, leading to edema and swelling…The state of vascular permeability continues throughout acute inflammation, permitting blood cells and plasma proteins to move continuously into inflamed tissues. Once in the tissues, these cells and proteins (1) stimulate and control subsequent inflammatory processes and (2) interact with components of the immune response.”
7. Describe the effect of kinins and prostaglandins in a soft tissue injury/inflammatory process
(page 157&160) Induce pain, increase vascular permeability and induce smooth muscle contraction.
8. Identify 2 chemical mediators (inflammatory cytokines) responsible for induction of fever. Explain the process
(page 169) TNF-alpha; IL-1. They have a direct effect on the hypothalamus. “Systemically, TNF-alpha acts directly on the hypothalamus in the brain to induce fever…”
9. Describe the local manifestations of acute inflammation
(page 170) Heat, pain, swelling, redness.
10. Describe the purpose of exudates
(page 170) “(1)to dilute toxins produced by bacteria and toxic products released by dying cells; (2) to carry plasma proteins (including anti-body) and leukocytes (both phagocytes and lymphocytes) to the site; and (3) to carry away bacterial toxins, dead cells, debris and other products of inflammation.”
11. describe the different types of exudates and examples of conditions
(page 170-171) Serous exudates-“In early or milde inflammation the exudates is watery with very few plasma proteins or leukocytes, like fluid in a blister.”
Fibrinous exudates-“In more severe or advanced inflammation the exudates may be thick and clotted, as in the lungs of individuals with lobar pneumonia.
Purulent (suppurative exudates)- “If many leukocytes accumulate, as in persistent bacterial infections, the exudates consists of pus. Purulent exudates is characteristic of walled-off lesions (abscesses).”
Hemorrhagic exudates- “If bleeding occurs, the exudates is filled with erythrocytes.”
12. describe the differences between primary and secondary intention
(Page 173) Primary intention-Wounds that heal under conditions of minimal tissue loss are said to heal by primary intention.
Secondary intention-With an open wound, epithelialization, scar formation, and contraction take longer and healing occurs through secondary intention.
15. describe nutritional deficiencies that would impair healing
(page 176) “Most of the factors that interfere with the production of collage in healing tissues are nutritional. Scurvy, for example, is caused by lack of ascorbic acid-one of the cofactors required for collagen formation by fibroblasts.”
13. describe the difference in resolution and repair of injured tissue
(page 173)Resolution- Restoration of original structure and physiologic function is called resolution.
Repair-Is the replacement of destroyed tissue with scar tissue composed of collagen
14. define granulation tissue, and angiogenesis
(page 175)Granulation tissue-“In repair, granulation tissue grows inward from surrounding health connective tissue.”
(page 273) Angiogenesis-Development of new blood vessels.
16. differentiate between a keloid and hypertrophic scar
(page 176) “A keloid is a raised scar that extends beyond the original boundaries of the wound.”
“A hypertrophic scar is raised but remains within the original boundaries of the wound.”
17. define dehiscence and contracture and situations that would increase occurrence
(page 177) “A potential complication of wounds that are sutured closed is dehiscence, in which the wound pulls apart at the suture line.”
“Wound contraction, although necessary for healing, may become pathologic when contraction is excessive, resulting in a deformity or contracture.”
18. differentiate between symbiosis, mutualism, commensalism, and pathogenicity
(page 193 Box7-1) Symbiosis-benefits only the human; nor harm to the organism.
Mutualism-benefits the human and the organism.
Commensalism-benefits only the organism; no harm to the human.
Pathogenicity-benefits the organism; harms the human.
19. describe how pathogenic organisms defend themselves from the human immune response
(page 195) “For example, some bacteria produce capsules of carbohydrate or protein that are antiphagocytic, preventing efficient phagocytosis.”
20. define the term used to describe bacteria that produce endotoxin
(page 197) “Bacteria that produce endotoxins are called pyrogenic bacteria because they activate the inflammatory process and produce fever.”
21. differentiate between endotoxins and exotoxins
(page 197) “Endotoxins (lipopolysaccharides) are contained in the cell walls of gram-negative bacteria and are released during lysis, or destruction, of the bacteria.”
“Exotoxins are proteins released during bacterial growth.”
22. explain the pathophysiology of septicemia
(page 198) “Septicemia (bacteremia) is the presence of bacteria in the blood and is caused by a failure of the body’s defense mechanisms. The usual cause is proliferation of gram-negative bacteria, although a few gram-positive bacteria and fungi can cause it.”
23. what is the hallmark sign/symptom of most infectious diseases
(page 203) “However, the hallmark of most infectious diseases is fever.”
24. describe the process in which bacteria become resistant to antimicrobials. How can the risk of this happening be diminished.
(page 205) In my own words. Microbes mutate and adapt and become resistant to our antibiotics. Not completing your prescribed antibiotics is one variable.
25. Explain the GAS response (stress response). Explain which hormones are released (and from where) and how they effect (manifestations) the body
(page 222) “Three successive stages in development of the GAS were identified: (1) the alarm stage or reaction, in which the CNS is aroused and the body’s defenses are mobilized; (2) the stage of resistance or adaptation, during which mobilization contributes to “fight or flight”; and (3) the stage of exhaustion, in which continous stress causes the progressive breakdown of compensatory mechanisms (acquired adaptations) and homeostasis. The stage of exhaustion marks the onset of certain diseases (diseases of adaptation)
26. What is the purpose of B endorphin release during the GAS response
27. Exhaustion during GAS occurs if what important process does not?
(page 222) adaptation
28. Differentiate between acute and chronic pain (GAS?, Time line differences?)
(page 332-333) Acute less than six months.
Chronic greater than six months.
29. Give examples of somatic, visceral, referred pain
(page 332) “Somatic pain is superficial (coming from the skin or close to the surface of the body) and is either sharp and well localized or dull, aching, and poorly localized and accompanied by nausea and vomiting.”
“Visceral pain is pain in internal organs, the abdomen, or skeleton.”
“Referred pain is pain that is present in an area removed or distant from it point of origin. The area of referred pain is supplied by the same spinal segment as the actual site of pain. Impulses from many cutaneous and visceral neurons converge on the same ascending neuron, and the brain cannot distinguish between the two.”
30. Differentiate between pain tolerance and pain threshold
(page 334) “The pain threshold is the lowest intensity at which a stimulus is perceived as pain.”
“Pain tolerance is the amount of time or intensity of pain that an individual will endure before initiating overt pain responses.”
31. Give an example of neuropathic pain
(page 334) “Neropathic pain results from abnormal processing of sensory information by the peripheral and central nervous systems. Examples: phantom pain or reflex sympathetic dystrophy.”
32. What skin condition must be present for evaporation to function effectively
(page 336 Table 13-5) “ Body water evaporates from surface of skin and linings of mucous membranes; major source of heat reduction connected with increased sweating in warmer surroundings”
33. What will the release of epinephrine do to body temperature
(page 336 Table 13-5) “Epinephrine is released and produces rapid, transient increase in heat production by raising basal metabolic rate; quick, brief effect that counters heat lost through conduction and convection; involves brown adipose tissue, which decreases markedly in older adults.”
34. Describe the process of fever development
(page 337) “Exogenous pyrogens, or endotoxins, stimulate the release of fubstances such as tumor necrosis factor-alpha (TNF-alpha), interleukin-1 (IL-1), interleukin-6 (IL-6), and interferon (IF), which raise the set point by inducing the synthesis of prostaglandins. In response, the hypothalamus signals an increase in heat production and conservation to raise body temperature to the new level.”
***try saying that ten times fast***
35. What group of microbes are implicated in fever production
(page 337) “Exogenous pyrogens”
36. Explain the reasons why infants and elderly have problem managing temperature regulation and fluid regulation
(page 337) “Infants produce sufficient body heat but cannot conserve heat produced because of their small body size and greater ratio of body surface to body weight. Infants also have little subcutaneous fat and thus are not as well insulated as adults. Elderly persons respond poorly to environmental temperature extremes because of their slowed blood circulation, structural and functional skin changes, and overall decreased heat-producing activities. In addition, they have a decreased shivering response (delayed onset and decreased effectiveness), slowed metabolic rate, decreased vasoconstrictor response, diminished or absent sweating, decreased peripheral sensation, desynchronized circadian rhythm, decreased perception of heat and cold, decreased thirst, under nutrition, and decreased brown adipose tissue.
37. Differentiate between heat exhaustion and heat stroke.
(page 338) “Heat exhaustion-results from prolonged high core or environmental temperatures, which cause profound vasodilation and profuse sweating, leading to dehydration, decreased plasma volumes, hypotension, decreased cardiac output, and tachycardia. Symptoms include weakness, dizziness, confusion, nausea, and fainting.”
“Heat stroke-potentially lethal result of overstressed thermoregulatory center. With very high core temperatures (>40celcius), the regulatory center ceases to function and the body’s heat loss mechanisms fail. Symptoms include cerebral edema, degeneration of the CNS, swollen dendrites, renal tubular necrosis, and eventually death if treatment is not undertaken.”
38. Which age group is increased risk for febrile seizures
(page 338 Box 13-2) Children “Febrile seizures before age 5 years are not uncommon.”
39. Why is heat stroke so dangerous (life threatening)
(page 338) “Heat stroke-potentially lethal result of overstressed thermoregulatory center. With very high core temperatures (>40celcius), the regulatory center ceases to function and the body’s heat loss mechanisms fail. Symptoms include cerebral edema, degeneration of the CNS, swollen dendrites, renal tubular necrosis, and eventually death if treatment is not undertaken.”
40. What disease/condition(s) would effect oncotic pressure in the capillaries
(pages 107&108) “CHF and renal failure are associated with salt and water retention, which cause plasma volume overload and edema.” “Lost or diminished plasma albumin production (liver disease or protein malnutrition) contributes to decreased plasma oncotic pressure.”
41. Which electrolyte is closely related to water balance? Why?
(page 109) “Because water follows the osmotic gradients established by changes in salt concentration, sodium and water balance are intimately related.”
42. Describe the etiology (causes) and manifestations of each acid base imbalance
(pages 122-124) Metabolic acidosis-DKA; chronic renal failure. HA, lethargy, kussmaul respirations.
Metabolic alkalosis-primarily excess of bicarbonate in ECF. GI losses
Respiratory acidosis-primary excess of carbonic acid in ECF. Aspirin; vital sign center, drug toxicity, ventilator, increase ICP.
Respiratory alkalosis-primary deficit of carbonic acid in ECF. Increased respirations.
43. Explain why plasma proteins are not usually found in the urine and if found what it probably indicates
Normally not able to be filtered due to their size. Probably kidney problems. (PAGE # ???)
44. What condition is commonly associated with both hyperkalemia and metabolic acidosis
(pages 118&122) Renal failure
45. How does the body try to compensate (acute) metabolic acidosis
(page 122) “Hyperactive breathing to “blow off” CO2…Kidneys conserve HCO3 and eliminate H+ ions in acidic urine.”
46. What does the GFR tell us about kidney health, and perfusion pressure in the glomerular capillaries
(page 823) “The glomerular filtration rate (GFR) is the filtration of plasma per unit of time and is directly related to the perfusion pressure of renal blood flow.”
47. Explain the rennin angiotensin system pathway. In what situations would it be initiated (what is trigger)
(page 110 also 814) “When circulating blood volume is reduced, rennin, an enzyme secreted by the juxtaglomerular cells of the kidney, is released. Renin stimulates the formation of angiotensin 1, an inactive polypeptide, which is then converted into angiotensin 2 by angiotensin-converting enzyme (ACE) located in the lung, which stimulates the secretion of aldoserone and also causes vasoconstriction.”
48. Signs and symptoms of renal calculus obstruction
(page 828) “Renal colic, described as moderate to sever pain often originating in the flank and radiating to the groin, usually indicates obstruction of the renal pelvis or proximal ureter.”
49. Most common organism responsible for UTI’s (why??)
(page 832) “Most UTI’s are caused by gram-negative bacteria commonly found in the intestinal tract. Escherichia coli accounts for about 80% of all uncomplicated infections.”
50. Signs and symptoms of pyelonephritis
(page 834 Table 29-3) “Pyelonephritis is an infection of the renal pelvis and interstitium…The onset of symptoms is usually acute, with fever, chills, flank or groin pain, frequency, dysuria, and costovertebral tenderness. Children and older adults may have nonspecific symptoms, such as fever and malaise.”
51. Pathophysiology of acute poststreptococcal glomerulonephritis
(page 836-837) “Acute glomerulonephritis often is associated with a streptococcal infection. The disease begins abruptly and usually occurs 7 to 10 days after a streptococcal infection of the throat or skin, commonly in children…The streptococcal antigen carries a positive charge that deposits in the negatively charged glomerular basement membrane.” ***More there to read in book***
52. Lab values that reflect renal failure
(page 840) “elevated creatinine levels”
53. Signs and symptoms of renal failure
(page 842; 841 for acute) “The clinical manifestations of chronic renal failure are often described using the term uremia. Uremia refers to a number of symptoms caused by decline in renal function with the accumulation of toxins in the plasma. Generally the symptoms include hypertension, anorexia, nausea, vomiting, diarrhea, weight loss, pruritus, edema, anemia, and neurologic changes.” ***TABLE 29-11***
54. Why are pathological fractures and anemia probable problems in renal failure
(page 843-844; TABLE 29-11) “Bone resorption associated with hyperparathyroidism, vitamin D deficiency, and demineralization; lowered calcium and raised phosphate levels.”
“Reduced erythropoietin secretion associated with loss of renal mass, leading to reduced red cell production in the bone marrow; uremic toxins associated with shortened red cell survival.”
55. Reason for pruritus in ESRD
(page 844; TABLE 29-11) “Retention of urochromes contributing to sallow, yellow color, high plasma calcium levels and neuropathy associated with pruritus”
56. List dietary restrictions/fluid considerations in a pt in renal failure
(page 842) “Management involves dietary control, including protein restriction, sodium and fluid evaluation, potassium restriction, adequate caloric intake, and erythropoietin as needed.” ***More there to read in book***
57. What causes lymphedema
(page 108) “The lymphatic system normally absorbs interstitial fluid and a small amount of proteins. When lymphatic channels are blocked or surgically removed, proteins and fluid accumulate in the interstitial space causing lymphedema.”
58. Causes of edema
(pages 107-109) “Edema is the accumulation of fluid within the interstitial spaces. The forces favoring fluid movement from the capillaries or lymphatic channels into the tissues are increased hydrostatic pressure, lowered plasma oncotic pressure, increased capillary membrane permeability, and lymphatic channel obstruction.” “CHF, renal failure, liver disease or protein malnutrition (diminished plasma albumin production), trauma, lymphedema.”
59. Type of fluid/electrolyte imbalance in a patient with SIADH
(page 114) “water excess”
60. Identify the role of ADH, aldosterone and natriuretic hormone in water and electrolyte imbalance
(pages 109-111) “Water balance is regulated by the secretion of ADH and the perception of thirst…ADH is secreted when plasma osmolality increases or circulating blood volume decreases and blood pressure drops.”
“Hormonal regulation of sodium balance is mediated by aldosterone, a mineralocorticoid synthesized and secreted from the adrenal cortex. Aldosterone increases the reabsorption of sodium and the secretion of potassium by the distal tubule of the kidney. As a result, sodium concentration of the ECF is enhanced, and potassium is excreted with the urine.”
“Natriuretic hormones (peptides) promote urinary excretion of sodium and water and decrease blood pressure. Atrial natriuretic peptide is produced by the atrial muscle of the heart and functions in renal elimination of sodium to control sodium and water balance. Naturiuretic hormone is sometimes called the “third factor” in sodium regulation, after increased glomerular filtration rate and aldosterone. Its effect is apparent when there is prolonged aldosterone elevation from chronic retention of fluid or excessive secretion from an adrenal tumor. The sodium-retaining action of aldosterone is overcome by the action of natriuretic hormone, and salt is excreted, followed by a water diuresis.”
61. What organ is especially at risk of dysfunction in the event of potassium imbalance
(page 118) “Hyperkalemia causes decreased cardiac conduction and more rapid repolarization of heart muscle.”
62. Define and identify the common etiologies for prerenal, intrarenal and postrenal disease
(pages840-841)“Prerenal-is the most common cause of ARF (acute renal failure) and is caused by impaired renal blood flow.”
“Intrarenal acute renal failure usually results from acute tubular necrosis (ATN). ATN caused by ischemia occurs most often after surgery but is also associated with sepsis, obstetric complications, or severe burns.”
“Post acute renal failure usually occurs with urinary tract obstruction that affects the kidneys bilaterally (e.g., bladder outlet obstruction, prostatic hypertrophy, bilateral ureteral obstruction.)
63. Describe chronic renal failure, identify the systemic manifestations of uremia
(page 842) “Progressive and irreversible loss of nephrons (chronic renal failure) decreases GFR and affects these vital processes with changes manifest throughout all organ systems…The clinical manifestations of chronic renal failure are often described using the term uremia. Uremia refers to a number of symptoms caused by decline in renal function with the accumulation of toxins in the plasma. Generally, the symptoms include hypertension, anorexia, nausea, vomiting, diarrhea, weight loss, pruritus, edema, anemia, and neurologic changes.”