Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what are some internal factors that might cause cell injury?

A
  • immunologic
  • genetic
  • metabolic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what are the two types of cell death?

A

apopotosis & necrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what are the 4 types of necrosis?

A
  1. coagulative- infraction
  2. liquefactive- abscess
  3. caseous- tuberculosis
  4. gangrene- with infection
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

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

A

Hypertrophy (bigger cells)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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*

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What can cause hypertrophy?

A

can be physiological or pathological:

  • increasing work load (muscles)
  • hormonal stimulation (uterus, mammary gland)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what is Hyperplasia?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

hyperplasia frequently occurs together with with ________

A

hypertrophy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what is metaplasia?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
Q

what is Lipidosis?

A

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
Q

What are the ultrastructural changes of reversible cell injury?

A
  • 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
Q

What characterizes the transition from reversible to irreversible injury ?

A
  • 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
Q

what types of nuclear changes are their in irreversible injury?

A
  1. Pyknosis (nuclear condensation)
  2. Karyorrhexis (nuclear fragmentation)
  3. Karyolysis (dissolution of the nucleus)
29
Q

what is necrosis or oncosis?

A

necrotic cell death due to external causes (cell degradation)

30
Q

what is apoptosis?

A

apoptotic cell death programmed by the cell (cellular suicide)

31
Q

why does apoptosis occur normally (physiologically)?

A
  • to eliminate unwanted or potentially harmful cells (immune system)
  • eliminate cells that have outlive their usefulness
32
Q

when does apoptosis occur physiologically ?

A
  • 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
Q

what are some examples of apoptosis in pathologic situations?

A
  • 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
Q

what are some symptoms of an apoptotic cells?

A
  • 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
Q

which are the executioner caspases?

A

Casp 3, 6 & 7

36
Q

what activates apoptosis?

A
  • 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
Q

members of what family of proteins either inhibit or promote cell’s death

A

Bcl-2

38
Q

what do executioner caspases do?

A

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
Q

what is the end result in the intracellular cascade during apoptosis?

A

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
Q

consequences of cell injury depend on what?

A
  • cause
  • duration and severity of the injury
  • cell type
  • cell state
  • cell adaptability
41
Q

what are the two mechanisms which mediate non apoptotic cell injury?

A
  • alteration of energy supply
  • direct damage to cell membranes
42
Q

what are the functional and morphological consequences of decreased intracellular ATP during cell injury?

A
  • 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
Q

what happens in mitochondrial dysfunction in response to less ATP production?

A
  • cytochrome c released
  • MPT or mitochondrial permeability transition (H + released)
44
Q

what are the consequences of increased cytosolic calcium in cell injury?

A
  • 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
Q

what is the role of reactive oxygen species in cell injury?

A
  • DNA fragmentation
  • membrane disruption
  • lipid peroxidation
46
Q

what are some examples of free radicals or ROS?

A
  • superoxide anion (O2-)
  • hydrogen peroxide (H2O2)
  • hydroxyl radical (OH)
47
Q

what do free radicals do to cause cell injury?

A
  • 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
Q

what can stop further damage of free radicals?

A

antioxidants (Vit E and A, Glutathione) can attract and inactivate free radicals preventing further damages

Animal Health & Disease (7 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions