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Block 3 Found Sci > 1-Cellular Adaptations and Accumulations > Flashcards

1-Cellular Adaptations and Accumulations Flashcards

1
Q

adaptation

A

state b/t normal/unstressed cell and injured/over stressed cell, reversible changes

new but altered steady state to survive

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2
Q

cellular responses to stress

A
  1. adaptive responses
  2. cell injury
  3. metabolic/subcellular alterations- intracellular accumulations, pathologic calcification
  4. cell aging
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3
Q

categories of adaptation

A
  1. physiologic- normal stimulation like hormones/endogenous chemical mediators
  2. pathologic- some same underlying mechanisms to modulate environment and escape irreversible injury
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4
Q

types of adaption

A
  1. hypertrophy
  2. hyperplasia
  3. atrophy
  4. metaplasia
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5
Q

hypertrophy

A

-inc in size of indiv cells and inc size of an organ
-no new cells just bigger bc inc syn of structural proteins and organelles
-coexist with hyperplasia (# of cells)

physio or pathologic

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6
Q

physiologic examples hypertrophy

A
  1. weight lifters- inc skeletal muscle with hypertrophy of indiv cells,
  2. pregnant uterus
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7
Q

pathologic examples hypertrophy

A

cardiac enlargement- hypertension, aortic valve disease (stenosis), MI
-myocytes nuclei enlarge (boxcar)

esp left ventricle

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8
Q

hypertrophy signals

A

signals:
1. mechanical (stretching)
2. vasoactive agents (alpha adrenergic agonist)
3. growth factors(TGF-beta)

limit reached when enlargement not be compensated

degenerative changes

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9
Q

hypertrophy mechanism

A
  1. trigger mech/agonist/GF
  2. inc signal transduction for protein syn and transcription
  3. induction of embryonic/fetal genes (mechanical) OR syn of contractile proteins (agoinsts) OR inc growth factors (GFs)
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10
Q

why happens?

hypertrophy

A
  1. in response to inc demand since most adult cells cannot divide
  2. balance to inc proteins and myofilaments, nuc with higher DNA content
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11
Q

hyperplasia

A

inc in # of cells in response to stimulus or persisten injury
-usually inc size(hypertrophy) and weight of organ

patho or physiologic

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12
Q

physiologic hyperplasia

A
  1. hormonal: puberty, pregnancy, proliferative endometrium
  2. compensatory: inc tissue mass after damage or resection (i.e liver fast regeneration)
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13
Q

pathologic hyperplasia

A

usually due to xs hormones or GF on target cells, will dissapear with stimulus so controlled process

  1. endometrial hyperplasia from estrogen/progesterone imbalace
  2. BPH, benign prostatic, from over exuberant mitotic activity from androgens

could also be from stem cells

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14
Q

atrophy

A

reduced size of organ from dec in cell size and organelles

-dec workload
-loss innervation
-dec blood supply
-inadequate nutrition
-loss endocrine stimulation
-pressure

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15
Q

atrophy process

A
  1. initial dec cell size reduces metabolic needs of cell to survive
  2. new equilibrium
  3. diminished function but not dead
  4. progress to irreversible cell injury/ death
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16
Q

atrophy mechanism

A

dec protein syn + inc protein degradation via ubiquitin proteasome pathway

autophagy of starved cells to find nutrients and survive

inc # of autophagic vacuoles bound and residual bodies (lipfuscin) if resist digestion

reversible

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17
Q

metaplasia

A

reversible change in one differentiated cell type to another cell type
-replaced by cells better able to withstand stress of a particular stressor
-from epithelial stem cells or undifferentiated mesenchymal cells thru genetic reprogramming

18
Q

metaplasia examples

A

bronchi in smokers ciliated columnar cells replaced with stratified squamous

cancer if protective mechanisms lost

columnar to squamous most common, but could be oppo in esophagus

connective tissue- cartilage, bone, adipose tissue,

not usually physiologic, pathologic from injury

19
Q

metaplasia mechanism

A

-reprogramming stem cells in normal tissues or undifferentiated mesenchymal in CT
-precursor cells diff along diff pathway
-signals like cytokines, GF, extracellular matrix components

20
Q

dysplasia

A

disordered growth in squamous epithelial after common injury

progression of metaplasia into cancer

variations in size/shape, disorder arrangement, enlarge irregular nucleus, hyperchromasia,

21
Q

intracellular accumulations categories

A
  1. normal endogenous substance: normal or inc rate, metabolism inadequate to remove, i.e fat
  2. abnormal endogenous: secondary to genetic or defects in metabolism/packaging/ transport/secretion
  3. abnormal exogenous: deposited and cannot be removed
22
Q

mechanisms of intracellular accumulation

A
  1. abnormal metabolism
  2. alteration in protein folding and transport
  3. deficiency of critical enzymes
  4. inability to degrade phagocytosed particles
23
Q

steatosis

fatty change

A

abnormal acc of triglycerides w/i parenchymal cells @ liver, heart, muscle, kidney

from toxins, protein malnutrition, diabetes mellitus, obesity, anoxia, alcohol

24
Q

cholesterol and esters diseases

A
  1. atherosclerosis
  2. xanthomas- foamy cells under skin, acquired or hereditary, look like masses
  3. inflamm and necrosis
  4. cholesterolosis in gall bladder, foam cells
  5. niemann pick disease type C- lysosomal storage

foam cells can rupture so lipids into extracellular space = cholesterol cleft

25
Q

atherosclerosis

A

@ plaques, smooth muscle, macrophages within intimal layer or aorta/large arteries

lipid vacuoles/foam cells yellow cholesterol laden atheromas

26
Q

protein accumulations

A

less common than lipid acc

appear pink “hyaline” droplets in cytoplasm

from reabsorption droplets in proteinuria @proximal renal tubules, syn xs amounts, defects in folding
-Russell bodies immunoglobulins by plasma cells
-Mallory body from alcoholic liver disease

27
Q

cytoskeletal abnormalities

A

defects in cell function locomotion, organelle movement
xxxxxxx

28
Q

defects in protein folding

A

ER stress from misfolding of alpha helix or beta sheet (lead to apoptosis via caspases)

ubiquitin tags for degradation, chaperones help facilitate degradation and folding

29
Q

examples of protein defects

A
  1. alpha 1 antitrypsin deficiency, buildup of intermediate so acc and trap in hepatocytes, emphysema and cyrosis of lungs
  2. amyloid- acc extracellularly, stiff tissues, interfere with normal function,
30
Q

hyaline changes

A

nonspecific morphologic change of proteins to glassy, pink homogenous

intra: protein droplets @ tubules, russell bodies, mallory bodies, viral inclusions
extracellular: collagenized scars, damage glomeruli, atherosclerosis, amyloid

descriptive term

31
Q

glycogen

A

abnormal metabolism of glucose or glycogen = xs intracellular deposits, clear vacuoles

diabetes @renal tubule epi, hepatocytes, cardiac myocytes, islets langerhand
glycogen storage diseases- enzyme defect, massive acc, i.e pompe

32
Q

pigments

A

endogenous or exogenous colored substances from normal constituents or special

most common exo is carbon

33
Q

exogenous pigments

A
  1. carbon- inhaled and transport to regional lymph nodes, darken tissue, emphysema or fibroblastic rxn
  2. tattoos: localized pigmentation of skin into dermal macrophages
34
Q

endogenous pigments

A

aka lipofuscin
-insoluble brown/yellow from wear and tear ‘aging’ around nucleus

marker of free radical injury

35
Q

melanin

endogenous

A

essential pigment for UV protection
-formed in melanocytes by tyrosine oxidation in epidermis
-can acc in basal keratinocytes or dermal macrophages

36
Q

hemosiderin

endogenous

A

granular or crystalline storage of iron, hemoglobin derived

ferritin forms hemosiderin granules/aggregates if local or systemic xs of iron

from inc absorption of dietary, impaired use, anemias, transfusions

normal in small amounts

37
Q

hemosiderosis progression

A

limited to liver,BM, spleen, LN
then liver, pancreas, heart, endocrine organs

maybe liver fibrosis, heart failure, diabetes

38
Q

bilirubin

endogenous

A

normal in bile from hemoglobin
jaundice if xs

39
Q

pathologic calcification

A

abnormal deposition of Ca salts mixed with iron, Mg, mineral salts

dystrophic (local in injured/dying tissues not in serum tho, necrosis) or metastatic (inc serum levels)

40
Q

hypercalcemia

A

from bone cancer, high PTH in parathyroid, vitamin D disorders (sarcoid, renal failure)

in metastatic calcification @blood vessels, kidneys, lungs, gastric mucosa

Block 3 Found Sci (60 decks)

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