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Unit 4 - Pathology

Intro, Cell injury, inflammation, wound healing

syndrome signs and symptoms that occur together in a particular morbid process
etiology cause of a disease - primary, immediate, and intervening
pathogenesis sequence of events in the development of a disease
Natural History usual course of a disease if it were to be untreated
lesion structural alteration in a tissue and can help distinguish b/w diseases
clinical manifestations of disease functional disturbances of a disease - early in disease, these often only detectable (if even present) by labs
physical sign objective findings (murmurs, feet swelling, jaundice) that are confirmed by Dr.
Anatomic pathology study of structure (morphology) of cells, tissues, and organs in disease. If microscopic study = histopathology
cytopathology study of smears of cells
surgical pathology study of organs/tissues removed surgically - is specimen is specifically for diagnosis, it = "biopsy"
differential diagnosis consideration of which of 2+ diseases a person has by examining history of present illness, past history, family history, social history, abnormalities of physical exam, and any clinical studies (labs, EKG, X-ray, consults)
degenerative disease result of aging or wear-and-tear ; most common diseases of the elderly
molecular disease metabolic disease where the molecular products of cell activity are abnormal in composition (ex: sickle cell)
psychosomatic disease begin in emotions and are mediated through the autonomic nervous system
factitious disease produced artificially/deliberately
After a person dies, the body becomes the property of the next of kin. What is the order of authorization? 1. Spouse 2. Adult child 3. Parent 4. Adult Sibling
manner of death natural or unnatural (ie suicide, homocide, acident), or undetermined
rigor mortis stiffening of mm 2-24 hr after death- unnatural position suggest body was moved after rigor started
livor mortis settling of blood after death - eventually becomes fixed; not present where pressure prevents pooling
algor mortis cooling of the body after death
adipocere lipids in the body become waxy
Hyperplasia (what is it and its 4 causes) increase in NUMBER of cells in an organ - causes = physiologic (ex increase in cell of uterus during pregnancy), pathologic, growth factor induced, or cytokine induced (via interleukin 6 or TNF)
Hypertrophy (what is it and its 2 causes). What feature in heart cells indicates hypertrophy? increase in SIZE of cells - causes = increased work, or weight training. Box Car nuclei (causes by increased DNA from an inability of nuclei to divide)
Atrophy (what is it and its 8 causes) SHRINKAGE of cell size - causes = disease, loss of innervation, decreased blood supply, inadequate nutrition, loss of endocrine nutrition, aging (aka senile atrophy), loss of neurons (aka cerebral atrophy), return to original/normal size
Metaplasia (what is it, its 3 causes, and its most common type) reversible change where one cell type is replaced by another cell type - causes = inflammation, cytokines, or growth factors. Most common change is columnar to squamous, a more protective cell type
Describe the progression of morphological alteration with cell injury initially, damage is reversible, until cell fxn decreases to a point where it becomes irreversible, at which point biochem. alternations occur (cell death), then ultrastrucal change, light micoscopic changes, and finally gross morphological changes
cloudy swelling REVERSIBLE cell swelling - decrease in ATP causes the Na+/K+ ATPase to cease working causing Na+ to rush in the cell and cause water to follow (membrane becomes "leaky"). Mt may swell, but cristae inside will not swell. Ribosomes dis-aggregate from ER
what are the 4 ultrastructural changes in reversible cell injury plasma membrane alterations (swelling), mt changes (swelling), dilation of ER, nuclear alterations (swelling, but DNA intact)
What is necrosis and what are the 5 types of necrosis? pathological Cell death (more than one!) in living tissue - types = coagulative, liquefactive, caseous, fat, gangrenous
Coagulative (coagulation) necrosis most common type of necrosis that occurs due to ischemia (hypoxia). Histologcially, the basic outline of cells will still be visible, but there will be a loss of the nucleus - karyolysis (fading), Karyorrhexis (breakup), pyknosis (shrinkage)
Ultrastructural changes with necrosis/early ischemia(x5) discontinuous membranes, marked dilation of Mt. and Mt. cristae, densities and calcifications in Mt, myelin figures, chromatin clumping in nucleus
Liquefactive necrosis seen in abcesses (collection of pus/broken down cells from bacterial and neutrophilic enzymes) and brain infarcts/strokes (due to neurons having their own enzymes that break down cell wall). Injured area starts creamy, becomes cystic mass
caseous necrosis mixture of coagulative and liquefactive necrosis. Associated with granuloma (collection of microphages) seen in TB & fungal infections. Looks like cream cheese
what are giant cells several macrophages that clump together to form one large cell - seen in caseous necrosis
enzymatic fat necrosis enzymatic break down of adipose tissue. Usually caused by trauma to pancreas breaking the pancreatic duct and releasing lipases. Causes soap formation
gangrenous necrosis coagulation necrosis with a superimposed bacterial infection. Typically seen in limbs and is painless due to nerve death. *not a real type of necrosis, because outside agent "necrosis" tissue
4 intracellular systems vulnerable to injury integrity of cell membranes, aerobic resp. and production of ATP, protein synthesis, integrity of genetic apparatus
What cell injuries lead to necrosis ATP depletion, O2 derived free radicals (partially reduced free radicals can damage lipid membranes), rise in normally low intracellular Ca2+ (causes activation of cleaving enzymes), ↑ membrane permeability, irreversible Mt. damage
↓ ATP in cell injury caused by ↓ fxn of mt. - leads to malfxning of ion pumps (causes swelling/blebbing & loss of microvilli), ↑ anaerobic resp (↑ lactic acid leading to ↓pH causing chromatin clumping), ribosome detachment→protein synthesis→lipid deposition
Mt. injury in cell injury Caused by ↑Ca2+ or oxidative stress - causes ↑ in mt. memb. permeability leads to loss of electrochem. gradient causing a ↓ ATP that can lead to necrosis. OR release of Cyt c (apoptosis)
Rise in intracellular Ca2+ in cell injury Ca2+ sequestered in Mt. & ER increase mt. permeability to ↓ ATP, and activate cell enzyme to lead to membrane and nuclear damage
Causes of Free Radical Induced Cell injury created by the absorption of radiant energy, metabolism of exogenous chem. (toxins), reduction of oxidative rxns from normal metabolic processes, transition metals, or NO
role of reactive Oxygen species in cell injury react with FA to disrupt membranes, proteins to lose enzymatic activity and protein folding, and DNA to cause mutations/breaks. Removed by catalase in peroxisomes, and glutathione peroxidase & SOD in Mt.
role of chemical injury in hepatocyte cell injury FATTY CHANGE - ↑ lipid radicals that damage RER membrane to cause ↓ Apo protein leading to fatty liver. Release of lipid peroxidation leads to cell swelling and eventually necrosis
When does cell damage become irreversible? certain amount of cell membrane is lost to render malfxnal and cause lysis of lysosomes, cristae swelling of Mt., and nuclear condensation
Cellular fetures of Apoptosis cell shrinkage, chormatin condensation, formation of cytoplasmic blebs, phagocytosis of apoptotic cells or bodies, typically only one cell dies, and NO INFLAMMATION!!!
Apoptosis mechanism 1) Cell signaling either via receptor binding or a lack of survival factor binding induced by cell injury, 2) initiator capases activated, 3)executioner capases activated which cause the breakdown of cytoskeleton and endonuclease activation
what initiates the extrinsic death receptor pathway? The intrinsic? Extrinsic: T-cells, TNF (cytokine), growth factor withdraw. Intrinsic: DNA damage causing p53 to arrest the cell cycle and trigger apoptosis
What is a cell's unfolder protein response? increased synthesis of chaperones, decreased translation of proteins, activation of ub-proteasome pathway
Dystrophic calcification calcium accumulates in damaged tissues (atherosclerosis)
Metastatic Calcification cacification accumulates in normal tissues (hypercalcemic states such as hyperthyroidism)
What is the physical appearance of a hyaline? Homogenous, glassy pink appearance
What type of hyalin change is Mallory's alcoholic hyalin? Amyloid hyalin in the brain? intracellular hyalin change; Extracellular hyalin change;
Steatosis (Fatty Change) abnormal accumulation of fat INSIDE parenchymal cells, mostly due to alcohol, drugs, poison, and/or morbid obesity.
Mechanism of Steatosis (fatty change) increased mobilization of FAs, increased conversion of FAs to cholesterol/phospholipids/TAG, ↓ oxidation of TAG to acetyl-CoA or ketones, and ↓ production of Apoproteins leading to decreased transport of FA to blood
Fatty Infiltration infilration of fat cells BETWEEN parenchymal cells. Mainly due to increased body weight and has little clinical significance
Carbon is what type of pigment? exogenous (outside cells)
Lipofuscin (fatty residues), melanin, hemosiderin (iron), and bilirubin (hemoglobin) are examples of what type of pigments? Endogenous (inside cells
Created by: c.phill