Physiopath Exam 1 Unit 1: Basic terms, cellular adaptations, and abnormal physiological processes Flashcards Preview

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Flashcards in Physiopath Exam 1 Unit 1: Basic terms, cellular adaptations, and abnormal physiological processes Deck (99):
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principle

-generalization that is accepted as true & that can be used as a basis for reasoning or conduct
-a rule or law concerning a natural phenomenon or function of a complex system

1

homeostasis

the ability of cells to handle normal physiological demands

2

4 aspects of a disease that form the core of patho

-etiology
-pathogenesis
-morphologic changes
-function derangements and clinical manifestations

3

etiology

cause of

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pathogenesis

series of steps that occur that manifest the disease

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morphologic changes

changes in shape of cell

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function derangements & clinical manifestations

-signs: something that can be seen
-symptoms: something that can be felt

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focal (vs. diffuse)

localized, exact spot

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diffuse (vs. focal)

spread out multiple areas, large area, poorly defined

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eosinophilic

looks red, cytoplasm, eosin-loving

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basophilic

looks blue, nucleus, hemotoxyin-loving

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hyaline ("hyaline change")

tissue starts to look like cartilage

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endogenous

from within

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exogenous

from exterior

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reactions of body to injury and/or stress

-cellular adaptation
-reversible cell injury

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factors affecting ability of a tissue/organ to adapt to an injury/stress

-potential for regeneration
-severity of injury
-duration of injury
-condition of cell
-location of cell
-degree of cell specialization

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labile cells

-continuously renewing cell population
-ex. epithelial cells

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stable cells

-a (potentially) expanding cell population
-increase # if need to
-ex. hepatocytes, anything with "blast"

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permanent cells

-a static cell population
-ex. CNS neurons, cardiac myocytes

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how can cells adapt

-atrophy
-hypertrophy
-hyperplasia
-metaplasia
-dysplasia

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atrophy

-an adaptation to diminished need or resources for a cells activities
-shrinkage of a cell or organ due to the loss of organelles
-changes in production & destruction of cellular constituents

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physiological atrophy

-normal loss of endocrine stimulation
-ex. muscle shrinking with disuse

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pathological atrophy

-diminished blood supply, inadequate nutrition, loss of innervation, abnormal loss of endurance stimulation, decreased workload
-ex. skinny legs in fat hyperlipidic person: common iliac artery occluded: loss of blood supply to legs
-brain w focal atrophy from stroke

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hypertrophy

-increase in cell size and functional capacity
-due to an increase in the production and number of intracellular organelles (increased metabolic demands on the cell/hormonal stimulation)

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physiological hypertrophy

-occurs due to increased functional demand
-ex. muscles getting bigger from working out

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pathological hypertrophy

-goiter: hyperactivity of an endocrine gland
-hormone secreting tumor: hyperactivity of an endocrine gland
-excessive demands on an organ: myocardial hypertrophy due to valve damage/hypertension

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hyperplasia

increase in the size of an organ or tissue due to an increase in the number of cells (increased functional and/or metabolic demands on the cell or compensatory proliferation)

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physiological hyperplasia

-Lactating hormone stimulation > lactating breast
-increase in RBC's at high altitude

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pathological hyperplasia

-endometriosis: higher conc. endometrium
-psoriasis: skin cells have longer cell life>plaque on skin
-liver regeneration following damage

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metaplasia

-a change where one terminally differentiated cell type is replaced by another terminally differentiated cell type

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reason for metaplasia

response to persistent injury/irritation

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most common cell type metaplasia

glandular epithelium is replaced by squamous epithelium

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examples metaplasia

-squamous metaplasia: bronchus, bladder
-Barret esophagus: squam > columnar
-Myositis ossificans: blow to soft tissue > lymph doesn't go away> bone devel. w/in muscle

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dysplasia

-disordered growth & maturation of cellular components of a tissue
-loss of uniformity & architectural oreintation of cells

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dysplasia is response to

persistent injurious influence and may regress

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dysplasia > ?

-dysplasia is a pre-neoplastic lesion
-a necessary stage in the cellular evolution of cancer

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cellular adaptations that can give rise to neoplasia

-dysplasia
-hyperplasia
-metaplasia

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cellular adaptations that cannot give rise to neoplasia

-atrophy
-hypertrophy

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dysplasia: application of CIN grading method

-CIN I: 25% - mild
-CIN II: 50% - moderate
-CIN III: 75% - severe
-100% : carcinoma in situ or microinvasie carcinoma

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3 categories of accumulations of material w/in a cell/organ

-normal cellular constituent
-abnormal substance
-pigment

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features of intracellular accumulations

-steatosis
-hydropic change
-pigments
-protein
-glycogen
-cholesterol

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steatosis

-accumulation of triglycerides within parenchymal cells
-reversible
-most common organ involved: liver

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causes of steatosis

-protein malnutrition
-toxins (alcohol, CCL4 dry cleaning, obesity, anoxia

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histological features of steatosis

-peripheralized nucleus
-signet ring structure

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hydropic change

-cellular swelling
-increase in H2O accumulation within parenchymal cells
-water accumulation within cytoplasm & cytoplasmic organelles
-reversible

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most common cause of hydropic change

-loss of ATP resulting in failure of Na/K ATPase pump > lack of free energy

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histological features of hydropic change

swollen cells but centralized nucleus

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pigment accumulations

-accumulation of iron within parenchymal cells and within interstitium
-golden brown granules

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localized hemosiderosis

-localized/focal pigment accumulations
-common bruise (derived from hemoglobin=RBC breakdown

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systemic hemosiderosis

-systemic pigment accumulations
-blood transfusions
-hemolytic anemia (body attacks its own RBCs)
-host vs. graft reaction
-looks like big bruise over entire body

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lipofuscin

-undigestable mixture of lipids and proteins thought to be the result of oxidative stress
-increases with age
-"wear and tear pigment"
-type of pigment accumulation

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glycogen storage diseases

caused by enzyme deficiency
-Pompe
-McArdle
-Cori
-Von Geirke

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Pompe

-glycogen storage disease
-enzyme: acid alpha glucosidase

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McArdle

-glycogen storage disease
-enzyme: myophosphorylase

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Cori

-glycogen storage disease
-enzyme: debranching enzyme

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Von Geirke

-glycogen storage disease
-enzyme: glucose-6-phosphatase

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cholesterol accumulation

-can accumulate in macrophages and vascular smooth muscle cells within blood vessel walls: atherosclerosis

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xanthomas

-disorders of cholesterol accumulation
-cholesterol gets deposited in random places: under eyes, bones, etc

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causes of cell injury

-hypoxia
-physical agents
-chemical agents
-infectious agents
-immunological rxns
-genetic defects
-nutritional imbalances

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hypoxia

due to ischemia or decreased O2 carrying capacity of blood

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physical agents

trauma, temp, radiation, shock

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lack of oxygen causes ?

decrease of synthesis of ATP (so can excess oxygen)

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increases in intracellular calcium and loss of calcium homeostasis causes

-activation of Calcium-dependent enzymes
-ex. apoptosis depends on Ca++ release

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depletion of ATP causes

loss of membrane function and intracellular processes

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defects in membrane permeability causes

cell = like balloon, poke it and it'll pop

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reversible cell injury: subcellular changes

-subcellular changes occur in reversibly injured cells
-cellular swelling: loss of activity of Na/K ATPase pump activity
-steatosis: fatty change: altered metabolism/transport of triglycerides
-REVERSIBLE CAN BECOME IRREVERSIBLE

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reversible cell injury: structural cellular changes

-plasma membrane bleb
-increase intracellular volume
-mitochondrial swelling & calcification
-disaggregated ribosomes
-dilated, vesicular endoplasmic reticulum
-aggregated cytoskeletal elements

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irreversible injury

-vacuolization of the mitochondria
-rupture of lysosomes (ex. lactate dehydrogenase, creatine kinase)
-nuclear changes

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irreversible injury: rupture of lysosomes

-ex. lactate DH, creatine kinase
-shouldn't have any in blood
-when cells die they perform autolysis and explode then the stuff in them is present in blood when it isn't normally there

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irreversible injury: nuclear changes

-pyknosis: small, shrunken and dark nucleus
-karryorrhexis: fragmented
-karyolysis: faded, nucleus disappears

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hypoxic/ischemic injury: reversible

-compromised aerobic respiration
-increased rate of anaerobic glycolysis
-decreased cellular pH
-acute cellular swelling
-detachment of ribosomes from RER
-mitochondrial swelling

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hypoxic/ischemic injury: irreversible

-severe mitochondrial vacuolization
-lysosomal membrane rupture/activation of Ca dependent enzymes
--> cell death "point of no return"

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free radical

-a final common pathway in a variety of cell processes
-chemical and radiation injury, cellular agin, oxygen toxicity, microbial killing by phagocytes
-highly reactive, autocatalytic, and unstable

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free radical as part of normal metabolism

1. everytime you break or make a covalent bond
2. immune response to unknown objects

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damage by free radicals

-lipid peroxidation of cell membranes
-oxidative metabolism of cellular proteins
-damage to cellular DNA: > mutations

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hydrogen peroxide - H2O2

-free radical
-forms free radicals via Fe catalyzed Fenton reaction

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superoxide anion (O2-)

-free radical
-generated by leaks in ETC and some cytosolic reaction

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hydroxyl radical (OH)

-free radical
-generated from H2O2 by Fenton rxn

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peroxynitrate (ONOO)

-free radical
-formed from NO + O2-

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calcification

-deposition of calcium salts (no trabeculae or cortex)
-can be normal or abnormal

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pathologic calcification

-abnormal deposition of calcium salts on soft tissues
-types: dystrophic calcification, metastatic calcification

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dystrophic calcification

calcium deposition in dead/necrotic or non-viable tissues

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metastatic calcification

calcium deposition in normal tissues due to hypercalcemia

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necrosis

-morphological changes that occur in cells following cell death in living tissue
-different from apoptosis

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necrosis = sum of what 2 processes that follow cell death in living tissue/organs

1. denaturation of proteins
2. enzymatic digestion of organelles

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hypochlorous acid (HOCl)

-free radical
-produced by macrophages and neutrophils during respiratory burst that accompanies phagocytosis
-dissociates to yield hypochlorite radical (OCl-)

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endocrine disturbances that can cause calcification

-PTH secreting tumor: increase blood Ca, decrease renal CA production
-bone tumors: attack bone > release of Ca salts

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coagulative necrosis

a pattern of cell death characterized by preservation of cellular outline w/ slow degradation of tissue/cells

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liquefactive necrosis

a pattern of cell death characterized by:
-loss of tissue architecture
-cellular debris
-infiltration of WBCs
-ex. brain after stroke, purulent (bacterial/pus infection)

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gangrenous necrosis

a pattern of cell death characterized by color change usually due to compromised blood supply
-easily observable
-usually blue, black, green
-ex. nose falls off climbing Everest

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caseous necrosis

a pattern of cell death characterized by looking like cheese
-most commonly found with tuberculosis

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enzymatic fat necrosis

a pattern of cell death characterized by enzymatic disruption of fat
-ex. pancreas

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causes of apoptosis

-embryogenesis
-hormone-dependent involution in adult (ex. breast feeding>back to norm)
-cell deletion in population of cells which have normal turnover

93

morphological pattern of death by apoptosis

-cell shrinkage
-chromatin condensation
-apoptotic bodies (blebbing)
-phagocytosis of apoptotic bodies by phagocytic cells

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features of apoptosis

-considered a natural event: plays imp. role in regulation of normal cell population density
-apoptosis "looks" different than necrosis
-apoptosis may play a role in the pathogenesis of neoplasms (some cells lose ability to become apoptotic: keep growing: fundamental cause of cancer)

95

heat shock proteins def

-proteins involved in adaptation to stressful/injurious stimuli

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heat shock proteins features

-induced and constitutively synthesized
-play an important role in normal cell metabolism
-essential for cell survival in all species subjected to injury
-induced during myocardial and cerebral ischemia
-increased heat shock expression is correlated with attenuation of cell injury/death

97

HSP 60 & HSP 70

-ex. of heat shock protein
-chaperonins
-involved in protein folding and targeting to final destination

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ubiquitin

-ex. of heat shock protein
-facilitates the degradation of proteins
-"surveilance role": tags proteins to be destroyed not doing their job