Chapter 1. Adaptation to Cell Injury: Growth Alterations Flashcards Preview

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Flashcards in Chapter 1. Adaptation to Cell Injury: Growth Alterations Deck (31)
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1

causes of atrophy

1. decreased hormone stimulation
2. decreased innervation
3. decreased blood flow
4. decreased nutrients
5. increased pressure

2

mechanisms of atrophy

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

3

what is brown atrophy?

tissue discoloration from lysosomal accumulation of lipofuscin

4

what are causes of hypertrophy

increase in cell size
1. increased workload
2. cell enlargement in cytomegalovirus infections

5

mechanisms of cardiac muscle hypertrophy

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

6

causes of hyperplasia

(increase in cell number)
1. hormone stimulation
2. chronic irritation
3. chemical imbalance
4. stimulating Ab
5. viral infections

7

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

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

8

what is Barrett's esophagus?

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

9

what is intestinal metaplasia?

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

10

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

1. mainstem bronchus epithelium becomes squamous in response to cigarette smoke
2. endocervical epithelium develops squamous metaplasia in response to acid pH in vagina

11

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

S. hematobium infection causes transitional epithelium to undergo squamous metaplasia

12

what are mechanisms of metaplasia?

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

13

what is dysplasia? risk factors?

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

14

what are microscopic features of dysplasia?

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

15

coagulation necrosis and mechanism

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

16

coagulation necrosis microscopic features

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

17

how are infarctions related to coagulation necrosis? the types?

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

what is dry gangrene?

form of infarction that results from ischemia
-coagulation necrosis is primary type of necrosis present

19

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

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

liquefactive necrosis and its mechanisms

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

21

what kind of necrosis is cerebral infarction?

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

22

what is wet gangrene?

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

23

what is caseous necrosis and its mechanisms?

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

what are microscopic features of a granuloma?

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

25

what is enzymatic fat necrosis and its mechanisms?

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

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

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

what is traumatic fat necrosis

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

28

what is fibrinoid necrosis and the mechanism?

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

what are the mechanisms of apoptosis?

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

what are genes that regulate apoptosis via intrinsic pathway?

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