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What are pathologic responses to stimuli?
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Pathology Lect2&3
Pathology Lect2&3 Cell adaptation, Injury, and Death.
| Question | Answer |
|---|---|
| what is a physiologic response to stimuli? | Adaptations (reversible changes to cell stress) |
| What are pathologic responses to stimuli? | 1.Injury (morphologic chanes and outcomes). 2.Death (apoptosis & necrosis). **result from altered cell structure and function in response to cell stress (cells lose ability to withstand stress). |
| Allostasis Vs Homeostasis in terms of the cells response to stress. | 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 |
| What is the ultimate endpoint of uncompensated state of injury? | Death |
| What is the goal of cell adaptation | to new conditions/demands for optimal functioning. **reflects cells ability to alter cell cycle acitivity (G1,G2, S, and M/Proliferation). |
| 4 major kinds of Adaptive cellular responses | 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. |
| When is Hyperplasia Physiologic? Pathologic? | PHYSIO: 1.Hormonal (meet functional demands). 2.Compensatory (regain functional capacity after loss of cells). PATH: 1.Proliferation for protection. |
| examples of physiologic hormonal hyperplasia? | 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 |
| What is the main cause of Hypertrophy? Where does it generally occur? | 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) |
| List 2 examples of adaptive responses involving both hyperplasia & Hypertrophy | 1.Gravid Uterus. 2.Mammary tissue during lactaion. |
| What is atrophy? why is substance lost? | Dec cell size resulting from Dec cellular substance. Substance is lost b/c the cell environment cannotsupport current size OR b/c functional stimuli is dimished (dec cell protein). |
| Causes of Atrophy | 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. |
| What is Metaplasia? | 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 |
| Is metaplasia a protective process? is it a reversible process? | YES to BOTH. It is protective to noxious stimuli b/c cells change from susceptible cell type to more resistant/protective type of cell. |
| 7 causes of cell injury | 1.Hypoxia (Norm BF, dec O2 delivery). 2.Physical agents/mechanical forces (Temp extremes, radiation, etc..). 3.Chemicals/Drugs (direct toxic effect). 4.Infectious agents. 5.Immunologic reactions. 6.Genetic mutations/ derangements. 7.Nutritional Imba |
| Thickening of what layer would indicate proliferative cell process indicating hyperplasia in squamous cells? | Granular cell layer as well as keratin layer. |
| Exmaples of Pathologic hyperplasia | 1.Lichen simplex. 2.Psoriasis. 3.Endometrial hyperplasia (Pre-cancerous). |
| Where is hypertrophy of cells normal? | Adipocytes. |
| Cachexia | general physical wasting. (cause of atrophy) |
| Where does cervical cancer usually occur? | At the endo/ecto cervical junction b/c there is a change in epithlium from columnar to squamous cells |
| When would you have a metaplastic change in the airway not due to stomach acid? what does this cause? | In response to cigarette smoke. **will change from stratified columnar to stratified squamous in order to protect against cigarette smoke. This means cilia is lost in the bronchi and cough reflex will be more active. |
| What does Hypoxia cause in the tissues? How is it different from Ischemia? | CAUSES: 1.Dec BF. 2.Anemia. 3.Poor oxygenation. **Ischemia is impaired BF which leads to dec O2 AND nutrients. |
| What organ will affected first by 1st overdose of chemicals and drugs? | LIVER b/c of the CYP450 system |
| Underlying Mechanisms of Cell Injury | Disruptions of Normal Structure/Function: 1.Disruption of Ox Phos (due to ischemia): Dec ATP. 2.disruption in removal of ROS. 3.Cell membrane integrity. 4.Ca+ Homeostasis. |
| What determines the reversibility of cell damage? | 1.Severity. 2.Duration. |
| Hypertrophy in the heart in adaptation to chronic stress and injury is due to what? | Inc mRNA. |
| What does the threshold of irreversibility on the continuum of cell injury represent? | When self function declines below the cell death risk level. **there is greater chance of cell death than cell function. |
| Morphologic changes in Cell injury | REVERSIBLE: 1.Cell swelling (due to disruption of fluid homeostasis): Dec ATP-dependent ion pump activity. 2.Fatty change (accumulation of lipid vacuoles): seen in cells using FA metab (heart, liver). IRREVERSIBLE: 1.Ultimately Cell death |
| What is occuring during Necrosis? | Mitochondria become swollen, membrane Does NOT maintains integrity. **Cells are consumed by phagocytes so they dont damage other cells. |
| Ischemia-Reperfusion Injury | Some cells recover when BF is restored, but others do not, could be due to: 1.generation of ROS. 2.Some inflammatory mechanisms. **Especially important in CNS & heart. |
| Compare and Contrast Apoptosis and Necrosis | 1.Both undergo nuclei shrinkage & fragmentation. 2.Membrane Integrity: lost w/ necrosis (leakage of cell material), blebbing with apop. 3.Area of tissue: Large w/ nec, small/isolated w/ apop. 4.No inflamm repsonse w/ apop. 5.Apop isnt ALWAYS pathologi |
| Does Apoptosis or Necrosis result from "Un-programmed" cell death? What are the 4 different types? | NECROSIS: 1.Coagulative. 2.Liquefactive. 3.Caseous. 4.Fat necrosis. |
| What type of Necrosis is most commonly seen w/ ischemia? | Coagulative (except in brain) |
| Nuclear changes seen with Coagulative Necrosis | 1.Pykonsis (nuclear shrinkage). 2.Karyolysis (nuclear dissolution). 3.Karyorrhexsis (fragmentation of pyknotic nucleus). **Nuclei disappears in a few days, ghost cells left behind. |
| Morphology and process behind coagulative necrosis | 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). |
| What are the only 2 times Liquefactive necrosis occurs? | 1.Bacterial Infection. 2.CNS necrosis. |
| Morphology and process behind Liquefactive necrosis | MORPHOLOGY: 1.Tissue architecture is lost, no cell outlines (Pink blob with NO nuclei). 2.Associated with dead inflammatory cells & pus. PROCESS: 1.Complete enzymatic digestion of dead cells (released from neutrophils). |
| Morphology of Caseous necrosis | 1.No tissue architecture remains. 2.Surrounded by granulomatous inflammation . 3.Cheesy white/yellow friable material. **seen with TB. |
| What is the Process involving Fat Necrosis? Where all does it occur? | PROCESS: Destruction of adipocytes within fatty tissue. Seen in: 1.Acute pancreatitis (lipases leak into fat surrounding pancrease). 2.Traumatic destruction of fat (surgical). 3.Inflamm destruction of fat. 4.Neoplastic destruction of fat. |
| Since fat necrosis is such a large-scale destruction, what can it lead to? what will be seen in tissue? | SOPONIFICATION. **deposition of Ca+ salts in tissue (Ca is released from stores in damaged tissue). |
| Dry Vs Wet Gangrenous Necrosis | 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 |
| 4 examples of Apoptosis as a physiologic process | 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. |
| Pathologic Apoptosis is seen with | 1."Insults" (such as radiation, drugs, DNA damage). 2.Viral infection. 3.Autoimmunity. 4.Neoplastic cells |
| Main Pathways of Apoptosis | 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) |
| What are 2 Pro-apoptotic proteins? 2 Anti-apoptotic proteins? | PRO: 1.Bax. 2.Bak. ANTI: 1.bcl-2. 2.bcl-x |
| Mechanism behind the Itrinsic Injury stimulus pathway leading to Apoptosis | 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. |
| Mechanism behind the Intrinsis withdrawal of growth factor stimulus pathway leading to apoptosis | 1.Growth factor withdrawal alters the balance of bcl family proteins. 2.Inc Bax & Bak. 3.Dec bcl-2 & bcl-x. |
| Mechanism behind the extrinsic Death receptor stimulus pathway leading to Apoptosis | 1.Death receptors (Fas & FasL) bind a ligand (TNFR1 & TNF). 2.Increases Bax & Bak. |
| Important molecule in the extrinsic cytotoxic T-cell mediated cell death stimulus pathway leading to Apoptosis | Granzyme B |
| Are the Pro-apoptosis & Anti-apoptosis noramlly in balance? What happens if they aren't? | YES. **Disruption of this balance can participate in disease processes |
| What 2 things can occur if there is too little Apoptotic activity? | 1.Cancers: Neoplastic cells proliferate despite DNA damage (p53 has failed). 2.Autoimmunity: Failure to eliminate self-reacting lymphocytes |
| What 3 things can occur if there is too much apoptotic activity? | 1.Neurodengenerative disorders (parkinson's). 2.Ischemic injury. 3.Death of virally infected cells. |
| 2 main forms of Normal Lipid that can build up in excess causing accumulations | 1.Fatty Acid: w/in cells w/ normally very active FA metabolism (heart & liver). 2.Cholesterol: Atherosclerosis (extracelluarly), Xanthalamas (intracellularly) |
| Steatosis | Part of cell injury in the liver causing Fatty change. **reversible process (unlike cirrhiosis) |
| Xanthelasma | Cutaneous xanthomas deposited around the eyelids and neck. **50% associated with hypercholesterolemia due to genetic mutation. |
| Endogenous & exogenous Pigment Acculumations | EXO: 1.Carbon dust (coal, soot, smog): anthracosis. ENDO: 1.Melanin. 2.Lipofuscin (NOT iron). 3.Hemosiderin (iron stored in cells) |
| 2 different types of pathologic calcifications | 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. |
| 2 major contributors to Cellular Senescence | 1.Replicative senescence (cells have limited capacity to replicate: telomeres). 2.Declining Function of proteosome (Cell loses its main method of disposing of unwated protein within the cell). |
Created by:
WeeG