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COM - MOD 1 > Ch 2 - 5/4 Dobson > Flashcards

Ch 2 - 5/4 Dobson Flashcards

1
Q

What kind of cellular adaptation is a result of increased demand and stimulation?

A

Hyperplasia or hypertrophy

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2
Q

What kind of cellular adaptation is a result of chronic irritation (physical or chemical)?

A

Metaplasia

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3
Q

What cellular adaptation is most common in the uterus during pregnancy?

Endometrium from estrogen?

A

Hypertrophy

Hyperplasia

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4
Q

What cellular adaptation is most common in muscle disuse?

Barrett esophagus?

A

Atrophy

Goblet cell Metaplasia

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5
Q

Metabolic alterations to a cell that are due to chronic injury result in what?

A

Intracellular accumulations, calcification

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6
Q

Cumulative sub lethal injury over long life span induce what cellular response?

A

Cellular aging

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7
Q

What type of necrosis is associated with tuberculous infection?

What type specifically?

A

Caseous

Myobacterium tuberculosis

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8
Q

Caseous necrosis is described as what?

How does it look on microscopic examination?

A

Yellow-white and “cheese-like”

Appears as a structure less collection of fragmented or lysed cells and amorphous granular debris enclosed within a distinctive inflammatory border (Granuloma)

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9
Q

If there is ischemia to a cell, what happens in the mitochondria?

A

DEC ox-phosph and DEC ATP production

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10
Q

What are the 3 consequences of DEC ATP production in the mitochondria?

A

DEC Na pump
INC anaerobic glycolysis
Detachment of ribosomes (dec protein synthesis)

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11
Q

What are the major sequellae of increased anaerobic synthesis in the cell?

What happens structurally in the cell?

A

DEC glycogen
INC lactic acid and Dec pH

Clumping of nuclear chromatin

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12
Q

What are the consequences of DEC activity in the Na+ pump?

What structural changes seen in the cell?

A

INC influx of Ca, H2O, and Na
INC effluent of K+

ER swelling, cellular swelling, loss of Microvilli and Blebbing

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13
Q

What are the major causes of ATP depletion?

A

Reduced supply of oxygen and nutrients, mitochondrial damage, and actions of toxins (Cyanide)

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14
Q

What are the consequences of membrane damage?

A

Loss of cellular components

Enzymatic digestion of cellular components

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15
Q

What are the microscopic features of coagulative necrosis in the heart?

A

Wavy fibers

Widened spaces bw dead fibers containing edema fluid and scattered neutrophils

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16
Q

What pathological conditions lead to apoptosis?

A

DNA damage
Accumulation of misfolded proteins
Cell death in infection
Pathological atrophy in parenchymal organs after duct obstruction

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17
Q

Li-Fraumeni syndrome is a result of DNA damage to what gene?

A

TP53

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18
Q

What kind of cellular adaptation is a result of decreased nutrients and and decreased stimulation?

A

Atrophy

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19
Q

What are the 3 basic steps in the molecular pathogenesis of cardiac hypertrophy?

A

Actions of mechanical sensors
Signals that activate a signal transduction pathways
Signaling pathways activating TFs

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20
Q

What are the the GFs of mechanical sensors in hypertrophy?

Vasoactive agents?

A

TGF-B, IGF-1, FGF

A-adrenergic agonists, Endothelin-1, Angiontensin II

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21
Q

What are the TFs which increases the synthesis of muscle proteins responsible for muscle hypertrophy?

A

GATA4
NFAT
MEF2

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22
Q

Cardiac hypertrophy is associated with INC/DEC gene expression of ANF?

What does this do?

A

Increased

Decreases blood volume and pressure

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23
Q

What is an example of hormonal hyperplasia?

Compensatory hyperplasia?

Pathologic hyperplasia?

A

Enlargement of breast tissue during puberty

Liver regeneration

Endometrial, BPH

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24
Q

What are the 6 different causes of atrophy?

A 
Dec workload
Loss of innervation
Diminished blood supply
Inadequate nutrition / malnutrition 
Loss of endocrine stimulation
Pressure (tissue compression)
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25
Q

How does the degradation of cellular protein mainly occur?

A

Ubiquitin-proteasome pathway

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26
Q

Some of the cell debris within autophagic vacuoles may resist digestion and persist in the cytoplasm as what?

Example of one?

A

Residual bodies

Lipofuscin granule (brown color)

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27
Q

What is the order of change in a cell during irreversible cell injury? (Fig. 2-7)

A

Biomechanical alterations leading to cell death
Ultrastructural
Light microscopic
Gross morphologic

BULGe

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28
Q

How does the cell size change in necrosis?

Apoptosis?

A

Swell

Shrinks

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29
Q

Describe the plasma membrane in necrosis?

Apoptosis?

A

Disrupted

Intact with altered structure

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30
Q

What happens to the cellular contents in necrosis?

Apoptosis?

A

Enzymatic digestion, may leak out of cell

Intact, released into apoptotic bodies

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31
Q

What is it called on microscopic examination, small clear vacuoles may be seen within the cytoplasm, representing distended and pinched-off segments of the ER?

The may show what kind of staining?

A

Hydropic change or vacuolar degeneration

Increased eosinophilic staining

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32
Q

What are the Ultrastructural changes of reversible cell injury?

A

Blebbing, blunting, loss of Microvilli
Mitochondrial swelling and amorphous densities
Dilation of the ER with detachment of polysomes
Nuclear alterations -> disaggregate on of granular and fibrillar elements

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33
Q

What do necrotic cells show in a H&E stain?

Due to what?

A

Increased eosinophilia

Loss of cytoplasmic RNA and denatured cytoplasmic proteins

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34
Q

Dead cells may be replaced by whirled phospholipid masses called what?

Derived from where?

A

Myelin figures

Damaged cell membranes

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35
Q

In living patients, if necrotic cells and cellular debris are not promptly destroyed and reabsorbed, what happens to them?

A

Dystrophic calcification

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36
Q

What kind of necrosis is characteristic of malignant hypertension and vasculitis?

A

Fibroid necrosis

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37
Q

What are the major causes of depletion of ATP?

A

Reduced supply of oxygen and nutrients, mitochondrial damage, toxins

38
Q

What are 3 consequences of mitochondrial damage?

A

Formation of the mitochondrial permeability pore
Formation of ROS
Increased permeability of the outer mitochondrial membrane

39
Q

Increased intracellular calcium activates what enzymes?

What do they do?

A

Phospholipase and proteases do membrane damage
Endonucleases do nuclear damage
ATPases hasten ATP depletion

40
Q

How does intracellular calcium affect mitochondrial membrane permeability?

A

Increases it, thus decreasing ATP production

41
Q

What ROS is the most reactive and principally responsible for damaging lipids, proteins, and DNA?

A

OH radical

42
Q

How is hydrogen peroxide converted to oxygen?

A 
Catalase (in Peroxisomes) and 
Glutathione peroxidase (cytosol, mitochondria)
43
Q

What agents act as antioxidants??

A

Vitamins A, C, E and glutathione

44
Q

What are the pathological effects of ROS?

A

Lipid peroxidation in membranes
Protein modification (misfolding and breakdown)
DNA damage -> mutations

45
Q

How is membrane permeability damaged and what is responsible?

A

Phospholipid loss due to decreased phospholipid synthesis (ROS)
Increase in phospholipid breakdown via INC in intracellular Ca2+
Cytoskeleton damage via activation of proteases

46
Q

If there is duct obstruction that may occur in the pancreas, parotid, or kidney what may this lead to?

A

Pathologic apoptosis

47
Q

What is the most characteristic feature of apoptosis?

Describe it

A

Chromatin condensation

Chromatin aggregates peripherally and becomes dense, may fragment

48
Q

What are the anti-apoptotic proteins?

What domains do they contain?

What do they prevent?

A

BCL2, BCL-XL, MCL

BH1-4

Cytochrome c leakage

49
Q

What are the pro-apoptotic proteins?

What domains do tha even have?

A

BAX and BAK

BH1-4

50
Q

What are the major sensors of apoptosis?

Domains?

A

BAD, BIM, BID, Puma, Noxa

BH3 ONLY

51
Q

What happens once cytochrome c is released into the cytosol?

A

Binds APAF-1 forming apoptosome

Binds caspase 9 which activates caspase 3

52
Q

What is responsible for inhibiting anti-apoptotic proteins?

A

Smac and Diablo

53
Q

What are the death receptors of the extrinsic pathway?

A

TNFR1 and Fas (CD95)

54
Q

What is the adaptor protein that begins the pathway of apoptosis once Fas binds FasL?

55
Q

Once the adaptor protein of the extrinsic pathway is activated what happens leading up to apoptosis?

A

Caspase 8 and 10 are activated, which will activate executioner caspases 3 and 6

56
Q

What protein is capable of inhibiting the death receptor pathway of apoptosis?

How?

What contains this protein?

A

FLIP

Binds pro-caspase-8

Viruses and normal cells

57
Q

What are the most prominent signals for cells indicating apoptosis?

A

Phosphatidlyserine
Thrombospondin
C1q

58
Q

What is triggered when abnormal proteins accumulate in the ER?

A

Unfolded protein response

59
Q

What does the unfolded protein response trigger?

A

INC production of chaperones
INC proteasomal degradation of abnormal proteins
Slows protein translation (and DEC protein synthesis)

60
Q

Tay-Sachs disease is due to what defective protein?

A

Hexoaminidase Beta subunit

61
Q

Familial hypercholesterolemia disease is due to what defective protein?

A

LDL receptor

62
Q

Creutzfeldt-Jacob disease is due to what defective protein?

A

Prions (abnormal folding of PrPsc)

63
Q

Alzheimer’s disease is due to what defective protein?

A

AlphaBeta peptide

64
Q

What is the distinguishing feature of necroptosis?

Triggered by mostly what? What else?

A

NO activation of Caspases

TNFR1 and by viruses

65
Q

Ligation of TNFR1 recruits what in necroptosis?

A

RIP1 and RIP3

66
Q

Necroptosis occurs where?

Associated with what diseases?

A

Formation of mammalian bone growth plate

Cell death in steatohepatitis, acute pancreatitis, reperfusion injury, neurodegenerative diseases

67
Q

Caspase-1 is involved of what?

It activates what?

A

Pyroptosis

IL-1

68
Q

What cell processes involves inward invagination of lysosomal membranes for delivery?

A

Microautpohagy

69
Q

What marker is used to identify cells in which Autophagy is occurring?

70
Q

Deletion of what gene leads to increased susceptibility to tuberculosis?

71
Q

Autophagy plays a role in what main diseases?

A 
Cancer
Alzheimer's 
Huntington's
IBD and Crohn's 
Infections diseases
72
Q

Intracellular accumulation of cholesterol within macrophages is also characteristic of acquired and hereditary hyperlipidemic states is called what?

Found where?

A

Xanthomas (clusters of foamy cells)

Us epithelial CT of the skin and tendons

73
Q

The focal accumulations of cholesterol-laden macrophages in LP of the gallbladder is referred to what?

A

Cholesterolosis

74
Q

What is the name of a lysosomal storage disease caused by mutations affecting enzyme involved in cholesterol trafficking, resulting in cholesterol accumulation in organs?

A

Niemann-Pick type C disease

75
Q

Large, homogenous eosinophilic inclusions produced from a distended ER are called what?

A

Russell bodies

76
Q

This subclass of intermediate filaments resists forces applied to it in epithelial cells?

Muscle cells?

CT cells?

A

Keratin filaments

Desmin

Vimentin

77
Q

What is the most common exogenous pigment?

Accumulations of this tissue in the lung is called what?

A

Carbon (coal dust)

Anthracosis

78
Q

What is an insoluble pigment produced from wear-and-tear?

A

Lipofuscin

79
Q

What is the only endogenous brown-black pigment?

80
Q

What is of a yellow-brown color and is a tell-tale sign of free radical injury and lipid peroxidation?

A

Lipofuscin

81
Q

What is of a golden yellow-to-brown, granular or crystalline pigment?

Major storage form of what?

A

Hemosiderin

Iron

82
Q

When there is local or systemic excess of iron, what will form hemosiderin granules?

83
Q

What are the major causes of hemosiderosis?

A

INC absorption of dietary iron (hemochromatosis)
Hemolytic anemia
Repeated blood transfusions

84
Q

What is the abnormal deposition of calcium salts, together with iron and magnesium called?

A

Pathologic calcification

85
Q

What kind of calcification occurs locally in dying tissues with normal serum levels of calcium?

Frequently occurs where?

A

Dystrophic

Aging or damaged heart valves

86
Q

Deposition of calcium salts in normal tissues is what?

Results from what?

A

Metastatic calcification

Hypercalcemia secondary to disturbance in calcium metabolism

87
Q

What may be formed in the focus of calcification?

A

Heterotopic bone

88
Q

Papillary cancers (thyroid) are apt to develop what?

Describe them

A

Psammoma bodies

Grains of sand, lamellated configurations

89
Q

Where does metastatic calcification most often occur?

A

Gastric mucosa, kidneys, lungs, systemic arteries, PV

90
Q

patients with Werner syndrome show what?

Defective gene is what?

A

Premature aging

DNA helicase

91
Q

What does the CDKN2A locus encode for?

Controls what phase progression of the cell cycle?

A

p16

G1 to S

COM - MOD 1 (7 decks)

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