Cellular Adaptation Flashcards

1
Q

What is Cellular Adaptation?

A

The cell’s ability to maintain their structure/function when exposed to stressful situations and return to normal after the stimulus ceases.

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

When does Cell Injury or Death occur?

A

When the stress is too overwhelming

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

What do the molecular mechanisms that mediate cellular adaptations do?

A

Alter gene function (change depends on chemical messengers)

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

The genes that are altered are:

A
  1. Housekeeping (necessary for normal function)

2. Differentiating (differentiate characteristics of particular cell type)

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

In many cases _________ gene is altered. Why?

A

Differentiating

Cell can change size/form without compromising normal function

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

Implies that an organism remains within a certain range of physiological parameters to maintain stable function

A

Homeostasis

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

Implies that an organ constantly varies and adjusts physiological parameters to maintain stable function

A

Allostasis

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

Difference between homeostasis vs. allostasis

A

Homeostasis: Organism stays within a certain range
Allostasis: Constantly varies and adjusts

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

Decrease in cell size

A

Atrophy

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

Why Atrophy Responds

A
  • Decrease in work demands

- Adverse environmental conditions

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

What happens in Atrophy?

A

Cells revert to smaller size and lower/more efficient level of functioning (compatible with survival)

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

Causes of Atrophy (5)

A
  1. Disuse
  2. Denervation
  3. Loss of Endocrine Stimulation
  4. Inadequate Nutrition
  5. Ischemia (decrease blood flow)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Increase in cell size with increase in functioning tissue mass

A

Hypertrophy

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

Reason for Hypertrophy

A

Increased workload imposed on an organ or body part

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

Where is Hypotrophy commonly seen?

A

Skeletal/Cardiac muscle-where muscle tissue cant form more cells by mitosis

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

Causes of Hypertrophy (2)

A
  1. Normal Physiological Conditions
  2. Abnormal Pathological Conditions
    - Adaptive Hypertrophy
    - Compensatory Hypertrophy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Normal Physiological Conditions

A

Increase mm mass associated with exercise

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

Adaptive Hypertrophy Examples

A
  • Thickening of urinary bladder from long continued obstruction of urinary outflow
  • Myocardial hypertrophy that results from heart disease or hypertention
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Explain Compensatory Hypertrophy

A

Enlargement of a remaining organ or tissue after a portion has been removed or rendered inactive (Kidney removal)

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

Increase in the number of cells in an organ or tissue

A

Hyperplasia

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

Where does Hyperplasia occur?

A

In tissue with cells that can undergo mitosis

Epidermis, Intestinal Epithelium, Glandular Tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Causes of Hyperplasia

A
  1. Physiological Hyperplasia
    a. Hormonal
    b. Compensatory
  2. Non-Physical Hyperplasia
    a. Hormonal
    b. Effects of Growth Factors on Target Tissue
    (Is Reversible)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Breast/Uterine enlargement during pregnancy as a result of estrogen stimulation

A

Hormonal Physiological Hyperplasia

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

Regeneration of the Liver after partial hepatectomy or wound healing

A

Compensatory Physiological Hyperplasia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Abnormal menstrual bleeding as a result of too much estrogen
Hormonal Non-physiological Hyperplasia
26
Skin warts caused by growth factors produced by a certain virus
Effects of Growth Factors on Target Tissue (Non-Physiological Hyperplasia)
27
Reversible change in which one adult cell type is replaced by another
Metaplasia
28
Metaplasia occurs as a result of:
Chronic Irritation and Inflammation
29
Example of Metaplasia
Habitual Smoker: Stratified squamous epithelial cells into columnar epithelial cells
30
Deranged cell growth of a specific tissue. Results in cells varying in size, shape, and organization
Dysplasia
31
What is Dysplasia associated with?
Chronic Irritation and Inflammation (Reversible after irritation is removed )
32
Metaplasia and Dysplasia's relation to cancer
Metaplasia: continued exposure to stimulus, predispose to cancer transformation of the metaplastic reticulum Dysplasia: Strongly implicated as a precursor of cancer
33
Difference between cell injury and cell death
Injury: Reversible Death: Irreversible (comes from an injury)
34
Types of Cell Injury
1. Sublethal/Reversible cellular damage | 2. Irreversible injury with cell destruction or death
35
Two observed patterns of reversible cell injury
1. Cellular Swelling | 2. Intracellular Accumulations
36
Usually occurs as the result of hypoxic cell injury (ischemia, virus, bacteria, extreme heat/cold)
Cellular Swelling
37
Types of Irreversible Cell Injury
1. Apoptosis or programmed cell death | 2. Necrosis or cell death
38
Disintegration of cells into membrane-bound particles that are then phagocytosed by other cells
Programmed Cell Death or Apoptosis
39
The number of cells in tissues is regulated by _____
Cell Death (therefor controlling tissue regeneration)
40
Physiological processes of Apoptosis
1. Programmed destruction of cells during embryonic development 2. Hormone dependent involution of tissues 3. Death of immune cells
41
Apoptosis links to Pathological processes
1. Contributes in carcinogenesis 2. Cell death with viral infections (Hep B/C) 3. Implicated in neurodegenerative disorders (Alzheimer's, Parkinson's, ALS)
42
Cell death in an organ or tissue that is still part of living tissue
Necrosis
43
How does necrosis differ from apoptosis?
1. Unregulated enzymatic digestion of cell components 2. Loss of membrane integrity 3. Initiation of inflammatory response 4. Interference with cell replacement and tissue regeneration
44
How does necrosis present?
1. Coagulative (Ischeima, Viruses, Toxins) 2. Liquefaction Necrosis (Bacterial Infection) 3. Caseous Necrosis (TB) 4. Gangrene
45
When does Gangrene occur?
When a considerable mass of tissue undergoes necrosis (usually due to deficient or absent blood supply)
46
Gangrene can be:
1. Dry (extremities arteries) 2. Wet (Veins flow impaired and bacteria) 3. Gas (from infection of devitalized tissue by bacteria)
47
Causes of Cell Injury (6) Most common
1. Hypoxia (Most common) 2. Injury from physical agent 3. Radiation Injury 4. Chemical Injury 5. Injury from biological agents 6. Injury from nutritional imbalances
48
Caused by lack of oxygen, respiratory disease, ischemia, anemia, physical or pathological injury to delivery method
Hypoxia
49
Hypoxia Outcomes
1. Cell Swelling 2. Denaturation of enzymes 3. Chromosome clumping 4. Autolysis 5. Coagulative Necrosis
50
Common causes of injury due to environmental exposure, occupational and transportation accidents, and physical violence and assault
Injury from physical agents
51
3 Sections of Injury from Physical Agents
1. Mechanical Forces 2. Extremes of Temperature 3. Electrical Injuries
52
Impact of body with another object. Injuries split and tear tissue
Mechanical Forces (Physical Agent)
53
Extremes of heat and cold cause damage to the cells, its organelles and its enzyme systems
Extremes of Temperature (Physical Agent)
54
What happens with low intensity heat (43-46' C)
- Vascular injury - Accelerated cell metabolism - Disrupt Cell Membrane
55
What happens with high intensity heat
Coagulation of blood vessels and tissue proteins
56
What happens with exposure to cold
-Increased blood viscosity -Induces vasoconstriction (could lead to hypoxic tissue injury)
57
Leads to disruption of neural and cardiac impulses
Electrical Injuries
58
3 Sections of Radiation Injury
1. Ionizing Radiation 2. Ultraviolet Radiation 3. Non-ionizing Radiation
59
Can immediately kill cells, interrupt cell replication, or cause a variety of genetic mutations. (May/May Not be lethal)
Ionizing Radiation
60
Where is ionizing radiation used? What are its outcomes?
Treatment for cancer - Direct: cell death - Indirect: Free radicals (division impairment, mutations, enzyme inactivation)
61
Most vulnerable cells to ionizing radiation
- GI tract - Bone Marrow - Cells with high mitotic activity
62
Cause sunburn and increases risk of skin cancer
Ultraviolet Radiation
63
What is damaged by ultraviolet radiation?
- Reactive oxygen species - Melanin producing process in the skin - DNA
64
Includes infrared light, ultrasound, microwaves, and laser energy
Non-ionizing Radiation
65
Affects of non-ionizing radiation
- Causes vibration and rotation of atoms and molecules | - Bc deep penetration, involve dermal and subcutaneous tissue
66
Drugs, Lead Toxicity, and Mercury Toxicity injure the cell membrane and other cell structure.
Chemical Injury
67
Results of Chemical Injury
- Injure cell membrane and other cell structures - Block enzymatic pathways - Coagulate Cell Proteins - Disrupt the osmotic and ionic balance of the cell
68
Differ from other injurious agents because they are capable to replicate (continue to produce injurious effects)
Biological Agent
69
Nutritional excesses and nutritional deficiencies predispose cells to injury
Nutritional Imbalances
70
Nutritional excess leads to:
- Obesity | - Increase risk of many diseases
71
Diets in saturated fats lead to:
Predispose person to atherosclerosis
72
Nutritional deficiencies of protein lead to:
Malnutrition
73
Deficiencies in vitamin C
Scurvy
74
Deficiencies in vitamin B1 (thymine)
Beri Beri
75
Deficiencies in vitamin D
Rickets