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FPP Weeks 1 & 2 > Cell Injury, Adaptations, and Death I and II > Flashcards

Cell Injury, Adaptations, and Death I and II Flashcards

1
Q

Name the cellular response to:

Altered physiological stimuli or nonlethal injurious stimuli ⇒

  1. Increased demand, increased stimulation (e.g., by growth factors, hormones) ⇒
  2. Decreased nutrients, decreased stimulation ⇒
  3. Chronic irritation (physical or chemical) ⇒
A

⇒ Cellular adaptations

  1. ⇒ Hyperplasia, hypertrophy
  2. ⇒ Atrophy
  3. ⇒ Metaplasia
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2
Q

Name the cellular response to:

Reduced oxygen supply, chemical injury, microbial infection ⇒

  1. Acute and transient ⇒
  2. Progressive and severe (including DNA damage) ⇒
A

⇒ Cell injury

  1. ⇒ Acute reversible injury (cellular swelling and fatty change)
  2. ⇒ Irreversible injury (cell death)
    • Necrosis
    • Apoptosis
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3
Q

Name the cellular response to:

**Metabolic alterations, genetic or acquired, chronic injury ⇒ **

A

⇒ Intracellular accumulations, calcification

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4
Q

Name the cellular response to:

Cumulative sub-lethal injury over long life span ⇒

A

⇒ Cellular aging

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5
Q

How are tissues grouped based on their proliferative properties?

A
  1. Labile cells
    • Continuously dividing cells
    • Hematopoietic cells, surface epithelia (ex.: linings of upper airways, gastrointestinal tract, skin, etc.)
  2. Stable tissues
    • Quiescent; minimal replicative activity normally
    • Proliferate in response to injury
    • Parenchyma of most solid organs (liver, kidney, pancreas)
    • Endothelial cells, fibroblasts, smooth muscle cells
  3. Permanent tissues
    • Non-proliferative
    • Neurons, cardiac muscle cells
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6
Q

Cellular Adaptations: Hypertrophy

A
  • Increase in size of cells = increase of size of organ
    • Increased amounts of proteins and organelles
    • Mechanisms: trophic or mechanical triggers to cell
  • Occurs in cells that have limited or no capacity to divide
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7
Q
  1. Physiological Hypertrophy
  2. Pathological Hypertrophy​​
A
  1. Physiological Hypertrophy
    • Increased functional demand or hormonal stimulation
    • Examples: Skeletal muscle hypertrophy in weight lifting athlete and uterus in pregnancy
  2. Pathological Hypertrophy​​
    • Example: Cardiac muscle hypertrophy seen in hypertension
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8
Q

Generally describe left ventricular hypertrophy:

A
  1. Thick left ventricle & increased mass
  2. Adaptation in response to increased work load in hypertension (chronic hemodynamic overload)
    • Also occurs with aortic valve stenosis
  3. Myofibers enlarge: synthesis of more filaments
  4. Clinical manifestations:
    • initially no clinical signs, but eventually, heart reaches a limit beyond which enlargement of muscle mass cannot compensate for increased work & heart failure occurs.
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9
Q

Cellular Adaptations: Hyperplasia

A

Increase in cell number

  • Occurs in cells capable of division
    • labile and stable cells
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10
Q
  1. Physiologic Hyperplasia
  2. Pathologic Hyperplasia
A
  1. Physiologic Hyperplasia
    • Hormonal hyperplasia of female breast at puberty and in pregnancy
    • Compensatory hyperplasia of liver after partial resection
    • Connective tissue response with wound healing
  2. Pathologic Hyperplasia
    • Excessive stimulation by growth factors or hormones
    • Example:
      • Hormonal imbalance stimulates endometrial hyperplasia
      • Skin warts and mucosal lesions associated with viral infections
        • papilloma viruses
    • Reversible
    • Cells respond to normal regulatory mechanisms
    • Clinical significance: Increases risk for cancer
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11
Q

Describe benign prostatic hyperplasia. What makes it different from other hyperplasias?

A
  • Very common in men > 50 years old
  • Results in formation of nodules in prostate gland in the periurethral region ⇒ varying degrees of urinary obstruction
  • Underlying cause is unknown
  • Mechanism: androgen-induced release of growth factors increases proliferation of stromal cells ⇒ decreases death of epithelial cells
  • Differs from endometrial hyperplasia in that it is not associated with increased risk of prostate cancer
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12
Q

Give a clinical example of both hyperplasia and hypertrophy:

A

Enlargement of uterus during pregnancy (gravid)

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13
Q

Cellular Adaptations: Atrophy

A

Decrease in size of a cell due to loss of cell substance

  • If severe ⇒ decreased organ size
  • Decreased protein synthesis & increased degradation
  • Decreased function, but not death
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14
Q
  1. Physiologic Atrophy
  2. Pathologic Atrophy
A
  1. Physiologic Atrophy
    • ​​Loss of hormonal stimulation
    • ex: endometrium at menopause
  2. Pathologic Atrophy
    • Decreased functional demand
      • ex: broken arm in cast
    • Loss of innervation
      • ex: trauma to peripheral nerve
    • Inadequate nutrition
      • calorie or protein deficit
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15
Q

Cellular Adaptations: Metaplasia

A

One adult cell type is replaced by another adult cell type (that is better able to handle the stress)

  • Adaptive process to chronic stress +/or persistent cell injury
    • Examples: Chronic smokers, Chronic gastric acid reflux
  • Cells are “reprogrammed”
    • Stem cells differentiate along a new pathway
  • Reversible
  • May be associated with risk of cancer
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16
Q

Describe the two types of metaplasia:

A
  1. Epithelial metaplasia
    • Ciliated columnar epithelium becomes squamous epithelium
      • _​_ex. Trachea/bronchi of smokers
    • Squamous epithelium becomes gastric/intestinal type epithelium
      • ex. Distal esophagus in those with reflux
  2. Mesenchymal metaplasia
    • Bone formation in soft tissue (muscle/connective tissue) at sites of injury
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17
Q

Describe squamous metaplasia of trachea & bronchi in smokers:

A
  • Respiratory epithelium:
    • ciliated columnar epithelium
      ⇒ squamous epithelium
  • Stimulus that causes metaplasia may predispose to development of malignant neoplasm (squamous cell carcinoma)
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18
Q

Describe the process of Barrett Esophagus:

A

Squamous epithelium (distal esophagus) ⇒ glandular epithelium (stomach)

  • protects against reflux of stomach acid
    • predisposes to development of glandular carcinoma (adenocarcinoma)
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19
Q

What happens with squamous metaplasia in the endocervix?

A
  • columnar becomes squamous
  • increases risk of HPV infection
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20
Q

What are the 2 types of oxygen deprivation?

A

hypoxia and ischemia

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21
Q

What is the difference between hypoxia and ischemia?

A
  1. Hypoxia
    • Inadequate oxygenation of blood
      • ex: lung disease, lack of oxygen in ambient air
    • Reduced oxygen-carrying capacity of blood
      • ex: anemia, cyanide
  2. Ischemia
    • lack of blood supply to site
      • ex: coronary artery disease/heart attack, stroke
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22
Q

Besides oxygen deprivation, what are the other etiologies of cell injury?

A
  • Physical agents
    • Trauma, temperature extremes, radiation, etc.
  • Chemical agents
    • Chemicals (sodium, glucose), poisons, asbestos, etc.
  • Infectious agents
    • Viruses, fungi, bacteria, parasites, etc.
  • Immunologic reactions
    • Autoimmune diseases, hypersensitivity
  • Genetic derangements
    • Point mutations, polymorphisms, etc.
  • Nutritional imbalances
    • Protein / calorie imbalance, vitamin & mineral deficiencies, etc.
  • Aging: decreased ability to repair damage
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23
Q

What is cell injury a result of?

A

Continued severe stress (intrinsic and extrinsic) to a point that the cell reaches its limit and can no longer adapt

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24
Q

Irreverisble Cell Injury (cell death):

Causes and Types (2)

A
  • Inability to reverse mitochondrial dysfunction
    • lack of oxidative phosphorylation & ATP generation
  • Disturbance of membrane function

​Two Types:

  1. Necrosis
  2. Apoptosis
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25
Q

Cell Death: Necrosis vs. Apoptosis

  1. Cell size:
  2. Nucleus:
  3. Plasma Membrane:
  4. Cellular Contents:
  5. Adjacent Inflammation:
  6. Physiologic or Pathologic Role:
A

Necrosis

  1. Cell size: Enlarged
  2. Nucleus: Pyknosis, karyorrhexis, karyolysis
  3. Plasma Membrane: Disrupted
  4. Cellular Contents: Enzymatic digestion: may leak out of cell
  5. Adjacent Inflammation: Frequent
  6. Physiologic or Pathologic Role: Invariable pathologic

Apoptosis:

  1. ​Cell size: Reduced
  2. Nucleus: Fragmentation into nucleosome-size fragments
  3. Plasma Membrane: Intact: altered structure
  4. Cellular Contents: Intact: may be released in apoptotic bodies
  5. Adjacent Inflammation: No
  6. Physiologic or Pathologic Role: Often physiologic: elminating unwanted cells. May be pathologic
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26
Q

Morphology of Reversible Cell Injury

  • Fatty change
  • Cellular Swelling
A
  • Fatty change
    • Lipid vacuoles in cytoplasm
    • Occurs with toxic and hypoxic injury
    • Primarily in cells dependent on fat metabolism
    • Example: fatty liver secondary to toxins (alcohol)
  • Cellular Swelling
    • Hydropic change or vacuolar degeneration
    • Results from failure of membrane pumps to maintain homeostasis: membrane blebs
    • Vacuoles appear in cells corresponding to distended endoplasmic reticulum
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27
Q

Describe the pathogenesis and clinical manifestations of fatty liver:

A
  • Yellow color and “greasiness” indicates steatosis (fat accumulation)
  • Hepatocytes are injured resulting in an intracellular accumulation of triglycerides, liver enlargement and elevated liver enzymes
    • leak from injured hepatocytes
  • Clinical manifestations: depend upon specific cause & how severe the injury
  • It is reversible if cause is removed.
    • Mild: no effect on cell function.
    • Severe: impairs cell function, may lead to cell death, eventual cirrhosis if injury continues
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28
Q

What are some causes of fatty liver? What other organs accumulate fat?

A
  • Common causes:
    • toxins (including alcohol)
    • obesity
    • malnutrition
    • carbon tetrachloride
    • anoxia
    • diabetes
    • viral infections
  • Other organs accumulate fat also:
    • heart, skeletal muscle, kidney
29
Q

Why would the liver accumulate fat?

A
  1. impairment of microsomal & mitochondrial functions
  2. decreased fatty acid oxidation
  3. decreased apoprotein formation
  4. increased mobilization of fatty acids from periphery
30
Q

Describe Vacuolar (hydropic) Change:

A

Hydropic change (cellular swelling) of kidney tubules:

  • First manifestation of many types of cell injury
  • Corresponds to distended endoplasmic reticulum
    • Also seen:
      • plasma membrane blebs
      • swollen mitochondria
      • clumped nuclear chromatin
  • When many cells in an organ are affected ⇒ organ weight is increased and appears swollen
31
Q

Morphologic Features of Necrosis

A
  • increased eosinophilia
  • nuclear shrinkage
  • fragmentation
  • breakdown of plasma membrane & organelle membranes
32
Q

List the types of necrosis (6):

A
  1. Coagulative necrosis
  2. Liquefactive necrosis
  3. Caseous necrosis
  4. Gangrenous
  5. Fat necrosis
  6. Fibrinoid necrosis
33
Q

Coagulative Necrosis:

  • Etiology:
  • Morphology:
  • Areas affected:
A
  • Etiology:
    • ​Results from hypoxic or anoxic injury due to ischemia (infarct)
  • Morphology:
    • Persistence of dead cells with intact outlines but with loss of cellular details
    • Injury denatures both cellular proteins and enzymes (no proteolysis takes place)
  • Areas affected:
    • ​Occurs in all solid organs (except for the brain)
34
Q

Liquefactive Necrosis

  • Etiology:
  • Pathogenesis:
  • Morphology:
A
  • Etiology:
    • ​Complete digestion of the dead cells
  • Pathogenesis:
    • Commonly seen with bacterial and fungal infections
    • Microbes stimulate accumulation of WBC
    • WBCs release digestive enzymes
    • Necrotic cells together with acute inflammatory cells = pus
    • EXCEPTION: brain infarcts results in liquefactive necrosis (reasons not understood)
  • Morphology:
    • Tissue is semi-liquid as it has been dissolved by hydrolytic enzymes
      • from lysosomes in WBCs attracted to the area
35
Q

Caseous Necrosis:

  • Etiology:
  • Morphology:
A
  • Etiology:
    • ​Characteristic of tuberculous infection
  • Morphology:
    • Gross appearance resembles cheese
      • Crumbly (friable) appearance of necrosis
    • Fragmented and coagulated cells with loss of tissue architecture (no cell outlines)
    • Usually surrounded by a border of inflammatory cells forming a distinctive pattern (granuloma)
36
Q

Gangrenous Necrosis

  • Dry gangrene vs. wet gangrene
A
  • Not a specific type of necrosis but a term used for ischemic coagulative necrosis of lower or upper extremity
  • Dry gangrene vs. wet gangrene:
    • When a bacterial infection is also present, the necrosis has liquefactive characteristics (wet gangrene)
  • Also used for severe necrosis of other organs:
    • Ex: gangrenous bowel, gangrenous appendix, gangrenous gallbladder
37
Q

Fat Necrosis:

  • Areas affected:
  • Pathogenesis:
A
  • Areas affected:
    • ​Typically seen in the pancreas in acute pancreatitis
  • Pathogenesis:
    • ​Injury to pancreas releases lipase which liquefies fat and splits triglycerides
    • Fatty acids combine with calcium to form chalky white material (saponification)
    • Can also occur as a result of trauma to fatty tissue with release of lipases and triglycerides
      • Example: Fat necrosis of breast
38
Q

Fibrinoid Necrosis:

A
  • Deposition of immune complexes (antigens & antibodies) in vascular wall
  • Fibrin-like (suffix “-oid” means “like”)
    • Bright pink amorphous appearance
  • Occurs in vasculitis syndromes
    • Polyarteritis nodosa, giant cell arteritis, etc.
39
Q

What are the principal targets for cellular injury? By what mechanism are the targets affected?

A
  • Mitochondria
    • depletion of ATP & ↑ reactive oxygen species-ROS
  • Calcium homeostasis
    • intracellular entry of calcium
  • Cellular membranes
    • increase permeability
  • DNA & cellular proteins
    • damage to DNA, protein misfolding
40
Q

Mitochondrial damage results in ___ ________.

  • Major Causes:
A

ATP depletion

  • Major Causes:
    • Decreased oxygen
    • Decreased nutrients (glycogen)
    • Specific toxins (cyanide)
  • ATP: required for synthetic & degradative cell processes
41
Q

What happens as a result of ATP depletion in the mitochondria?

A

Production of reactive oxygen species (ROS)

42
Q

Effects of increased intracellular calcium:

A
43
Q

Accumulation of Oxygen-derived Free Radicals
(Oxidative damage)

A
44
Q

What are the mechanisms of membrane damage? What are the etiologies of membrane damage?

A
  • Causes:
    1. ischemia
    2. microbial toxins
    3. complement
    4. other physical/chemical agents
45
Q

Ischemic vs. Hypoxic Injury

A
  • Ischemia (decreased blood flow) injures tissues faster than hypoxia (decreased oxygen level)
    • No delivery of substrates for glycolysis
      • Both aerobic & anaerobic glycolysis cease
    • No removal of metabolites by blood flow
    • Most common cause of cell injury
  • Hypoxia: anaerobic glycolysis continues
  • In each: reduced supply of oxygen
    • Results in reduced production of intracellular ATP
    • Leads to failure of other energy dependent systems
46
Q
  • *Factors affecting cell injury and death**
  • *Cell response depends upon:**
A
  1. Type of injury
    • Ischemia vs. hypoxia; toxins, infection, etc.
  2. Duration & severity of insult
    • Example:
      • IF complete ischemia: death in 15 to 20 minutes
      • IF blood flow reduced by half: it takes 3-4 hours for cell death
47
Q

Factors affecting cell injury and death

Outcome depends upon:

A
  1. Cell type:
    • Example: Neurons are particularly sensitive to lack of oxygen
    • In other tissues: skeletal muscle dies in 2-3 hours; cardiac muscle in 20-30 minutes, etc.
  2. Extent of collateral flow:
    • from vessels around the area affected
48
Q

What are other factors that affect cell injury and death (besides injury and cell type)?

A

Additional factors:

  1. genetics
  2. hormones
  3. nutritional status of cell/organ
49
Q

Reperfusion Injury

  • Definition:
  • Mechanisms:
A
  • Definition: Restoration of blood flow to ischemic tissue may increase cell injury
    • Occurs most frequently in brain and heart
  • ​Mechanisms:
    1. Increased free radical generation
    2. Incomplete reduction of oxygen occurs with ischemia
      • Restoration of oxygen allows production of free radicals which increase tissue damage
    3. Increased leukocytes, plasma proteins, & complement (inflammation)
      • Production of adhesion molecules and cytokines by damaged tissue attract inflammatory cells that increase extent of injury
50
Q

Chemical (toxic) injury:

Mechanims (2)

A

Many drugs/toxins are metabolized in liver; it is often site of drug toxicity

  1. Direct toxins:
    • Bind to cellular organelle or molecular component
  2. Toxic metabolites:
    • Toxin is “activated”
    • Often by P-450 oxidases in liver smooth ER
51
Q

Give an example of a direct toxin that causes cell injury:

A

Example:

  • Mercuric chloride binds to cell membrane proteins
  • Results in decreased membrane transport and increased membrane permeability
52
Q

Give an example of a toxic metabolite that causes cell injury:

A

Examples:

  1. Acetominophen (tylenol)
  2. Carbon tetrachloride converted to toxic free radical which breaks down ER membranes
53
Q

Apoptosis characteristics:

A
  1. The plasma membrane is intact
  2. No leakage of cell contents
  3. No inflammation
54
Q

Causes of apoptosis:

Physiologic Conditions

A
  1. during embryogenesis
  2. involution of hormone dependent tissues after hormone deprivation (ex. pregnancy)
  3. cell loss in proliferating cells maintains constant number (ex. GI epithelium)
  4. death of inflammatory cells (neutrophils, lymphocytes) after completion of immune response
  5. elimination of self-reactive lymphocytes
  6. death induced by cytotoxic-T lymphocytes
55
Q

Causes of apoptosis:

Pathologic condtions

A
  1. Eliminates cells with DNA damage (ex. radiation, chemo, etc.)
    • If repair processes fail, apoptosis is activated and the cell dies
    • Radiation & many chemo drugs work via apoptosis
  2. Accumulation of misfolded proteins (ex. Alzheimer disease)
  3. Cell injury induced by viral infections (ex. HIV), induced by the virus or the host
  4. Organ atrophy with duct obstruction (example: Pancreas)
56
Q

Morphology of Apoptosis

A
  • Cytoplasmic eosinophilia
  • Chromatin condensation & aggregation
    • eventually karyorrhexis
  • Cell shrinkage with cytoplasmic blebs & apoptotic bodies
  • Phagocytosis without inflammation
57
Q

Describe the intrisnic mitchonidrial pathway for apoptosis:

A

Intrinsic pathway:

Bcl-2 proteins increase permeability of the mitochondria ⇒ allow cytochrome C to enter cyotplasm ⇒ resulting in caspase activation

58
Q

Cystic fibrosis, familial hypercholesterolemia, Tay-Sachs disease, Creutzfeldt-Jakob disease, Alzheimer disease, Huntington disease, Parkinson disease are all caused by what process?

A

Unfolded protein response & diseases caused by mis-folding of proteins ⇒ leads to apoptosis

59
Q

Subcellular responses due to cell injury:

A
  • Alterations of the cell resulting in distinctive morphology involving specific organelles
    • Occur in acute (lethal) & chronic (on-going) injury as an adaptive response to injury
  • Results may be accumulation of abnormal substances
    • Lipid accumulation already discussed
    • May be seen in lysosomes, endoplasmic reticulum, mitochondria, etc.
    • Examples: lipofuscin, carbon, iron, etc.
60
Q

Lipofuscin in heart muscle:

A
  • Indigestible material resulting from lipid peroxidation
  • “Wear & tear” pigment, occurs predominantly with aging
  • Particularly in heart, liver, & brain
61
Q

What type of disease of Tay-Sachs Disease?

A

Lysosomal Storage Disease

  • Abnormal metabolism
    • increased production of normal substance (gangliosides) because of lack of enzyme to degrade it
62
Q

Anthracosis in lung:

A

Inhaled in air ⇒ **phagocytosed by alveolar macrophages **⇒ transported to regional lymph nodes

63
Q

Give an example of hypertrophy of smooth ER in liver:

A

adaptative response to barbiturates & alcohol in hepatocytes (to maximize toxin removal)

64
Q

What could cause mitochondrial change?

A
  1. mitochondria response to starvation (atrophy)
  2. alcohol (enlarge)
  3. myopathy due to respiratory chain enzyme abnormality (increase in number & show abnormal structure)
65
Q

Cytoskeleton Abnormalities

A
  • Consists of actin, myosin, microtubules & intermediate filaments
  • Accumulations occur with:
    • Toxins: Alcohol - Mallory hyaline in liver
    • Unknown causes: Alzheimer’s disease - Neurofibrillary tangle
  • Abnormal organization of microtubules
    • Kartagener Syndrome: immotile cilia: sterility & lung infections
66
Q

Describe the morphology and pathogenesis of hemosiderin in the liver:

A
  • Hemoglobin-derived pigment containing iron:
    • yellow to golden-brown
  • Occurs locally where there has been hemorrhage
  • Systemic deposition occurs:
    • with increased absorption of iron, in anemias, with many transfusions, and in hereditary conditions
  • Hemosiderin is found in many organs
    • liver, bone marrow, spleen, lymph nodes
67
Q

Pathologic Calcification:
Dystrophic

A
  • Non-viable, damaged or dying tissues
  • Normal serum calcium
  • Examples:
    • Atheromas
    • Aortic valves in elderly
    • Lymph nodes with old TB
  • Gross: white gritty deposits
  • Microscopically: basophilic
68
Q

Pathologic Calcification:

Metastatic

A
  • Normal tissues
  • Hypercalcemia
    • Increased parathyroid hormone
    • Destruction of bone
    • Vitamin D intoxication
    • Renal failure (most common cause)
  • Most common locations:
    • Interstitial tissues (lung, kidney, gastric mucosa)
69
Q

Cellular Aging

A
  • DNA damage increases with age
    • Possible role of free radicals
  • Decreased cellular replication (“progressive replicative senescence”)
    • Progressive shortening of telomeres (short DNA sequences at ends of chromosomes) over time in each cell division
    • Lack of telomerase (maintains telomere lengths) in somatic cells
  • Defective protein homeostasis
    • Decreases cell survival, replication, & function

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