Patho Exam 2

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Patho Exam 2
2011-03-08 00:04:52

patho exam 2
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  1. Hyponatremia
    too little Na+
  2. Causes of edema (4 main)
    • 1. increase hypostatic pressure
    • 2. decrease capillary osmotic
    • 3. increased interstitial osmotic pressure
    • 4. decreased protein in the plasma
  3. What can hypokalemia cause?
    muscle problems=heart problems
  4. What is the major problem with decreased Mg?
    decreased Mg leads to decreased K. Must fix decreased Mg first or K will never fix
  5. what does increased CO2 lead to?
    decreased pH of blood
  6. How does the body get rid of acid?
    Acid is turned into H2CO3 (bicarb) and converted into C02. C02 is only let out thru lungs.
  7. What happens with untreated type 1 diabetes?
    ketoacidosis. The body produces more acid. Not necessarily acidemia but a change in the pH of blood...which is very bad
  8. skeletal muscles in GI
    Sphincters in upper GI.
  9. Agenesis
    didn't happen. Just didn't grow an arm
  10. Aplasia
    started but then stopped before done. Arm stopped growing at elbow
  11. Atrophy
    Reaches fully developed but then shrinks.
  12. hypertrophy
    increase in cell size
  13. hyperplasia
    increase in cell number.Normally occurs in breast and calluses
  14. Metaplasia
    cells begin to change and act like other cells
  15. Neoplasia
    New cell growth. Can be CA but maybe not. describes as abnormal cell growth or tumors.
  16. tumors
    growths, lumps, or swelling. sign of inflammation. don't have to be cancerous, and cancer doesn't have to have tumors
  17. What is cancer
    abnormal, unregulated cell growth
  18. What do cancers arise from? in most cases
    breakdown in control of cellular growth.
  19. Benign
    not necessarily dangerous. used more in the predicted outcome. don't spread to different areas. inclosed.
  20. carcinoma
    cancer in epithilioid cells
  21. sarcoma
    cancer in cell from supporting tissues. muscles, bone and other connective tissue
  22. most (90%) of cancers are...
    carcinomas- epithelial cells constantly have to be replaced, makes it much easier for CA
  23. Malignant cancer
    have a much higher tendency to spread.
  24. Metastasize
    move to a secondary location and cause tumors to grow
  25. good thing about primary tumor
    keeps secondary tumors from growing. if cut out may cause a bunch of other tumors to suddenly pop up
  26. if primary tumor in leg, secondary goes where
  27. if primary in lymph where secondary
  28. primary in GI secondary where
  29. carinogenesis
    development of CA. Has to do with cellular replication
  30. proto-oncogene
    normal gene that might become cancer. very good at telling cells to grow.
  31. tumor suppressor gene
    keeps cells from growing too much
  32. oncogenes
    protooncogenes gone bad. something damaged the gene.
  33. oncogenes occur from 4 main mechanisms
    • 1. point mutations
    • 2. gene amplification (too many genes being produced)
    • 3. chromosomal rearrangements (chunks of chromos getting stuck together)-might be CA or fetal death
    • 4. insertion of viral genomes
  34. Rb
    tumor suppressor gene. codes for a protein which soaks up transcription factors. keeps transcription from happening too much
  35. p53
    tumor suppressor gene. very common gene defect in CA normally inhibits cells from going through cell cycle
  36. BRCA1 and BRCA2
    breast CA. women with one or both have much higher probability of breast and ovarian CA
  37. DNA repair genes
    making millions of copies each day. fix errors, when there is a problem with these genes the errors never get fixed.
  38. best thing about CA
    cancer cells look different than other cells makes it easier to detect
  39. Type 1 hypersensitivity
    way too much. doesnt just go to place needed goes to whole body.
  40. IgE
    antibodies involved in most allergic reactions. binds to antigen and stimulates others to come
  41. urticaria
  42. asthma
    comes and goes
  43. deep breathing by asthmatics causes what over time
    hyperinflated chest
  44. possible that what is impaired in asthmatics
    B-adrenergic innervation of bronchioles. (receptors in flight/fight response) this is why b-agonist are helpful in some pt.
  45. asthma tx
    • 1. b-agonist inhalants
    • 2. drugs that prevent mast cells from releasing histamine
    • 3. blockers of acetylcholine receptors
    • 4. leukotriene
  46. atopic
    person has a type I response (lotsa IgE) and has symptoms in other areas of the body
  47. serum sickness
    illness due to circulation immune complexes. occurs when lotsa ag introduced. ab sticks to and deposits somewhere (kidneys, blood vessel walls, etc.)
  48. Main targets of HIV
    CD4 cell (t helper cell), makes immune response not very helpful cells appear to commit suicide when infected with HIV. therefore no immune system
  49. when is HIV AIDS?
    • 1. when CD4 cells are lower than 200
    • 2. or presence of indicator condition (TB, invasive cervial CA, pneumonia (recurrent), or kaposi sarcoma)
  50. Macrocytic, normochromic
    large RBC's cells supposed to divide and don't still norm Hgb
  51. microcytic, hypochromic
    small cells with less color (decreased hgb)
  52. increased RBC loss
    • 1. bleeding
    • 2. hemolysis (something causes RBC to die too fast)
    • 3. Malaria (infection of RBC's causes them to be cleared by spleen)
  53. lack of production of RBC
    • 1. leukemias
    • 2. lymphomas
    • 3. multiple myelomas
    • 4. chemicals
    • 5. radiation
  54. aplastic anemia
    stem cells don't work properly not producing enough RBC's
  55. polycythemia
    too many RBC's, increases blood volume and viscosity. fix by drinking.
  56. Lymphomas
    lymph cells in the periphery. reproducing away from the bone marrow.
  57. two classifications of leukemia
    • 1. lymphocytic- malignant transformation of stem cell
    • 2. myelocytic- malignant tranformation of granulocyte cell
  58. two types of lymphomas
    • 1. hodgkin's just know what it's going to do next
    • 2. non-hodgkins unpredictable..everything else
  59. Renal control of acid-base balance
    kidneys can get rid of any acid except carbonic. bicarb goes into urine and h follows. bicarb reabsorbed into blood leaving h to pee. getting rid of acid
  60. metabolic acidosis
    too much HCO3
  61. respiratory acidosis
    too much CO2
  62. metabolic alkalosis
    too little HCO3
  63. respiratory alkalosis
    too little CO2
  64. what happens with metabolic acidosis
    ABG show low bicarb, hyperventilation will try to compensate
  65. what happens with respiratory acidosis
    too much carbonic acid, ABG will have too much CO2 (lungs not doing very good job), compensation via renal excretion of acid
  66. what happens with metabolic alkalosis
    loss of lots of non-carbonic acid (could be an increase in bicarb or decrease in non-carbonic acid or both; also maybe too much bicarb ingestion i.e. antacids (rolaids--mag), also loss of stomach acid-vomiting); plasma bicarb is increased, hypoventalation will try to compensate, ABG increase CO2 concentration PaCO2
  67. what happens with respiratory alkalosis
    from hyperventilation PaCO2 will be very low. reduction of bicarb will compensate
  68. what is amazing thing about esophagus
    relaxation and contraction at same time. just knows what to do.
  69. dysphagia
    difficulty swallowing
  70. pyrosis
  71. achalasia
    weak and uncoordinated contraction in builds up in lower esophagus
  72. diffuse esophageal spasm
    contractions good but not coordinated. antacids may help sometimes surgery
  73. esophagitis
    many times due to acid coming up from esophagus
  74. chronic esophagitis
    reflux disease. over long period causes Barrett's esophagus (metaplasia-looks like skin)
  75. gastrin
    hormone produced by g-cells (stomach, pancreas and duodenum)
  76. enteric plexus
    tells alkaline to come (secretin) when detects acid in the intestine
  77. CCK
    chole (bile-from cholesterol), cysto (bladder) kinin (activator). causes pancreas to release digestive enzymes and tells nervous system full (satiety sense)
  78. peptic ulcer disease-gastric location
    20% of all ulcers. weakening of mucosal barrier. from aspirin, ETOH, bacteria, other. tx: coating meds or surgery
  79. peptic ulcer disease- duodenal location
    80% of all peptic ulcers. increased HCl and pepsins
  80. why ulcers bad
    risk of hemorrhage, gastric carcinoma increases.
  81. celiac disease
    a gluten in wheat causes autoimmune responce in mucosa of the sm intestine. only tx is to eliminate gluten from diet
  82. peritonitis
    inflammation of abdominal lining
  83. most cancers in whole GI tract is where?
    lower GI- colon and rectum
  84. two flavors of ulcerative colitis
    • 1. nonspecific ulcerative colitis: involves the whole colon, inflames then goes away then comes back later
    • 2. crohn's disease: inflam the entire thickness of the bowel wall appears in discrete places but can be anywhere from mouth to anus
  85. risk factors of large bowel CA
    colitis, polyps, low fiber, and other things we don't know about
  86. conjugation of bilirubin occurs where and why?
    liver cells and so bilirubin is soluble in water allows it to be excreted in bile
  87. unconjugated bilirubin why bad
    not soluble in water means liver cells not working. bili in blood gets big (jaundice, sickle cell, meds)
  88. hyperbilirubinemia
    excess conjugated bilirubin not secreted in bile, (hep, cirrhosis, gallbladder problems