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Pathology > Cellular Reaction to Injury Overview and Adaptations > Flashcards

Cellular Reaction to Injury Overview and Adaptations Flashcards

1
Q

what are the 2 major categories of etiological factors

A
  1. genetic

2. acquired (environmental, infectious, something exposed to)

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2
Q

most illnesses have a —- etiology

A

multifactoral

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3
Q

pathogenesis

A
  • succession of events in response to causative agent

- molecular and morphologic changes

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4
Q

clinical manifestations

A
  • functional consequence of tissue alterations
  • signs and symptoms (clinical diagnosis)
  • clinical course and outcome (progress)
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5
Q

in response to harm the cell may undergo

A
  1. adaptive changes
    a. reversible changes –> new steady-state
  2. cell injury
    a. reversible
    b. irreversible
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6
Q

in response to harm the cell may undergo adaptive changes such as

A
  1. hypertrophy (size)
  2. hyperplasia (number)
  3. metaplasia (type - cell changes phenotype)
  4. atrophy (size and function - cell becomes smaller and function is not as necessary)
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7
Q

are adaptive changes reversible

A

YES!

reversible changes –> new steady state

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8
Q

what is hypertrophy

A

-increase in the SIZE of individual cells within an organ (same number of cells but larger, leading to larger organ)

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9
Q

hypertrophy results from an increased production of

A

cellular proteins (growth factors) generally triggered by an increase in workload (STRESS)

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10
Q

hypertrophy is mostly seen in what type of cells

A

non-dividing cells (ie. heart)

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11
Q

in most other organs hypertrophy co-exists with

A

hyperplasia

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12
Q

hypertrophy can be — and —

A

physiologic or pathologic

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13
Q

hypertrophy is caused by

A

functional (workload) or hormonal (growth factor)

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14
Q

examples of functional (workload) or hormonal (growth factors)

A

Myocardium
Uterus
Skeletal muscle
Mammary glands (puberty)

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15
Q

PHYSIOLOGY of myocardial hypertrophy occurs due to

A
  • exercise (also pregnancy) leading to an increase in the heart’s muscle mass and pumping ability
  • this type of hypertrophy is reversible (ie. after giving birth HR goes back to steady state)
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16
Q

PATHOLOGY of myocardial hypertrophy

A
  • chronic hemodynamic overload (hypertension, vascular disease) leads to an increase in muscle mass
  • the heart attempts to increase its pumping ability, often enlargement cannot compensate increased burden leading to injury
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17
Q

is hypertrophy a fast or slow process

A

slow

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18
Q

increase in cell size results from what

A

increase protein production and # of myofilaments increase myocyte force and work capacity of the heart

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19
Q

mechanisms of hypertrophy

A
  1. mechanical stretch (increased work load)
  2. agonists (eg. adrenergic hormones, angiotensin)
  3. growth factors (eg. IGF-1)
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20
Q

treatment with barbiturates leads to

A

hypertrophy of the SER in hepatocytes

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21
Q

barbiturates increase the amount of what enzyme

A

cytochrome P450 in the liver to detoxify the drugs (catalyzes metabolism of drugs via oxidation)

22
Q

progressively what will happen in cytochrome P450 is increased in the liver

A

the pt will respond less to the drug bc of adaptation (catalyzes and metabolizes the drug via oxidation)

23
Q

normal genetic variations (polymorphisms) in P-450 lead to what

A

different levels of activity and sensitivity to drugs in pts

24
Q

what is hyperplasia

A

increase in the # of cells that make up the tissue/organ

25
Q

hyperplasia can be — or —

A

hormonal or compensatory

26
Q

hyperplasia often occurs with what

A

hypertrophy

27
Q

what is hormonal hyperplasia

A

hormones/growth factors stimulating cells leading to increase in the functional capacity of the tissue/organ

28
Q

what is mammary gland hyperplasia/hypertrophy (puberty/pregnancy)

A

increased proliferation of the glandular epithelium in the female breast leading also to increase in size of cells

29
Q

when does compensatory hyperplasia occur

A

when an organ that has regenerative capability increases the # of cells to compensate for loss of mass

30
Q

example of compensatory hyperplasia

A

liver regeneration in donors - following partial hepatectomy, remaining liver cells proliferate to regain original size and function

31
Q

what is pathologic hormonal hyperplasia

A

-results from excessive hormonal stimuli to target cells

32
Q

over stimulation and excess proliferation of cells can allow for

A

mutations to occur that can lead clonal formation and development of cancer

33
Q

patients with certain types of hyperplasias can have

A

an increased risk for developing cancer

34
Q

describe how the prostatic gland can undergo pathologic hormonal hyperplasia

A

under excess adrogenic stimulation, prostatic glands undergo hyperplasia leading to enlargement of the prostatic gland

35
Q

characteristics of atrophy

A
  • reduced organelles
  • reduced metabolic need
  • decreased in cell size
  • decrease in # of cells
  • decreased in organ size
  • decrease in function of tissue
36
Q

main causes of atrophy

A
  1. disease
  2. denervation
  3. decreased blood supply
  4. malnutrition
  5. hormonal under-stimulation
37
Q

what is atrophy

A
  • an adaptation to changes in steady-state

- cell decreases in size and organelles, reducing its metabolic needs to adapt to the change

38
Q

atrophy: disure/inability to use

A
  • skeletal muscle and bone can become atrophic if not used (ie. immobilized pt or post fracture)
  • in some cases, is reversible to normal state if activity is resumed
39
Q

atrophy: denervation

A

loss of nerve supply leads to loss of normal skeletal muscle function

40
Q

atrophy: decreased blood supply (schema/compression)

A

decrease in blood flow secondary to atherosclerosis will lead to senile atrophy

41
Q

atrophy: malnutrition

A

consumption of muscle as source of energy in malnourished pt leads to muscle wasting (cachexia)

42
Q

atrophy: hormonal under-stimulation

A

female reproductive organs become atrophied in absence of hormonal stimulation

43
Q

mechanism of atrophy

A
  • decrease in cell # = apoptosis

- decreased in cell size (decreased protein synthesis, increased protein degradation)

44
Q

what are 2 protein degradation pathways that occurs with atrophy

A
  1. ubiquitin degradation pathway - protein that needs to be degraded is tagged or ubiquinated
  2. autophagy - cell will autodigest some of its own components
45
Q

what is metaplasia

A

change in phenotype (morphologic and functional type of a cell)

46
Q

why do phenotypic changes of a fully differentiated cell occur

A

to better endure the stressful envrionment

47
Q

is metaplasia reversible or reversible

A

reversible

48
Q

what is the most common type of metaplasia

A

columnar –> squamous

Can be seen in respiratory, salivary, pancreatic, cervical, glands, etc.

49
Q

if stress continues what happens to the metaplasia

A

metaplasia –> dysplasia –> cancer

50
Q

vitamin A deficiency can lead to

A
  • squamous metaplasia

- deficiency due to general malnutrition or any condition with fat malabsorption

51
Q

what is vitamin A need for

A
  • differentiation of specialized epithelium
  • ocular conjunctiva (lacrimal/mucus secreting epithelium)
  • upper respiratory passage (musociliary epithelium)
  • urinary tract (transitional epithelium)
52
Q

what is the mechanism of metaplasia

A
  • the change in phenotype occurs through the reprogramming of stem cells that have the ability to differentiate through a different cell pathway
  • this occurs via cytokines and growth factors stimulating expression of proteins that will drive cells toward a specific differentiation

Pathology (18 decks)

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