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pathology > Cell injury > Flashcards

Cell injury Flashcards

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

A

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

20
Q

Hypertrophy Morphologic Features

A

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

21
Q

Def of hyperplasia

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 :

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 :

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

A

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

25
Q

Diff betw Hyperplasia & Neoplasia

A

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
Q

Deff of Metaplasia

A
  • 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
Q

Metaplasia Pathogenesis

A

genetic reprogramming of epithelial stem cells or UMCs in CT.

28
Q

Although metaplastic changes lead to stronger epithelium it may be less well-specialized. Explain

A

**Squamous metaplasia in Respiratory epithelium will result in deprivation of mucus secretion & ciliary clearence => infection. **

29
Q

Metaplasia may revert back in case of …………. /// but in case of …………… it may lead to malignant transformation

A
  • Absence of stimulus
  • Persistent stimulus
30
Q

EX of Epithelial Metaplasia

Metaplasia types : Epithelial & mesenchymal

A

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
Q

EX of Mesenchymal Metaplasia

A
  1. Osseous: In muscles in myositis ossoficans
  2. Cartilagenous: in long-standing fibrosis as capsule of spleen in chronic venous congestion.
32
Q

What are causes of cell injury ?

A

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
Q

Cell injury may result in a state of reversible or irreversible injury depending on …………….. & ………………

A
  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
Q

What are the mechanisms of Cell injury ?

A
  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
Q

Explain ATP depletion

Cause & Consequences

A

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
Q

Explain Mitochodrial Damage

A
  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
Q

Explain loss of Ca2+ Homeostasis

Cause & Consequences

A

**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
Q

Explain Accumulation of reactive O2 species (ROS)
/O2 derived free radicals

Def & Causes & Consequences

A

**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
Q

Explain Memb. damage

A

**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
Q

Morphologic feature following the memb. damage

A

Dead cells are further replaced by phospholipids masses calles myelin figures that will be phagocytosed by macrophages or form Ca+2 soaps

41
Q

During Memb. damage, Leaked enzymes can also
mark ” the cell type damaged. Explain.

A

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
Q

Explain nuclear damage

A

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
Q

What is morphology of reversible CI ?

2 processes

A
  1. Hydropic change
  2. Fatty change
44
Q

What can distinguish betw irreversible from reversible CI ?

A
  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
Q

Explain the Hydropic change during reversible CI

DEF, Pathogenesis, Features, ultrastructural changes

A

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
Q

What cellular adaptations may lead to Neoplasia if persistent ?

A

hyperplasia & Metaplasia

pathology (4 decks)

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