Preweek Sublethal Cellular Responses Flashcards
1
Q
Causes of cell injury/cell stress
A
- food
- inherited/congenital
- physical stimuli (temperature, trauma, radiation)
- chemical stimuli (toxins, medications)
- microorganisms
- time
- altered oxygen delivery (hypoxia)
2
Q
Pathobiology: process of disease
A
- Etiology
- Pathogenesis
- Molecular and morphologic changes
- Clinical manifestations (symptoms)
3
Q
Two ways cells deal in homeostasis to a change
A
- Cells respond and return to normal
2. Cells adapt to new altered homeostatic state
4
Q
Cellular responses
- reversible (3 types)
- Irreversible (2 types)
A
- Reversible:
- resolution and return to normal homeostasis
- Adaptation (hypertrophy, atrophy, hyperplasia; metaplasia)
- Alterations (cellular aging, neoplasia/dysplasia, accumulation of cell constituents) - Irreversible: necrosis or apoptosis
5
Q
Hyperplasia
- what is it
- In what cells does it occur (and where can it not occur)?
- Examples (2 specific types of hyperplasia)
A
- Adaptational, reversible change where number of cells increases, increasing size of tissue/organ
- Cells capable of DNA replication and cell division
- Hormonal hyperplasia (increase in breast tissue; endometrium undergoes hyperplasia in response to estrogen to regenerate after every menstrual cycle)
Compensatory hyperplasia (loss of tissue or increased need for tissue) - e.g. liver resected; blood loss (precursors in blood marrow undergo hyperplasia
6
Q
Hyperplasia MOA
A
Stimulation of cell proliferation by growth factors/hormones binding to the cells, resulting in cell division
- increased proliferation of mature cells
- increased production of new cells from stem cells
7
Q
Issues with hyperplasia
A
- there is a fine line between physiologic and pathologic hyperplasia
- what may start out as physiologic hyperplasia may become pathologic (could have exact same etiologic agent; sometimes agent occurs more strongly, over longer duration of time)
e. g.: endometrial hyperplasia; ductal hyperplasia of breast; prostate hyperplasia; response to certain viruses - HPV - response to viruses can become pathologic (wart from HPV is stimulus to grow and proliferate)
- some of these pathogenic hyperplasias have an increased risk for development of cancer
8
Q
Hypertrophy
- what is it?
- In what cells?
- examples (2 types and examples)
A
- Adaptational, reversible process, where there is an increase in the size of cells of a tissue, resulting in larger tissue or organ mass
- Could occur in any cells, often co-occurs with hyperplasia, but is the preferred method in cells that can’t undergo cell division (like terminally differentiated cells - skeletal muscle, cardiac muscle, nerve, etc.)
- Hormonal hypertrophy: uterus myometrium (smooth muscle) undergoes hypertrophy during pregnancy (to accommodate fetus, and to generate force for delivery)
Compensatory hypertrophy (exercise-induced hypertrophy) - big muscles
9
Q
Hypertrophy MOA
- explain
- plus example
A
- An increased synthesis of structural proteins and cellular components in response to growth factors and hormones
e. g. skeletal muscle: - mechanical sensors triggered by increased work load; production of growth factors
10
Q
Problems with hypertrophy
A
- cardiac muscle hypertrophy (muscle that needs to work harder because must push harder against a work load); there is a certain point where hypertrophy becomes detrimental to cardiac function. Risk factor for heart attacks, myocardial infarctions, or CHF (congestive heart failure)
- bladder muscle hypertrophy (usually when there’s an obstruction)
NOT TYPICALLY ASSOCIATED WITH INCREASED RISK FOR CANCER
11
Q
Atrophy
- What is it?
- examples (2 types)
A
- A reversible decrease in size and number of cells in a tissue or organ, resulting in decreased size or mass of the tissue or organ (reversible process)
- Physiological Atrophy: reversal of physiological hypertrophy/hyperplasia (uterus must atrophy after childbirth as it hypertrophied for pregnancy)
Normal embryogenesis and development (during development of fetus, certain structures form which aren’t needed later on in life so they undergo programmed atrophy)
12
Q
Atrophy MOA
A
- decreased protein synthesis and increased degradation of proteins
- decrease in cellular constituents and size/number of organelles
13
Q
Pathologic atrophy (6)
A
pathologic atrophy:
- Atrophy of disuse (decreased workload - cast on limb, muscles smaller)
- loss of innervation or stimulation of muscle
- inadequate nutrition
- loss of hormonal stimulation
- pressure (wheelchair)
- diminished blood supply
e. g. Alzheimer’s disease (atrophy of brain - smaller gyri, larger sulci)
14
Q
Metaplasia
- what is it? when does it occur?
- In what cells does this occur
- is it reversible
- example (one)
A
- When one mature cell type changes to become another mature cell type
- due to persistent damage and inflammation; adaptive substitution of cells that are better able to withstand adverse environment - Occurs in epithelial or mesenchymal cells
- It is not completely reversible (once adaptational adaptation has started, cell won’t convert back to what it used to be) after chronic stimulus is gone, metaplastic change may persist.
- Only one physiologic example: squamous metaplasia of the uterine cervix
15
Q
Metaplasia of uterine cervix
A
- happens in all girls during puberty, when cervix everts and becomes exposed to vagina:
- delicate columnar epithelium of endocervix is exposed to harsh, acidic environment of the vagina, and inflammation occurs
- undergoes universal metaplastic change to stratified squamous epithelia (tougher, more protective, protects that area of the cervix from damage all the time)
