Pathology Lect2&3 Cell adaptation, Injury, and Death.
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| what is a physiologic response to stimuli? | show 🗑
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| What are pathologic responses to stimuli? | show 🗑
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| show | Homeo: • Cells possess an innate ability to stress in such a way to work to maintain normal structure/function & viability.
Allo:cells respond to stresses by making substantive changes to structure and fnc that still allow for maintenance of viability
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| show | Death
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| show | to new conditions/demands for optimal functioning.
**reflects cells ability to alter cell cycle acitivity (G1,G2, S, and M/Proliferation).
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| show | 1.Hyperplasia: increased number of cells.
2.Hypertrophy: increased size of cells.
3.Atrophy: decreased size of cell.
4.Metaplasia: change from one mature cell type to another.
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| show | PHYSIO:
1.Hormonal (meet functional demands).
2.Compensatory (regain functional capacity after loss of cells).
PATH:
1.Proliferation for protection.
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| show | 1.Endometrial proliferation in response to estrogen (proliferatice phase prepares for implantation).
2.Increased cell number in mammary glands during lactaion (producing milk for infants).
3.The body's natural suturing of scars
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| show | 1.Occurs Due to increased protein synthesis, not cellular swelling.
2.Generally occurs in cells that would not typically divide (e.g., muscle cells ® cardiac hypertrophy)
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| List 2 examples of adaptive responses involving both hyperplasia & Hypertrophy | show 🗑
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| What is atrophy? why is substance lost? | show 🗑
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| show | 1.Dec Workload (skeletal muscle, bone).
2.Loss of nerve supply (skeletal m).
3.Ischemia (brain in elderly).
4.Poor nutrition.
5.Reduced endocrine stimulation (mammary, uterus, ovaries.
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| show | Change from one mature cell type to another type due to reprogramming the gene expression of stem cells.
**Can be:
1.Epithelial tissues: squamous to columnar (Barret's esophagus) or columnar to squamous (cervix, airways).
2.Mesenchymal: muscle to bon
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| show | YES to BOTH. It is protective to noxious stimuli b/c cells change from susceptible cell type to more resistant/protective type of cell.
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| 7 causes of cell injury | show 🗑
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| show | Granular cell layer as well as keratin layer.
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| Exmaples of Pathologic hyperplasia | show 🗑
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| show | Adipocytes.
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| Cachexia | show 🗑
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| Where does cervical cancer usually occur? | show 🗑
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| When would you have a metaplastic change in the airway not due to stomach acid? what does this cause? | show 🗑
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| show | CAUSES:
1.Dec BF.
2.Anemia.
3.Poor oxygenation.
**Ischemia is impaired BF which leads to dec O2 AND nutrients.
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| show | LIVER b/c of the CYP450 system
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| Underlying Mechanisms of Cell Injury | show 🗑
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| show | 1.Severity.
2.Duration.
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| show | Inc mRNA.
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| show | When self function declines below the cell death risk level.
**there is greater chance of cell death than cell function.
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| Morphologic changes in Cell injury | show 🗑
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| show | Mitochondria become swollen, membrane Does NOT maintains integrity.
**Cells are consumed by phagocytes so they dont damage other cells.
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| Ischemia-Reperfusion Injury | show 🗑
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| Compare and Contrast Apoptosis and Necrosis | show 🗑
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| show | NECROSIS:
1.Coagulative.
2.Liquefactive.
3.Caseous.
4.Fat necrosis.
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| show | Coagulative (except in brain)
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| Nuclear changes seen with Coagulative Necrosis | show 🗑
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| show | MORPHOLOGY:
1.Cell outline & tissue architecture remain for 48 hrs.
2.Cytoplasmic changes: Shrunken, Inc eosinophilia.
3.Nuclear changes.
PROCESS:
1.Denaturation of cytosolic proteins (due to Dec pH).
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| show | 1.Bacterial Infection.
2.CNS necrosis.
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| Morphology and process behind Liquefactive necrosis | show 🗑
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| show | 1.No tissue architecture remains.
2.Surrounded by granulomatous inflammation .
3.Cheesy white/yellow friable material.
**seen with TB.
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| What is the Process involving Fat Necrosis? Where all does it occur? | show 🗑
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| Since fat necrosis is such a large-scale destruction, what can it lead to? what will be seen in tissue? | show 🗑
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| show | DRY: Coagulative necrosis of tissues secondary to profound ischemia (toes of diabetes pt, intestine of ischemic bowel pt).
WET:o Liquefactive necrosis from inflammatory necrosis superimposed on ischemic necrosis (usually secondary to bacterial infectio
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| show | 1.Involution of structures during dev (webbing).
2.Elimination of immune cells.
3.Involution following hormonal withdrawal (Endometrium).
4.Cytotoxic T-cell mediated elimination of infected/neoplastic cells.
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| Pathologic Apoptosis is seen with | show 🗑
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| show | STIMULUS PATHWAYS:
1.Intrinsic ("Injury" such as ROS/toxins/radiation or withdrawal of growth factors).
2.Extrensic (Death receptors or cytotoxic T cell mediated).
**COMMON PATHWAY (shared by all):
1.Execution pathway (caspase enzyme cascade)
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| show | PRO:
1.Bax.
2.Bak.
ANTI:
1.bcl-2.
2.bcl-x
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| show | 1.Injury (from ROS, toxin, radation) causes Inc p53 tumor suppressor gene production.
2.Cell is arrested in G1 phase to repair DNA.
3.If repair is unsuccessful: Apoptosis.
4.Inc production of Bax and Bak.
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| show | 1.Growth factor withdrawal alters the balance of bcl family proteins.
2.Inc Bax & Bak.
3.Dec bcl-2 & bcl-x.
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| Mechanism behind the extrinsic Death receptor stimulus pathway leading to Apoptosis | show 🗑
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| show | Granzyme B
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| Are the Pro-apoptosis & Anti-apoptosis noramlly in balance? What happens if they aren't? | show 🗑
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| show | 1.Cancers: Neoplastic cells proliferate despite DNA damage (p53 has failed).
2.Autoimmunity: Failure to eliminate self-reacting lymphocytes
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| What 3 things can occur if there is too much apoptotic activity? | show 🗑
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| 2 main forms of Normal Lipid that can build up in excess causing accumulations | show 🗑
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| Steatosis | show 🗑
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| show | Cutaneous xanthomas deposited around the eyelids and neck.
**50% associated with hypercholesterolemia due to genetic mutation.
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| Endogenous & exogenous Pigment Acculumations | show 🗑
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| show | 1.Dystrophic: normal Ca levels, associated with dying/degenerating cells (seen in: calcific atheroscl, fat necrosis, psammona body).
2.Metastatic: Hypercalcemia due to Inc PTH, destruction of bone, and excess Vit D.
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| 2 major contributors to Cellular Senescence | show 🗑
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