Path Intro Test 1

  1. What are some of the causes of plasma membrane pathology?
    • Lysis
    • Free radicals
    • Complement system
  2. What are some of the things that can cause lysis (disruption) of plasma membranes?
    • Enzymes
    • Detergents
    • Metals (mercury, lead, iron)
    • Chemotherapy
    • Acetaminophin (liver, kidney)
  3. What are the antioxidant defense mechanisms/H2O2 reducing enzymes most cells have? What are some dietary sources for antioxidants?
    • Cytosol and mitochondria: catalase, superoxide dismutase, glutathione peroxidase
    • Foods: beans (red, kidney, pinto), berries (blue-, rasp-, straw-, black-, cran-), russet potatoes, other fruits, vegetables
  4. What are the cell-type specific proteins found in intermediate filaments of a cell's cytoskeleton?
    • Keratin: epithelial cells
    • Vimentin: mesenchymal cells
    • Desmin: muscle cells
    • Glial acidic fibrillary protein: glial cells
    • Neurofilament: neural cells
  5. What protein is responsible for cell movement and is found in microfilaments?
  6. What cellular structure is responsible for processing proteins?
    Endoplasmic reticulum
  7. What cellular structure is involved in cell division and transport of vesicles?
  8. What are the three types of cytoskeleton pathologies? What diseases do these cause?
    • Abnormal RBC shape: sickle cell disease
    • Abnormal myosin in muscle cells: muscular dystrophy
    • Abnormal actin in brain cells: Alzheimer's disease
  9. What is the amount of cytoplasm in a highly differentiated cell such as liver or kidney cells? What is the amount in undifferentiated cells such as cancer cells, embryonic cells, and stem cells?
    • Very abundant
    • Scant (larger nuclei)
  10. What is the site of glycolysis for a cell? What else resides in this site?
    • Glycolysis (anaerobic respiration)
    • Many organelles/membrane bound structures
  11. What substance disrupts the cytochrome C oxidase step of oxidative phosphorylation causing decreased utilization of O2 and decreased ATP production?
    Cyanide (result in hypoxia WITHOUT hypoxemia) (decreased O2 utilization, paO2 in blood not affected)
  12. Explain what happens with hypoxia resulting in mitochondrial pathology.
    • Hypoxia causes decreased production of ATP and failure of the N-K pump.
    • N-K pump keeps intracellular K concentration inside cell higher than outside the cell, and extracellular Na concentration outside the cell higher than inside the cell. Na "tries" to get into the cell but the N-K pump prevents this.
    • If the pump fails, too much Na and water enter cell (flowing down the gradient), cellular edema ensues, dysfunction, and maybe lysis.
  13. What disease is caused by mitochondrial dysfunction?
    Parkinson's disease
  14. What are the intracellular granules, composed of RNA, active in protein synthesis? What are the functions of this structure?
    • Ribosomes
    • Free floating: produce proteins and enzymes needed for basic cell function
    • Attached to ER (RER): contain proteins to be excreted
  15. What are the main functions of the rough endoplasmic reticulum (RER)?
    • Receive amino acid chains from ribosome to complete protein synthesis, sends proteins to Golgi apparatus.
    • Calcium homeostasis
  16. What are the main functions of the smooth endoplasmic reticulum?
    • Produce enzymes for lipid and steroid synthesis.
    • Cytochrome P450 for break down of drugs.
  17. What condition is a result of chronic exposure to high glucose and fatty acids, which lead to endoplasmic reticulum stress in cells and ultimately pancreatic beta-cell failure?
    Type 2 diabetes
  18. What is the function of the Golgi apparatus?
    • Receives proteins from ER for excretion (glyco/lipoproteins are incorporated into inner cell membrane to form vesicles).
    • Vesicles fuse with outer cell membrane to release products.
  19. What cellular structures are membrane bound organelles rich in lytic enzymes, come from the Golgi apparatus, contain acid hydrolases which are activated in low pH, engulf particles in cytoplasm and destroy them, and dispose of particles by fusing with the plasma membrane?
  20. T-lymphocytes-->produce interleukins-->stimulate T-lymphocytes-->signals cell growth, is an example of what kind of stimulation?
    Autocrine: "self stimulation"
  21. G cells in the stomach produce gastrin-->stimulates chief cells in stomach-->signals cell growth, is an example of what kind of stimulation?
    Paracrine: "adjacent cells"
  22. Pancreatic β cells produce insulin-->carried in bloodstream-->acts on liver, muscle, fat cells, is an example of what kind of stimulation?
    Endocrine: via bloodstream
  23. What are the causes of cell injury (pathology)?
    • O2 deprivation (hypoxia/anoxia)
    • Toxin (harmful substance accumulating in body)
    • Microbes (bacteria, viruses, protozoans, etc)
    • Inflammation & immune reactions
    • Genetic & metabolic disorders
    • Nutritional imbalances (deficient/excess)
    • Physical agents
  24. What is the mechanism of cell injury? What does cell pathology depend on?
    • Loss of function, then cell death.
    • Depends on type of injury, duration/severity, and type of cell.
  25. What are the cellular systems vulnerable to injury?
    • Cell integrity: cell membrane
    • ATP production: mitochondria (primary source)
    • Protein synthesis: rough ER
    • Genetic integrity: nucleus
  26. What is a reversible cell injury? How can the damage be stopped?
    • Hypoxia (failure to produce adequate ATP, switches to anaerobic glycolysis, disruption of N-K pump, "cellular swelling").
    • If its not too late, restoring O2 can stop the damage.
  27. What are irreversible (not recoverable) cell injuries?
    • Membrane dysfunction: plasma membrane breaks (cytoplasmic enzymes AST and LDH released increasing concentration in blood which is clue to illness)
    • Disruption of nuclear function: clumping & fragmentation of chromatin, destruction by enzymes (nucleases)
    • Irreversible mitochondrial dysfunction: not enough energy for cell function (one cause is hypoxia)
  28. What is the most common cell injury, causing damage to tissues faster than hypoxia?
    Ischemia (deficient blood flow)- causes injury faster because wastes cannot be cleared
  29. What does the PaO2 reflect? What is "normal" and how is it measured?
    • Unbound O2 dissolved in arterial blood (O2 available to tissues)
    • Normal >95 mmHg
    • Measured by ABG
  30. What does O2 saturation show? What is "normal" and how is it measured?
    • Percentage of O2 bound to Hgb
    • Normal >95%
    • SpO2 measured by pulse oximetry
    • SaO2 measured with ABG (more invasive & expensive)
  31. What is the difference between hypoxia and hypoxemia?
    • Hypoxia: reduced availability of O2
    • Hypoxemia: low concentration of O2 in arterial blood
  32. What can cause hypoxemic hypoxia (O2 deficiency due to low paO2)?
    • Hypoventilation (respiratory arrest)
    • Shunts (rt-lt shunts in heart) or (vent/perf mismatch- Pulmonary Embolism)
    • High altitude (low partial pressure of Atm O2)
  33. What can cause anemic hypoxia (PaO2 nl, but total O2 decreased due to Hgb)?
    • Anemia: low O2 carrying capacity (few RBCs)
    • Carbon monoxide: CO displaces O2 on Hgb
  34. What is the cause of histotoxic hypoxia?
    Cyanide (inhibits Cyt C oxidase)
  35. What is the normal partial pressure of O2 at sea level in arterial blood (PaO2)?
    Between 75 and 100 mmHg
  36. What is the normal oxygen tension in venous blood at sea level (PvO2)?
    Between 30 and 40 mmHg
  37. What are the steps to ischemia-reperfusion injury?
    • Blood flow interrupted-->
    • Accumulation of anaerobic metabolites and free radicals-->
    • O2 available with reperfusion-->
    • Oxidative cell damage, cytokine and adhesion molecule synthesis and activation-->
    • Leukocyte-mediated tissue injury-->
    • Microcirculation "white" clots + release of free radicals and toxic substances-->
    • Increased vascular permeability (tissues swell)
  38. When O2 interacts with certain molecules causing oxidation, what is a result?
    Atoms/molecules with odd number of electrons ("free radicals")
  39. How do the odd electrons of free radicals cause cellular damage? How are they neutralized?
    • They interact with cell components and damage cell membranes or DNA.
    • Anti-oxidants react with free radicals to neutralize their effect.
  40. Name the five cellular adaptations and briefly describe them.
    • Atrophy: decreased size/growth of cell, tissue, organ (diminished function, not dead)
    • Hypertrophy: increase in the size of tissues/organs due to enlargement of individual cells
    • Hyperplasia: increase in size of tissues and organs due to increase in the number of cells
    • Metaplasia: reversible replacement of one differentiated cell type with another mature differentiated cell type (due to normal maturation process or abnormal stimulus)
    • Dysplasia: disorderly arrangement and layering of cells (nuclear atypia might become cancer)
  41. Where does pure hypertrophy occur exclusively?
    • Heart
    • Striated muscles
  42. How does pure hyperplasia typically occur?
    As a result of hormone stimulation.
  43. How can metaplasia due to abnormal stimulus recover (cell type reverts)? What can happen if cells can't recover?
    • If abnormal stimulus resolves cell type can recover.
    • If stimulus persists metaplasia can progress to dysplasia, then neoplasia and eventually cancer (smokers, reflux esophagitis).
  44. Is dysplasia reversible? What can happen if it is not reversed?
    • Yes if stimulus is stopped (however it usually progresses).
    • If it progresses it goes to neoplasia then cancer.
  45. Described as premature or unnatural death of organs and tissue; loss of membrane integrity.
  46. What are the forms in which necrosis take place? Describe them.
    • Coagulative (most common): tissue appears as solid mass, typically involves solid internal organs
    • Liquefactive: in an abscess or the brain
    • Fat: in adipose tissue as in areas of trauma
    • Caseous: typically seen in TB and some fungal infections (histoplasmosis)
    • Fibrinoid: necrosis of blood vessel walls
  47. Described as orderly, genetically programmed cell death which is necessary for normal form and function.
  48. How is apoptosis activated? Why is it important?
    • Activated by "suicide genes"
    • Important in formation of body parts, fingers/toes, intestine
  49. What are the pathological abnormalities associated with apoptosis?
    • Syndactyly, intestinal atresia
    • Chronic lymphocytic leukemia mutation of the proaptotic gene (too many WBCs)
Card Set
Path Intro Test 1