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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

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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24
Q

physiological hypertrophy

A
  • occurs due to increased functional demand

- ex. muscles getting bigger from working out

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25
Q

pathological hypertrophy

A
  • 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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26
Q

hyperplasia

A

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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27
Q

physiological hyperplasia

A
  • Lactating hormone stimulation > lactating breast

- increase in RBC’s at high altitude

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28
Q

pathological hyperplasia

A
  • endometriosis: higher conc. endometrium
  • psoriasis: skin cells have longer cell life>plaque on skin
  • liver regeneration following damage
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29
Q

metaplasia

A

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

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30
Q

reason for metaplasia

A

response to persistent injury/irritation

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31
Q

most common cell type metaplasia

A

glandular epithelium is replaced by squamous epithelium

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32
Q

examples metaplasia

A
  • 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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33
Q

dysplasia

A
  • disordered growth & maturation of cellular components of a tissue
  • loss of uniformity & architectural oreintation of cells
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34
Q

dysplasia is response to

A

persistent injurious influence and may regress

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35
Q

dysplasia > ?

A
  • dysplasia is a pre-neoplastic lesion

- a necessary stage in the cellular evolution of cancer

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36
Q

cellular adaptations that can give rise to neoplasia

A
  • dysplasia
  • hyperplasia
  • metaplasia
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37
Q

cellular adaptations that cannot give rise to neoplasia

A
  • atrophy

- hypertrophy

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38
Q

dysplasia: application of CIN grading method

A
  • CIN I: 25% - mild
  • CIN II: 50% - moderate
  • CIN III: 75% - severe
  • 100% : carcinoma in situ or microinvasie carcinoma
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39
Q

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

A
  • normal cellular constituent
  • abnormal substance
  • pigment
40
Q

features of intracellular accumulations

A
  • steatosis
  • hydropic change
  • pigments
  • protein
  • glycogen
  • cholesterol
41
Q

steatosis

A
  • accumulation of triglycerides within parenchymal cells
  • reversible
  • most common organ involved: liver
42
Q

causes of steatosis

A
  • protein malnutrition

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

43
Q

histological features of steatosis

A
  • peripheralized nucleus

- signet ring structure

44
Q

hydropic change

A
  • cellular swelling
  • increase in H2O accumulation within parenchymal cells
  • water accumulation within cytoplasm & cytoplasmic organelles
  • reversible
45
Q

most common cause of hydropic change

A

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

46
Q

histological features of hydropic change

A

swollen cells but centralized nucleus

47
Q

pigment accumulations

A
  • accumulation of iron within parenchymal cells and within interstitium
  • golden brown granules
48
Q

localized hemosiderosis

A
  • localized/focal pigment accumulations

- common bruise (derived from hemoglobin=RBC breakdown

49
Q

systemic hemosiderosis

A
  • systemic pigment accumulations
  • blood transfusions
  • hemolytic anemia (body attacks its own RBCs)
  • host vs. graft reaction
  • looks like big bruise over entire body
50
Q

lipofuscin

A
  • 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
51
Q

glycogen storage diseases

A

caused by enzyme deficiency

  • Pompe
  • McArdle
  • Cori
  • Von Geirke
52
Q

Pompe

A
  • glycogen storage disease

- enzyme: acid alpha glucosidase

53
Q

McArdle

A
  • glycogen storage disease

- enzyme: myophosphorylase

54
Q

Cori

A
  • glycogen storage disease

- enzyme: debranching enzyme

55
Q

Von Geirke

A
  • glycogen storage disease

- enzyme: glucose-6-phosphatase

56
Q

cholesterol accumulation

A

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

57
Q

xanthomas

A
  • disorders of cholesterol accumulation

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

58
Q

causes of cell injury

A
  • hypoxia
  • physical agents
  • chemical agents
  • infectious agents
  • immunological rxns
  • genetic defects
  • nutritional imbalances
59
Q

hypoxia

A

due to ischemia or decreased O2 carrying capacity of blood

60
Q

physical agents

A

trauma, temp, radiation, shock

61
Q

lack of oxygen causes ?

A

decrease of synthesis of ATP (so can excess oxygen)

62
Q

increases in intracellular calcium and loss of calcium homeostasis causes

A
  • activation of Calcium-dependent enzymes

- ex. apoptosis depends on Ca++ release

63
Q

depletion of ATP causes

A

loss of membrane function and intracellular processes

64
Q

defects in membrane permeability causes

A

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

65
Q

reversible cell injury: subcellular changes

A
  • 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
66
Q

reversible cell injury: structural cellular changes

A
  • plasma membrane bleb
  • increase intracellular volume
  • mitochondrial swelling & calcification
  • disaggregated ribosomes
  • dilated, vesicular endoplasmic reticulum
  • aggregated cytoskeletal elements
67
Q

irreversible injury

A
  • vacuolization of the mitochondria
  • rupture of lysosomes (ex. lactate dehydrogenase, creatine kinase)
  • nuclear changes
68
Q

irreversible injury: rupture of lysosomes

A
  • 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
69
Q

irreversible injury: nuclear changes

A
  • pyknosis: small, shrunken and dark nucleus
  • karryorrhexis: fragmented
  • karyolysis: faded, nucleus disappears
70
Q

hypoxic/ischemic injury: reversible

A
  • compromised aerobic respiration
  • increased rate of anaerobic glycolysis
  • decreased cellular pH
  • acute cellular swelling
  • detachment of ribosomes from RER
  • mitochondrial swelling
71
Q

hypoxic/ischemic injury: irreversible

A
  • severe mitochondrial vacuolization
  • lysosomal membrane rupture/activation of Ca dependent enzymes
  • -> cell death “point of no return”
72
Q

free radical

A
  • 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
73
Q

free radical as part of normal metabolism

A
  1. everytime you break or make a covalent bond

2. immune response to unknown objects

74
Q

damage by free radicals

A
  • lipid peroxidation of cell membranes
  • oxidative metabolism of cellular proteins
  • damage to cellular DNA: > mutations
75
Q

hydrogen peroxide - H2O2

A
  • free radical

- forms free radicals via Fe catalyzed Fenton reaction

76
Q

superoxide anion (O2-)

A
  • free radical

- generated by leaks in ETC and some cytosolic reaction

77
Q

hydroxyl radical (OH)

A
  • free radical

- generated from H2O2 by Fenton rxn

78
Q

peroxynitrate (ONOO)

A
  • free radical

- formed from NO + O2-

79
Q

calcification

A
  • deposition of calcium salts (no trabeculae or cortex)

- can be normal or abnormal

80
Q

pathologic calcification

A
  • abnormal deposition of calcium salts on soft tissues

- types: dystrophic calcification, metastatic calcification

81
Q

dystrophic calcification

A

calcium deposition in dead/necrotic or non-viable tissues

82
Q

metastatic calcification

A

calcium deposition in normal tissues due to hypercalcemia

83
Q

necrosis

A
  • morphological changes that occur in cells following cell death in living tissue
  • different from apoptosis
84
Q

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

A
  1. denaturation of proteins

2. enzymatic digestion of organelles

85
Q

hypochlorous acid (HOCl)

A
  • free radical
  • produced by macrophages and neutrophils during respiratory burst that accompanies phagocytosis
  • dissociates to yield hypochlorite radical (OCl-)
86
Q

endocrine disturbances that can cause calcification

A
  • PTH secreting tumor: increase blood Ca, decrease renal CA production
  • bone tumors: attack bone > release of Ca salts
87
Q

coagulative necrosis

A

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

88
Q

liquefactive necrosis

A

a pattern of cell death characterized by:

  • loss of tissue architecture
  • cellular debris
  • infiltration of WBCs
  • ex. brain after stroke, purulent (bacterial/pus infection)
89
Q

gangrenous necrosis

A

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
90
Q

caseous necrosis

A

a pattern of cell death characterized by looking like cheese

-most commonly found with tuberculosis

91
Q

enzymatic fat necrosis

A

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

92
Q

causes of apoptosis

A
  • embryogenesis
  • hormone-dependent involution in adult (ex. breast feeding>back to norm)
  • cell deletion in population of cells which have normal turnover
93
Q

morphological pattern of death by apoptosis

A
  • cell shrinkage
  • chromatin condensation
  • apoptotic bodies (blebbing)
  • phagocytosis of apoptotic bodies by phagocytic cells
94
Q

features of apoptosis

A
  • 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
Q

heat shock proteins def

A

-proteins involved in adaptation to stressful/injurious stimuli

96
Q

heat shock proteins features

A
  • 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
Q

HSP 60 & HSP 70

A
  • ex. of heat shock protein
  • chaperonins
  • involved in protein folding and targeting to final destination
98
Q

ubiquitin

A
  • ex. of heat shock protein
  • facilitates the degradation of proteins
  • “surveilance role”: tags proteins to be destroyed not doing their job

5 semestre (19 decks)

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