patho_exam1

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notton
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110912
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patho_exam1
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2011-10-25 00:22:28
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patho felver notton midterm1
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Study for Pathophysiology midterm 1 Fall 2011
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  1. Name 3 ways diabetic ketoacidosis cause hyperkalemia?
    • 1. A decrease of insulin, which normally pumps K+ from ECF into cells.
    • 2. Polyuria due to osmotic effect of glucose in the urine leads to volume depletion & oliguria.
    • 3. Oliguria decreases potassium excretion, which leads to hyperkalemia.
  2. What are mechanisms of chronic alcoholism that cause predisposal to hypomagnesmia?
    • 1. Poor dietary intake of Mg
    • 2. Decreased Mg absorption from GI tract
    • 3. Increased Mg excretion in urine due to (repeated) rising blood alcohol.
  3. Chronic oliguria due to renal failure causes plasma excesses of which electrolytes?
    • - Potassium
    • - Magnesium
    • *NOT calcium - vitamin D activation does not occur effectively, which leads to low plasma calcium.
  4. What are the most common fluid/electrolyte imbalances seen wtih oliguric renal failure?
    • - ECV excess
    • - hyperkalemia
    • - hypermagnesemia
    • - hyperphosphalemia
    • - hypocalcemia
  5. Describe what happens with excessive ADH production.
    • - Hyponatremia
    • - Sometimes hypevolemia
    • Why? ADH acts in the distal portion of the renal tubule and the collecting duct and causes the retention of water, but NOT solute. Hence, ADH activity effectively dilutes the blood (decreasing the concentrations of solutes such as sodium).
  6. What are hallmarks of chronic inflammation?
    With chronic inflammation, there is evidence of tissue repair & damage happening at the same time, so the inflammation persists (ie, cirrhosis).
  7. What determines whether necrosis is coagulative or liquefactive?
    The type of cells involved.
  8. What are the 4 types of necrosis, and what tissue does each affect?
    • 1. Coagulative (heart, kidney, most other tissues)
    • 2. Liquefactive (brain, areas of bacterial infection with pus)
    • 3. Fat (adipose tissue)
    • 4. Caseous (pulmonary)
  9. What are the 3 types of gangrene?
    • 1. Dry
    • 2. Wet
    • 3. Gaseous
  10. What is a major risk factor for hyperkalemia?
    • Chronic oliguric renal disease.
    • Note: Before giving extra potassium (ie, in IV solution), check that urine output is normal.
  11. What is steatosis?
    Abnormal retention of fatty substances within a cell.
  12. What are risk factors for hypermagnesemia?
    • - Near drowning (intake)
    • - Excessive use of antacids (ie, Milk of Magnesia)
    • - Chronic oliguric renal disease (excretion)
    • - Adrenal insufficiency (excretion)
  13. What is wound dehiscence?
    • A wound breaks open along surgical suture.
    • Risk factors are age, diabetes, obesity, poor knotting or grabbing of stitches, and trauma to the wound after surgery.
  14. What can be caused by effervescent antacids? Why?
    ECV excess. Many contain extremely high amounts of sodium, which leads to water retention.
  15. What's the difference between "infarction" and "ischemia"?
    • Infarction = tissue death (necrosis) that is caused by a local lack of oxygen due to obstruction of the tissue's blood supply.
    • Ischemia = restriction in blood supply, generally due to factors in the blood vessels, with resultant damage or dysfunction of tissue
  16. What are the phases of tissue healing?
    • Inflammation
    • Proliferation/reconstruction
    • Maturation/Remodeling
  17. What are the phases of inflammation? What happens in each?
    • Hemostatic phase: blood clotting occurs
    • Vascular phase: blood vessels dilate
    • Cellular phase: chemotaxis causes phagocytes move to area via margination and diapedesis; Phagocytic cells release cytokines that promote tissue healing.
  18. What causes the pain in inflammation?
    Bradykinins and pressure
  19. What causes the fever in inflammation?
    Cytokines circulate to the hypothalmus.
  20. What happens in regeneration?
    • Necrotic tissues are replaced by tissues of the same type.
    • Note: This restores tissue function, if the supporting framework has not been destroyed.
  21. Why does edema slow healing?
    It makes it harder for nourishment to reach cells.
  22. What do adhesion factors do?
    Allow WBCs to stick to the sides of the capillaries and small venules, which is necessary to enable them to squeeze through the vessel walls and enter tissue to fight microorganisms
  23. What are functions of macrophages?
    Macrophages secrete growth factors and cytokines that stimulate fibroblasts to produce collagen.
  24. What are functions of histamines?
    Cause vasodilation and increased vascular permeability.
  25. What are functions of neutrophils?
    Arrive first and clean up debris
  26. Excessive amounts of which hormone cause ECV excess?
    Aldosterone
  27. How does aldosterone work?
    Aldosterone causes reabsorption of sodium and water, and excretion of potassium at the distal convoluted tubules.
  28. What happens with fluid balance in diabetes insipidus?
    The kidneys are unable to conserve water, though they do retain sodium. This results in hypernatremia.
  29. An excess of what hormones would cause an ECV excess?
    Aldosterone, cortisol.
  30. What is the appropriate therapy for ECV excess? Why?
    Salt restriction. This will reduce the amount of serum sodium, and the reduced sodium concentration will allow water to be lost as well.
  31. An excess of which hormone will lead to hyponatremia? Why?
    ADH. ADH causes water to be retained by the kidneys, but NOT salt. More water is retained for a given volume of salt, leading to sodium dilution.
  32. What is the clinical reason for giving a D5W solution?
    Increase ECF volume. It's like giving water, but with enough solutes to not cause RBCs to lyse.
  33. What are symptoms of hypernatremia? What causes them?
    Lethargy, confusion. Too high sodium concentration in ECF causes water to leave cells, causing them to shrivel. In the CNS, this leads to "nonspecific signs of cerebral dysfunction".
  34. What hormone is released in response to surgery, and what effects can it have on the body?
    ADH. It can lead to hyponatremia (low serum sodium).
  35. What are clinical assessments for ECV deficit?
    • Sudden weight loss (unless 3rd space accumulation)
    • Postural BP decrease substantially with postural tachycardia
    • Prolonged capillary & small vein rill time
    • Flat neck veins when supine
    • Sunken fontanel (infants)
    • General dryness (mucous membranes, skin, eyes,
    • Dizziness/fainting
    • Oliguria
  36. What imbalance would be caused by adrenal insufficiency? What are signs/symptoms?
    ECV deficit from loss of sodium-containing fluid due to lack of cortisol/aldosterone.
  37. What are the general causes of hyponatremia? Give examples.
    • - Gain of relatively more water than salt. (Too much D5W, tap water enemas, too much water, irrigating with distilled water, excessive ADH (SIADH), NSAIDs)
    • - Loss of relatively more salt than water. (diuretic use; sweating/vomiting/diarrhea while replacing water but not electrolytes).
  38. What two things are important to give to someone with clinical dehydration?
    • Salt (to help hold water in the blood)
    • Water (to offset fluid deficit)
  39. What are general causes of hypernatremia? Give examples.
    • - Gain of relatively more salt than water. (Decreased thirst sensation in elderly; unable to swallow, unable to access water, tube feedings with more solute than water)
    • - Loss of relatively more water than salt. (diabetes insipidus due to insufficient ADH, diarrhea without fluid replacement, urine water excretion due to particulates in tube feedings).
  40. Is D5W isotonic, hypotonic, or hypotonic with sodium?
    Hypotonic without sodium
  41. What is the distribution of D5W IV solution?
    • 1/3 extracellular (1/3 of that vascular, 2/3 interstitial)
    • 2/3 intercellular
  42. What is the purpose of D5W solution?
    To get water into cells. It's a cell-friendly way to infuse the equivalent of "plain water".
  43. Ascending bilateral muscle weakness & flaccid paralysis are characteristic of what electrolyte imbalances?
    • - hypokalemia
    • - hyperkalemia
  44. What electrolyte imbalance would most likely be caused by a fistula?
    - Electrolyte deficit in serum
  45. What is the similarity between hypokalemia and hypomagensemia?
    They may both result from loss of gastrointestinal fluids.
  46. What electrolyte disorder is caused by impaired calcium absorption?
    Hypocalcemia.
  47. What condition would cause a higher risk for pathologic fractures associated with electrolyte imbalance?
    Hyperparathyroidism, which would pull lots of calcium from bones.
  48. What test would you use to check a chronic alcoholic for hypomagnesemia?
    Trousseau sign
  49. If a patient has chronic diarrhea and has already received 1000 mL .9% NaCl solution, what would you want to assess before giving him a new IV that contains 20 mEq KCl plus .9% NaCl?
    • Urine output.
    • You want to.make sure kidneys are working before giving ANY extra solute (KCl, Magnesium sulfate, etc.)
  50. If a patient has chronic diarrhea, what nutrients would you encourage them to get plenty of in their diet?
    • Potassium
    • Calcium
    • Magnesium
    • Note: This would necessitate a variety of foods.
  51. If a patient is severely hemorrhaging and is being given lots of replacement blood (9+ units), what electrolyte imbalances would they be at risk for? What are the symptoms?
    • - hypocalcemia (due to citrated blood)
    • - hypomagnesemia (due to citrated blood)
    • - hyperkalemia (K leaks out of stored blood cells into plasma)
    • Tests:
    • - Apply cardiac monitor
    • - Test Chvosktek sign
    • - Tell pt to watch for tingling in fingers/around mouth
  52. Too much insulin can cause which electrolyte imbalance? Why?
    • Hypokalemia.
    • Insulin causes K+ to move from plasma into cells.
    • Note: Alkalosis and Beta-andrenergic stimulation also moves K+ from plasma into cells.
  53. What causes edema in pregnancy?
    Venous congestion increases capillary hydrostatic pressure and causes increased movement of fluid into the tissues.
  54. What are some symptoms of ECV excess? What would you NOT expect to see?
    • Distended neck vein when upright (due to extra fluid)
    • Rapid weight gain (due to retention of extra fluid)
    • Edema (due to extra fluid leaking out)
    • Crackles/rails (due to fluid in lungs)
    • Dyspnea/Orthopnea (due to increased fluid volume making it hard to breathe)
    • Bulging fontanels (infants)
    • Note: You would not expect to see abnormal sodium levels. The concentration would be normal.
  55. What electrolyte disorder is caused by too much insulin (either from overdose or total parenteral nutrition)?
    Hypokalemia (low serum potassium), because insulin moves it into cells.
  56. What are some examples of magnesium-rich foods?
    • Dark/Brown Foods
    • Cocoa
    • Coffee
    • Dark green veggies
    • Legumes
    • Meat
    • Milk
    • Nuts
    • Whole-grains
  57. What are common symptoms of hypercalcemia? Try to name all 8.
    • Constipation
    • Lethargy
    • Muscle weakness
    • Fatigue
    • Nausea
    • Vomiting
    • Polyuria
    • Personality/mood changes
  58. 3 days of diarrhea puts you at risk for what electrolyte disorders?
    • Hypokalemia (acute or chronic: people with diarrhea excrete more potassium in feces)
    • ECV deficit (loss of sodium-containing fluid)
    • Hypernatremia (diarrhea WITHOUT fluid replacement = clinical dehydration)
    • Hyponatremia (diarrhea with water replacement but NO salt replacement)
    • Hypocalcemia (chronic diarrhea)
    • Hypomagnesemia (chronic diarrhea)
  59. What happens after somatic death?
    • 1. Algor mortis (body cools off to environmental temp)
    • 2. Livor mortis: Blood starts to pool & settle
    • 3. Rigor mortis starts (2-6 hrs after death)
    • 4. Putrefication (with the help of bacteria)
  60. Define "Poikilothermia"
    Where body temperature equals environmental temperature.
  61. Define "Postmortem autolysis"
    Tissue degradation after death.
  62. What are "capsases"?
    • Capsases are "executioner enzymes" in apoptosis.
    • Cells have "PROCASPASES" inside the cell. "Pro-" = inactive; "-ase" = enzyme. If a trigger happens, the procaspases become activated caspases.
  63. What are the 5 phases of bone healing?
    • 1. Hematoma formation
    • 2. Fibrocartilage formation
    • 3. Callus formation
    • 4. Ossification
    • 5. Consolidation and remodeling.

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