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PATHO > CELL INJURY > Flashcards

CELL INJURY Flashcards

1
Q

4 mechanisms of TRUE ADAPTIVE CHANGE of cell injury

A 
atrophy
hypertrophy
hyperplasia
metaplasia
( AHMM)
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2
Q

Physiological Adaptation of atrophy

A

Developmental;

Involution

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3
Q

Pathologic Adaptation of atrophy

A

Constant Pressure;
Dec workload, nutrition,
Loss of blood supply, nervous & endocrine
stimulation

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4
Q

Dec metabolism - dec protein synthesis

Activate ubiquitin- proteasome pathway - inc protein degradation

A

ATROPHY

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5
Q

Proteasome

A
  • complex 26S molecules comprised of TWO alter 19S
    regulatory particles with Lid and a Base sandwiching
    20s core with alpha and beta cell units
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6
Q

Proteasome activity

A

step 1 Deubiquitination(Deconjugation)
step 2 Protein unfolding
step 3 Proteolysis/Degradation

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7
Q
  • ones that recognize polyubiquitin
    conjugates tag on target proteins
  • also cause a conformational change in 20s
    catalytic core to open this chamber
A

19s regulatory particles

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8
Q

In atrophy :
decrease in protein synthesis coupled w rapid protein degradation will significantly reduce cells protein content causing

A

AUTOPHAGY

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9
Q

ATROPHY AUTOPHAGY contains

A

DEC ER , DEC mitochondria & DEC cytoskeleton

  • DEC ( C E M )

Cytokeleton
ER
Mitrohondria

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10
Q

HYPERTROPHY
REGARDLESS of physiologic and pathologic cause the effect is ___ leading to ___ protein synthesis which eventually leads to ______

A

INC METABOLISM –> INC PROTEIN SYNTHESIS –> enlargement of cytoplasmic volume and number of cell organelles

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11
Q

GROWTH FACTOR RELEASE —>mature cells undergo ____ thus ____ -

____ stem cells to differentiate into more cells
of the same type that leads inc to total number of cells

A

mature cells undergo cell division, leading to increase proliferation in cells

Immature stem cells to differentiate into more cells
of the same type that leads INC to total number of cells

HYPERPLASIA

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12
Q

HYPERPLASIA IN COMMON WITH HYPERTROPHY

A

CAN CAUSE IN INC IN OVERALL SIZE OF THE
ORGAN BUT NOT ALL CELLS CAN UNDERGO
HYPERPLASIA

** PROCESS CAN OCCUR ONLY IN CELLS CAPABLE OF CELL DIVISION / LABILE/ STABLE CELLS

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13
Q

HYPERPLASIA and HYPERTROPHY INC size of cell but not all cells can undergo ___hypertrophy or hyperplasia?__ because

** PROCESS CAN OCCUR ONLY IN CELLS CAPABLE OF CELL DIVISION / LABILE/ STABLE CELLS

A

NOT ALL CELLS CAN UNDERGO

HYPERPLASIA

HYPERPLASIA CAN OCCUR ONLY IN CELLS CAPABLE OF CELL DIVISION / LABILE/ STABLE CELLS

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14
Q

METAPLASIA hallmark mechanism

A

stem cells

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15
Q

DYSPLASIA/ ATYPICAL HYPERPLASIA is a combination of?

A

metaplasia and hyper plasia that is confined to EPITHELIAL CELLS

” masyadong hype yung discord”

metaplasia+ hyperplasia = Displasia

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16
Q

HINDI ITO NORMAL ADAPTATION NOT A TRUE ADAPTIVE CHANGE ABNORMAL ITO

A

DYSPLASIA / ATYPICAL HYPERPLASIA

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17
Q

INSTEAD CHANGES IN AFFECTED CELLS PREDISPOSES

THEM TO DEVELOP IN MALIGNANT NEOPLASM

A

DYSPLASIA

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18
Q

results exposure to persistent severe injury or irritation that leads mature epithelial cells to undergo a disordered development leading to a change in its SIZE SHAPE ARRANGEMENT from basal to apical layer

A

DYSPLASIA

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19
Q

DYSPLASIA often occurs in

A

EPITHELIAL CELLS

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20
Q

a cell is considered injured if there is damage in any of
the cellular components that maintain cell viability

T or F?

A

TRUE

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21
Q

results from a functional, structural and
bio-chemical of disruption of one or more of the essential cellular
components that maintain cell viability.

T or F?

A

TRUE

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22
Q

MAIN CELLULAR MECHANISMS of REVERSIBLE CELL INJURY

A
  1. ATP depletion
  2. Loss of calcium homeostasis
  3. Oxidative stress (excess Reactive Oxygen Species)
  4. Damage and increased permeability of membranes
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23
Q
  1. ATP DEPLETION: REVERSIBLE CELL INJURY

Failure of CALCIUM ATPASE leads to

A

INC OF CALCIUM IN CYTOSOL -

CYTOPLASM

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24
Q
  1. ATP DEPLETION: REVERSIBLE CELL INJURY

Failure of Na/ K pump leads to

A

INC H20
INC Na
Dec K

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25
Q
  1. ATP DEPLETION: REVERSIBLE CELL INJURY
    INC ___
    DEC___
A

INC CHNa ( Inc in china)

Inc Ca , H20, Na

Dec K

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26
Q
  1. ATP DEPLETION: REVERSIBLE CELL INJURY

processes that happens here which leads to what ph of the cell?

A

process that happens :
1. GLYCOLYSIS - breaking down glucose , an ineffective anaerobic generating ATP and Lactic acid

Leads to Acidic Ph

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27
Q

GLYCOLYSIS generates

A

ATP and Lactic acid

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28
Q
  1. LOSS OF CALCIUM HOMEOSTASIS : REVERSIBLE CELL INJURY

loss of calcium homeostasis which is precipitated by ATP
depletion most often secondary to ____?

A

HYPOXIA aka HYPOXIC INJURY

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29
Q
  1. LOSS OF CALCIUM HOMEOSTASIS : REVERSIBLE CELL INJURY

- an uncontrolled influx of?? in cytosol

A

Calcium leading to Calcium Accummulation

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30
Q

Calcium goes out of ___ ER to go to cytosol

A

Smooth ER

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31
Q

a pore across the inner mitochondrial membrane;
formed from interactions between several
transmembrane proteins

A

Mitochondrial Permeability Transition (MPT)

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32
Q

MPT ( MITOCHONDRIAL PERMEABILITY TRANSITION) why is ti called transition

A

CALLED TRANSITION BECAUSE IT WILL REVERSE
FLOW OF CALCIUM OUT OF MITOCHONDRIAL
MATRIX FURTHER INCREASING CALCIUM LEVELS
IN CYTOPLASM/ CYTOSOL

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33
Q

OTHER STUFF THAT MPT allows to go inside of the cell that causes the cell to swell

A

SODIUM AND WATER

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34
Q

CALCIUM TOXICITY causes 2 main events

A

-Activation of multiple cellular enzymes
-Calcium is required in activation of several
enzymes including

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35
Q

MPT - ATP depletion and formation of more ROS leads to

A

apoptosis or necrosis

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36
Q

INCREASE MPT mitochondrial permeability
transition leads to ____ _____
production

A

DEC IN ATP PRODUCTION

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37
Q

in CALCIUM TOXICITY , the Calcium is required in activation of several enzymes including

A

PHOSPHOLIPASES
PROTEASES
ENDONUCLEASES
ATPASe

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38
Q

in CALCIUM TOXICITY , the Calcium is required in activation of several enzymes which enzyme is this?

calcium breakdowns phospholipids
major component of cellular membranes
cellular damage

A

PHOSPHOLIPASES

39
Q

in CALCIUM TOXICITY , the Calcium is required in activation of several enzymes which enzyme is this?

calcium activates proteases that degrades cellular proteins

A

PROTEASES

40
Q

in CALCIUM TOXICITY , the Calcium is required in activation of several enzymes which enzyme is this?

induce DNA fragmentation
NUCLEAR DAMAGE

A

ENDONUCLEASES

41
Q

in CALCIUM TOXICITY , the Calcium is required in activation of several enzymes which enzyme is this?

breaks down ATP

A

ATPASe

42
Q

d

A
  1. Oxidative stress Excess Reactive Oxygen

Species (ROS): REVERSIBLE CELL INJURY

43
Q

When Reactive Oxygen

Species (ROS) interacts with fat what happens

A

causing damage to all lipid containing cellular organelles

especially the cell membrane

44
Q

When Reactive Oxygen

Species (ROS) interacts with proteins what happens

A

protein misfolding or protein modification

45
Q

When Reactive Oxygen

Species (ROS) interacts with DNA what happens

A

damages DNA

46
Q

When Reactive Oxygen
Species (ROS) interacts with DNA

____ stops the cell cycle at ___phase to allow DNA to be repaired before it is replicated. HOWEVER IF THE DAMAGE IS TOO GREAT TO BE REPAIRED, IT UNDERGOES APOPTOSIS

A

p 53 gene stops the cell cycle at G1 phase

47
Q

Damage and increased permeability of

membranes - mitochondria, plasma membrane & lysosome REVERSIBLE CELL INJURY

A

,

48
Q

elevated cytosolic CALCIUM FROM HYPOXIA AND DIRECT INNER MITOCHONDRIAL MEMBRANE BY TOXINS AND

REACTIVE OXYGEN SPECIES FROM RADIATION WILL
RESULT IN HEIGHTENED MPT thereby :

A

DECREASE ATP GENERATION and ELEVATED/ INCREASE PRODUCTION OF ROS .

49
Q

DECREASE ATP GENERATION and ELEVATED/ INCREASE PRODUCTION OF ROS leads to

A

NECROSIS

50
Q

DECREASED SURVIVAL SIGNALS, DNA DAMAGE .

PROTEIN DAMAGE leads to ?

A

ACTIVATES PRO APOPTOTIC PROTEINS ( APAP)

INACTIVE / DECREASE ANTI APOPTOTIC PROTEINS ( DAAP)

51
Q

ASIDE FROM MITOCHONDRIAL MEMBRANE,

OTHER IMPORTANT MEMBRANES SUCH AS

A

PLASMA MEMBRANE and LYSOSOMAL MEMBRANE

52
Q 
\_\_\_\_\_ membrane INJURY RESULTS TO EFFLUX
OF DIGESTIVE ENZYMES like
acid phosphatases, araneses,
dnases, proteases,
and glucosidases into the cytoplasm
thereby eliciting the destruction
of cell components in a process
known as autophagy
A

LYSOSOMAL MEMBRANE

53
Q 
LEAKAGE
OF
CELLULAR
COMPONENTS INTO
THE
EXTRACELLULAR
SPACE
RESULTING IN NECROSIS
A

PLASMA MEMBRANE

54
Q

REVERSIBLE
Cell Injury
Main Morphologic (Retrogressive) changes

A
  1. Hydropic change (Acute cell swelling) injury

2. Fatty changes (Steatosis)

55
Q

Hydropic change (Acute cell swelling) main cause is

A

cellular hypoxia proceeds from any condition THAT DAMAGES

CIRCULATION BY “ PASS”

56
Q

cellular hypoxia proceeds from any condition THAT DAMAGES

CIRCULATION BY “ PASS” what is PASS

A

pneumonia
anemia
suffocation
shock

57
Q
  1. Hydropic change (Acute cell swelling) Injury

ATP production (dec or inc?)
Sodium and water move ___ cell ( Influx or Efflux?)
Potassium moves ___ of cell (Influx or Efflux?)

A

ATP production decreases

Sodium and water move INTO cell (Influx )
Potassium moves OUT of cell ( Efflux ) “POTA, GO OUT!”

58
Q
  1. Hydropic change (Acute cell swelling) Injury

Sodium ( Influx or Eflux?) will lead to raise osmotic pressure in cytoplasm leading to cell enlargement

A

Sodium (Influx) “SIn”

59
Q

• It is related to a dysfunction in
céllular regulation of triglyceride
synthesis, metabolism and elimination.

A

Fatty changes (Steatosis)

60
Q

Fatty changes (Steatosis) :

______ process Caused by hypoxia, toxins and metabolic injuries
which in turn causes fat degeneration this process will PRIMARY AFFECTS all CELL MEMBRANE since they mainly comprise of PHOSPHOLIPIDS

A

LIPID PEROXIDATION CAN TAKE PLACE

61
Q

TRIGLYCERIDES BIND WITH ___ so that they can be

released for transportation out of the cell

A

TRIGLYCERIDES BIND WITH APOPROTEIN so that they can be

released for transportation out of the cell

62
Q

The main pathways of abnormal intracellular accumulations:

A
  1. Inadequate removal and degradation
  2. Excessive production of an endogenous substance
  3. Deposition of an abnormal exogenous material
    into the cytosol of the cell
63
Q

Substances that accumulate in cells:

A 
1. Triglycerides
2 Cholesterol and cholesterol esters
3. Proteins
4. Glycogen
5- Pigments

TA GO CA PA PA

64
Q

most common pigment , esp during

smoking. THE ONLY EXOGENOUS one

A

Carbon

  • found in smoking
65
Q

ENDOGENOUS PIGMENTS

A

Lipofuscin
Melanin
Hemosiderin

66
Q

Brownish yellow pigment

Free radical Peroxidation of fats

A

Lipofuscin

67
Q

Golden yellow to brown

Iron catabolism

A

Hemosiderin

68
Q

Brown to black

Normal pigment of the skin

A

Melanin

69
Q

an abnormal deposition of calcium salts, together with
smaller amounts of iron, magnesium, and other minerals,
pathologic

A

Pathologic Calcification

70
Q

Calcium deposits in injured or dead tissue

A

DYSTROPHIC CALCIFICATION

71
Q

HIGH CALCIUM LEVELS : HYPERCALCEMIA

A

METASTATIC CALCIFICATION

72
Q

METASTATIC CALCIFICATION EFFECTS

A
  • Hyperparathyroidism
  • INC BONE DESTRUCTION
  • hyper vitaminosis D
  • renal failure
  • sarcoidosis
  • Paget’s disease
  • phosphate retention leads to secondary hyperparathyroidism
73
Q

Calcium deposits in normal tissues

A

METASTATIC CALCIFICATION

74
Q

Occurs in normal calcium metabolism

A

DYSTROPHIC CALCIFICATION

75
Q

METASTATIC CALCIFICATION diseases

A 
BONE
renal failure
sarcoidosis
Paget's disease
Vitamin D intoxication
76
Q

DYSTROPHIC CALCIFICATION diseases

A

intima of blood vessels

damaged parts of heart and valves

77
Q

PATHOLOGIC ADAPTATION OF

APOPTOSIS / ACTIVE / ENERGY DEPENDENT involves the enzymes called

A

CASPASES

C ysteine dependent
ASP artate specific
prote ASE

CASPASES

78
Q

PATHOLOGIC ADAPTATION OF

APOPTOSIS / ACTIVE / ENERGY DEPENDENT involves the enzymes called

A

CASPASES

C ysteine dependent
ASP artate specific
prote ASE

CASPASES

79
Q

PATHOLOGIC ADAPTATION OF

APOPTOSIS / ACTIVE / ENERGY DEPENDENT caused by

A

DNA damage,
Accumulation of misfolded CHON,
Graft rejection, Infection

80
Q

CASPASES in apoptosis functin to

A

cleave proteins containing cysteine after

aspartic acid residues

81
Q

CASPASES in apoptosis function to

A

cleave proteins containing cysteine after

aspartic acid residues

82
Q

EXECUTIONER CASPASES

A

executioner 367

83
Q

APOPTOSIS / ACTIVE / ENERGY DEPENDENT

2 pathways for apoptotic cell death

A 
Mitochondrial pathway (Intrinsic)
Death receptor pathway (Extrinsic)

Mnemonic : De for DE- Death , Extrinisc

84
Q

APOPTOSIS / ACTIVE / ENERGY DEPENDENT

2 pathways for apoptotic cell death

A 
Mitochondrial pathway (Intrinsic)
Death receptor pathway (Extrinsic)

Mnemonic : De for DE- Death , Extrinsic

85
Q

Involvement of both inflammation and aspects of both

necrosis and apoptosis

A

PYROPTOSIS

86
Q

OTHER PATHWAYS OF CELL DEATH

A

NECROPTOSIS

PYROPTOSIS

87
Q

hybrid that shares aspects of both necrosis

and apoptosis

A

NECROPTOSIS

NECRO- necrosis + PTOSIS - apoptosis

88
Q

NECROPTOSIS

trigger

A

triggered by the activation of death

receptors

89
Q

PYROPTOSIS

trigger

A

Trigger: inflammasome

90
Q

NECROPTOSIS

Subsequent sequence

A

protein activation ( kinases)

91
Q

NECROPTOSIS

effect

A

Effect: destruction of cellular membranes

w/ inflammation

92
Q

PYROPTOSIS

effect

A

Effect: Intact nucleus with cell membrane

destruction

93
Q

PYROPTOSIS

Subsequent sequence

A

Sequential caspase activation, some induce
the production of cytokine inflammation

cytokines are used in fever, “pyro”

94
Q

Reperfusion occurs in several mechanisms:

A

Oxidative stress.
Intracellular calcium overload.
Inflammation.
Activation of the complement system

PATHO (8 decks)

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