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Cell Injury, Death And Adaptation Flashcards

1
Q

Implicated for accelerated proteolysis in catabolic conditions (cachexia in CA, TB)

Drives atrophy by decreasing cell size
Posted in intermediate filaments of cytoskeleton
Proteasome recognizes and tags them for degradation

A

Ubiquitin Proteosome Pathway

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2
Q

REVERSIBLE change in which one adult cell type (epi or mesen) is replaced by another adult

A

Metaplasia

Replacement better able to withstand environment

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3
Q

Metaplasia occurs by

A

reprogramming stem cells to differentiate along a different pathway vs phenotypic transdifferentiation change

But inc propensity for malignant transformation

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4
Q

Inc cell and organ size in resp to inc workload in cells incapable of cell division

A

Hypertrophy

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5
Q

Hypertrophy esp in cardiac tissue are induced by

A

1) mechanical trigger

2) trophic chemical trigger

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6
Q

Inc cell number in response to 1) hormone 2)compensation

in cells with abundant tissue stem cells

A

Hyperplasia

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7
Q

Dec cell organ and size due to dec nutrient and disuse

Inc protein degradation dec protein synthesis

A

Atrophy

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8
Q

First lost after stress and noxious influence in the cell

A

Cellular function

Lag with morphologic change and cell death

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9
Q

Irreversibility in cell damage occurs (2)

A

1) inability to correct mitochondrial dysfunction (lack of oxphos and ATP generation) despite resolution
2) profound disturbance in membrane function

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10
Q

targetting membrane of this organelle promotes progression to necrosis

A

Lysosome

Enzymatic dissolution by hydrolases

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11
Q

Barbiturates cause tolerance in the long run bec

A

Hypertrophy of ER and inc CYP450 activity in liver

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12
Q

Morphologic changes in reversible injury (2)

A

Cellular swelling

Fatty change

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13
Q

Small clear vacuoles within cytoplasm which pinched off from SER

A

Hydrophic change

Vacuolar degeneration

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14
Q

Failure of energy dependent ion pumps in plasma mem leading to inability to maintain ionic and fluid homeostasis

A

Cellular swelling

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15
Q

Occurs in hypoxic injury, toxic or metabolic charac by appearance of lipid vacuoles in cytoplasm

A

Fatty change

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16
Q

Intracellular changes assoc with reversible injury (4)

A

1 plasma membrane blebbing and loss of microvilli
2 mitochondrial swelling
3 dilation of ER
4 eosinophilia due to dec cytoplasmic RNA, nuclear alteration chromatin clumping

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17
Q

Loss of basophilia of chromatin in necrotic cell

A

Karyolysis

due to DNase

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18
Q

Nuclear shrinkage and inc basophilia in necrotic cells

A

Pyknosis

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19
Q

Fragmentation of pyknotic nucleus in necrotic cell

A

Karyorrhexis

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20
Q

Necrotic cells become calcified by

A

Necrotic cell -> myelin figure -> degraded to fatty acid -> FA with calcium salt -> calcified

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21
Q

Architecture preserved with tissues having firm texture
Structural proteins and enzymes denatured halting proteolysis of dead cell
Infarcts, solid organs

A

Coagulative necrosis

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22
Q

Focal bacterial, fungal infection stimulating leukocytic digestion of tissue
Completely digested -> liquid viscous mass
Creamy yellow pus
Brain

A

Liquefactive necrosis

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23
Q

Limb losing blood supply undergoing coagulative necrosis

Bacterial superimposition -> coagulative necrosis (modified)

A

Gangrenous necrosis

Wet gangrene

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24
Q

Cheese like friable yellow like
Collection of lysed cell with pink appearance complete obliteration of architecture
Enclosed in an inflammatory border
Focus of inflammation:

A

Caseous necrosis

Granuloma

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25
Q

Focal areas of fat destruction resulting from release of pancreatic lipase liquefying fat cells
FA combine with Ca to form chalky white areas (saponification)

A

Fat necrosis

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26
Q

Deposition of immune complex with fibrin in walls of arteries producing :

Seen in PAN

A

Fibrinoid

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27
Q

Inc eosinophilia
Nuclear shrinkage, fragmentation, dissolution (pyknosis, karyorrhexis, karyolysis)
Breakdown of plasma and organelle membrane
Abundant myelin
Leakage and digestion of enzyme to cell content

A

Necrosis

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28
Q

Principal targets and biochem mech of cell injury (4)

A

1) mitochondria (ATP and ROS generation)
2) calcium homeostasis disturbance
3) plasma and lysosomal membrane damage
4) DNA damage and protein misfolding

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29
Q

Restoring of blood flow to ischemic but viable tissue results in death of cells undergoing irreversible injury

A

Ischemia-reperfusion injury

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30
Q

Ischemia reperfusion injury occurs due to (2)

A

Generation of ROS

Inflammation bec of influx of leukocytes and plasma protein and complement

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31
Q

Cell death where cells activate enzymes that degrade its own nucleur DNA and cytoplasmic proteins

A

Apoptosis

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32
Q

Apoptosis does not elicit inflammatory response bec

A

Membranes remain intact and fragments are cleared before contents have leaked

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33
Q

Apoptosis is induced in pathologic conditions (4) by

A

1) DNA damage
2) misfolded protein accumulation
3) cell injury in infection
4) Pathologic atrophy

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34
Q

Reduced cell size
Fragmentation into nucleosome
Intact altered structure and orientation of lipid
Intact cellular contents released into apoptotic bodies
No inflammation

A

Apoptosis

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35
Q

Cysteine proteins that cleave proteins after aspartic residues activated in apoptosis

A

Caspases

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36
Q

Survival and death of cell depends on

A

Permeability of mitochondria

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37
Q

Permeability of mitochondria is controlled by

A

20 proteins prototype BLC 2

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38
Q

Apoptosis mitochondrial pathway

A

Lack of survival signals (DNA damage, protein misfolding) -> activation of sensors Bax and Bak channels inhibiting BCL-2 -> leak of cytochrome c and proteins -> capsase activation

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39
Q

Loss of CFTE leading to defect in chloride transport

A

Cystic fibrosis

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40
Q

Loss of LDL receptor leading to hyperchole

A

Familial hypercholesterolinemia

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41
Q

Lack of lysosomal enzyme leading to storage of GM2 gangliosides in neuron

Hexosaminidase B2 unit

42
Q

Absence of alpha 1

Antitrypsin in lungs causing destruction of elastic tissue -> emphysema

A

Alpha 1 antitrypsin deficiency

43
Q

Eliminates self reactive lymphocytes and damage by cytotoxic T lymphocytes
Initiated by engagement of death receptors (TNF)

A

Death receptor extrinsic pathway

44
Q

Mechanisms of intracellular accumulation (4)

A

1 abnormal metabolism (fatty change)

2) protein misfolding and transport (intracellular accum of defective protein)
3) enzyme deficiency (substrate accumulation, storage disease)
4) ingestion of indigestible material (exogenous material accumulation)

45
Q

Most common exogenous pigment

A

Carbon

Anthracosis

46
Q

Wear and tear pigment
Brownish yellowish granular
Marker of past free rad injury (age or atrophy)
Lipid perox

A

Lipofuscin

47
Q

Golden yellow to brown from hg due to excess iron

A

Hemosiderin

48
Q

Deposition of calcium at sites of cell injury and necrosis (dead cell)

A

Dystrophic

49
Q

Deposition of Ca at normal tissue by hypercalcemia inc PTH

A

Metastatic

50
Q

Results from accumulating cell damage (ROS), reduced capacity to divide (replicatice senescence), reduced ability to repair damaged DNA

A

Cellular aging

51
Q

Defective DNA repair mech reversed by calorie restriction

A

Accumulation of DNA damage

52
Q

Reduced capacity of cell to divide secondary to progressive shortening of chromosomal ends (telomeres)

A

Replicative senescence

53
Q

Progressive accumulation of metabolic damage, role of growth factors promoting aging

A

Other causes of aging

54
Q

Hemosiderin-laden alveolar macrophage

A

Heart failure cell

55
Q

Earliest symptom of LSHF

A

Dyspnea

Cardiomegaly
Tachycardia
S3 
Rales
MR systolic murmur
56
Q

Early latent phase syphilis is until

A

1 year after infection

Mucocutaneous lesion recurrence

57
Q

Untreated syphilis patients enter an asymptomatic period

A

Latent phase

1/3 will develop new sx in 5-20 years

58
Q

Progression from latent phase develops into

A

Tertiary syphilis (late symptomatic phase)

Lesions in CV, CNS other organs

59
Q

In tertiary stages, spirochetes are

And patients are

A

Less likely to be demonstrated

Less likely to be infectious

Common in HIV and promotes its transmission (bec ulceration)

60
Q

Pathognomonic microscopic syphilitic lesion

A

Proliferative endarteritis with plasma cell-rich infiltrate

61
Q

Responsible for endothelial cell activation and proliferation
Hallmark of endarteritis
Leading to perivascular fibrosis and lumen narrowing

A

Host immune response

62
Q

3 instances of Hypoxia

Most important cause of injury

A

Ischemia
Hypoxemia
Decreased capacity of blood to carry oxygen

63
Q

Decreased blood flow

Atherosclerosis
CVD (Brain 3-5mins)
Skeletal muscle (CS)

64
Q

Low partial pressure of oxygen in the blood (PaO2 less than 60mmHg, SaO2 <90%)

COPD
Interstitial fibrosis

65
Q

RBC incapable of carrying right amount of oxygen

Methemoglobinemia
Anemia (dec in RBC mass, PaO2 normal, SaO2 normal)

CO poisoning (binds hgb 100x affinity compared to O2, PaO2 normal, SaO2 dec)

Cherry red appearanc of akin because of co tightly bound to Hb

Early sign of exposure = headache

A

Decreased oxygen carrying capacity

66
Q

Uncommon bone disorder in which scar-like fibrous tissue develops in place of normal bone

A

Fibrous dysplasia

67
Q

Most common cause of budd-chiari blocking the hepatic vein

A

Polycythemia vera

68
Q

FiO2 (atm)-> PAlveolar -> Parterial pressure -> SaO2 RBCs

In high altitude, FiO2

A

Do not be confused

Decreases

FiO2 -> PAO2 will decrease if PACO2 increases (hypoventilation, COPD); interstitial fibrosis (thickened alveolar sac)

69
Q

Fe binds to O2
Fe2 to Fe3
PaO2 is normal, SaO2 is decreased

Clasically seen in oxidant stressors such as sulfa and nitrate drugs

A

Methemoglobinemia

70
Q

Impaired oxidative phosphorylation

Consequence

A

Dec ATP
Na-K pump promotes cell swelling
Ca pump active enzymes (promotes Ca in cytosol)
Aerobic glycolysis -> shift to anaerobic glycolysis (low ATP, lactic acid, precipitates DNA and proteins)

71
Q

Able to proliferate all the time

Epidermis
Hematopoietic cells
Excretory ducts

72
Q

Few divisions
Capable of rapid division when activated

Hepatocyte
Renal tubular epithelial cells

A

Stable

quiescent

73
Q

Incapable of cell division
Responds to injury by repair or producing a fibrous of scar

Neurons
Myocardial cells
Skeletal muscle

A

Permanent
Nondividing

Fibrosis
Gliosis

74
Q

associated change in fibrocystic change of breast

can it progress to dysplasia?

A

Apocrine metaplasia blue dome cyst

No this metaplasia does not transform into dysplasia

75
Q

Low Vit A induces metaplasia in the lungs to become squamous

Other uses

A

Maturation of immune system
Conjunctiva and cornea: highly specialiazed
Keratomalacia: thickening of surface epithelium
Night blindness
Vitamin A/Retinol
Retinaldehyde: for normal vision
Retinoic: normal morphogenesis

76
Q

Only leukemia than can be treated with all trans retinoic acid (Vit A)

chromosome translocation?

A

Acute Promyelocytic Leukemia

T 15;17

77
Q

CT: bone, cartilage
Metaplasia

Ex:
Inflammation of skeletal muscle results in metaplastic production of bone

A

Mesenchymal type of tissue can withstand stress

Myositis ossificans

78
Q

Cell consumes some components in vacuole and these fuse with lysosomes which contains hydrolytic enzymes

Tagged with:

Shrink and break the cytoskeleton

A

Autophagy

Mannose-6-phosphate

79
Q

What lysosomal storage disease is associated with defective phosphotransferase hence there is failure to transfer phosphate to mannose residues (No mannose 6 phosphate)

A

I cell inclusion cell disease

80
Q

Hallmark of irreversible cell damage

A

Membrane damage

81
Q

Plasma membrane damage

82
Q

Mitochondrial membrane damage

A

Cytochrome C

83
Q

Enzyme leak in cytosol, will synergize with calcium to digest the cell itself

A

Lysosomal membrane

84
Q

Correct sequence of morphologic changes

A 
Cell function
Biochemical
Ultrastructural 
Light microscopic 
Gross
85
Q

Frequently overexpressed due to chromosomal translocations and resulting rearrangements in certain B cell lymphomas

Controls release of pro-apoptotic proteins

A

BCL-2 family of proteins

86
Q

Anti-apoptotic proteins

A

BCL2
BCL XL
MCL1

87
Q

Pro-Apoptotic

88
Q

Sensors

A 
BIM
BID
Puma
Noxa
BAD
89
Q

Best known death receptors (Death Receptor Pathway)

A

Fas

TNFR 1

90
Q

Mitochondrial intrinsic pathway

Critical Inititator

91
Q

Death Receptor Pathway extrinsic

Critical initiator

92
Q

Execution Phase

A

Caspase 3

Caspase 6

93
Q

Combinations of both

Morpho (necrosis) plasma membrane damage, loss of AT, release of enzyme

Genetically programmed signal transduction (apoptosis-like) -> CASPASE INDEPENDENT

Grossly looks necrotic
Biochemically apoptotic

A

Necroptosis

94
Q

Receptor for necroptosis

A

RIP -> Receptor Associated Kinase 1

95
Q

Programmed cell death accompanied by IL - 1

A

Pyroptosis

96
Q

Immunoglobulin in plasma cells

A

Russel bodies

97
Q

Premature aging is seen in Werner syndrome because of the enzyme defect?

A

DNA helicase

Wherner

98
Q

Caloric restriction increases longevity by

A

Reducing signal intensity IGF-1 pathway (dec IGF or GH)

Increasing sirtuins

99
Q

Speeds up aging

100
Q

Decrease in IGF-1 driven by caloric restriction promotes

A

slowing of aging

101
Q

Prolongs longevity by expression of several genes that increase longevity

Caloric restriction increases this protein

Pathology (24 decks)

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