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FPP Block 1 > Cell Injury, Adaptations, and Death I and II > Flashcards

Cell Injury, Adaptations, and Death I and II Flashcards

1
Q

Define Homeostasis and list 2 types of stress that cells respond to

A

-maintenance of normal function within physiologic parameters

  • physiologic stimuli/stress: normal stimuli
  • pathologic stimuli/stress: cells modify to decrease or avoid injury
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2
Q

Define Hypoxia and Ischemia and what do they both result in?

A

They both result in oxygen deprivation

  • Hypoxia: oxygen deficiency/inadequate oxygenation of blood (ex lung disease, lack of oxygen/air)
  • Ischemia: reduced blood supply to site (ex: myocardial infarct)
    • also results in deficiency in nutrient supply and build up of toxic metabolites
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3
Q

List 8 etiologies of cell injury

A
  1. Hypoxia & Ischemia
  2. Toxins
  3. Infectious agents
  4. Immunologic reactions
    • autoimmune, allergies, hypersensitivity
  5. Genetic derangements
  6. Nutritional imbalances
  7. Physical agents
    • trauma, temperature extremes, radiation
  8. Aging
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4
Q

Define reversible cell injury and what are the typical functional derangements and morphologic changes

A
  • stage of injury at which the injured cell can return to normal if damaging stimulus is removed
  • typical changes
    • failure of membrane pumps to maintain homeostasis and accumulation of degenerated organelles and lipids in cell
      • causes cell swelling as intracellular organelles take on water leads to organelle changes
        • Specific changes to organelles: distended endoplasmic reticulum,
          detached ribosomes, membrane blebs, loosening of intercellular
          attachments, swollen mitochondria, clumping of nuclear chromatin
      • results in enlargement of entire organ
      • hydropic change/vaculoar degeneration or fatty change
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5
Q

Describe Vacuolar (hydropic) change in reversible injury

A
  • hydropic change is cellular swelling
  • its the first manifestation of a lot of cell injury
  • multiple cells affected leads to organ swelling
    • corresponds to distended ER, plasma membrane blebs, swollen mitochondria, and clumped nuclear chromatin
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6
Q

Descibe the example of hydropic changes in a yellow liver

A
  • yellow color means steatosis
  • injured hepatocytes=intracellular triglyceride accumulation, liver enlargemnet and elevated liver enzymes
  • nucleus is pushed aside due to liposomes

if cause is removed this is reversible

mild=no effect on cell function

severe=impairs cell function

*caused by toxins, obesity etc

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7
Q

What is Necrosis

A
  • a major pathway of cell death
  • it is uncontrolled and leads to damage that is too severe to be repaired
  • caused by: ischemia, toxin exposure, infection, trauma
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8
Q

What is regulated cell death

A
  • occurs with less severe injury
  • cells are eliminated as part of normal process
  • therapeutic agents and genetic mutation modify this
  • morphologically seen as apoptosis
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9
Q

Describe: what happens to the cell during necrosis and the morphology of necrosis

A
  • What happens to the cell
    • membrane falls apart
    • enzymes leak out of lysozomes an cell
    • inflammation is inuced
    • cell is digested by enzymes leaked from lysozomes or from recruited leukocytes
  • Morphology
    • Cytoplasmic changes: increased eosinophilia, homogenous cytoplasm, vacuolation
    • Nuclear chnages:
      • pyknosis: shrinkage and increased basophilia
      • karyorrhexis: fragmentation of the (pyknotic) nucleus
      • karyolysis: nuclear basophilia dissapears due to digetsion by DNase
    • Dead cells
      • may be completely digestion/dissapear
      • debris may be phagocytosed and further degraded
      • results in fatty acids that may calcify
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10
Q

List the types ot tissue necrosis

A
  • coagulative necrosis
  • liquefactive necrosis
  • caseous necrosis
  • gangrenous
  • fat necrosis
  • fibrinoid necrosis
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11
Q
  1. What causes Coagulative Necrosis?
  2. What do you see microscopically ?
  3. Where in the body does it happen?
A
  1. Results from hypoxic or anoxic injury due to ischemia
  2. Microscopically you see persistence of dead cells with intact outlines with loss of cellular details
  3. Coagulative necrosis occurs in all solid organs except for the brain
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12
Q
  1. What is Liquefactive Necrosis
  2. When do we see it
  3. What is an exception?
A
  • Liquefactive necrosis is complete digestion of dead cells
    • tissue is semi-liquid bc it was dissolved by hydrolytic enzymes (from lysosomes in WBCs attracted to area)
      • se no residual architecture
      • karyorrhexis
      • later you see mostly macrophages with little debris
  • Seen with bacterial and fungal infections
    • microbes stimulate accumulation of WBC which release digetsive enzymes
    • pus=necrotic cells + acute inflammatory cells
  • Exception: brain infarcts result in liquefactive necrosis (typically that would result in coagulative necrosis)

***no residual tissue architecture is preserved (remember that coagulative is preserved outlines with no cell details)

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13
Q

Caseous Necrosis

-what do you see microscopically?

A
  • characteristic of TB infection
  • gross appearance resembles cheese (crumbly/friable)
  • you see fragmented and coagulated cell with loss of architecture (No cell outlines) (remember cell outlines is coagulative) Usually surrounded by a border of inflammatory cells forming a distinctive pattern (granuloma)
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14
Q

Gangrenous Necrosis

  • wet gangrene vs. dry gangrene
A
  • not a specific type of necrosis however is a term to describe ischemic coagulative necrosis of lower or upper extremity
  • Wet or Dry
    • when a bacterial infection is also present, the necrosis has liqufactive characteristics (wet)
  • ​Also used for severe ecrosis of other organs (eg gangrenous bowel, appendix, gallbladder)
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15
Q

Fat Necrosis

A
  • typically in pancreas during acute pancreatitis
    • pancrease injury releases lipase which liquifies fat and splits triglycerids
    • saponification: fatty acids combine w calcium to form white chalky material
  • Also a result of trauma to fatty tissue with release of lipases and triglycerides (ex: fat necrosis of breast)
  • smudgy purple areas
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16
Q

Fibrinoid Necrosis

A
  • deposition of immune complexes (antigens and antibodies) in vascular walls
  • fibrin-like (bc oid means like) Bright pink amorphous appearance
  • occurs in vasculitis syndormes
    • polyarteritis nodosa, giant cell arteritis etc.
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17
Q

What is apoptosis and what are the key features

A
  • pathway of cell death-cells activate enzymes that degrade DNA and proteins
  • key features
    • plasma membrane intact
    • no leakage of cell contents
    • fragments of cell are pinched off
      • APOPTOTIC BODIES
    • no inflammation
    • cell fragments are consumed by macropahges
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18
Q

Describe the physiologic conditions that cause apoptosis

A
  • during embryogenesis
  • involution of hormone depenedent tissues after hormone deprivation (breasts in pregnancy)
  • turnover of proliferative tissues (ex GI eptihelium)
  • death of leukocytes after completion of inflammatory response
  • elimination of self-reactive lymphocytes
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19
Q

Describe pathologic conditions that lead to apoptosis

A
  • eliminates cells with DNA damage (afterradiation or chemo) if repeair process fails
  • accumulation of misfolded proteins (alzheimers)
  • cell injury from viral infection (HIV) induced bu virus or host
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20
Q

Describe the 3 Mechanisms of apoptosis

  • Mitochondrial (intrinsic pathway)
  • Death receptor (extrinsic pathway)
  • Clearance of apoptotic cells
A

Mitochondrial (intrinsic) Pathway

  • cytochrome C leaks from mitochondria after BH3 sensors are activated and Bax Bak are released

Death receptor

  • cell sexpress Fas ligand or TNF bind to cell surface “death receptors” and trigger caspase activation

Clearance of apoptotic cells

  • apoptotic cells express ligands for phagocyte cell receptors and secrete factors that attract phagocytes
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21
Q

describe the morphology of apoptosis

A
  • cytoplasmic eosinphilia
  • chromatin condensation and aggregation; eventually karyorrhexis (fragmentation of nucleus and break up of chromatin into granules)
  • cell shrinkage with cytoplasmic blebs and apoptotic bodies
  • phagocytosis without inflammation
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22
Q

Necrosis vs. Aoptosis

  • Cell size
  • Nucleus
  • Plasma membrane
  • Cellular contents
  • Adjacent inflammation
  • Physiologic or pathologic role
A
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23
Q

List the factors affecting cell injury and death

A
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24
Q

Describe how hypoxia/ischemia leads to necrosis

A
  • Decreased ATP production (bc less oxygen)
  • decreased energy-dependent functions
  • cell injury
  • necrosis
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25
Q

Describe how multiple simutaneous injuries may lead to necrosis

A
  • increase in ROS
  • damage to lipids, proteins, nucleic acids
  • cell injury
  • necrosis
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26
Q

Describe how mutations, cell stress and infections can lead to apoptosis

A

accumulation of misfolded proteins

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27
Q

describe how radiation and other insults can lead to apoptosis

A

leads to DNA damage in nucleus which elads to apoptosis

28
Q

Describe how infections, and immunologic disorders can lead to necrosis or apoptosis

A

they lead to inflammation which reates toxic metabolites. This leads to necrosis or apoptosis

29
Q

List common casues of cell injury/necrosis

A
  1. ischemic or hypoxic injury
  2. reperfusion injury
  3. oxidative stress
  4. chemical (toxic) injury
  5. Endoplasmic reticulum stress
  6. DNA damage
  7. inflammation
30
Q

Describe the difference between ischemic and hypoxic injury

A
  • ischemic injuries are the most common cause of cell injury and cause damage faster than hypoxic bc its not just not enough oxygen (like hypoxia) its
    • no delivery of substrates for glycolysis
      • stoppin aerobic and anaerobic glycolysis
    • no removal of metabolites by blood flow (build up of toxins)
  • Whereas a hypoxic injury aerobic glycocsis stops but anaerobic continues

But in both….

  • reduced supply of oxygen leads to reduced production and depletion of intracellular ATP which leads to failure of other energy dependent systems
31
Q

What does reduced supply of oxygen in both ischemic and hypoxic injuries elad to

A
  • reduced production and depletion of intracellular ATP
  • failure of other energy dependent systems
    • reduced activity of plasma membrane ATP-dependent sodium pumps results in swelling
    • increase in anaerobic glycolysis leads to increased lactic acid and decreased pH resulting in decreased activity of intracellular enxzmes
    • disruption of protein synthesis apparatus leads to decreased protein synthesis (detachment of ribosomes decreases protein synthesis)
    • possible ROS generation
    • eventual irreversible damage to mitochondrial and lysozomal membranes
32
Q

what happens o th N/K pump when thee is ischemia

A

stops working! bc there is decreased ATP

  • leads to influx of Ca, water and sodium
  • and efflux of K
  • this causes ER and cellular swelling and loss of micovili
33
Q

describe reperfusion injury

A
  • restoration of blood flow to ischemic tissue may increase cell injury
  • most frequently in brain and heart
  • mechansims:
    • increased generation of ROS: incomplete reduction of oxygen occurs with ischemis and restoration of oxygen allows production of ROS whihc increase tissue damage
    • increased leukocytes, plasma proteins, and complement (inflammation)
      • ​production of adhesion molecules and cytokines by damaged tissue attract inflammatory cells that increase the extent of the injury and repurfusion allows inflammatory cells to come back to the area and attract more inflammatory cells leading to injury
34
Q

Describe oxidative stress as a cause of cell injury and 3 patholgic effects of it!

A
  • oxidative stress causes _cellular abnormalitie_s induced by ROS and can lead to apoptotic and/or necrotic cell death
  • pathologic effects
    • lipid peroxidation-membrane damage
    • protein modification-breakdown, misfolding
    • DNA damage-mutations
  • generation of ROS increased with
    • absorption of radiant energy, ultraviolet, light, x-rays
    • selected exogenous toxins 9ex: carbon tetracloride
    • reperfusion of ischemic tissues
35
Q

Describe endoplasmic reticulum stress as a cause of cell injury/necrosis

A
  • ER stress is when there are misfolded proteins
    • typically when misfolded proteins accumulate the unfolded protein response is induced and things are fixed. however if more unfolded proteins continue to accumulate then apoptosis occurs
      *
36
Q

How do misfolded proteins accumulate? What causes this? What is the pathogenesis and what are some examples?

A
  1. accumulate due to increased production or decresed elimination
  2. caused by: aging, infections, changes in pH/redox sttae, ischemia/hypoxia, increased insulin demand (insulin resistance) and several neurodegenerative diseases (Alzheimer’s Parkinsons, Huntington)
  3. Pathogenesis: misfolded proteins don’t function normallt and are degraded, leading to eventual cell injury/death
  4. Examples of misfolded protein diseases: CF, Tay-Sachs, type II diabetes
37
Q

Describe the adaptive infolded protein response and the terminal unfolded protein response

A
  • increased synthesis of chaperone, reduced protein synthesis and increased protein degradation.
  • terminal is apoptosis. too many unfolded proteins leads to signaling and BH3 proteins are activated which activated caspases
38
Q

Describe DNA damage as a cause of cell injury

-causes and mechanism

A
  • DNA damage is caused bu radiation, cheomtheraeutic agents, intracellular generation of ROS, acquisition of mutations
  • mechanism leading to apoptotic death
    • with DNA damage, p53 accumulates, stops the cell cycle to allow DNA repair but if damage is too great then p53 triggers apoptosis
39
Q

Inflammation can cause cell injury. What causes this and what is the mechanism leading to death

A
  • causes: pathogens, necrotic clls and dysregulated immune response (autoimmune diseases and allergies)
  • mechanism leading to cell death is necrosis OR apoptosis
    • inflammatory cells damage the host tissue while they are destroying the pathgen. *hypersensitivity reactions)
    • they may also damage the host tissue beacsue of abnormal immune response against self antigens (autoimmune)
40
Q

Does mitochondrial dysfunction occur in necrosis apoptosis or both

A
  • Mitochondrial dysfunction occurs in BOTH necrotic and apoptoti cell death
41
Q

Do defects in membrane permeability occur in necrosis, apoptosis or both

A

defects in membrane permeability occur in necrotic cell death

42
Q

where are the most important location of membrane damage?

A

mitochondrial membrane

plasma membrane

lysososmal membrane

43
Q

There are 3 groups of proliferative capacities of tissues what are they and describe them

A
  • Continuously dividng (labile cells)
    • hematopoetic cells, surface epithelia (ex linings of airways, GI ract, skin etc)
  • Stable tissues
    • Quiescent (quiet); minimal replicative activity normally, bu they have a proliferative response to injury
    • parenchyma of most solid organs (liver kidney pancreas), endotelial cells, fibroblasts, smooth muscle cells
  • Permanent tissue
    • non-proliferative, ex: neurons, cardiac muscle cells
44
Q

Describe hypertrophy and the two types!

A
  • hypertrophy is when the increase in size of cells= the increase in size of organs. Amount of proteins and organelles increase and the mechanism can be trophic or mechanical triggers to the cell
  • the cells have limited to no capacity to divide
  • PHYSIOLOGIC:i ncreased functional demand or hormonal stimulation causes hypertrophy. ex: sleletal muscle hypertrophy when weight lifting and uterus in pregnancy
  • PATHOLOGIC: not natural cause. ex: cardiac muscle hypertrophy seen in hypertension
45
Q

Describe ventricular hypertrophy

A
  • pathologic hypertrophy: left ventricl increases in mass as an adaptation to the increased work load on the heart during hypertension or aortic valve stenosis.
  • myofibers enlarge (but number stays the same) leads to heart failure
46
Q

Hyperplasia

  • definition
  • physiologic vs pathologic
A
  • hyperplasia in an increas in cell NUMBER (remember hypertropic is increase in size, plasia is number) often occurs in cells capable of division (labile and stable)
  • PHYSIOLOGIC: hormonal hyperplasia of female breast at puberty and in pregnancy, compensatory hyperplasi of liver after partial resection
  • PATHOLOGIC: excessive stimulation by growth factors or hormone (not natural cause) ex: hormonal imbalance stimulate endometrial hyperplasia
  • reversible
  • cells respond to normal regulatory mechanism and clinical significance is that it increases risk for cancer
47
Q
  • Describe BPH
A
  • Benign prostatic hyperplasia
    • common in men over 50yo.
    • results in formation of nodules in prostate glans in the periurethral region, results in varying degree of urinary obstruction
    • cause is unknown
    • mechanism: androgen-induced release of growth factors increases proliferation of stromal cells and decreases death of epithelial cells (so number of cells increases)
    • not associated with increased risk for prostate cancer (unlike endometrial hyperplasia)
48
Q

Is connective tissue response to wound healing physiologic or pahologic and is it hypertrophy or phyperplasia

A
  • connective tissue response to wound healing is physiologic hyperplasia
49
Q

Are skin warts and mucosal lesions associated with viral infections (Papilloma viruses) physiologic or pathologic and is is hypertrophy or hyperplasia

A

warts and mucosal lesions from viruses are pathology hyperplasia

50
Q

Is enlargement of the uterus hypertrophy or hyperplasia

A

BOTH

51
Q

Define atrophy and what are some causes

A
  • decrease in size of a cell due to loss of cell subtance (decreased protein synthesis and increased degradation)
    • severe-decreasd organ size
    • leads to decreased function but not death
  • causes:
    • physiologic: loss of hormonal stimulation (endometrium at menopause)
    • pathologic: decreased functional demand (broken arm), loss of innervation (peripheral nerve trauma), inadequate nutrition (calorie or protein deficit)
52
Q

does skeletal muscle myopathy lea to hypertrophy or atrophy

A

BOTH

53
Q

Define metaplasia ang give 2 examples

A

when one adult cell type is replaced by another adult cell type.The cells are reprogrammed and the stem cells differentiate along a new pathway (that is better able to handle the stress)

  • can be an adaptive process to chronic stress/injury (smokers, reflux)
  • reversible but may be associated with increased risk of cancer
  • epithelial metaplasia:
    • ciliated columnar epithelium become ssquamous epithleium (ex trachea/bronchi of smokers)
    • squamous epithelium becomes gastric/intestinal type epithleium (distal esophagus of reflux pts.)
  • mesenchymal metaplasia:
    • ​bone formation in soft tissue (muscle/connective) at sites of injury
54
Q

Describe squamous metaplasia or trachea and bronchi

A

respiratory epithelium was ciliated columnar epithelium and becomes squamous

55
Q

describe Barrett esophagus

A
  • simple squamous epithelium in the distal esophagus becomes glandular epithelium (like what is found in the stomach) to protect against acid reflux. this predisposes pts. to adenocarcinoma
56
Q

Describe Squamous metaplasia in the endocervix

A
  • columnar becomes squamous and this increases risk of HPV infection
57
Q

Describe intracellular Accumulations

  • when do they occur and what are some examples
A
  • They are lterations of the cells resulting in distinctive morphology involving specific organelles (lysosomes, ER, mitochondria, nuclei, cytoskeleton)
  • intracellular accumulations occur in actue and chonic situations as a response to injury
    • excessive production and/or inadequate removal of substances, endogenous substance or exogenous substances
  • ex: lipid accumulation, cholesterol, proteins, glycogen, pigments (like lipofuscin, carbon, melanin, hemosiderin)
58
Q

how is cholesterol often and intracellular accumulation

A

found in the intima of atherosclerotic plaques in arteries

59
Q

examples of proteins as intracellular accumulations

A

neurofibrillary tangles in Alzheimer’s disease and Mallory hyaline in liver

60
Q

Describe Lipofuscin in heart muscle as an intracellular accumulation

A

Lipfuscin is indigestable material resulting from lipid peroxidation “wear and tear” pigment that occurs in the heart, brain and liver and is associated with aging

61
Q

Descibe anthracosis in lungs as an intracellular accumulation

A

carbon is inhaled in air and is phagocytosed by alveolar macrophages and transported to regional lymph nodes

62
Q

Describe hemosiderin in the liver

A
  • is a hemoglobin derived pigment containing iron that occurs locally where there has been a .ehmorrhage
  • systemic deposition occurs with an increased absoprtion of iron, in anemias, with many transfusions an in herditary conditions. found in many organs (liver, bone marrow, spleen, lymph nodes)
63
Q

What is dystrophic pathologic calcification

  • examples, what does is look like grossly and microscopically
A
  • non-viable, damaged or dying tissues with noraml serum calcium
  • ex: atheromas, aortic valves in elderly, lymph nodes with old TB
  • gross: white gritty deposits
  • microscopically: basophillic
64
Q

What is metastatic pathologic calcification

A
  • normal tissues
  • hypercalcemia
    • increased PTH
    • destruction of bone
    • Vitamin D intoxication
    • renal failure
  • most common locations: interstitial tissues (lung, kidney, gastric mucosa)
65
Q

How do cell aging and people aging relate?

A
  • people age bc their cells age. increased age measn inedependent risk factor for many chrnic diseases (cancer, alzheimers, ischemic heart disease)
  • cellular aging is the progressive decline in life span and functional activity of cells
  • persistant inflammation induces chronic diseases (atherosclerosis, diabetes) and chrnoic cytokine activation whihc may induce cellular alteration that exacerbate aging
  • telomere shortening
    • replicative senescence:
      • reduced capcity of cells to divide due to progressively shortening of chromosome ends (telomeres)
      • telomere shortening results in cell cycle arrest nd eventually results in somtic cells exit from cell cycle

FPP Block 1 (18 decks)

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