Patho Week 1 Cell death.txt

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Patho Week 1 Cell death.txt
2012-01-17 08:56:36
Patho Week Cell Death

Patho Week 1 Cell Death
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  1. Is necrosis pathological or physiological? What
    about apoptosis?
    • Necrosis is pathological and apoptosis can be
    • both
  2. Define hypoglycemia, what is it, why is is so critical and what part of the body is most affected?
    Hypoglylcemia is low blood glucose (sugar), it is important because cells need glucose for blycolysis (production of ATP). The brain is most affected.
  3. Is glycolysis aerobic or anaerobic? Is this where most of the ATP is stored?
    Blycolysis is anaerobic. Most of the glycolysis is made/stored through aerobic means. Goycolysis requieres two molecules of ATP and only produces 4.
  4. What is the most common cause of hypoglycemia?
    Diabetes. Note, the role of insulin is to lower blood glucose levels, so if a diabetic takes too much insuline, or does not eat after taking insulin it may result in hypoglycemia.
  5. What is the most common cause of impaired energy production at the cellular level?
  6. What is the differences between hypoxia and hypoxemia?
    Hypoxia is low oxygen levels in the Tissue, Hypoxemia is low oxygen levels in the Blood.
  7. Hypoxia involves decreased O2 delivery to the ______________ whtere ATP is produced.
  8. List four causes of hypoxia.
    • 1. Respiratory obstruction or disease
    • 2. Ischemia
    • 3. Anemia
    • 4. Alteration of Hemoglobin (hemoglobinopathies)
  9. What is the earliest clinical signs of hypoxia and hyperglycemia?
    The earliest clinical signs are distubances of the normal level of consciousness. This happens becaue failure of energy production will first affect cells with the highest demand for oxygen beause of their high basal metabolic rate which makes brain cells maximally affected.
  10. Hypoxia and hypoglycemia lead to decreased energy production. how does this lead to cell swelling/rupture?
    When ATP is not available, the Na+ pumps cannot function. This means the sodium is left inside the cell with the calcium, and since water follows sodium, the cells swells and ruptures. This also leaves elevated potassium in the ECF.
  11. How does decreased energy production affect organelles?
    When the cell swells, the endoplasmic reticulum sweels as well, this causes detachment of ribosomes that hang on to the rough ER. Since protein synthesis happens in the ribosomes, when they pop off protein sysnthesis stops. When protein synthesis stops it causes lipid buildup in the cell an dthe cell stops functioning.
  12. Describe the effectss of decreased energy production on a cell's ability to continue aerobic metabolism. What is the bi-product of the metabolism switch?
    Aerobic metabolism requires oxygen, thereofre when there is not enough oxygen our cells switch to anaerobic metabolism (glycolysis). Since the cells need glycogen for glycolysis our glycogen levels quickly decrease and the bi-product of glycolysis is lactic acid. when lactic acid builds up, the intracellular pH goes down, making the cell more acidic.
  13. What are the effects on a cell due to lowering of pH within the cell?
    When the pH lowers, it causes Pyknosis (nuclear chromatic clumping) which leads to Karyorrhexis (nuclear clumping fragments/ruptures). Karyolysis then occurs (auto-digestion of cell contents). A low pH also causes lysomomes to be lyse, which releases lysosomal enzymes (hydrolases) which promote cellular auto-digestion.
  14. What are lysosomes?
    Lysosomes are cellular organelles that contain acid hydrolase enzymes used to break down waste and cellular debris.
  15. What is another name for Free Radical?
    ROS: Reactive Oxygen Species
  16. What do ROS have in their outer shell that makes them so dangerous?
    Odd number of electrons
  17. Why are oxygen-based ROS most dangerous?
    They disrupt to the structure of the cell membrane by interacting with the lipids in the membrane
  18. When a cell ruptures, ________stored in the ER can enter the cytoplasm of another cell. This release in free radical ________ can lead ot activation of enzymes leading to cell auto-digestion.
  19. What are the effects of cell membrane damage?
    The effects of cell/plasma membrane damage are loss os structural integrity and loss of function.
  20. How does Clostridium perfringens damage cell membranes? Why does it do this?
    Clostridium perfringens, the causative agent of Gas Gangrene, uses lipase-like enzyems to damage cell membranes, it does this to get deeper into the tissue.
  21. How do cytopathic viruses damage cell membranes? What are two viruses that do this?
    Cytopathic viruses damage cell membanes by direct insertion into the cell membrane. As the virus leaves it forms a bud that tears off and causes cell membrane damage. Both HIV and Hep B do this.
  22. Is HPV a genetic or acquired genetic alteratkon? What does it do to a cell?
    HPV is an acquired genetic alteration, it alters the DNA which promotes cancer growth in the cervix.
  23. List four effects of genetic altreations.
    - abnormalities in: structural proteins, enzymes, mitosis, or regulator proteins
  24. What are txi agents that come into our body from the outside called?
    Exogenous toxic agents
  25. Describe four causes of fatty liver.
    • 1. Increased mobilization of fatty acids: If breakdown occurs too fast, such as starvation or diabetes mellitus, there is an accumluation of fat in the liver.
    • 2. Increased conversion of faty acids to lipids: This happnes with chronic alcohol abuse because alcohol is a hepatic enzyme inducer which converts fatty acids to lipids
    • 3. Decreased oxygenation: hypoxia/krebs gets backed up du to decreased ATP production, therefore things like cholesterol, triglycerides, and pholpholipids get accumulated.
    • 4. Decreased synthesis of lipoproteins: a sick liver can't make proteins, so there isnothing for lipids to bind with. Therefore, you get a backup of lipids because of the lack of protein.
  26. Describe the two types of fatty liver.
    • 1. Acute: sudden and severe. Ex: poisoning with carbon tetrachloride
    • 2. Chronic: slowly progresses, such as in alcoholism
  27. What is bilirubin?
    The breakdown product of RBCs
  28. List three causes of Hyperbilirubinemia.
    • 1. Hemolytic jaundice
    • 2. Hepatocellular jaundice
    • 3. Obstructive jaundice
  29. Descibe Hemolytic Jaundice.
    Increased RBC desctruction; the increased RBC destruction ovewhlems the liver so it cannot conjugate it all, since teh bilirubin is bound to albumin in the blood, it stays in the blood stream instead of bein excreted from the body. Pathologic would be sickle cell - Physiologic would be a new born baby who was born with an excessive amount of RBCs
  30. Describe Hepatocellular Jaundice.
    When the liver is sick there is a decreased uptake, conjugation or excretion of bilirubin, the bilirubin will build up in the liver.
  31. Describe Obstructive Jaundice
    Biliary tract obstruction of the flow of bilirubin, perhaps due to a stone.
  32. W
  33. What is the term used to describe the condition when bilirubin corsses the bloodbrain barrier and causes disease?
  34. What does bilirubin nomally bind with? Why is this an issue for babies?
    Normally, bilirubin binds with albumin. This can be an issue for babies because they have immature livers that are not able to produce enough albumin.
  35. What is the disorder called when too much bilirubin collects in an infants brain? What part of the brain does it collect in?
    Kernicterus. Basil ganglia
  36. Describe the three morphologic/biochemical changes of a nucleus due to cell necrosis.
    • 1st stage is Pyknosis where the chromatic (nucleic acid and proteins) clump
    • 2nd stage is Karyorrhexis where the clumps fragment/ruptue
    • 3rd stage is Karyolysis where the fragments are digested
  37. Describe Coagulative Necrosis.
    The cell retains some fo its shape, but the insdie of the cell looks like a scrambled egg. An example of this is gangrene.
  38. Describe Dry Gangrene.
    Dry gangrene usually occurs on an extremity, the necrotic area appears black, dry and mummified.
  39. Describe Wet Gangrene.
    Wet Gangrene resuts from evere bacterial infection superimposed on necrosis. Wet gangrene can be internal or external, it is very smelly and appears red.
  40. Describe Gas Gangrene.
    Gas Gangrene is Wet gangrene that has gas bubbles (with crepitus), usually caused by Clostridium perfringens.
  41. What is the surgical removal of dead tissue called that is frequently used for treatment of dry gangrene?
  42. What is Crepitus and when might a nurse encounter it?
    Crepitus is a crackling sound or feeling. We can encounter this under the skin with gas gangrene, in the lungs when gas and liquid mix, or in the joints due to joint wear.
  43. What type of necrosis makes tissue look like blue cheese and is commin TB patients?
    Caseous necrosis
  44. What type of necrosis has cell contents that get mushy and lyse and when do we see it?
    Liquefactive necrosis, we see it in the brain with stroke patients becuase of ischemia
  45. Provide an example of physiological cellular apoptosis.
    We develop as a fetus with webbed feet, at a particular point the webbing is removed by apoptosis.
  46. Give an example of pathological apoptosis.
    In HIV, infected CD4 cells can signal other non-infected CD4 cells to undergo apoptosis.
  47. Where are labile cells found and can the regenerate?
    Labile cells are found in the skin, GI system and the lining of our lungs. Yes, the regenerate often.
  48. Where are permanent cells found and what is their regenerating capability?
    Permanent cells are found in the brain and they cannot regenerate.
  49. Where are stable cells found and can they regenerate?
    Stable cells are found in the liver and yes, they can regenrate but at a slow pace.
  50. What is atrophy?
    Cell shrinkage and weakening. The cell becomes smaller.
  51. List four causes of cellular atrophy.
    • 1. Disuse
    • 2. Loss of nutients to the cell
    • 3. Loss of trophic hormones
    • 4. Denervation
  52. Give an example of physiologic and pathologic hypertophy.
    • Physiologic: lifting weights - muscles get bigger but will return to their smaller size when you stop.
    • Pathologic: cells will not return to normal size, Ex: when we develop heart failure, the heart tries to overcompensate and the cells will get bigger and stay that way, plus they develop scar tissue instead of getting stronger.
  53. How does hyperplasia differ from hypertrophy?
    Hyperplasia is an increase in the number of cells, hypertrophy is an incresae in the size of a cell.
  54. Which type of cell cannot experience hyperplasia, why?
    Permanent cells cannot experience hyperplasia because they cannot reproduce.
  55. What is the difference between metaplasia and dysplasia?
    • Metaplasia is when normal cells of one type are replaced by norlal cells of another type.
    • Dysplasia is when normal cells of one type are replaced by precancerous cells of another type.
  56. What is the difference between rouch ER and smooth ER?
    • The Rough ER has the ribosomes on it which are responsible for protein synthesis.
    • The smooth ER is involved with the synthesis of steroids, lipids, morphine as well asregulates calcium levels and drug metabolism.
  57. What is an example of hypoxia by enzyme tampering?
    Cyanide poisoning
  58. What are the normal serum values for bilirubin; Total, Direct (conjugated) and Indirect (unconjugated)
    • Total: 0.2 - 1.5 mg/dl
    • Direct: 0.0 - 0.3 mg/dl
    • Indirect 0.2 - 0.8 mg/dl
  59. What type of bilirubin do we find in Bile? If there is an increase of this bilirubin what could be the problem?
    We find Direct (conjugated) bilirubin in bile because it has already been to the liver. If there was an excess in Direct bilirubin we might suspect a biliary obstruction.
  60. If the liver is not producing protein, whymight this affect a newborn with regards to bilirubin?
    Bilirubin adheres to proteins which make it a large molecule, if the vilirubin does not bind with protein it is very small and can cross the blood/brain barrier of a newborn causing Kernicterus.
  61. List three causes of decreased energy production.
    • 1. Hypoglycemia
    • 2. Hypoxia
    • 3. Enzyme Tampering
  62. What are three effects of decreased energy production?
    • 1. Intreacellular accumulation of water
    • 2. Changes in organelles
    • 3. Switch to anaerobic metabolism
  63. What are three causes for cell membrane damage?
    • 1. Production of ROS
    • 2. Activation of Compliment
    • 3. Lysis by enzymes
    • 4. Lysis by Virus
    • 5. Lysis by physical or chemical agents
  64. What are three causes of hyperbilirubinemia?
    • 1. Hemolytic
    • 2. Hepatocellular
    • 3. Obstructive
  65. An increase in amylase could indicate necrosis in what organ?
  66. An increase in troponin, MB isoenzyme, and AST-GOT would indicate cell necrosis in what organ?
  67. An increase in ALP, AST, ALT and GPT levels would indicate cell necrosis in what organ?
  68. An increase in GGT levels would indicated cell necrosis in what two areas?
    Liver or bile ducts