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NRS 250: Exam 1 > Module 2: Alterations in Cells and Tissues > Flashcards

Module 2: Alterations in Cells and Tissues Flashcards

1
Q

Atrophy

A
  • Cell size decreases or shrinks
  • Normal example: thymus
  • Pathological ex: loss of blood circulation, hormones, aging = loss of brain cells
  • Mechanism: decrease in protein synthesis
    • upregulation of proteasome activity
    • autophagy by lysosomes
      • cellular debris breaks down
  • Visible Changes: smaller cell size
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2
Q

Hypertrophy

A
  • Cell size increases
  • Normal ex: increased demand by hormones or growth factors
    • i.e. construction worker with hypertrophied upper body
  • Pathological Ex: chornic hemodynamic overload
    • leads to cardiomegaly
  • Mechanism: Increased protein synthesis
    • increased DNA synthesis
    • does NOT occur due to swelling caused by fluid
  • Visible Changes: increase total cell size
    • increased number of organelles
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3
Q

Hyperplasia

A
  • the number of cells increases due to increased cell divison
  • Physiological Ex:
    • compensatory hyperplasia: hepatocytes of the liver regenerate and replicate in the liver after they are damaged by alcohol
    • hormonal hyperplasia: hormone dependent organs experience replication of cells when exposed to certain hormones
      • i.e. endometrium of uterus grows with increased hormone production
  • Pathological Ex: abnormal proliferation of cells
    • i.e. cancer/tumors
  • Mechanism: hormonal and growth facotrs increase
    • failure of normal growth regulation
  • Visible changes:
    • excess cells
    • enlarged nucleus with enlarged nucleoli
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4
Q

Metaplasia

A
  • a type of cell is replaced with another type of cell, often becoming more homogenous (less differentiated)
  • New cell type may be more suitable for new environment–> prolonged exposure can lead to neoplasia
  • Mechanism: cytokines and growth factors related to inflammation and injury cause precursor cells to reprogram
  • Visible changes: cells look more homogenous (less differentiated)
    • abnormal cells that are not typical of surrounding cells are present
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5
Q

Dysplasia

A
  • mature cells end up with abnormal shapes, size, and organization
  • aka atypical hyperplasia
    • caused by persistent cell injury or irritation
  • NOT a good adaptive change
  • can be classified as low or high grade; or mild, moderate, or severe
  • can be associated with neoplastic growths in the cervix, respiratory tracts, or breast cancer
  • Mechanism: increased cell division
  • visible changes: increased number of cells, abnormal shape, and organization
    • Enlarged nucleus as inm hyperplasia and hypertrophy
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6
Q

Cellular Injury

A

a change occurs that can result in death

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7
Q

cellular adaptation

A

changes that occur in the cell as a result of changes in the environment

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8
Q

Causes of cellular injury (8)

A
  1. hypoxia
  2. free radicals
  3. chemical agents
  4. infectious agents
  5. physical or mechanical stress
  6. immune reactions
  7. genetic factors
  8. nutritional imbalance
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9
Q

Early Reversible Stages of Cellular Injury

A
  • Trigger is low oxygen
    • mitochondria reduce ATP production (only glycolysis can occur)
      • results in loss of Na/K pump acitvity
        • Na builds up intracellularly
          • water no longer block by Na in the ECF and enters the cell
        • K build up in the ECF
      • Results in loss of Na/Ca exchanger
        • intracellular build up of Ca in the ICF
      • Water enters the cell
        • causes cellular swelling, endoplasmic reticulum dilation, detached ribosomes, decreased protein synthesis, and lipid deposition
      • anaerobic glycolysys occurs
        • increased production of lactic acid leads to a decrease in pH in the cell which causes the nuclear chromatin to clump
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10
Q

Prolonged Hypoxic Cellular Injury

A
  • swelling continues which causes vacuolation: the formation of cavities within the cell; and blebs to occur
  • swelling of lysosomes:
    • becuase they are digesting cytoplasm and nuclear components
  • swelling of mitochondria
  • Ca2+ activates intracellular enzymes
    • proteases, phospholipases, and endonucleases
  • cell membrane damage occurs
    • influx of Ca2+
    • Further loss of proteins, degradation of nucleic acids, loss of ATP
  • Becomes irreversible–>cell death
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11
Q

Hypoxic Cellular Injury Causes

A

***Most common type of cellular injury*** Caused by lack of O2

  1. loss of local blood supply
  2. low oxygen in the air
  3. loss or alteration of hemoglobin
  4. decreased number of red blood cells ie anemia
  5. damage to oxidation enzymes (Cytochromes)
  6. insufficient systemic respiration
  7. insufficient system circulation
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12
Q

Ischemia

A
  • reduced blood supply
  • but if it is gradual then adaptations can occur
    • ex. thrombus that is growing and reducing blood supply
      • can adapt by creating new vessels that circumvent the thrombus
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13
Q

Anoxia

A
  • total lack of oxygen–> not tolerated by most tissues
    • ex. an embolus that gets stuck in a vessel
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14
Q

Oxidative Stress

A
  • Caused by reactive oxygen species(ROS)
  • ROSs causes cell, membrane, and organelle damage by:
    • peroxidation of lipids–> breakdown of unsaturated fatty acids
    • alteration of proteins
    • DNA damage
  • MITOCHONDRIA are very important in this oxidative stress
    • they produce and are damaged by ROS
      • they generate them during the electron transport chain
    • if ROS levels are high they can overhwlem the peroxisomes which carry antioxidant enzymes
  • Lipids, proteins, and mtDNA are all affected by ROS
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15
Q

Free Radicals

A
  • Definition: they are uncharged atoms with unpaired electrons that are unstable and often damage other molecules
  • Formed by: neutrophils and other inflammatory cells
    • endothelial cells, vascular smooth muscle, fibroblasts
    • they are possible in all cell types to different degrees
  • Formed due to:
    • energy sources that hve excess energy: UV and other radiation
    • redox reactions
    • enzymatic breakdown of exogenous molecules or drugs
  • They cause:
    • peroxidation of lipids–> breakdown of unsaturated fatty acids
    • alteration of proteins
    • DNA damage
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16
Q

Chemical Injury

A
  • Examples of chemicals that cause injury
    • carbon tetrachloride (CCl4)
    • lead
    • carbon monoxide
    • ethanol/alcohol
    • mercury
    • drugs
  • exposure via inhalation, ingestion, and absorption
  • Common mechanisms:
    • direct toxicity to the cell, membrane or organelles
    • production of free radicals
    • cellular enzymes or proteins may be altered
      • blocked synthesis of molecules
      • blocked cellular functions
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17
Q

Reperfusion Injury

A
  • Reperfusion can lead to apoptosis of cells
    • calls accumulate xanthine and hypoxanthine during ischemia
      • these two molecules combine with oxygen to form the ROS superoxide and hydrogen peroxide
    • causes cell membrane damage
    • mitochondrial Ca2+ overload
      • mitochondrial permability transition pore (MPTP)
        • results in loss of ATP and loss of solutes
    • Apoptosis–> activation of cell death by activation of Caspases
      • caspases are activated by the release of cytochrome C from the mitochondria
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18
Q

Caspases

A
  • pro-apoptotic enzyme
  • lead to a cascade that breaks down DNA \
  • can be activated by the release of Cytochrome C from the mitochondria
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19
Q

4 types of necrosis

A
  1. coagulative necrosis
  2. liquefactive necrosis
  3. casseous necrosis
  4. fat necrosis
20
Q

4 mechanisms of cellular accumulations

A
  1. abnormal metabolism
  2. defect in protein folding or transport
  3. enzyme defects
  4. cellular uptake of substances
21
Q

Examples of Types of Cellular Accumulations

A

Can be transient or permanent; can also be harmless or toxic

  • waters
  • lipids
  • carbohydrates
  • glycogen
  • proteins
  • pigments
  • calcium
  • urate
22
Q

Cellular Accumulations and Ethanol

A

Ethanol–> acetaldehyde and free radicals in the liver–> leads to inflammation, fatty liver, membrane damage–>depresses the CNS by acting on reticular formation which normally inhibits unacceptable behavior

23
Q

Storage Disease *

A

These are a set of diseases that lead to abnormal accumulations within the body

  • accumulation of substances caused by:
    • rare, genetic disease
    • loss of a specific enzyme function
    • accumulation of metabolic products due to defect in catabolism
  • Macrophage uptake these accumulations:
    • may be expelled into extracellular matrix
    • taken up by macrophages
    • may be stored in the liver or spleen
24
Q

Systemic Manifestations of Cellular Injury

A
  • fatigue
  • malaise
  • decreased appetite
  • fever–> endogenous pyrogens
  • increased heartrate
  • increased white blood cells(5000-9000mm3)
  • pain
  • release of enzymes from damaged cells
25
Q

Mechanisms Leading to Necrotic Cells

A
  1. Decreased ATP
  2. Mitochondrial damage
    1. results in leakage of pro-apoptotic proteins
  3. entry of Ca2+
    1. increases mitochondrial permability
    2. activation of multiple cellular enzymes
  4. Increased ROS
    1. damage to lipids, proteins, and DNA
  5. Membrane Damage
    1. Plasma membrane
      1. loss of cellular components
    2. lysosomal membrane
      1. releases enzymes that begin to digest cellular components
  6. protein misfolding and DNA damage
    1. activates pro-apoptotic proteins
26
Q

Coagulative Necrosis

A

The area that has undergone coagulative necrosis is also called an infarct

  • follows hypoxia
  • commonly affects heart, kidneys, and adrenal glands
  • ***proteins become denatured*** and become firm and opaque
    • albumin becomes firm “cooked egg white”
27
Q

Caseous Necrosis

A
  • Coagulative+ Liquefactive
  • common with Tuberculosis
  • clumped cheese appearance
28
Q

Liquefactive Necrosis

A

Generally affects the brain the most and is caused by excessive hydrolases

  • following ischemia in the brain
    • excessive hydrolases (break down water/-OH groups)
      • liquifies neural tissue, forms cysts
  • following certain bacterial infections
    • excessive hydrolases from pathogens
      • liquifies bacteria and causes nearby cell pus
29
Q

Fat necrosis

A

Caused by excess lipases

  • lipids get broken down and combine with Ca2+, Mg2+, and Na2+​
    • leads to saponification
  • occurs in breast, pancreas, and abdomen
    • where there is more fatty tissue
30
Q

Gangrene

A
  • Tissue level necrosis
  • its a result of severe hypoxic injury usually as a result of atherosclerosis or severe blockage of arteries
31
Q

Dry Gangrene

A

Causes by coagulative necrosis

  • appearance:
    • dry, shrunken, dark brown to black
      • there are no blood vessels that supply neutrophils which would make it wet
32
Q

Wet Gangrene

A

Caused by liqufactive necrosis

  • liquefactive necrosis due to neutrophil (anitgen presenting cell) invasion and inflammation
  • characteristics:
    • pus, foul odor
    • cold, swollen, and black
33
Q

Gas Gangrene

A

Caused by Clostridium perfringens (anaerobe) which releases excess hydrolytic enzymes

  • causes crepitous:
    • gas bubbles in the muscle cell
34
Q

Intrinsic Pathway for Apoptosis

A
  • cell receives signals from inside the cell
    • endoplasmic reticulum stress
    • causes mitochondria to produce enzumes and DNAses that break down everything
      • DNA is the first thing to break down
    • Pro-apoptotic enzymes
      • caspases–> lead to cascade that breaks down DNA
    • membrane itself does not break down right away
35
Q

Apoptosis

A
  • Size:
    • cellular shrinkage
    • one cell affected
  • Uptake:
    • cell contents ingested by neighboring cells
    • no inflammatory response
  • Membrane:
    • blebbing but integrity is maintained
    • apoptotic bodies form
  • Organelles:
    • mitochondria release pro-apoptotic proteins
    • chromaticn condensation and non-random DNA degradation
  • example: breast tissue when mothers ween after breastfeeding
36
Q

Necrosis

A
  • Size:
    • cellular swelling
    • many cells affected
  • Uptake:
    • cell contents ingested by macrophages
    • significant inflammation
  • Membrane:
    • loss of membrane integrity
    • cell lysis occurs
  • Organelles:

organelle swelling and lysosomal leakage

  • random degradation of DNA
37
Q

pyknosis

A

nucleus shrinks and condenses

38
Q

karyolysis

A

nucleus dissolves

39
Q

Extrinsic Pathway for Apoptosis

A

cell receives death signals through FAS ligand pathway that activate caspase 8/10 which triggers the cascade to break down

40
Q

Autophagy

A

when a cell eats itself, result in the delivery of cargo (organelles, etc.) to the lysosome for degradation and RECYCLING

  • membrane remains intact
  • 3 types:
  1. microautophagy
  2. macroautophagy
  3. chaperone-mediated autophagy
41
Q

Microautophagy

A
  • eats external things
  • occurs at the level of the peroxisome
42
Q

Macroautophagy

A
  • type of autolysis
  • eats its entire self
  • occurs through the phagophore
    • the phagophore is a double membrane that encloses the cytoplasmic components during macroautophagy
43
Q

Chaperone-mediated autophagy (CMA)

A

uses a receptor

44
Q

Cellular Aging

A

characterized by atrophy, decreased function, and loss of cells (through apoptosis)

45
Q

Sarcopenia

A

loss of muscle mass and strength

46
Q

Tissue and Systemic Aging

A

every physiological process declines with age

  • progressive stiffness and rigidity
    • arterial, pulmonary, and musculoskeletal
47
Q

Frailty

A
  • Can be a wasting syndrome of aging
  • decreased mobility, balance, muscle strength, motor activity, cognition, nutrition, endurance, and bone density in creased falls and fractures
  • accompanied by declining hormone levels and increased levels of pro-inflammatory cytokines

NRS 250: Exam 1 (11 decks)

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