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Pathology > Cellular Adaptation > Flashcards

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.

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2
Q

When does Cell Injury or Death occur?

A

When the stress is too overwhelming

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3
Q

What do the molecular mechanisms that mediate cellular adaptations do?

A

Alter gene function (change depends on chemical messengers)

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4
Q

The genes that are altered are:

A
  1. Housekeeping (necessary for normal function)

2. Differentiating (differentiate characteristics of particular cell type)

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5
Q

In many cases _________ gene is altered. Why?

A

Differentiating

Cell can change size/form without compromising normal function

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6
Q

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

A

Homeostasis

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7
Q

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

A

Allostasis

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8
Q

Difference between homeostasis vs. allostasis

A

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

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9
Q

Decrease in cell size

A

Atrophy

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10
Q

Why Atrophy Responds

A
  • Decrease in work demands

- Adverse environmental conditions

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11
Q

What happens in Atrophy?

A

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

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12
Q

Causes of Atrophy (5)

A
  1. Disuse
  2. Denervation
  3. Loss of Endocrine Stimulation
  4. Inadequate Nutrition
  5. Ischemia (decrease blood flow)
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13
Q

Increase in cell size with increase in functioning tissue mass

A

Hypertrophy

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14
Q

Reason for Hypertrophy

A

Increased workload imposed on an organ or body part

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15
Q

Where is Hypotrophy commonly seen?

A

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

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16
Q

Causes of Hypertrophy (2)

A
  1. Normal Physiological Conditions
  2. Abnormal Pathological Conditions
    - Adaptive Hypertrophy
    - Compensatory Hypertrophy
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17
Q

Normal Physiological Conditions

A

Increase mm mass associated with exercise

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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
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19
Q

Explain Compensatory Hypertrophy

A

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

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20
Q

Increase in the number of cells in an organ or tissue

A

Hyperplasia

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21
Q

Where does Hyperplasia occur?

A

In tissue with cells that can undergo mitosis

Epidermis, Intestinal Epithelium, Glandular Tissue

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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)
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23
Q

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

A

Hormonal Physiological Hyperplasia

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24
Q

Regeneration of the Liver after partial hepatectomy or wound healing

A

Compensatory Physiological Hyperplasia

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25
Q

Abnormal menstrual bleeding as a result of too much estrogen

A

Hormonal Non-physiological Hyperplasia

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26
Q

Skin warts caused by growth factors produced by a certain virus

A

Effects of Growth Factors on Target Tissue (Non-Physiological Hyperplasia)

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27
Q

Reversible change in which one adult cell type is replaced by another

A

Metaplasia

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28
Q

Metaplasia occurs as a result of:

A

Chronic Irritation and Inflammation

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29
Q

Example of Metaplasia

A

Habitual Smoker: Stratified squamous epithelial cells into columnar epithelial cells

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30
Q

Deranged cell growth of a specific tissue. Results in cells varying in size, shape, and organization

A

Dysplasia

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31
Q

What is Dysplasia associated with?

A

Chronic Irritation and Inflammation (Reversible after irritation is removed )

32
Q

Metaplasia and Dysplasia’s relation to cancer

A

Metaplasia: continued exposure to stimulus, predispose to cancer transformation of the metaplastic reticulum
Dysplasia: Strongly implicated as a precursor of cancer

33
Q

Difference between cell injury and cell death

A

Injury: Reversible
Death: Irreversible (comes from an injury)

34
Q

Types of Cell Injury

A
  1. Sublethal/Reversible cellular damage

2. Irreversible injury with cell destruction or death

35
Q

Two observed patterns of reversible cell injury

A
  1. Cellular Swelling

2. Intracellular Accumulations

36
Q

Usually occurs as the result of hypoxic cell injury (ischemia, virus, bacteria, extreme heat/cold)

A

Cellular Swelling

37
Q

Types of Irreversible Cell Injury

A
  1. Apoptosis or programmed cell death

2. Necrosis or cell death

38
Q

Disintegration of cells into membrane-bound particles that are then phagocytosed by other cells

A

Programmed Cell Death or Apoptosis

39
Q

The number of cells in tissues is regulated by _____

A

Cell Death (therefor controlling tissue regeneration)

40
Q

Physiological processes of Apoptosis

A
  1. Programmed destruction of cells during embryonic development
  2. Hormone dependent involution of tissues
  3. Death of immune cells
41
Q

Apoptosis links to Pathological processes

A
  1. Contributes in carcinogenesis
  2. Cell death with viral infections (Hep B/C)
  3. Implicated in neurodegenerative disorders (Alzheimer’s, Parkinson’s, ALS)
42
Q

Cell death in an organ or tissue that is still part of living tissue

43
Q

How does necrosis differ from apoptosis?

A
  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
Q

How does necrosis present?

A
  1. Coagulative (Ischeima, Viruses, Toxins)
  2. Liquefaction Necrosis (Bacterial Infection)
  3. Caseous Necrosis (TB)
  4. Gangrene
45
Q

When does Gangrene occur?

A

When a considerable mass of tissue undergoes necrosis (usually due to deficient or absent blood supply)

46
Q

Gangrene can be:

A
  1. Dry (extremities arteries)
  2. Wet (Veins flow impaired and bacteria)
  3. Gas (from infection of devitalized tissue by bacteria)
47
Q

Causes of Cell Injury (6) Most common

A
  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
Q

Caused by lack of oxygen, respiratory disease, ischemia, anemia, physical or pathological injury to delivery method

49
Q

Hypoxia Outcomes

A
  1. Cell Swelling
  2. Denaturation of enzymes
  3. Chromosome clumping
  4. Autolysis
  5. Coagulative Necrosis
50
Q

Common causes of injury due to environmental exposure, occupational and transportation accidents, and physical violence and assault

A

Injury from physical agents

51
Q

3 Sections of Injury from Physical Agents

A
  1. Mechanical Forces
  2. Extremes of Temperature
  3. Electrical Injuries
52
Q

Impact of body with another object. Injuries split and tear tissue

A

Mechanical Forces (Physical Agent)

53
Q

Extremes of heat and cold cause damage to the cells, its organelles and its enzyme systems

A

Extremes of Temperature (Physical Agent)

54
Q

What happens with low intensity heat (43-46’ C)

A
  • Vascular injury
  • Accelerated cell metabolism
  • Disrupt Cell Membrane
55
Q

What happens with high intensity heat

A

Coagulation of blood vessels and tissue proteins

56
Q

What happens with exposure to cold

A

-Increased blood viscosity
-Induces vasoconstriction
(could lead to hypoxic tissue injury)

57
Q

Leads to disruption of neural and cardiac impulses

A

Electrical Injuries

58
Q

3 Sections of Radiation Injury

A
  1. Ionizing Radiation
  2. Ultraviolet Radiation
  3. Non-ionizing Radiation
59
Q

Can immediately kill cells, interrupt cell replication, or cause a variety of genetic mutations. (May/May Not be lethal)

A

Ionizing Radiation

60
Q

Where is ionizing radiation used? What are its outcomes?

A

Treatment for cancer

  • Direct: cell death
  • Indirect: Free radicals (division impairment, mutations, enzyme inactivation)
61
Q

Most vulnerable cells to ionizing radiation

A
  • GI tract
  • Bone Marrow
  • Cells with high mitotic activity
62
Q

Cause sunburn and increases risk of skin cancer

A

Ultraviolet Radiation

63
Q

What is damaged by ultraviolet radiation?

A
  • Reactive oxygen species
  • Melanin producing process in the skin
  • DNA
64
Q

Includes infrared light, ultrasound, microwaves, and laser energy

A

Non-ionizing Radiation

65
Q

Affects of non-ionizing radiation

A
  • Causes vibration and rotation of atoms and molecules

- Bc deep penetration, involve dermal and subcutaneous tissue

66
Q

Drugs, Lead Toxicity, and Mercury Toxicity injure the cell membrane and other cell structure.

A

Chemical Injury

67
Q

Results of Chemical Injury

A
  • Injure cell membrane and other cell structures
  • Block enzymatic pathways
  • Coagulate Cell Proteins
  • Disrupt the osmotic and ionic balance of the cell
68
Q

Differ from other injurious agents because they are capable to replicate (continue to produce injurious effects)

A

Biological Agent

69
Q

Nutritional excesses and nutritional deficiencies predispose cells to injury

A

Nutritional Imbalances

70
Q

Nutritional excess leads to:

A
  • Obesity

- Increase risk of many diseases

71
Q

Diets in saturated fats lead to:

A

Predispose person to atherosclerosis

72
Q

Nutritional deficiencies of protein lead to:

A

Malnutrition

73
Q

Deficiencies in vitamin C

74
Q

Deficiencies in vitamin B1 (thymine)

75
Q

Deficiencies in vitamin D

Pathology (7 decks)

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