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MOD - 2 - Cells: Adaptation, Injury, and Death > Robbins - Ch. 2 - Cell Response to Stress and Insult > Flashcards

Robbins - Ch. 2 - Cell Response to Stress and Insult Flashcards

1
Q

what are the four aspects of a disease process that make up the core of pathology?

A

etiology (cause)

pathogenesis (mechanism/ development)

morphogenesis (structural alterations)

clinical manifestations

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2
Q

what does adaptation mean?

A

that the functional and structural responses to change in physio state or pathologic stimuli are reversible

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3
Q

what are the 4 adaptation responses?

A

1) hypertrophy
2) hyperplasia
3) atrophy
4) metaplasia

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4
Q

what does hypertrophy refer to?

A

an increase in the size of cells that result in an increase in the size of the affected organ

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5
Q

how do cells get bigger?

A

incr protein synthesis

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6
Q

what is physiologic hypertrophy caused by?

A

incr in functional demand, or by stimulation by hormones or growth factors

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7
Q

what is the most common stimulus for hypertrophy of muscle?

A

increased workload

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8
Q

what is the stimulus for hypertrophy in the heart?

A

chronic hemodynamic overload

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9
Q

what is a good example of massive physiologic growth due to hormone-induced enlargement?

A

the uterus during pregnancy

  • uterine hypertrophy is stimulated by estrogenic hormones acting on smooth m. resulting in incr. synthesis of smooth m. proteins - increasing its size
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10
Q

what is hypertrophy a result of?

A

increased production of cellular proteins!

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11
Q

what are the 3 basic steps in molecular pathogenesis of cardiac hypertrophy?

A

1) the integrated actinos of mechanical sensors (which are triggered by Incr. workload), growth factors, and vasoactive agents.
2) two biochem pathways: PI3K/AKT pathway (physiologic), and signaling downstream of G-protein coupled receptors (pathologic)
3) these singnals activate tf’s: GATA4, NFAT, and MEF2

***THESE TFs INCR. SYNTHESIS OF PROTEINS = HYPERTROPHY***

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12
Q

what is hyperplasia?

A

an incr in the number of cells in an organ or tissue in response to a stimulus

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13
Q

where can hyperplasia not occur?

A

skeletal muscle

cardiac cells

neurons

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14
Q

what is physiologic hyperplasia due to? when does it occur?

A

the action of hormones or growth factors

  • when there is a need to increase functional capacity of the hormone sensitive organ; or when there is a need for compensatory increase after damage or resection
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15
Q

whats an example of hormonal hyperplasia?

A
  • the proliferation of the glandular epithelium of the female breast at puberty and during pregnancy, which is accompanied by enlargement of the glandular epithelial cells
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16
Q

what is a good example of compensatory hyperplasia?

A

liver regeneration after hepatectomy

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17
Q

what is the 3rd example of physiologic hyperplasia?

A

bone marrow: undergoes rapid hyperplasia in response to a deficiency of terminally differentiated blood cells; like in the event of acute bleeding or hemolysis

growth factor: erythropoeitin

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18
Q

what is pathologic hyperplasia caused by?

A

excessive or inapproapriate actions of hormones or growth factors acting on target cells

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19
Q

what are examples of a hormone-induced hyperplasia?

A

endometrial hyperplasia

benign prostatic hyperplasia

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20
Q

what is important to note about pathologic hyperplasia?

A

although they are abnormal, the process remains controlled and the hyperplasia regresses If stimulus is removed

- while hyperplasia Is distinct from cancer, pathologic hyperplasia consittutes a fertile soil in which cancerous prolferations may eventually arise

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21
Q

hyperplasia is a characteristic response to which viral infection?

A

papillomavirus; skin warts and several mucosal lesions composed of masses of hyperplastic epithelium

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22
Q

what drive hyperplasia?

A

its a result of growth factor-driven proliferation of mature cells

(in some cases, theres an increased output of new cells from stem cells, too)

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23
Q

what is atrophy?

A

a reduction in size of an organ or tissue due to a decrease in cell size and number

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24
Q

what are physiologic atrophy examples?

A

embryonic: notochord, thyroglossal duct
- decrease in uterus size after birth

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25
Q

what are the 6 common causes of pathologic atrophy?

A

1) decreased workload (atrophy of disuse)
2) loss of innervation (denervation atrophy)
3) diminished blood supply
4) inadequate nutrition
5) loss of endocrine stimulation
6) pressure

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26
Q

what is the initial response in atrophy?

A

decrease in cell size and organelles, which reduces metabolic needs of the cell (sufficient enough to survive)

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27
Q

what is the main mechanism of atrophy?

A

atrophy results from:

1) decreased protein synthesis

2) Increased protein degradation

in cells

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28
Q

what is the mechanism of degradation of cell proteins?

A

mainly ubiquitin-proteasome pathway

nutrient deficiency and disuse may activate ubiquitin ligases, which tag and target proteins for degradation via proteasomes

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29
Q

what may atrophy be accompanied by?

A

autophagy, marked by the appearance of increased numbers of autophagic vacuoles

autophagy is the process in which starved cells eat its own components in an attempt to reduce nutrient demand to match the supply

  • some vacuoles resist digestion: residual bodies

eg; lipofuscin granules

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30
Q

what is metaplasia?

A

the reversible change in which one differentiated cell type (epithelial or mesenchymal) is replaced by another cell type

31
Q

what is the most common epithelial metaplasia?

A

columnar to squamous; eg: respiratory tract in response to chronic irritation (smokers)

eg: stones in excretory ducts of salivary glands, pancrease, or bile ducts, may do this too

32
Q

why is the change to metaplastic squamous cells in the respiratory tract a double-edge sword?

A
  • important protection against infection (musuc and ciliary action) are lost
  • also, the influences that predispose to metaplasia, can initiate malignant transformation in metaplasitc epithelium (thus, common form of cancer in resp. tract is composed of squamous cell)
33
Q

what is Barrett esophagus an example of?

A

metaplasia from squamous to columnar type

34
Q

what is connective tissue metaplasia?

A

formation of cartilage, bone, or adipose tissue in tissues not normally containing these elements

eg: myositis ossificans: bone formation in muscle after intramuscular hemorrhage

35
Q

describe the mechanism of metaplasia

A

important to note that metaplasia does not result from a change in the phenotype of an already differentiated cell type;

its the result of a reprogramming of a stem cell, or of undifferentiated mesenchymal cells present in the connective tissue

36
Q

what is the differentiation of a stem cell to a particular lineage due to?

A

signals generated by cytokines, growth factors, and EXCmatrix components in the environment

37
Q

what are the 7 causes of cell injury?

A

1) oxygen deprivation
2) physical agents
3) chemical agents and drugs
4) infectious agents
5) immunologic reactions
6) genetic derangements
7) nutritional imbalances

38
Q

describe oxygen deprivation

A
  • hypoxia is a deficiency of oxygen, which reduces aerobix oxidative respiration causing injury

= causes of hypoxia:

  • ischemia
  • hypoxemia
  • decr. oxygen-carrying capacity (Hb related [CO-poinsoning] or blood loss)
39
Q

what do physical agents include?

A

mechanical trauma, temp change, sudden changes in atmospheric pressure, radiation, electric shock

40
Q

in regards to cell injury or death, what is there a time lag between?

A

the stress and the morphologic changes;

41
Q

when can you expect to see light microscopic changes of myocadium cell death?

A

4-12 hours

42
Q

what is reversible injury characterized by?

A
  • swelling of cell and its organelles
  • blebbing of plasma membr.
  • detacchment of ribosomes from ER
  • clumping of nuclear chromatin

*these morphologic changes are associated with decr generation of ATP, loss of cell membr. integrity, defects in protein synthesis, cytoskeletal damage, and DNA damage

43
Q

what two features of reversible cell injury can be recognized under a light microscope?

A
  • cellular swelling
  • fatty change
44
Q

what is hydropic change?

A

aka vacuolar degeneration

  • small clear vacuoles are seen within the cytoplasm; these represent distended and pinched-off segments of the ER
45
Q

what are the morphologic changes of necrosis due to?

A

denaturation of intracellular proteins and enzymatic digestion of the lethally injured cell

46
Q

what do necrotic cells show, histologically?

A
  • increased eosinophilia (H&E stain)
  • glassy homogenous appearance
  • dead cells may be replaced by large, whorled phospholipid masses called myelin figures (they come from damaged membranes)
  • these phospholipid precipitates are either phagocytosed by other cells or further degraded to fatty acids; they can also generate calcium soaps, if Ca binds the fatty acids = calcification
47
Q

what are the nuclear changes that appear in one of 3 patterns, in necrosis?

A

1) karyolysis: basophilia of chromatin may fade
2) pyknosis: nuclear shrinkage and increased basophilia
3) karyorrhexis: the pyknotic nucleus undergoes fragmentation

48
Q

describe coagulative necrosis

A

form of necrosis in which the architecture of dead tissue is preserved for a span of at least some days

  • exhibit a firm texture
  • this happens cuz the injury not only denatures the structual proteins, but also the enzymes; so it blocks proteolysis of the dead cells
  • eosinophilic, anucleate cells persist for days
  • Ischemia caused by obstruction In a vessel may lead to coagulative necrosis of the supplied tissue in all organs except the brain

- a localized area of coagulative necrosis is called an infarct

49
Q

describe liquefactive necrosis

A
  • digestion of dead cells transforms the tissue inot a liquid viscous mass
  • seen in focal (localized) bacterial infection or fungal

eg: hypoxic death of cells within the central nervous system

50
Q

how does the necrosis liquify the tissue?

A

microbes stimulate the accumulation of leukocytes (neutrophils; pus) and the liberation of enzymes from these leukocytes

  • the material is often creamy yellow + dead leukocytes = pus
51
Q

describe gangrenous necrosis

A
  • often a limb, lower leg, that has lost its blood supply and has undergone necrosis involving multiple tissue planes.
52
Q

describe caseous necrosis

A

encountered most often in foci of tuberculous infection

  • microscopic exam: structureless collection of fragmented or lysed cells and amorphous granular debris enclosed within a distinctive inflammatory border

*this appearance lets you know theres a granuloma! meaning a “focus of inflammation”*

53
Q

describe fat necrosis

A
  • refers to focal areas of fat destruction

typical finding: pancreas (pancreatitis)

  • results from release of activated pancreatic lipases Into the substance of the pancreas and the peritoneal cavity
54
Q

describe what happens in acute pancreatitis

A

enzymes leak out of acinar cells and liquefy the membranes of fat cells in the peritoneum.

  • the released lipases split the triglyceride-esters contained within fat cells
  • the fatty acids combine with calcium to produce fat saponification
55
Q

what can you expect in histologic examination of fat necrosis?

A
  • foci of shadowy outlines of necrotic fat cells
  • with basophilic calcium deposits

surrounded by an inflammatory reaction

56
Q

describe fibrinoid necrosis

A
  • seen in immune reactions involving the blood vessels

= pattern occurs when complexes of antigens::antibodies are deposited in the walls of the arteries

  • deposits of these complexes + fibrin that leaked out of vessels = bright pink and amorphous appearance in HnE stains called FIBRINOID
57
Q

how does dystrophic calcification happen?

A

when necrotic cells and cell debris is not destroyed and reabsorbed- they provide a nest for the deposition of calcium salts and other minerals

58
Q

what are key concepts of reversible cell injury

A

= cell swelling

fatty change

plasma membrane blebbing and loss of microvilli

mitochondrial swelling

dilation of ER

eosinophilia

59
Q

what are the key concepts of necrosis in regards to morphologic alterations?

A

incr. eosinophilia

nuclear shrinkage, fragmentation and dissolution

breakdown of plasma membr and organelles

abundant myelin figures

leakage and enzyme digestion of cell contents

60
Q

what does apoptosis serve to do?

A

eliminate cells that are no longer needed, and to maintain a steady number of various cell populations in tissues

61
Q

what are some examples of physiologic apoptosis?

A

1) destruction of cells during embryogenesis
2) involution of hormone-dependent tissues upon hormone withdrawal (eg: endometrial cell breakdown, ovarian follicular atresia, regression of lactating breast, prostatic atrophy after castration)
3) cell loss in proliferating cell populations (immature lymphocytes in bone m. and thymus, and B lymphs in germinal centers that fail to express useful antigen receptors; and epithelial cells in intestinal crypts)
4) elimination of potentially harmful self-reactive lymphocytes

62
Q

what are some examples of apoptosis in pathologic conditions?

A
  • DNA damage
  • accumulation of misfolded proteins
  • cell death in certain infections
  • pathologic atrophy in parenchymal organs after duct obstruction (such as the pancreas, parotid gland, and kidney)
63
Q

describe apoptosis in regards to accumulation of misfolded proteins

A

if there is excessive accum. of improperly folded proteins in the ER, it leads to ER Stress, which ends up in apoptosis

64
Q

whats an example of pathologic apoptosis in regards to cell death in certain infections

A

ie: when you get infected with a virus and the cells die out to contain the virus. can lead to a lot of tissue damage

65
Q

what are some morphologic features of apoptosis seen under the electron microscope?

A
  • cell shrinkage
  • chromatin is condensed; it aggregates peripherally
  • formation of cytoplasmic blebs and apoptotic bodies
  • phagocytosis of apoptotic cells or cell bodies, usually by macrophages
  • does not elicit inflammatory response
66
Q

what does apoptosis result from, in regards to its mechanism?

A

the activation of caspases

  • so called becasue they are cysteine proteases that cleave proteins after aspartic residue
67
Q

what is the major mechanism of apoptosis in all mammalian cells?

A

the mitochondrial pathway aka intrinsice pathway

68
Q

what does the intrinsice pathway result from?

A
  • results from an incr permeability of the mitochondrial outer membrane
  • cytochrome is released (resides in the intermembrane space)
  • the release of this protein is tightly controlled by BCL2 proteins (a protein family)
69
Q

what are the anti-apoptotic proteins found on the outer mitochondrial membrane?

A

BCL2, BCL-XL, and MCL1

(they also reside in the cytosol and ER membranes)

  • they keep the outer membrane impermeable and prevent leakage of cytochrome c
70
Q

what are the two pro-apoptotic proteins? what happens when they are activated?

A

BAX and BAK

  • when activated, they oligomerize within the outer mito protein and promote membrane permeability, releasing cytochrome C
71
Q

what are the “sensors” of the intrinsic pathway?

A

BAD, BIM, BID, Puma and Noxa

theyre all BH3-only proteins

-they act as sensors of cellular stress and damage, and regulate the balance between apoptotic and anti-apoptotic proteins

72
Q

what happens when cytochrome c is released to the cytosol?

A

cyto-c binds to a protein called APAF-1 (apoptosis-activating factor-1)

  • forms the apoptosome
  • apoptosome binds caspase-9
  • caspace-9 is the initiator of the mirochondrial pathway, and cleaves other adjacent C9’s - thus its autoamplifying
73
Q

what other proteins leave the mitochondria

A

Smac and Diable

  • they enter cytoplasm, bind to and neutralize IAPs (inhibitors of apoptosis proteins)
  • IAPs blocks the activation of capsases, esp caspase-3, which Is the executioner caspase.
  • thus, they add on to the inititation of caspase cascade
74
Q
A

MOD - 2 - Cells: Adaptation, Injury, and Death (10 decks)

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