Cell Adaptations- (Exam 1) Flashcards

1
Q

Define atrophy

A

decrease in size and/or number of the cells and their metabolic activity after normal growth has been reached

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

Define hypertrophy

A
  • increased size of cells and their functions

- more common in cells with little replication

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

Define hyperplasia

A
  • increase in the number of cells of an organ

- cells capable of replication

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

What is metaplasia?

A
  • change in phenotype of a differentiated cell
  • reversible if cause is removed
  • most often in epithelial cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is dysplasia?

A
  • refers to abnormal development

- mostly of epithelial cells

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

What is etiology?

A
  • the study or theory of the factors that cause disease and the method of their introduction to the host
  • the causes or origin of a disease or disorder
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is acute swelling?

A

early, sub-lethal manifestation of cell damage, characterized by increased cell size and volume due to water overload

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

What is the etiology of acute swelling?

A
  • loss of ionic and fluid homeostasis
  • failure of cell energy production
  • cell membrane damage
  • injury to enzymes regulating ion channels of membranes
  • hypoxia, toxic agents
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Describe the gross appearance of acute cell swelling

A
  • slightly swollen organ with rounded edges
  • pallor compared to normal
  • in cut surface: tissue bulges and cannot be easily put in correct apposition
  • slightly heavy (wet organ)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is fatty change?

A

sub-lethal cell damage characterized by intracytoplasmic fatty vacuolation

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

What are the main causes of fatty change?

A

hypoxia, toxicity, metabolic disorders

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

Describe the gross appearance of fatty change

A
  • diffuse yellow
  • edges rounded and bulge on section
  • tissue is soft, friable, greasy texture
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Irreversible injury is associated morphologically with:

A
  • severe swelling of mitochondria
  • extensive damage to plasma membranes, giving rise to myelin figures
  • swelling of lysosomes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Describe the gross appearance of necrosis

A

pale, soft, friable, and sharply demarcated from viable tissue by a zone of inflammation

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

Describe coagulative necrosis

A
  • architecture of dead tissues is preserved

- necrotic cells removed by phagocytosis or digestion by lysosomal enzymes

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

Describe liquefactive necrosis

A
  • architecture is liquified
  • dead cells are digested and transformed into a liquid viscous mass
  • occurs in tissues with high lipid content, high neutrophil recruitment, and high enzymatic release
17
Q

Describe an abscess

A

a localized collection of pus in a cavity formed by disintegration of tissues surrounded by fibrous connective tissue

18
Q

What is fibrinoid necrosis?

A
  • usually seen in immune reactions involving blood vessels

- occurs when Ag-Ab complexes are deposited in walls of arteries

19
Q

What can happen when there is too little apoptosis?

A
  • mutations in p53 give rise to neoplasia
  • lymphocytes react against self antigens
  • failure to eliminate dead cells
20
Q

What can happen when there is too much apoptosis?

A
  • neurodegenerative disease
  • ischemic injury
  • death of virus-infected cells
21
Q

Describe Phosphatidylserine and its actions

A
  • phospholipid on inner membrane
  • carries a negative charge
  • flips to outer membrane to signal macrophages
22
Q

What are the two types of endocytosis?

A
  • potocytosis: caveolae mediated

- pinocytosis: receptor mediated

23
Q

What are 3 causes of cell injury?

A
  • oxygen deficiency
  • infectious agents
  • immunologic dysfunction
24
Q

What are the 6 mechanisms of cell injury?

A
  • depletion of ATP
  • mitochondrial damage
  • entry of calcium
  • increased ROS
  • membrane damage
  • protein misfolding, DNA damage
25
Q

What is the fundamental cause of necrotic cell death?

A

depletion of ATP

26
Q

What are the 3 major consequences of mitochondrial damage?

A
  • formation of the mitochondrial permeability transition pore
  • increased production of ROS
  • activation of apoptotic pathways
27
Q

What are the 3 major forms of damage resulting from accumulation of calcium?

A
  • membrane damage
  • nuclear damage
  • ATP depletion
28
Q

How are ROS formed?

A
  • normal metabolic processes
  • absorption of radiant energy
  • inflammation
  • transition metals
  • nitric oxide
29
Q

How are ROS removed?

A
  • spontaneous decay
  • antioxidants
  • storage and transport proteins
  • enzymes
30
Q

What types of cells can undergo hypertrophy?

A
  • cardiomyocytes
  • skeletal muscle cells
  • neurons
31
Q

What is the order of injury you will see?

A
  • biochemical alterations
  • ultrastructural changes
  • light microscope changes
  • gross changes
32
Q

Describe the histological appearance of cellular swelling

A
  • dilated cytoplasm from water uptake
  • enlarge cells with pale cytoplasm
  • increased cytoplasmic eosinophilia
  • nucleus in normal position
33
Q

Describe the ultrastructural changes of cellular swelling

A
  • blebbing and blunting of plasma membrane, and loss of microvilli
  • swelling and appearance of small densities in mitochondria
  • dilation of ER with detachment of ribosomes
  • nuclear alterations such as clumping of chromatin