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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
1. ATP DEPLETION: REVERSIBLE CELL INJURY INC ___ DEC___
INC CHNa ( Inc in china) Inc Ca , H20, Na Dec K
26
1. ATP DEPLETION: REVERSIBLE CELL INJURY | processes that happens here which leads to what ph of the cell?
process that happens : 1. GLYCOLYSIS - breaking down glucose , an ineffective anaerobic generating ATP and Lactic acid Leads to Acidic Ph
27
GLYCOLYSIS generates
ATP and Lactic acid
28
2. LOSS OF CALCIUM HOMEOSTASIS : REVERSIBLE CELL INJURY loss of calcium homeostasis which is precipitated by ATP depletion most often secondary to ____?
HYPOXIA aka HYPOXIC INJURY
29
2. LOSS OF CALCIUM HOMEOSTASIS : REVERSIBLE CELL INJURY | - an uncontrolled influx of?? in cytosol
Calcium leading to Calcium Accummulation
30
Calcium goes out of ___ ER to go to cytosol
Smooth ER
31
a pore across the inner mitochondrial membrane; formed from interactions between several transmembrane proteins
Mitochondrial Permeability Transition (MPT)
32
MPT ( MITOCHONDRIAL PERMEABILITY TRANSITION) why is ti called transition
CALLED TRANSITION BECAUSE IT WILL REVERSE FLOW OF CALCIUM OUT OF MITOCHONDRIAL MATRIX FURTHER INCREASING CALCIUM LEVELS IN CYTOPLASM/ CYTOSOL
33
OTHER STUFF THAT MPT allows to go inside of the cell that causes the cell to swell
SODIUM AND WATER
34
CALCIUM TOXICITY causes 2 main events
-Activation of multiple cellular enzymes -Calcium is required in activation of several enzymes including
35
MPT - ATP depletion and formation of more ROS leads to
apoptosis or necrosis
36
INCREASE MPT mitochondrial permeability transition leads to ____ _____ production
DEC IN ATP PRODUCTION
37
in CALCIUM TOXICITY , the Calcium is required in activation of several enzymes including
PHOSPHOLIPASES PROTEASES ENDONUCLEASES ATPASe
38
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
PHOSPHOLIPASES
39
in CALCIUM TOXICITY , the Calcium is required in activation of several enzymes which enzyme is this? calcium activates proteases that degrades cellular proteins
PROTEASES
40
in CALCIUM TOXICITY , the Calcium is required in activation of several enzymes which enzyme is this? induce DNA fragmentation NUCLEAR DAMAGE
ENDONUCLEASES
41
in CALCIUM TOXICITY , the Calcium is required in activation of several enzymes which enzyme is this? breaks down ATP
ATPASe
42
d
3. Oxidative stress Excess Reactive Oxygen | Species (ROS): REVERSIBLE CELL INJURY
43
When Reactive Oxygen | Species (ROS) interacts with fat what happens
causing damage to all lipid containing cellular organelles | especially the cell membrane
44
When Reactive Oxygen | Species (ROS) interacts with proteins what happens
protein misfolding or protein modification
45
When Reactive Oxygen | Species (ROS) interacts with DNA what happens
damages DNA
46
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
p 53 gene stops the cell cycle at G1 phase
47
Damage and increased permeability of | membranes - mitochondria, plasma membrane & lysosome REVERSIBLE CELL INJURY
,
48
elevated cytosolic CALCIUM FROM HYPOXIA AND DIRECT INNER MITOCHONDRIAL MEMBRANE BY TOXINS AND REACTIVE OXYGEN SPECIES FROM RADIATION WILL RESULT IN HEIGHTENED MPT thereby :
DECREASE ATP GENERATION and ELEVATED/ INCREASE PRODUCTION OF ROS .
49
DECREASE ATP GENERATION and ELEVATED/ INCREASE PRODUCTION OF ROS leads to
NECROSIS
50
DECREASED SURVIVAL SIGNALS, DNA DAMAGE . | PROTEIN DAMAGE leads to ?
ACTIVATES PRO APOPTOTIC PROTEINS ( APAP) | INACTIVE / DECREASE ANTI APOPTOTIC PROTEINS ( DAAP)
51
ASIDE FROM MITOCHONDRIAL MEMBRANE, | OTHER IMPORTANT MEMBRANES SUCH AS
PLASMA MEMBRANE and LYSOSOMAL MEMBRANE
52
``` _____ 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 ```
LYSOSOMAL MEMBRANE
53
``` LEAKAGE OF CELLULAR COMPONENTS INTO THE EXTRACELLULAR SPACE RESULTING IN NECROSIS ```
PLASMA MEMBRANE
54
REVERSIBLE Cell Injury Main Morphologic (Retrogressive) changes
1. Hydropic change (Acute cell swelling) injury | 2. Fatty changes (Steatosis)
55
Hydropic change (Acute cell swelling) main cause is
cellular hypoxia proceeds from any condition THAT DAMAGES | CIRCULATION BY " PASS"
56
cellular hypoxia proceeds from any condition THAT DAMAGES | CIRCULATION BY " PASS" what is PASS
pneumonia anemia suffocation shock
57
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?)
ATP production decreases Sodium and water move INTO cell (Influx ) Potassium moves OUT of cell ( Efflux ) "POTA, GO OUT!"
58
1. Hydropic change (Acute cell swelling) Injury Sodium ( Influx or Eflux?) will lead to raise osmotic pressure in cytoplasm leading to cell enlargement
Sodium (Influx) "SIn"
59
• It is related to a dysfunction in céllular regulation of triglyceride synthesis, metabolism and elimination.
Fatty changes (Steatosis)
60
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
LIPID PEROXIDATION CAN TAKE PLACE
61
TRIGLYCERIDES BIND WITH ___ so that they can be | released for transportation out of the cell
TRIGLYCERIDES BIND WITH APOPROTEIN so that they can be | released for transportation out of the cell
62
The main pathways of abnormal intracellular accumulations:
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
Substances that accumulate in cells:
``` 1. Triglycerides 2 Cholesterol and cholesterol esters 3. Proteins 4. Glycogen 5- Pigments ``` TA GO CA PA PA
64
most common pigment , esp during | smoking. THE ONLY EXOGENOUS one
Carbon - found in smoking
65
ENDOGENOUS PIGMENTS
Lipofuscin Melanin Hemosiderin
66
Brownish yellow pigment | Free radical Peroxidation of fats
Lipofuscin
67
Golden yellow to brown Iron catabolism
Hemosiderin
68
Brown to black | Normal pigment of the skin
Melanin
69
an abnormal deposition of calcium salts, together with smaller amounts of iron, magnesium, and other minerals, pathologic
Pathologic Calcification
70
Calcium deposits in injured or dead tissue
DYSTROPHIC CALCIFICATION
71
HIGH CALCIUM LEVELS : HYPERCALCEMIA
METASTATIC CALCIFICATION
72
METASTATIC CALCIFICATION EFFECTS
- Hyperparathyroidism - INC BONE DESTRUCTION - hyper vitaminosis D - renal failure - sarcoidosis - Paget's disease - phosphate retention leads to secondary hyperparathyroidism
73
Calcium deposits in normal tissues
METASTATIC CALCIFICATION
74
Occurs in normal calcium metabolism
DYSTROPHIC CALCIFICATION
75
METASTATIC CALCIFICATION diseases
``` BONE renal failure sarcoidosis Paget's disease Vitamin D intoxication ```
76
DYSTROPHIC CALCIFICATION diseases
intima of blood vessels | damaged parts of heart and valves
77
PATHOLOGIC ADAPTATION OF APOPTOSIS / ACTIVE / ENERGY DEPENDENT involves the enzymes called
CASPASES C ysteine dependent ASP artate specific prote ASE CASPASES
78
PATHOLOGIC ADAPTATION OF APOPTOSIS / ACTIVE / ENERGY DEPENDENT involves the enzymes called
CASPASES C ysteine dependent ASP artate specific prote ASE CASPASES
79
PATHOLOGIC ADAPTATION OF APOPTOSIS / ACTIVE / ENERGY DEPENDENT caused by
DNA damage, Accumulation of misfolded CHON, Graft rejection, Infection
80
CASPASES in apoptosis functin to
cleave proteins containing cysteine after | aspartic acid residues
81
CASPASES in apoptosis function to
cleave proteins containing cysteine after | aspartic acid residues
82
EXECUTIONER CASPASES
executioner 367
83
APOPTOSIS / ACTIVE / ENERGY DEPENDENT | 2 pathways for apoptotic cell death
``` Mitochondrial pathway (Intrinsic) Death receptor pathway (Extrinsic) ``` Mnemonic : De for DE- Death , Extrinisc
84
APOPTOSIS / ACTIVE / ENERGY DEPENDENT | 2 pathways for apoptotic cell death
``` Mitochondrial pathway (Intrinsic) Death receptor pathway (Extrinsic) ``` Mnemonic : De for DE- Death , Extrinsic
85
Involvement of both inflammation and aspects of both | necrosis and apoptosis
PYROPTOSIS
86
OTHER PATHWAYS OF CELL DEATH
NECROPTOSIS | PYROPTOSIS
87
hybrid that shares aspects of both necrosis | and apoptosis
NECROPTOSIS | NECRO- necrosis + PTOSIS - apoptosis
88
NECROPTOSIS | trigger
triggered by the activation of death | receptors
89
PYROPTOSIS | trigger
Trigger: inflammasome
90
NECROPTOSIS | Subsequent sequence
protein activation ( kinases)
91
NECROPTOSIS | effect
Effect: destruction of cellular membranes | w/ inflammation
92
PYROPTOSIS | effect
Effect: Intact nucleus with cell membrane | destruction
93
PYROPTOSIS | Subsequent sequence
Sequential caspase activation, some induce the production of cytokine inflammation cytokines are used in fever, "pyro"
94
Reperfusion occurs in several mechanisms:
Oxidative stress. Intracellular calcium overload. Inflammation. Activation of the complement system

PATHO (8 decks)

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