Brainscape's Knowledge GenomeTM

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


See full index

Pathology > Cellular Adaptations and Accumulations > Flashcards

Cellular Adaptations and Accumulations Flashcards

1
Q

What are physiologic adaptations?

A

Responses of cells to normal stimulation by hormones or endogenous chemical mediators

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

What are pathological adaptations?

A

Can share same underlying mechanisms as physiologic adaptations; allows cells to modulate their environment and escape injury

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

True or false: pathological changes to cells can share the same underlying mechanisms as physiologic changes

A

True

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

What are the four adaptations that cells can undergo?

A

Hypertrophy
Hyperplasia
Atrophy
Metaplasia

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

What is hypertrophy?

A

Increase in cell size, not number

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is hyperplasia? Metaplasia?

A

Hyperplasia = Increase in number of cells

Metaplasia = Change in cell type

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is atrophy?

A

Decrease in cell size

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

What is the underlying MOA of hypertrophy?

A

Increase in structural proteins and organelles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

True or false: hypertrophy can coexist with hyperplasia

A

True

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Is hypertrophy pathologic or physiologic?

A

Either

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

How does hypertrophy signalled? (2)

A

via hormones or increased functional demand

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

In the pregnant uterus, which cellular adaptation(s) occur? How is this signalled?

A

Hypertrophy and hyperplasia via hormonal stimulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

When can pathologic cardiac enlargement occur? (3)

A

HTN
Aortic valve disease
MI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What happens to non-necrotic cardiomyocytes following MI?

A

Enlargement of the surrounding the myocytes

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

What major adaptation (of the four) occurs in a necrotic heart?

A

Hypertrophy (CANNOT undergo hyperplasia)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What happens to the nucleus during hypertrophy of a cell? Cytoplasm?

A

Increases in size

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

Why is a thicker ventricle problematic?

A

Increased resistance to coronary blood flow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Why do cardiac muscle cell nuclei/cytoplasm increase in hypertrophy (boxcar nuclei)?

A

Kicking out more proteins

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

Boxcar nuclei = ?

A

Increased nuclei size in hypertrophic myocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Hypertrophy is the result of what?

A

increased production of cellular proteins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What are the three types of signals involved in causing hypertrophy?

A
  1. Mechanical signals (stretch)
  2. Vasoactive agents (alpha adrenergic)
  3. Growth factors (TGF-beta)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is the limit to hypertrophy of the heart?

A

When enlargement of muscle can no longer compensate for increased burden

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is the mechanical signal for increased myocardial hypertrophy?

A

Increased stretch

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What are the vasoactive agents signaling heart hypertrophy?

A

Alpha adrenergic agonists, like angiotensin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What are the growth factors that signal myocyte hypertrophy?

A

TGF-beta

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

How is myocyte hypertrophy effected? (3)

A
  1. Synthesis of contractile proteins
  2. Production of growth factors
  3. Induction of embryonic genes to increase performance
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

True or false: hypertrophied cells have increased DNA content

A

True– need more proteins per cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What is the requirement of the cells of tissues that can undergo hyperplasia?

A

Must be capable of replication

29
Q

What are the two physiologic forms of hyperplasia?

A

Hormonal hyperplasia (breast enlargement)

Compensatory hyperplasia (e.g. liver regrowth)

30
Q

What is compensatory hyperplasia?

A

Increased tissue mass after damage or resection (think liver)

31
Q

Pathologic hyperplasia usually results from what?

A

excessive hormones or growth factors acting on target cells

32
Q

What is endometrial hyperplasia?

A

Hyperplasia d/t estrogen/progesterone imbalance

33
Q

What is benign prostate hyperplasia (BPH) caused by?

A

Increased mitotic activity d/t increased androgens

34
Q

True or false: pathologic hyperplastic processes remain controlled (except for CA)

A

True

35
Q

What happens histologically in BPH?

A

Increased infolding d/t hyperplasia (nodular hyperplasia)

36
Q

What are the histological changes in Grave’s disease to the thyroid?

A

Cells pile up on themselves

37
Q

What is Grave’s disease?

A

Autoimmune disease where the abs act like signals to produce more TSH

38
Q

Hyperplasia is the result of what?

A

Increased growth factor leading to increased output of new cells from stem cells

39
Q

What the MOA of atrophy (2)?

A

Decrease in organelles/proteins

Increased protein degradation via ubiquitin

40
Q

What are the signals of atrophy? (6)

A 
Decreased workload
Loss of innervation
Decreased blood supply
Inadequate nutrition
Low endocrine
Pressure

(BP, WINE)

41
Q

How does pressure relate to atrophy?

A

Tissue compression leads to atrophy

42
Q

What is senile atrophy?

A

Decreased blood supply to tissues, leading to atrophy

43
Q

What is the initial atrophy response?

A

Decrease in cell size and organelles to reduce the metabolic needs of the cell to extent that they can survive

44
Q

Atrophy immediately results in dead cells (true or false)?

A

False–just smaller

45
Q

What is lipofuscin?

A

Bound residual cell debris from destruction of plasmalemma

46
Q

What is autophagy? What process is it seen in?

A

Self=eating by starved cells to survive

Occurs in atrophy

47
Q

What are the two cellular accumulations in atrophy?

A

Autophagic vacuoles and lipofuscin

48
Q

How does aortic atherosclerosis result in kidney atrophy?

A

Decrease in blood supply to kidney

49
Q

True or false: metaplasia is reversible

A

True

50
Q

What is metaplasia?

A

reversible changes in which one differentiated cell types is replaced by another cell type that is better adapted to conditions

51
Q

What is the effect of smoking on bronchi? What can this lead to?

A

Columnar cells turn to stratified squamous cells

May lead to CA

52
Q

Barrett’s esophagus?

A

Changes of lower esophagus d/t changing from squamous epithelium to columnar with goblet cells

53
Q

What is muscular dystrophy the result of?

A

Dystrophin gene messed up

54
Q

What is CT metaplasia?

A

Formation of cartilage, bone, or adipose tissue in tissue that does not usually contain these elements

55
Q

What is CT metaplasia the result of?

A

May be the result of tissue injury, rather than metaplasia

56
Q

What type of CT metaplasia occurs in intramuscular hemorrhage?

A

Bone formation in muscle after intramuscular hemorrhage

57
Q

What is the cellular mechanism underlying metaplasia? What are the three types of signals?

A

Result of reprogramming of stem cells that exist in normal tissues via cytokines, growth factors, ECM components

58
Q

What is dysplasia?

A

Disordered growth

59
Q

What disease process is dysplasia seen in? What cell type usually?

A

Precancerous in squamous epithelial cells (usually)

60
Q

What are the histological changes is dysplasia? (2)

A

Disorderly arrangement of cells

Enlargement of nuclei, irregular borders, and hyperchromasia of individual cell nuclei

61
Q

Intracellular accumulations are due to what?

A

Metabolic derangements

62
Q

Pathological calcification are due to what?

A

Calcium deposition at site of cell death

63
Q

In chronic cardiac overload, what genes are turned on?

A

genes expressed normally only in the neonatal heart are reactivated, and contractile proteins can switch to fetal isoforms, which contract more slowly

64
Q

When does cell injury occur? Is cell injury reversible?

A

when limits of adaptive response to stimulus are exceeded. Can be reversible or irreversible

65
Q

What are the three stages of progressive impairment that occur during cellular injury?

A

Adaptation, reversible injury, and cell death

66
Q

What happens to myocytes when the limit of enlarged muscle mass is reached? (2)

A

Lysis and loss of myofibrillar contractile elements or myocyte death

67
Q

Atrophy will continue until what point?

A

Until a new equilibrium is achieved so all cell can survive

68
Q

How are proteins degraded in atrophy?

A

Poly ubiquitination and proteasomal destruction

Pathology (32 decks)

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