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Pathophysiology Test 1 > Cell Adaptation/injury/death: Class 1 > Flashcards

Cell Adaptation/injury/death: Class 1 Flashcards

0
Q

Nucleus

-Function

A
  1. Brain of the cell
  2. Contains DNA
  3. Responsible for making ribosomes
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1
Q

Cell Membrane

-function

A
  1. Protects
  2. Transports
  3. Boundary system for the cell
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2
Q

Rough & Smooth Endoplasmic Reticulum (ER)

-function

A
  1. Where most protein synthesis occurs
  2. Synthesize lipids
  3. Smooth ER helps in detoxification of harmful substances
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3
Q

Ribosomes

-Function

A
  1. Make proteins that the cell and body need
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4
Q

Golgi Complex

-function

A
  1. UPS

2. Sorts and ships proteins made in the ER

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5
Q

Mitochondria

-function

A
  1. Packages the energy from food into ATP molecules
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6
Q

Vesicles

-function

A
  1. Stores and transports products produced by the cell
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7
Q

Cell injury can be caused by?

A
  1. Physical injury
  2. Toxic injury
  3. Infectious injury
  4. Hypoxic injury
  5. Deficiency injury
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8
Q

Ischemia

-cell sensitivity

A
  1. Skeletal muscle can tolerate 2-3 hrs of ischemia

2. Cardiac muscle can only tolerate 20 min of ischemia

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9
Q

Liver Cells

-Susceptible to what type of injury

A
  1. Chemical injury
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10
Q

Free Radicals

A
  1. Unpaired electron
  2. Highly unstable & reactive
  3. Will attempt to steal an electron from nearby molecule causing a chain reaction
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11
Q

Initiation of Free Radicals

A
  1. Absorption of extreme energy sources
    - UV light & Radiation
  2. Endogenous reactions when O2 is reduced to Water
    - Cell growth and proliferation
  3. Enzymatic Metabolism
    - from external chemicals like Cigarette smoke and Alcohol
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12
Q

Samples of Free Radical Damage

A
  1. Lipid per-oxidation
  2. Attacking critical proteins
  3. DNA fragmenting
  4. Damaging mitochondria
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13
Q

Free Radicals

-Terminating them

A
  1. Antioxidant enzymes
    - block synthesis of free radicals / inactivate them / Decompose
  2. Endogenous
    - Super Oxide Dismutase
    - Catalase
  3. Exogenous
    - Vitamin A, “E”, C
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14
Q

Free Radicals

-Endogenous Termination

A
  1. Super Oxide Dismutase

2. Catalase

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15
Q

Free Radicals

-Exogenous termination

A
  1. Vitamin E

2. Vitamin A & C

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16
Q

Cell Alteration

A
  1. All forms of disease begin with alterations to cells
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17
Q

Altered Cells and tissues

-Result from…

A
  1. Adaptation
  2. Injury
  3. Neoplasia
  4. Aging
  5. Death
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18
Q

Cellular Adaptation

-Atrophy

A
  1. Reduction in the size of the cell
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20
Q

Cellular Adaptation

-Atrophy - Examples

A
  1. Disuse
  2. Nutritional Deprivation
  3. O2 Deprivation (Ischemia)
  4. Decreased Hormonal stimulation
  5. Aging
  6. Denervation pressure
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21
Q

Cellular Adaptation

-Hypertrophy

A
  1. Enlargement of Cell due to increased workload
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22
Q

Cellular Adaptation

-Hypertrophy - Examples

A
  1. Mechanical signals
    - Stretch muscles causing enlargement
  2. Trophic signals
    - Send hormones causing enlargement
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23
Q

Cellular Adaptation

-Hyperplasia

A
  1. An increase in the number of cells caused by:
    - increased workload
    - hormonal stimulation
    - decreased tissue
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24
Q

Cellular Adaptation

-Hyperplasia - Examples

A
  1. Hormonal
    - Occurs mostly in estrogen-dependent organs (Uterus & breast)
  2. Compensatory
    - Liver cells (hepatocytes)
    - Epidermal (callus)
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25
Q

Cellular Adaptation

-Metaplasia

A
  1. Replacement of one adult cell w/ another cell
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26
Q

Cellular Adaptation

-Metaplasia - Examples

A
  1. Barret’s Esophagus

- GERD

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27
Q

Cellular Adaptation

-Dysplasia

A
  1. Deranged cell growth of specific tissue results in abnormal size, shape, and appearance
  2. DOES NOT INDICATE CANCER & may not progress to cancer
  3. Often reversible
  4. Not considered true adaptive process but is related to hyperplasia and often called (ATYPICAL HYPERPLASIA)
28
Q

Cellular Adaptation

-Dysplasia - Examples

A
  1. Cervical pre-cancer and Cancer R/T

- Human Papillomavirus (HPV)

29
Q

Cells adapt in what 5 ways?

A
  1. Atrophy
  2. Hypertrophy
  3. Hyperplasia
  4. Metaplasia
  5. Dysplasia
30
Q

Organisms

-Must be able to do what 3 things?

A
  1. Detect changes in their external & internal environments
  2. Interpret changes
  3. React or respond

If these are not done the cell with DIE
DETECT / INTERPRET / REACT

31
Q

Necrosis

-Fat

A
  1. Caused by LIPASES (powerful enzymes)
  2. Affect in:
    - Breast
    - Pancreas
    - Other Abdominal Structures
32
Q

Necrosis

-Coagulative

A
  1. Causes gelatinous, transparent state of ALBUMIN to change to a firm, opaque state
  2. Affects:
    - Heart, kidneys, & adrenal glands
  3. Caused by:
    - Severe ischemia or hypoxia
33
Q

Necrosis

-Liquefactive

A
  1. Results from Ischemic injury to NEURONS & GLIAL CELLS in the BRAIN.
  2. Cells are digested by their own hydrolyses
  3. Tissue becomes soft, liquefies, and segregates from healthy tissue
  4. Forms cysts
34
Q

Necrosis

-Caseous

A
  1. Results from TUBERCULOSIS pulmonary infection
  2. Tissue resemble clumped cheese (soft and granular
  3. Granulomatous inflammatory wall encloses areas of caseous necrosis
35
Q

Necrosis

-Gangrene

A
  1. Results from severe hypoxic injury
  2. Occurs because of ARTERIOSCLEROSIS or blockage of major arteries PVD
  3. Wet Gangrene occurs when neutrophils invade the site, causing liquefactive necrosis (diabetic ulcer)
36
Q

Wet Gangrene

A
  1. Develops when neutrophils invade the site, causing liquefactive necrosis (diabetic ulcer).
37
Q

Necrosis

-Gaseous Gangrene

A
  1. Caused by infection of tissue by CLOSTRIDIUM species
  2. Produces
    - hydrolytic enzymes & toxins that destroy connective tissue & cell membranes
  3. Leads to gas bubbles to form in muscle cells
38
Q

Apoptosis

A
  1. Programmed cell death
  2. Determines the size, patterning, and function of tissues
  3. Physiologic
  4. Pathologic
  5. Absence
39
Q

Cell production and destruction

A
  1. You produce and destroy about 10 Billion cells per day
40
Q

Re-perfusion Injury

A
  1. Results from oxidative stress (oxygen free radicals)
  2. Neutrophils adhesion to endothelium
    - Treatment: blockage of inflammatory mediators
41
Q

Hypoxia

A
  1. Most common cause of cellular injury
  2. Lack of sufficient oxygen
  3. Most common cause of hypoxia is ischemia (Reduced blood supply)
42
Q

Hypoxia

-Results from

A
  1. Reduced amount of 02 in the air
  2. Loss of hemoglobin
  3. decreased efficacy of hemoglobin
  4. Decreased production of RBCs
  5. Diseases of the respiratory and cardiovascular systems
  6. Poisoning of oxidative enzymes w/in the cells
43
Q

Mitosis

A

Process of dividing the duplicated DNA of the cell into two new nuclei

44
Q

Mitosis

-Prophase

A
  1. DNA condenses, organizes and the classic chromosome structure appears
  2. Protein strands called microtubules are seen
  3. Nucleolus disappears
45
Q

Mitosis

-Pro-metaphase

A
  1. Microtubules attach to the chromosomes

2. Begins when nuclear membrane is broken down

46
Q

Mitosis

-Metaphase

A
  1. Chromosomes align
47
Q

Mitosis

-Anaphase

A
  1. Chromosomes separate after metaphase
48
Q

Mitosis

-Telophase

A
  1. Nuclear membranes reappear around the two sets of chromosomes
49
Q

Cytokinesis

A
  1. Separation of the cytoplasm into 2 parts, a process that follows the division of the cell nucleus
50
Q

Interphase

overview

A
  1. Most of the cells life is spent in interphase
  2. Interphase is made up of:
    - G1, S, and G2
51
Q

Interphase

-G1 (Gap 1)

A
  1. 1st growth phase of interphase

2. Cell grows to nearly its full size and performs many of its biochemical activities

52
Q

Interphase

-S phase (Synthesis Phase)

A
  1. DNA in the nucleus is replicated
53
Q

Interphase

-G2 (Gap 2)

A
  1. Cell finishes growing
54
Q

Cellular Injury

-Occurs when?

A
  1. Cellular Injury occurs if the cell is unable to maintain homeostasis
55
Q

Physical Injury

-Examples

A
  1. Trauma/Surgery

2. UV Radiation

56
Q

Toxic Injury

-Examples

A
  1. External
    - Inhale C02
  2. Internal
    - byproducts of inflammatory response or another mechanism
57
Q

Infectious Injury

-Examples

A
  1. Fungi
  2. Parasites
  3. Bacteria
  4. Viruses
58
Q

Hypoxic Injury TEST

A

MOST COMMON INJURY

  1. Decreased Perfusion
    - pt w/ an MI
  2. Sickle Cell ANEMIA
  3. Ischemia
  4. Hypoxia
59
Q

Cell Injury Can be?

A
  1. Reversible or Irreversible
60
Q

Cell Injury

-Reversible

A
  1. Obstruction of blood flow
  2. Ischemia
  3. Decreased ATP production
  4. Na+ pump breaks down
    - INcreased intracellular Sodium and Calcium
    - Increased Extracellular Potassium
  5. INcreased glycolysis and lactate w/ decreased pH
    - leads to swelling of lysosomes // increased Ca influx
61
Q

Vulnerable Cellular Systems to Injury

A
  1. Cell membrane integrity
  2. ATP generation/ Mitochondrial function
  3. Protein function / Enzyme function
  4. Genetic Integrity
62
Q

Mechanisms of Cell Injury TEST

A
  1. Decreased O2
  2. decreased ATP production
  3. Increased ROS
  4. Decreased Mitochondrial function
  5. Increased intracellular Calcium
  6. Decreased Plasma Membrane Integrity
63
Q

Initiation of Free Radicals

-Enzymatic Metabolism EX.

A
  1. External Chemicals
  2. Cigarette smoke
  3. Alcohol
64
Q

Cellular Alteration and DIsease?

A
  1. All forms of disease begin with alterations to cells

Types of Adaptation

  • Atrophy
  • Hypertrophy
  • Hyperplasia
  • Metaplasia
  • Dysplasia
65
Q

Altered Cellular & Tissue biology Results from?

A
  1. Adaptation
  2. Injury
  3. Neoplasia
  4. Aging
  5. Death

Pathophysiology Test 1 (10 decks)

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