PathSem3

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Author:
pandachowmein
ID:
155286
Filename:
PathSem3
Updated:
2012-05-22 17:55:59
Tags:
Pathology
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Description:
Path LO
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  1. four aspects of disease
    • eitology (cause)
    • pathogenisis (mechanism of disease)
    • molecular/morphologic change (mechanical and visual tests)
    • functional consequence (clinical)
  2. 8 causes of cellular injury
    • Oxygen depreivation (everyone needs O2)
    • Chemical (bad things getting you)
    • Physical
    • Infectious
    • Immune (you getting yourself)
    • Genetic
    • Aging
    • Nutritional imbalance (either too much or too little)
  3. Cellular adaptation
    • hypertrophy
    • hyperplasia
    • atrophy
    • metaplasia
    • Boxcar nuclei
    • large and more dense nucleus means increased need for protein production
    • blue is bad = hypertrophy or cancer
  4. Physiological vs pathological hypertrophy
    • Physio --> pregers, subceullar hypertrophy in response to barbituates and alcohol,
    • Patho--> Left ventricular hypertrophy (responds to growth factors, agonists and mechanical stretch)
  5. Physio and patho hyperplasia
    • Physio --> liver regrowth in response to damage
    • Patho --> BPH, Post menapausal endometrial hyperplasiam, cancer
  6. Physio vs path atrophy
    • Physio --> embroynic development , uterus after parturition
    • Patho --> decreases in workload, innervation, blood supply, nutrition, stimulation and increases in pressur
  7. Cachexia
    • patho atrophy--> due to chronic inflammatory cytokine and TNF production's supression of appetite
    • Cancer wasting
  8. muscle atrophy due to disuse
  9. Metaplasia
    • No physiological
    • Pathological due to external stimulus cytokines, growth factors, extracellular matric components
    • squamous cell metaplasia in response to smoking/stimuli in respiratory tract
    • may lead to neoplasia = cancer
    • squamous to columnar metaplasia
    • barretts esophagus
  10. Reversible cell injury morphological change
    Swelling and fatty change
  11. Morphology of cell swelling
    • Plasma membrane - blebbing -blunting -loss of microvilli
    • Mitochondrial changes - swelling - appearance of small amorphous densities
    • Dilation of the ER - Detachment of polysomes - myelin formation
    • Nuclear alterations - disaggregation of granular and fibrillar elements
  12. Macrospocic of cellular swelling
    • pallor
    • increase turgor
    • increased weight of organ
  13. Types of necrosis
    • Coagulative Necrosis
    • Liquefactive Necrosis
    • Gangrenous Necrosis
    • Caseous Necrosis
    • Fat Necrosis
    • Fibrinoid Necrosis
  14. Coagulative necrosis:
    • Caused by ischemia (called an infarct) --> except brain which is liquifactive
    • perserved archtecture for days or weeks
    • eosinophilic --> pink
    • firm texture
  15. coagulative necrosis
  16. Liquefactive necrosis of the brain
  17. Liquiefactive necrosis
    • Hypoxic death of cells within central nervous system
    • necrotic tissue is a creamy yellow
    • tissue is turned into liquid mass through cell digestion
  18. Gangrenous necrosis
    • ischemia plus bacerial infection of the limbs
    • coagulative and liquefactive
  19. gangrenous necrosis
  20. cacseous necrosis
    • Granuloma necrosis
    • Inflammation enclosed lysed cells and amorphous granular debris
    • Think TB
  21. inflammation surrounded pink necrotic area
  22. Fat necrosis
    • when fat is broken down by lipases
    • fatty acid plus calciu equals fat soponification
    • dystrophic calcification
    • can be enzymatic or due to trauma
    • fat necrosis on the right side
    • vague cells lines, left side intact
    • fibrinoid necrosis
    • immune complex deposition and fibrin leaks causes pink necrotic arterial wall
  23. mechanisms of necrotic cell injury
    • Depletion of ATP
    • Mitochondrial damage
    • Calcium influx and loss of homeostasis
    • Accumulation of oxygen derived free radicals (oxidative stress)
    • Defects in membrane permeability
  24. Depletion of ATP
    • Caused by reduced O2, mitochondrial damage, and toxins
    • Liver better able to handle O2 than brain due to glycogen storage (longer glycolysis run)
    • Failures of PUMPS, PROTEIN SYNTHESIS/RECYCLING AND ORGANELL MEMBRANE DAMAGE
  25. Defects in membrane permeability
    • ROS peroxidation
    • o Hypoxia/ATP exhaustion decreased synthesis
    • o Increased Ca2+ phospholipase and protease breakdown or skeleton and membrane
    • o Causes mitochondria/lysosomal membrane damage, MPTP, apoptosis, lysing enzymes.
    • o General plasma membrane damage means loss of osmotic balance, metabolite, and cell content
  26. Mitochondrial damage
    • o Caused by increases in cytosolic Ca2+, ROS, toxins, mutation or deprivation of O2
    • o MPTP mitochondrial permeability transition pore (excitotoxicity ,ischemia and reperfusion injury) leaks small molecules out
    • o Leaking activates apoptosis
  27. Calcium influx and loss of homeostasis
    • o Caused by infectious agent, organelle break with stores released or bad
    • o Closely linked to mito-damage, can cause mito damage and be caused by mito damage
    • o Activation of digestive enzymes
  28. Accumulation of oxygen derived free radicals (oxidative stress)
    • o Caused by, normal respiration, WBC cytotoxic agent, drug detox (CCL4 to CCL3), UV radiation, NO, metals being oxidized
    • o Damages by peroxidation of membranes(lipids), modification of proteins and DNA lesions
    • o Antioxidants superoxide dismutase, glutathione peroxidase, catalase, vita A, C, E
  29. Damage to DNA & proteins
    o If damage it too sever it goes through apoptosis
  30. Most consistent irresibility of cell death
    • Can’t reverse mitochondria dysfunction
    • Membrane function disturbances
  31. Hypoxia vs ischemia
    • Hypoxia means no O2 avaliable
    • Ischemia is the inability to bring O2 to site (this compromises both arobic and anaerobic ATP production)
    • Ischemia is worse because not only O2 but all transports are down
  32. Reprefusion injury
    • Occurs when blood flow is restored and normally cells continue to die
    • due to increase in ROS, inflammation, compliment system activation continue clear out cells that were tagged (IgM deposition)
  33. Chemical injry
    • Direct = by the actual chemical
    • indrect = by the product of P450 oxidase system of a chemical (CCl4-an radial after p450) EtOH and acetaminophen
  34. Physiological Apoptosis
    • Embyogenesis
    • Hormone cycles: Endometrial breakdown; prostatic atrohy after castration (castration was not physiological but the atrophy in response is)
    • Cell population control: lymphocyte selection and neutrophil post infection
  35. Pathological Apoptosis
    • Atrophy
    • Viral infection
    • DNA and protein damage
  36. Morphology of Apoptotic cells
    • cell shrinkage
    • Chromatin condensation and fragmentation--> peripherally
    • Cytoplasmic blebs
    • Apoptotic bodies that are still enclosed by membrane

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