5 semestre > Physiopath Exam 1 Unit 1: Basic terms, cellular adaptations, and abnormal physiological processes > Flashcards

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

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0
Q

homeostasis

A

the ability of cells to handle normal physiological demands

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1
Q

principle

A
  • 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
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2
Q

4 aspects of a disease that form the core of patho

A
  • etiology
  • pathogenesis
  • morphologic changes
  • function derangements and clinical manifestations
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3
Q

etiology

A

cause of

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4
Q

pathogenesis

A

series of steps that occur that manifest the disease

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5
Q

morphologic changes

A

changes in shape of cell

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6
Q

function derangements & clinical manifestations

A
  • signs: something that can be seen

- symptoms: something that can be felt

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7
Q

focal (vs. diffuse)

A

localized, exact spot

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8
Q

diffuse (vs. focal)

A

spread out multiple areas, large area, poorly defined

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9
Q

eosinophilic

A

looks red, cytoplasm, eosin-loving

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10
Q

basophilic

A

looks blue, nucleus, hemotoxyin-loving

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11
Q

hyaline (“hyaline change”)

A

tissue starts to look like cartilage

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12
Q

endogenous

A

from within

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13
Q

exogenous

A

from exterior

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14
Q

reactions of body to injury and/or stress

A
  • cellular adaptation

- reversible cell injury

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15
Q

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

A
  • potential for regeneration
  • severity of injury
  • duration of injury
  • condition of cell
  • location of cell
  • degree of cell specialization
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16
Q

labile cells

A
  • continuously renewing cell population

- ex. epithelial cells

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17
Q

stable cells

A
  • a (potentially) expanding cell population
  • increase # if need to
  • ex. hepatocytes, anything with “blast”
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18
Q

permanent cells

A
  • a static cell population

- ex. CNS neurons, cardiac myocytes

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19
Q

how can cells adapt

A
  • atrophy
  • hypertrophy
  • hyperplasia
  • metaplasia
  • dysplasia
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20
Q

atrophy

A
  • 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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21
Q

physiological atrophy

A
  • normal loss of endocrine stimulation

- ex. muscle shrinking with disuse

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22
Q

pathological atrophy

A
  • 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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23
Q

hypertrophy

A
  • 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
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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)
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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
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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
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