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FTCM > L3, L4- Cell Injury and Adaptations > Flashcards

L3, L4- Cell Injury and Adaptations Flashcards

1
Q

define the four aspects of disease process

A

1) etiology = cause
2) pathogenesis = mechanism
3) morphology = appearance
4) functional consequences = clinical significance

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2
Q

a normal cell in homeostasis can undergo (1) to induce an adaptation, or undergo (2) resulting in (3)

A

1- stress
2- injurious stimulus
3- cell injury
Note- if cell can’t adapt to stress, cell goes into cell injury

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3
Q

cell injury can be (1) resulting in (2) or (3) resulting in (4) or (5)

A 
1- mild / transient
2- reversible injury (--> back to normal once stimulus removed)
3- severe / progressive
4- necrosis
5- apoptosis
(4/5) = irreversible injury
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4
Q

list the 6 causes of cell injury

A
  • metabolic
  • physical
  • chemical
  • immunologic
  • genetic
  • biologic (microbes)
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5
Q

list the 4 most vulnerable mechanisms of cell injury

A

1) cell membrane integrity
2) ATP production (oxidative phosphorylation)
3) protein synthesis (RER)
4) genetic apparatus (DNA)

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6
Q

list the 5 organelles susceptible to cell injury

A
  • plasma membrane
  • SER
  • mitochondria
  • lysosomes
  • nucleus / nucleolus
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7
Q

Plasma membrane cell injury is usually due to (1) or (2), but may also include the following: (3). (T/F) Tears / damage to plasma membrane can never be repaired and result in cell death.

A

1- trauma
2- free radicals
3- enzymes, chemicals, poisons
4- False, if not too severe tears can be repaired

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8
Q

SER damage can occur via (1) or (2), where (2) is defined as (3). SER damage may also occur through accumulation of (4) leading to (5).

A 
1- direct toxins
2- latent toxins
3- activated by ER, causing damage via release of free radicals
4- misfolded proteins
5- apoptosis
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9
Q

describe how mitochondria cell damage can occur

A

-usually due to an agent that affects oxidative phosphorylation

  • hypoxia, hypoglycemia
  • free radicals
  • poisons / toxins
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10
Q

describe how lysosome cell damage can occur

A

1) activation of enzymes => autophagy; digestion of cell components, cells die via necrosis
2) incomplete degradation of phagocytosed material

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11
Q

list some causes of cell injury due to damage to nucleus/nucleolus

A
  • radiation, viruses, chemotherapy

- or ROS => mutations, or if severe enough -> death

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12
Q

hypoxia and ischemia lead to decreased O2 to cell which leads to decreased (1) production, yielding the following three key effects: (2), (3), (4)

A

1- ATP
2- dec Na/K ATPase pump
3- inc anaerobic glycolysis => dec pH (inc lactic acid)
4- dec protein synthesis (due to detachment of ribosomes)

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13
Q

dec pH in the cell as a result of hypoxia or ischemia results in….

A

clumping of nuclear chromatin (+ changes in activities of proteins / enzymes)

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14
Q

describe how dec Na/K ATPase pump activity affects the cell

A

-inc influx of Ca2+, Na+, H2O (follows Na+)
-inc efflux of K+
=> ER swelling and cellular swelling –> loss of microvilli + more blebs

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15
Q

dec Na/K pump activity leads to inc influx of Ca2+ into the cell, resulting in…..

A

Excessive Intracellular Ca2+ –> activation of cellular enzymes:

  • phospholipases –> membrane damage (phospholipid loss)
  • proteases –> disrupts membrane and cytoskeletal proteins –> membrane damage
  • endonucleases –> nuclear damage
  • ATPase –> dec ATP
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16
Q

protection from free radicals include…

A

(antioxidants)

  • catalase
  • glutathione
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17
Q

ROS can be produced by the following…..

A
  • chemical and radiation injury
  • ischemia-reperfusion injury
  • cellular aging
  • during microbial killing by phagocytes
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18
Q

list the pathological effects of ROS on cells (hint- 3)

A
  • lipid peroxidation => membrane damage
  • protein modifications => breakdown or misfolding
  • DNA damage => mutations
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19
Q

describe toxic effect of CCL4

A

(indirect toxin)

CCL4 –> CCL3 by P450 in hepatocytes => lipid peroxidation

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20
Q

compare cell damage by chemicals or toxins that are direct or indirect

A
  • Direct: binds protein and cell membranes

- Indirect: converted to toxic metabolite (usually in heptocytes) that produce free radicals

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21
Q

list some causes of cell damage via viruses

A
  • rapid replication w/in cell => immune response, inflammation, cell lysis
  • cytopathic effects related to specific cell receptors
  • effects cytoskeleton => multi-nucleation,and inclusion bodies
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22
Q

describe features of reversible cell injury

A
  • cell and intracellular organelle (ER, mitochondria) swelling (taking in water) = hydropic changes
  • sometimes lipids (TAGs) accumulate inside injured cell (i.e. fatty liver / hepatocytes)
23
Q

list the progression of irreversible cell injury

A

(Note- function dec in reversible cell injury state preceding irreversible state)

1) biochemical alterations => cell death
2) ultrastructural changes (electron microscopy)
3) light microscopy changes
4) gross morphological changes

24
Q

define hydropic changes

A

small clear vacuoles w/in cytoplasm due to cellular swelling resulting from reversible cell injury (seen by LM)

25
Q

describe morphology of reversible cell injury at ultrastructural level (hint- 5)

A

(seen by EM)

  • plasma membrane changes: bleb formation, blunting, loss of microvilli
  • mitochondrial swelling
  • ER dilation + detachment of polysomes
  • intracytoplasmic myelin figures (may be present)
  • mild disaggregation of nuclear granular elements
26
Q

list the factors that determine if cell injury is irreversible (hint- 5)

A
  • mitochondria unable to recover after re-oxygenation
  • massive phospholipid loss
  • damage to cytoskeleton
  • excessive free radicals and lipid breakdown products
  • Ca2+ influx after re-oxygenation with protein denaturation (cell coagulation)
27
Q

describe the 3 patterns nuclei might show in irreversible cell injury

A

1) Pyknosis: condensed nucleus
2) Karyorrhexis: fragmented nucleus
3) Karyolysis: complete disruption and disappearance of nucleus

28
Q

describe morphology of irreversible cell injury (hint- 5)

A
  • increased eosinphilia in H&E stain
  • severe vacuolization of mitochondria
  • damaged plasma membrane
  • disruption of lysosomes
  • marked intracellular acidosis => ruptured lysosomal membranes => cell digestion and death
29
Q

compare apoptosis to necrosis

A

Apoptosis: individual cell, normal/pathological, cell shrinkage, no inflammation, nuclear fragmentation, Blebs / maintains cell membrane integrity, phagocytosis

Necrosis: groups of cells, pathological, cell swelling, inflammation, loss of cell membrane integrity

30
Q

in apoptosis, enzymes are activated in order to….

A

degrade its own cells’ nuclear DNA, nuclear proteins, cytoplasmic proteins

31
Q

The (1) family of enzymes are responsible for apoptosis. Once activated it will activate (2) which leads to (3) and induce the breakdown of (4).

A

1- caspases (initiators –> executioners)
2- endonuclease activation
3- nuclear fragmentation
4- cytoskeleton

32
Q

Extrinsic apoptosis pathway, aka (1), occurs when a (2) binds to either (3) or (4) which activates initiator caspases`

A

1- death receptor pathway
2- ligand (normal signalling or pathogenic ligand)
3- Fas receptor
4- TNF receptor

33
Q

Intrinsic apoptosis pathway, aka (1), occurs in response to the following three cell changes: (2), (3), (4)

A

1- mitochondrial pathway
2- growth factor withdrawal
3- DNA damage (radiation, free radicals, toxins)
4- protein misfolding (ER stress)

34
Q

The mitochondrial/intrinsic apoptosis pathway is usually regulated/inhibited by (1). Once cell injury occurs that is beyond repair (2) is activated, which results in (3) and its release of (4), resulting in caspase activation.

A

1- BCL2 (+ BCL-XL)
2- BCL2 family
3- increased mitochondrial permeability
4- cytochrome c (+ other pro-apoptotic proteins)

35
Q

(T/F) in apoptosis and necrosis the nucleus can undergo Pyknosis, Karyhorrhexis, Karyolysis

A

F- in apoptosis, karyolysis can’t happen

36
Q

describe how cell death occurs through necrosis mechanism

A
  • cell membranes fall apart

- cell enzymes leak out and ultimately digest cell

37
Q

list the types of necrosis

A
  • coagulative
  • liquefactive
  • fat
  • caseous: combination of coagulative and liquefactive
  • gangrenous
38
Q

(1) necrosis results from ischemia and the (2) of structural proteins and enzymes which results in (3). This can be found in (4) places in the body and the lesion that is left is called a (5).

A

1- coagulative
2- denaturement
3- blocking of protolysis of dead cells
4- solid organs (heart, kidneys, spleen, ect.)
5- infarct
Note- cell architecture is preserved for at least several days after death of cells in tissues

39
Q

(1) necrosis is seen in ischemia of the brain, its due to the release of (2). (3) is also a common cause as inflammatory cells accumulate and their leukocytic enzymes cause (4).

A

1- liquefactive
2- hydrolytic enzymes
3- bacterial and fungal infections
4- ‘liquify’ the tissue with pus formation

40
Q

Fat necrosis only occurs in (1), and most typically (2) as a consequence of (3).

A

1- fatty tissue
2- pancreas
3- acute pancreatitis

41
Q

describe the events of fat necrosis

A
  • acute pancreatitis –> release of enzymes
  • lipased digest TAGs into free FAs
  • FAs combine with Ca2+ (salt) to create soap (Fat Saponification)
  • fat deposits onto pancreas
42
Q

TB infections lead to (1) necrosis and is described as (2) on gross examination and has the following histological features: (3).

A

1- caseous
2- ‘cheese-like’ (meaning of caseous)
3- collection of fragmened / lysed cells surrounded by dense chronic inflammatory cells –> pattern = caseating granuloma

43
Q

describe gangrenous necrosis and its two types

A
  • not a distinct pattern of necrosis, more a clinical than pathological term
  • DRY: limb ischemia –> coagulative necrosis
  • WET: bacterial infection –> liquefactive necrosis (appears shiny in comparison)
44
Q

(1) necrosis is seen in blood vessels and occurs due to (2) or (3). It has a (4) appearance on H&E histological stains.

A

1- fibrinoid
2- immune rxns –> Ag-Ab complexes deposited in vessel wall
3- malignant HTN, >160/110
4- fibrin-like amorphous deposits

45
Q

list the 4 types of cell adaptations (all reversible)

A

1- atrophy (cell shrinkage)
2- hypertrophy (cell enlargement)
3- hyperplasia (inc cell number)
4- metaplasia (change cell type)

46
Q

permanent cells undergo _____ as cell adaptation

A

atrophy and hypertrophy only (no hyperplasia or metaplasia)

47
Q

stable/labile cells undergo _____ as cell adaptation

A

atrophy, hypertrophy, hyperplasia, metaplasia

48
Q

list some causes of atrophy

A
  • dec blood supply
  • loss of innervation
  • loss of trophic signals (hormones)
  • dec workload
  • aging (brain)
49
Q

give 2 common examples of physiological hypertrophy and 1 of pathological hypertrophy

A
  • Phys: uterine enlargement in pregnancy due to hormonal stimulation (trophic), skeletal muscles after exercise due to inc workload
  • Path: cardiac muscle due to HTN / inc workload
50
Q

give 2 common examples of physiological hyperplasia and 3 of pathological hyperplasia

A

-Phys: glandular epithelium in breast development during puberty and pregnancy (hormonal), residual tissue grows after partial removal like in the liver (compensatory)

Path: excess Estrogen => endometrial hyperplasia, excess TSH => thyroid enlargement, prostate => BPH

51
Q

describe the progress of a normal cell to malignancy

A

1) normal
2) stress => metaplasia via stem cell reprogramming (reversible, not premalignant)
3) stress => dysplasia (reversible, premalignant)
4) stress => malignancy (irreversible)

52
Q

____ is a sign of cellular aging

A

lipofuscin

53
Q

give 2 common examples of metaplasia

A
  • respiratory epithelium in smokers: sqamous metaplasia (from ciliated columnar)
  • esophageal epithelium in GERD: columnar metaplasia (from squamous)

FTCM (16 decks)

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