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Animal Health & Disease > Lecture #4: Disease at the Cellular Level > Flashcards

Lecture #4: Disease at the Cellular Level Flashcards

1
Q

what is a definition of injury?

A

any stimulus bringing changes in cell physiology and or structure (disruption of homeostasis)

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2
Q

Adaptation results from the changes in a cell due to _________ injury

A

REVERSIBLE

if irreversible, cell fails to adapt and cell death occurs

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3
Q

a normal cell undergoing stress and increased demand will lead to what?

A

adaptation and if inability to adapt then cell injury and cell death

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4
Q

what are some external factors that might cause cell injury?

A
  • lack of O2 (hemorrhage, anemia)
  • physical agents (trauma, burn, freeze, radiation, electric shock)
  • chemical agents (drugs, poisons, heavy metals)
  • biological agents (bacteria, viruses, protozoa, fungi, parasites)
  • malnutrition (deficiencies, over-nutrition)
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5
Q

what are some internal factors that might cause cell injury?

A
  • immunologic
  • genetic
  • metabolic
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6
Q

what are the 4 types of adaptation a cell will undergo due to injury?

A
  1. Atrophy
  2. Hypertrophy
  3. Hyperplasia
  4. Metaplasia
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7
Q

what are the two types of cell death?

A

apopotosis & necrosis

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8
Q

what are the 4 types of necrosis?

A
  1. coagulative- infraction
  2. liquefactive- abscess
  3. caseous- tuberculosis
  4. gangrene- with infection
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9
Q

what do cell reactions to injury depend on?

A
  • type of injurious stimulus
  • duration and severity of injurious stimulus
  • type, state and adaptability of cells involved
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10
Q

myocardial cells adapt to hypertension or heart valve deficiency by what mechanism?

A

Hypertrophy (bigger cells)

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11
Q

what happens when the myocytes are irreversibly injured?

A
  • arteries can become blocked causing lack of oxygen to tissues which can cause necrosis
  • vacuoles with accumulation of water are formed
  • condensed nucleus and damaged nuclear membrane
  • chromatin damage
  • eventually leads to cell death
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12
Q

what is Atrophy?

A

decrease in the mass or a organ or tissue due to the reduction in the cell number or size.

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13
Q

what can cause atrophy ?

A
  • reduction in the work load
  • nutritional deficiencies
  • loss of innervations or hormone supply
  • reduced blood supply
  • aging
  • pressure (tumors- blocking blood suppy to neighbouring tissues)
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14
Q

what is hypertrophy?

A

the increase in the SIZE of a tissue or organ due to an increase in the size of the cells without increasing the cell number (no new cells, just larger cells)

* increases the total cellular proteins, mitochondria and ER*

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15
Q

What can cause hypertrophy?

A

can be physiological or pathological:

  • increasing work load (muscles)
  • hormonal stimulation (uterus, mammary gland)
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16
Q

what is Hyperplasia?

A

increase in organ size or tissue caused by an increase in the number of cells

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17
Q

hyperplasia frequently occurs together with with ________

A

hypertrophy

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18
Q

what can induce hyperplasia?

A

physiologic: hormone induced or pathologic (compensatory)

  • usually caused by activated of cellular pathways, local production of growth factors or its receptors
  • increased lvl of a normal stimulus
  • compensatory response (ex: kidneys)
  • excessive stimulation (ex: goiter- lack or iodine for thyroid to produce T3 and T4)
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19
Q

what is metaplasia?

A

one type of differentiated cell is replaced by a different type that is not normal of that tissue

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20
Q

give an example of metaplasia?

A

normal columnar ciliated epithelium becomes squamous epithelium in bronchi of smokers

21
Q

what does metaplasia depend on?

A

proliferation of stem cells

22
Q

where is metaplasia most frequent?

A

in epithelial cells in response to chronic irritations

23
Q

what are the hallmarks of reversible injury?

A
  • reduced oxidative phosphorylation
  • adenosine triphosphate (ATP) depletion
  • cellular swelling caused by changed in ion concentrations (more sodium causing osmotic pressure to increase and swelling) and water influx (increase in cell size and volume)
24
Q

what are the characteristics of cellular swelling?

A
  • enlarged cells
  • water accumulation (increased intracellular osmosis)
  • vacuoles in the cytoplasm (distended organelles- ER or small lipid droplet)
  • can evolve to necrosis (irreversible)
25
what is Lipidosis?
**Fatty change**: accumulation of excessive intracellular lipids characterized by lipid accumulation in vacuoles and is more common in cells that metabolize lipids (ex: hepatocytes, cardiac myocytes, renal tubular epithelial cells)
26
What are the ultrastructural changes of reversible cell injury?
* lost of surface microvilli * breakdown of intercellular attachments * formation of cytoplasmic blebs (blister like in cell) * mitochondrial swelling * dilatation of ER * ribosomes dis-aggregate and detach from RER * clumping of chromatin
27
What characterizes the transition from reversible to irreversible injury ?
* increasing swelling of the cell * swelling and disruption of lysosomes (release of proteases and decrease pH of cell) * presence of large amorphous densities in swollen mitochondria * disruption of cellular membranes * profound nuclear changes * laminated structures (myelin figures: derived from damaged membranes of organelles and the plasma membrane)
28
what types of nuclear changes are their in irreversible injury?
1. Pyknosis (nuclear condensation) 2. Karyorrhexis (nuclear fragmentation) 3. Karyolysis (dissolution of the nucleus)
29
what is necrosis or oncosis?
necrotic cell death due to external causes (cell degradation)
30
what is apoptosis?
apoptotic cell death programmed by the cell (cellular suicide)
31
why does apoptosis occur normally (physiologically)?
* to eliminate unwanted or potentially harmful cells (immune system) * eliminate cells that have outlive their usefulness
32
when does apoptosis occur physiologically ?
* during embryogenesis * implantation * organogenesis * metamorphosis * hormone-dependent involution: regression of lactating breast after weaning or ovarian follicular atresia * death of neutrophils in an acute inflammatory response (served their purpose) * destruction of self-reactive lymphocytes * cell death induced by cytotoxic T cells in defense against viruses, tumors, and cellular rejection of transplants
33
what are some examples of apoptosis in pathologic situations?
* in response to injurious stimuli: DNA damage (ex: radiation), heat and hypoxia * cell injury in certain viral diseases (ex: viral hepatitis) * pathologic atrophy after duct obstruction : pancreas and kidney * cell death in tumors
34
what are some symptoms of an apoptotic cells?
* cell shrinkage * membrane blebbing * chromatin condensation and DNA fragmentation (Karyolysis) * formation of apoptotic bodies (nuclear fragments within a cytoplasmic mass, usually with intact organelles) * phagocytic removal of dead cells * apoptotic cells do not release cellular constituents (do not provoke inflammatory response)
35
which are the executioner caspases?
Casp 3, 6 & 7
36
what activates apoptosis?
* specific death ligands (TNF and Fas ligand) * withdrawal of growth factors or hormones * injurious agents (ex: radiation) * cytotoxic cells can act as stimuli to directly activate execution caspases
37
members of what family of proteins either inhibit or promote cell's death
Bcl-2
38
what do executioner caspases do?
activate latent cytoplasmic endonucleases and proteases that degrade cytoskeletal and nuclear proteins which results in a cascade of intracellular degradation, including fragmentation of nuclear chromatin and breakdown of the cytoskeleton.
39
what is the end result in the intracellular cascade during apoptosis?
Formation of apoptotic bodies containing various intracellular organelles and other cytosolic components as well as new ligands for binding and uptake by phagocytic cells
40
consequences of cell injury depend on what?
* cause * duration and severity of the injury * cell type * cell state * cell adaptability
41
what are the two mechanisms which mediate non apoptotic cell injury?
* alteration of energy supply * direct damage to cell membranes
42
what are the functional and morphological consequences of decreased intracellular ATP during cell injury?
* hypoxia * ischemia = block of O2 to tissues * lactic acid build up from anaerobic glycolysis= lower pH * clumping of nuclear chromatin * influx of Ca2+ into cell causes cellular swelling * decrease in glycogen * decrease in protein synthesis
43
what happens in mitochondrial dysfunction in response to less ATP production?
* cytochrome c released * MPT or mitochondrial permeability transition (H + released)
44
what are the consequences of increased cytosolic calcium in cell injury?
* ATPase causing decreased ATP * phospholipase causing decrease phospholipids and membrane damage * proteases causing disruption of membrane and cytoskeleton proteins and membrane damage * endonucleases causing nucleus chromatin damage
45
what is the role of reactive oxygen species in cell injury?
* DNA fragmentation * membrane disruption * lipid peroxidation
46
what are some examples of free radicals or ROS?
* superoxide anion (O2-) * hydrogen peroxide (H2O2) * hydroxyl radical (OH)
47
what do free radicals do to cause cell injury?
* combine with polyunsaturated lipids (lipid peroxidation) leading to membrane damage * modify certain proteins affection ion pumps and transport * can affect DNA integrity (fragmentation) * can damage mitochondria
48
what can stop further damage of free radicals?
antioxidants (Vit E and A, Glutathione) can attract and inactivate free radicals preventing further damages

Animal Health & Disease (7 decks)

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