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Cell injury Flashcards

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1
Q

Defenition of cell injury

A

**A Variety of stresses the cell encounters as a change in external or internal environment causing morphological &/or functional chnages. **

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2
Q

The cellular response depends on ……… & ……..

A

1- Type of cell or tissue involved
2- extent & type of injury

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3
Q

What are types of cellular responses ?

A

1. Cellular adaptations
2. reversible Cell injury
3. Irreversible CI
4. Intracellular accumulations

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4
Q

In reversible CI, when the stress is …… to ……., the cell ……..

A

mild
moderate
may recover

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5
Q

In Irreversible CI, the stress is ……………, ………. may occur

A

severe, persistent
cell death (necrosis // Apotosis

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6
Q

Def of Cellular addaptations

def & types

A

Reversible changes in size, type, phenotype, metabolic activity or functions of cell in response to a stimuli (chnage in the environment).
There are 4 types :
1. Hypertrophy
2. Atrophy
3. Hyperplasia
4. Metaplasia

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7
Q

diff betw physiologic adaptations & Pathologic ones

A
  1. **Physiologic adaptations : ** represent responses of cell to normal stimulations as hormones or endogenous chemical mediators
  2. Pathologic Adaptations :represent responses of cell to stress allowing to modulate its structure & functions => escape injury.
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8
Q

Def of Atrophy

A

decrease in size of a normal organ due to decrease in size of its cells w/ or w/o decrease in nb of cells.

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9
Q

Diff betw Atrophy // Aplasia // Agenesis

A
  1. **Atrophy : **decrease in size of a normal organ due to decrease in size of its cells w/ or w/o decrease in nb of cells.
  2. **Aplasia : **extreme failure of develop. so only rudimentary tissue is present.
  3. **Agenesis : **Complete absence of an organ.
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10
Q

Atrophic cells are dead ?

A

No, they have diminished function but not dead.

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11
Q

…………. death may be induced by the same signals as Atrophy leading to decrease in nb.

A

Apoptotic death

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12
Q

EX of Physiologic Atrophy

A

Atrophy of
1. Lymphoid tissue, thymus, appendix
2. Brain & Heart w/ aging
3. gonads after menopause

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13
Q

EX of Pathologic Atrophy

A
  1. Disuse Atrophy: wasting of muscles of the limb immobilized
  2. Neuropathic Atrophy: Neuropathic due to loss of innervation => wasting of muscles (ex : traumatic nerve injury & poliomyelitis)
  3. Endocrine Atrophy: Loss of trophic hormones (hormones secreted by pituitary) (EX: hypopituitarism may lead to atrophy of thyroid, adrenal, gonads)
  4. Pressure Atrophy: Large aortic aneurysm => atrophy of vertebral bodies not intervertebral discs.
  5. Atrophy due to lack of nutrients: severe protein-calorie malnutrition (EX: Marasmus), => muscle atrophy.

disuse atrophy: not using muscles enough, body start break them down

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14
Q

Atrophy Pathogenesis (mechanism by w the lesions are produced)

A

Decrease in cells size due to :
decrease in protein synthesis
Increase in protein degradation

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15
Q

Atrophy Morphologic features

A
  1. Organ is small as cells are small due to reduction in cell organelles (mitochondira, ER, Myofil.)
  2. Numerous Autophagic vacuoles w/ cell debris => residual bodies EX: lipofuscin pigment granules in brown atrophy
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16
Q

Def of Hypertrophy

A

Increase in size of organ due to increase in size of its cells
Occurs in Non dividing cells (permenant cells)

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17
Q

EX of Physiologic Hypertrophy :

A
  1. Uterine smooth muscle hypertrophy during pregnancy (may be accompainied by Hyperplasia)
  2. Skeletal m. in athletes
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18
Q

EX of Pathologic Hypertrophy :

A

Hypertrophic left ventricle: in systemic Hypertension or Reduced aortic valve outflow

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19
Q

Hypertrophy Pathogenesis

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A

Cells become larger dur to :
Increase in protein synthesis
Decrease in protein degradation

20
Q

Hypertrophy Morphologic Features

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A

Organ is large & heavy due to increase if size in muscle fibers as well as of nuclei

21
Q

Def of hyperplasia

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A

Increase in size of an organ due to increase in nb of its cells
Occurs in Labile & Stable cells

22
Q

EX of Physiologic Hyperplasia :

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A
  1. Hormonal Hyper.:
    Hyperplasia of :
    Breast during puberty, during pregnancy & lactation /// pregnant uterus
  2. Compensatory Hyper.: following the removal of a part of sn organ or a conttralateral organ i paired organs. EX: Regeneration of liver following hepatectomy
23
Q

EX of Pathologic Hyperplasia :

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A

Hormonal (due to excessive hormonal stimulation):
1. Increase estrogen stimulation unopposed by progestrone as in *Fibrocystic breast disease (mammary hyper.) /// Endometrial Hyper. *
2. Prostatic Hyperplasia in old age
3. Thyroid Hyperplasia (Goiter) due to increase TSH (thyroid stimulating Hormone)

Epithelial due to chronic irritation or inflammation: as in Bilharizial cystitis.

24
Q

Hyperplasia Pathogenesis

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A

Cells increase in nb by proliferation of stem cells & parenchymal cells.

25
Diff betw Hyperplasia & Neoplasia
Both are icrease in nb of cells but **Hyperplasia**: controlled & reversible, but pathologic hyperplasia may be the soil of neoplastic proliferation. **Neoplasia **: uncontrolled & Irreversible => tumors
26
Deff of Metaplasia
- Reversible change in w one adult cell type (epithelial or mesenchymal) is replaced by another adult cell type, w/o crossing histogenetic boundries. - Occurs in response to chronic irritation & inflammation.
27
Metaplasia Pathogenesis
genetic reprogramming of epithelial stem cells or UMCs in CT.
28
Although metaplastic changes lead to stronger epithelium it may be less well-specialized. Explain
**Squamous metaplasia in Respiratory epithelium will result in deprivation of mucus secretion & ciliary clearence => infection. **
29
Metaplasia may revert back in case of ............. /// but in case of ............... it may lead to malignant transformation
- Absence of stimulus - Persistent stimulus
30
EX of Epithelial Metaplasia | Metaplasia types : Epithelial & mesenchymal
**Squamous metaplasia ** 1. From *Pseudostratified Columnar ciliated epithelium*: in bronchi in chronic bronchitis in chronic smokers 2. From *Simple columnar epithelium* : in gall Bladder in chronic cholecystitis w/ cholelithiasis (gall bladder stones fromation trapping the bile in the duct). 3. From* transitional epithelium* : in urinary bladder & renal pelvis in stones & chronic infection as schistosomiasis (caused by parasitic worms). **Columnar metaplasia**: *Barrett's esophagus*: change from normal squamous epithelium in the distal part of esophagus in case of *Chronic reflux Esophagitis*
31
EX of Mesenchymal Metaplasia
1. **Osseous**: In muscles in myositis ossoficans 2. **Cartilagenous**: in long-standing fibrosis as capsule of spleen in chronic venous congestion.
32
What are causes of cell injury ?
**Genetic Causes :** 1- Deficiency of proteins as enzymes functions. 2- Accumulation of damaged DNA => cell Death **Acquired causes :** 1. *Hypoxia*: has 3 causes : A. Ischemia => reduced B. Supply B. Ht & Lung diseases => Dminished blood oxygenation C. Anemia, CO poisoning => diminished oxygen carrying capacity. 2. Physical Agents : trauma, T, Radiation, Pressure ... 3. Chemical : poisons, organic & inorganic environ. agents, Therapeutic drugs. 4. Infectuous : virsus, parasites, bacteria.... 5. Immunologic : hypersens. reactions, Autoimmune 6. Nutritonal Imbalances : A. Nutritunal Deficency due to : Overall deficiency (Starvation) /// Protein calorie (marasmus,, Kwashiorkor), or minerals (anemia). B. Nutritunal Excess : obesity, Diabetes Mellitus, Atherosclerosis, Ht Disease, Hypertension. | CO => attaches to HB prevent its attachment to O2.
33
Cell injury may result in a state of reversible or irreversible injury depending on ................. & ..................
1. **Type, duration & severity of agents: ** A small dose of a chemical agent or brief ischemia => reversible cell injury. BUT, a large dose or persistent ischemia => Cell Death. 2. **Type, Status & Adaptability of the target cell: ** Skeletal muscle can endure hypoxic injury for 2-3 h, Cardiac muscle => 20-30 mins Brain 4-6 mins.
34
What are the mechanisms of Cell injury ?
1. ATP depletion 2. Mitochodrial damage 3. Nuclear damage 4. Plasma memb. damage 5. Generation of reactive oxygen species 6. Loss of Ca++2 Homeostasis.
35
Explain ATP depletion | Cause & Consequences
ATP depletion may be caused by ischemia that diminishs the oxidative phosphorylation in mitochodria causing => 1. Failure of Na+ pump => influx of Na+ & efflux of K+ => swelling 2. Failure of Ca2+ pump => its influx => damaging effects on cellular components. 3. Increases Anaerobic glycolysis => accumulation of Lactic acid => decrease Ph => damage enzymes + clumping of chromatin. 4. Detachment of ribososmes from rER => decrease in protein synthesis => damage to mitochodrial & plasma memb. => cell death.
36
Explain Mitochodrial Damage
1. **Increase cytosolic Ca2+, ROS (reactive O2 species) & Hypoxia:** appear as vacuoles & amorphous Calcium deposits. This damage affects oxifative phosphorylation w/ ATP depletion & generations of ROS => Necrosis. 2. **Decreased survival signals, Irrepairable DNA or Protein damage : **=> increase in permeability of mitochodrial memb => leaking of cytochrome C into cytop. => Apoptosis.
37
Explain loss of Ca2+ Homeostasis | Cause & Consequences
**Causes: ** Ischemia (ATP depletion => failure of Ca2+ pump) , Certain toxins => increase intracellular Ca2+. **Consequences** Activation of enzymes as : 1. Phospholipases & Proteases => CM damage. 2. Endonucleases => DNA & Chromatin fragmentation 3. ATPase => ATP depletion. 4. Caspases => Apoptosis.
38
Explain Accumulation of reactive O2 species (ROS) /O2 derived free radicals | Def & Causes & Consequences
**Def: **Chemical species w/ unpaired electron in their outer orbit, produced during Mitochondria respiration & energy generation, & degraded by cellular defense systemes (SOD & Glutathione superoxidase). **Causes** : Cell injury => accumulation of these ROS (superoxide, H2O2, Hydroxyl). **Consequences : ** 1. CM damage due to lipid peroxidations. 2. Protein oxidation => loss of enzymatic activity. 3. DNA damage.
39
Explain Memb. damage
**Causes : ** Increase in Cytosolic Ca2+ => activation of endogenous phospholipases => degradation of phospholipids causing memb damage of Cell, Lysosomes & Mitochondria. **Consequences :** 1. Loss of osmotic balance 2. Loss of cellular components depleting energy stores 3. Lysosomal memb damage => leakage of its Hydrolytic enzymes => their activation in cytosol as acidic Ph & lack of O2 => Cell death.
40
Morphologic feature following the memb. damage
Dead cells are further replaced by phospholipids masses calles myelin figures that will be phagocytosed by macrophages or form Ca+2 soaps
41
During Memb. damage, Leaked enzymes can also mark ” the cell type damaged. Explain.
As reflected by elevated serum level of specific izoenzymes as : **Creatine Kinase & Troponins** in case of **Myocardial infarction.** **Alanine aminotransferase (ALT), Aspartate aminotransferase (AST), Alkaline phosphatase** in case of **liver **problem.
42
Explain nuclear damage
**Cause :** Activated lysosomal enzymes such as proteases & endonucleases. This damage can occur in 3 forms : **Pyknosis** => condensation of nucleus w becomes dark basophilic **Karyorrhexis** => Fragmentation of nucleus into bits dispersed in cytopl. **Karyolysis** => Dissolution of the nucleus.
43
What is morphology of reversible CI ? | 2 processes
1. Hydropic change 2. Fatty change
44
What can distinguish betw irreversible from reversible CI ?
1. Inability of the cell to reverse mytochondrial dysfunction on reperfusion *(restoration of Blood Flow to a certain organ)* & Reoxygenation 2. Disturbance in CM function.
45
Explain the Hydropic change during reversible CI | DEF, Pathogenesis, Features, ultrastructural changes
**Def:**accumulation of water within the cytoplasm also known as *Cloudy swelling* (cytopl appears cloudy), & *Vacuolar degeneration* (due to cytopl vaculations). **Pathogenesis** Impairment distribution of Na & K at the level of the CM => accumulation of Na inside w/ efflux of K => swelling. **Morphological Features** *Grossly* : specialized organs as Heart, Kidney, Pancreas, Liver are enlarged + cut surface is bulged outwards & slightly pale. *Microscopically* : Cells are swollen, capillaries are compressed, small clear vacuoles repreenting distended cisternea of ER. **ultrastructural changes** 1. CM alterations : blunting, blebs, loss of microvilli 2. Mitochondrial swelling 3. Distention of rER w/ detachment of ribosomes 4. Nuclear alterations w/ chromatin clumping 5. Looseneing of intercellular attachment.
46
What cellular adaptations may lead to Neoplasia if persistent ?
hyperplasia & Metaplasia

pathology (4 decks)

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