Pathology Lect2&3 Word Scramble

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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