Brainscape's Knowledge GenomeTM

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


See full index

MSII Pathology > Chapter 1. Adaptation to Cell Injury: Growth Alterations > Flashcards

Chapter 1. Adaptation to Cell Injury: Growth Alterations Flashcards

1
Q

causes of atrophy

A
  1. decreased hormone stimulation
  2. decreased innervation
  3. decreased blood flow
  4. decreased nutrients
  5. increased pressure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

mechanisms of atrophy

A
  1. shrinkage of cells due to increased catabolism of cell organelles and reduction of cytosol
    - organelles and cytosol form autophagic vacuoles, which fuse with primary lysosomes for enzymatic degradation
    - undigested lipids are stored as residual bodies (lipofuscin)
  2. loss of cells by apoptosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what is brown atrophy?

A

tissue discoloration from lysosomal accumulation of lipofuscin

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

what are causes of hypertrophy

A

increase in cell size

  1. increased workload
  2. cell enlargement in cytomegalovirus infections
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

mechanisms of cardiac muscle hypertrophy

A

induction of genes for synthesis of growh factors, nuclear transcription, and contractile proteins
-increase in cytosol, number of cytoplasmic organelles, and DNA content

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

causes of hyperplasia

A

(increase in cell number)

  1. hormone stimulation
  2. chronic irritation
  3. chemical imbalance
  4. stimulating Ab
  5. viral infections
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what are mechanisms of hyperplasia for the different types of cells?

A

dependent on regenerative capacity of different types of cells

  1. labile (stem) cells divide continuously and may undergo hyperplasia as adaptation to cell injury
  2. stable (resting) cells divide infrequently b/c normally in G0 phase, and need to be stimulated to enter cell cycle
    - may undergo hyperplasia or hypertrophy as adaptation to cell injury
  3. permanent (nonreplicating) cells cannot divide, and only undergo hypertrophy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what is Barrett’s esophagus?

A

metaplasia from squamous to glandular epithelium

  • distal esophagus shows increased goblet cells and mucus-secreting cells in response to acid reflux
  • increased risk for developing dysplasia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what is intestinal metaplasia?

A

metaplasia from glandular to other types of glandular epithelium

  • pylorus and antrum epithelium show increase in goblet and Paneth cells in response to H. pylori chronic atrophic gastritis
  • increased risk for developing dysplasia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what are 2 examples of metaplasia from glandular to squamous epithelium?

A
  1. mainstem bronchus epithelium becomes squamous in response to cigarette smoke
  2. endocervical epithelium develops squamous metaplasia in response to acid pH in vagina
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what is an example of metaplasia from transitional to squamous epithelium?

A

S. hematobium infection causes transitional epithelium to undergo squamous metaplasia

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

what are mechanisms of metaplasia?

A

stem cells have array of progeny cells that have different patterns of gene expression

  • under normal physiologic conditions, differentiation is restricted
  • may result from reprogramming stem cells to use progeny cells with different pattern of gene expression
  • -ex: hormones, vitamins, chemical irritants
  • may be reversible if irritant removed
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what is dysplasia? risk factors?

A

disordered cell growth that is precursor to cancer

  • risk factors are infection, chemicals, UV light, chronic skin irritation, some types of hyperplasia and metaplasia
  • sometimes reversible if irritant is removed
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what are microscopic features of dysplasia?

A

nuclear features
-increased mitotic activity with normal mitotic spindles
-increased nuclear size and chromatin
disorderly proliferation of cells with loss of cell maturation as cells progress to surface

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

coagulation necrosis and mechanism

A

preservation of structural outline in dead cells

  • denaturation of enzymes and structural proteins (intracellular accumulation of lactate or heavy metals, exposure to ionizing radiation
  • inactivation of intracellular enzymes prevents autolysis of the cell
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

coagulation necrosis microscopic features

A

indistinct outlines of cells within dead tissue with absent nuclei or karyolysis (fading of nuclear chromatin)

17
Q

how are infarctions related to coagulation necrosis? the types?

A

gross manifestation of coagulation necrosis secondary to sudden occlusion of a vessel; usually wedge-shaped if dichotomously branching vessels

  • pale (ischemic) type: increased density of tissue prevents RBCs from diffusing through necrotic tissue
  • hemorrhagic (red) type: loose-textured tissue allows RBCs to diffuse through necrotic tissue
18
Q

what is dry gangrene?

A

form of infarction that results from ischemia

-coagulation necrosis is primary type of necrosis present

19
Q

what are 6 factors influencing whether infarction will occur in tissue?

A
  1. size of vessel occluded (unlikely if major branch of pulmonary artery, but likely if thrombus overlies it)
  2. state of development of collateral circulation
  3. presence of a dual blood supply
  4. sudden onset in organ with pre-existing disease
  5. tissues with high O2 requirement
  6. rapidity with which a vessel is occluded
20
Q

liquefactive necrosis and its mechanisms

A

necrotic degradation of tissue that softens and becomes liquefied
-lysosomal enzymes released by necrotic cells or neutrophils cause liquefaction of tissue

21
Q

what kind of necrosis is cerebral infarction?

A

liquefactive, NOT coagulative, as the autocatalytic effect of hydrolytic enzymes generated by neuroglial cells produce cystic space

22
Q

what is wet gangrene?

A

dry gangrene with superimposed anerobic infection, like C. perfringens
-leads to acute inflammation, where liquefactive necrosis is primary type of necrosis

23
Q

what is caseous necrosis and its mechanisms?

A

variant of coagulation necrosis, but associated with acellular, cheese-like material
-formed by release of lipid from cell walls of M. tuberculosis and systemic fungi after immune destruction by macrophages

24
Q

what are microscopic features of a granuloma?

A

acellular material in the center surrounded by activated mcrophages, CD4 helper T cells, and multinucleated giant cells

25
Q

what is enzymatic fat necrosis and its mechanisms?

A

adipose tissue located around acutely inflammed pancreas

  • due to activation of pancreatic lipase causing hydrolysis of TG in fat cells with release of FA
  • saponification (FA + Ca)
26
Q

what is the cross and microscopic appearance of enzymatic fat necrosis?

A

gross: chalky yellow-white deposits primarily in peripancreatic and omental adipose tissue
microscopic: pale outlines of fat cells filled with basophilic-staining calcified areas

27
Q

what is traumatic fat necrosis

A

occurs in fatty tissue as a result of trauma, but NOT enzyme mediated

28
Q

what is fibrinoid necrosis and the mechanism?

A

limited to small muscular arteries, arterioles, venules, and glomerular capillaries

  • deposition of pink-staining proteinaceous material in damaged vessel walls due to damaged basement membranes
  • associated with immune vasculitis and malignant HTN
29
Q

what are the mechanisms of apoptosis?

A
  1. extrinsic - binding of TNF to its receptor with eventual activation of caspases
  2. intrinsic - mitochondrial leakage of cyt c into cytosol with eventual activation of caspases
30
Q

what are genes that regulate apoptosis via intrinsic pathway?

A
  1. BCL2 gene family on Xm 18
    - manufactures gene products that inhibit apoptosis
    - gene products prevent mitochondrial leakage of cyt c into cytosol
  2. TP53 suppressor gene (guardian of cell)
    - temporarily arrests in G1 phase to repair DNA damage
    - promotes apoptosis of DNA is too great by activating BAX apoptosis gene to inactivate BCL2 antiapoptosis gene
31
Q

what are caspases?

A

group of inactive proenzymes that are activated by extrinsic and intrinsic system for apoptosis

  • changes in cell
  • activation of endonuclease leads to nuclear pyknosis and fragmentation
  • activation of protease leads to breakdown of cytoskeleton
  • formation of cytoplasmic buds on cell membrane, which break off to form apoptotic bodies

MSII Pathology (11 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions