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MOD Midterm > Cell Responses to Stress , Adaptation, Injury, Death - Dobson (Ch2) > Flashcards

Cell Responses to Stress , Adaptation, Injury, Death - Dobson (Ch2) Flashcards

1
Q

Etiology

A

Cause

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2
Q

Hypertrophy

A

Increased size in cells due to increased demand

= increased synthesis of cell proteins and myofilaments

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3
Q

Hyperplasia

A

Increased number of cells due to higher demand

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4
Q

Metaplasia

A

The increase in cells differentiated to new role (Change in phenotype), usually when a cell is sensitive to stress and replaced by a cell not as sensitive
Due to Chronic irritation
Reversible

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5
Q

What causes autophagy

A

Low nutrients

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6
Q

What can cause calcification or intracellular accumulations

A

Metabolic changes from genetically or acquired

Or Chronic Injury

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7
Q

what causes either the physiologic or pathological hypertrophy to activate

A

TGF-B, ,IGF-1, (a-adrenergic agonist, endthelin, angiotensin = vasoconstriction)

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8
Q

What are the factors activated for Physiologic Hyperplasia

A

= exercise induced
(PI3K/AKT pathway)
= (uterus grows when pregnant)

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9
Q

What are the factors activated in pathologic Hyperplasia

A

G-protein receptors and their pathway

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10
Q

What TF are activated to make more myosin and muscle proteins

A

GATA4, NFAT, MEF2

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11
Q

Cardiac hypertrophy usually is associated with what

A

Increased ANP production

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12
Q

Physiologic Hyperplasia

A

H or GFs needed in higher amount after damage or resection, so it can have normal function
(Breasts during puberty, adrenal gland)

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13
Q

Hormonal hyperplasia

A

Glands like breast growth

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14
Q

Compensatory hyperplasia

A

Liver

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15
Q

Pathologic Hyperplasia

A

Excessive H or GFs on target cells due to that cell not responding well
(Endometrial - E does not decrease like it should in period cycle and endometrium continues to grow, Prostate - T continuously stimulating growth)

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16
Q

Physiologic Atrophy

A

Embryologic and normal things

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17
Q

Pathologic Atrophy

A 
Low workload
X innervation 
X BF
Low nutrition or high TNF
X endocrine stimulation (endometrium, breasts, vagina)
Pressure on the tissue (tumor or bone)
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18
Q

Ex of metaplasia

A

Columnar to squamous epithelium in the respiratory track (irrigation like smoking, low VIT A, GERD), bile duct, pancreatic duct, salivary glands

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19
Q

Squamous metaplasia can cause what consequence

A

Low protection, mucus secretion, ciliary actions
Can lead to malignancy
For Cartilage or adipose or bone in muscles and other tissues = CT metaplasia

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20
Q

Bone formation in muscle (metaplasia) called what

A

Myositis Ossificans

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21
Q

How does metaplasia happen

A

Reprogramming or stem cells in tissues or mesenchyme cells that are undifferentiated

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22
Q

Hallmarks for reversible cell injury

A
  1. Cell swelling (ion changes)
  2. Reduced oxidative phosphorylation (low ATP storages)
  3. Altered mitochondria and cytoskeleton
  4. Light microscopy sees fatty change and swelled cells
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23
Q

Necrosis uses what to die

A

Lysosomes and cleaned up by inflammation

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24
Q

Necrosis and apoptosis physiologic and pathologic

A

Necrosis is always pathologic

Apoptosis is both

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25
Q

Necrosis nucleus

Apoptosis nucleus

A

N : Pyknosis = shrink, Karyorrhexis = fragmentation, Karyolysis = endonuclease degrade and it fades
A : Fragmentation to nucleosomes

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26
Q

What is seen in reversible cell injury

A

Lowered cell function

Ultra structural changes (mito, PM, ER, Nuclear changes)

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27
Q

What is seen in irreversible cell

A
  1. Biochemical alterations
    2 . Ultra structural changes
  2. Light microscopic changes
  3. Gross morphological changes
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28
Q

What is seen in necrotic cell

A
  1. High eosinophilia
  2. Glassy looking
  3. Myelin figures (phospholipid masses)
  4. Calcification
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29
Q

Coagulative necrosis

A

No digestion of cells (only denature proteins)
Ischemia due to obstructed vessel = all organs (except brain)
- if localized = infarct

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30
Q

Liquefaction necrosis

A

Digests cells - liquid, pus (creamy yellow)
Bacteria or fungal infection
CNS (brain)

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31
Q

Gangrenous Necrosis

A

Lowe limbs usually from coagulative necrosis, can undergo liquefactive necrosis is bacteria infects it

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32
Q

Caseous necrosis

A

TB ad fungal infection
= cheese Iike
= Lysed cells, granular debri = granuloma

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33
Q

Fat necrosis

A

Fat destruction, released pancreatic enzymes (lipases)

Calcium deposits

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34
Q

Fibrinoid necrosis

A

Immune reactions in BVs

Fibrinoids (fibrin leaks out)

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35
Q

In low ATP levels like from hypoxia

A

Body depends on anaerobic glycolysis from glycogen stores = lactic acid

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36
Q

Irreversible Mitochondrial and lysosomal damage causes

A

Necrosis

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37
Q

3 things that happen when there is mitochondrial damage

A
  1. Mitochondrial permeability transition pore = X membrane potential —> X oxphos —> X ATP (Cyclophilin D + Ca+2 causes this, targeted in transplantation)
  2. ROS
  3. Proteins leak inside —> apoptosis intrinsic pathway
38
Q

Increased CA+ 2 into cell causes what 3 things

A
  1. Mitochondrial permeability transition pore
  2. Activate ATPase, Protease, Phosphilipases, endonuclease
  3. Activate caspases
39
Q

How are ROS (free radicals also removed)

A

Add to H2O—-> O2 and H2O2

  1. Catalase
  2. SODs
  3. Glutathione peroxidase (makes GSSG)
40
Q

Which VIT are anti oxidants

A

E and A, C, glutathione

41
Q

What metals can cause ROS

A

Iron and copper

42
Q

What can you measure in blood to see if there is necrosis in

  1. Liver
  2. Liver by bile duct epithelium
  3. Cardiac myocardium
A
  1. Transaminase
  2. Alkaline phosphate
  3. Troponin
43
Q

Low ATP due to hypoxia or ischemia =

A

CA+ into the cell = changes and damage

44
Q

What stimulates new BVs to form

A

Hypoxia - induce blue factor -1

45
Q

Restoring O2 to ischemic tissues can do what

A
  1. If reversible : repair

2. If irreversible : make cells die (ischemia- reperfusion injury)

46
Q

ischemia- reperfusion injury how does this happen

A

Increasing O2 to damaged Mitochondria causes accumulation of ROS
Inflammation (from blood coming again)
CA+ increases more inside cell due to damaged mito

47
Q

Cyanide

A

Inhibits cytochrome oxidase = X oxidative phosphorylation

48
Q

What do you see in apoptosis

A
  1. Cell shrinks
  2. Chromatin condensation
  3. Cytoplasmic blebs + apoptotic bodies
  4. M that phagocytose (lysosomes)
49
Q

4 things causing apoptosis

A
  1. DNA damage
  2. Protein accumulation
  3. Infection like certain viruses
  4. Duct obstruction causing atrophy
50
Q

Intrinsic Apoptosis

A
  1. Mitochondria gets more permeable by inhibited Bcl-2 (from BAX/BAK activation)
  2. Cytochrome c released to cytoplasm binding to Apaf (apopsome) activating caspase 9
    * BH3= sensor activating this entire process when cell has stress*
51
Q

Over-expression of Bcl-2

A

B- cell lymphoma

52
Q

Extrinsic Apoptosis

A
  1. FAs —> FasL (death receptor on PM, CD95, TNF1)
  2. Activates FADD
  3. Activates caspase 8 + 10
53
Q

Caspases executing apoptosis

A

3 and 6 activated by both pathways

54
Q

Necroptosis

A

NO caspase = like necrosis
Programmed cell death = like apoptosis
= uses TNF and TNFR1, activating RIP1, RIP3, caspase 8 is not activated

55
Q

Pyroptosis

A

Programmed cell death with IL1 (fever) released

= IL1 activated inflammasome

56
Q

What is dysfunctional causing accumulation of something:

  1. CF
  2. Familial hyperlipidemia
  3. Tay-Sachs
  4. a-1-antitrypsin deficiency
  5. Crentzfeldt-Jacob
  6. Alzheimer’s
A
  1. CF : CFTR
  2. Familial hyperlipidemia : LDL receptor
  3. Tay-Sachs : Hexosaminidase B subunit (X lysosomal enzyme)
  4. a-1-antitrypsin deficiency : a1-antitrypsin (apoptosis in liver, emphysema in lungs)
  5. Crentzfeldt-Jacob : prions (misfolded PrPsc in neurons)
  6. Alzheimer’s : AB peptide
57
Q

3 features of autophagy

A
  1. Double membrane
  2. Lysosomes
  3. Sequestering vacuoles
    * *** usually during low nutrition
58
Q

What can caused by uncontrolled autophage

A

IBS (Crohns)
Cancers
Neurodegenerative disorders

59
Q

Steatosis

A

Fatty change : accumulation of TAGs in parenchymal cells due to DM, toxins, low protein diet, obesity, alcohol
(LIVER, heart, muscle, kidney)

60
Q

Atherosclerosis

A

accumulation of cholesterol in M and muscle cells on BVs

61
Q

Xanthomas

A

accumulation of cholesterol in M on skin and tendons

62
Q

Cholesterolosis

A

accumulation of cholesterol in GB lamina Propria

63
Q

Niemann- Pick disease , Type C

A

cholesterol trafficking enzyme mutation = accumulation cholesterol in many organs in lysosomes*

64
Q

Proteinuria and what accumulates

A

Loss of protein is high and this increases tubules in kidney to reabsorb proteins that go into the tubular epithelium

65
Q

Russell bodies

A

Are seen when protein is accumulated inside a cell especially immunoglobulins

66
Q

A1-antitrypsin

A

Is mutated accumulated protein causing either apoptosis(liver) or emphysema (lungs)

67
Q

Neurofibrillary tangles

A

Cytoskeleton accumulation can be seen in Alzheimer’s

68
Q

Hyaline in DM and HTN

A

Arteriolar wall in kidney become hyalinized

69
Q

Where can glycogen accumulation in DM

A

Kidney tubular epithelium, liver cells, B cells of Langerhans, heart muscle cells

70
Q

Coal workers pneumoconiosis

A

Carbon accumulation in lung M and stay there can cause emphysema

71
Q

Exogenous pigment

A

Carbon (anthracosis)

Tattoo ink

72
Q

Endogenous pigment

A
  1. Lipofuscin (lipids and phospholipids + protein from poly-sat lipids)
    = liver and heart gaining or cachexia
  2. Melanin
  3. Alkaptonuria (defect in protein metabolism = black color)
    4 .Hemosiderin : gold brown pigment
    ** usually lysosomal problem**
73
Q

Dystrophic Calcification

A

In necrotic areas

Organ dysfunction

74
Q

Metastatic Calcification

A

Normal tissues with hypercalcemia
(Can increase dystrophic calcification)
1. High PTH
2. High bone resorption (cancer, pager disease)
3. VIT D disorders (Williams D in infants)
4. Renal failure (cant excrete Phosphate —> secondary hyperparathyroidism)

75
Q

What can increase life

A

Low caloric intake = low IGF-1 and high sirtuins

76
Q

2 types of DAMPs released during necrosis

A

ATP : from damaged mitochondria

Uric Acid : broken down DNA

77
Q

which receptors have the FasL

A

T-cells and CTLs

78
Q

Extrinic pathwya inhibited by

A

FLIP

79
Q

Ferroptosis

A

Iron dependent pathway for cell death due to lipid peroxidation from Glutathione being overwhelmed

80
Q

increase in ROS and leakage of enzymes and proteins happens in what
and lowered ATP

A

necrosis

81
Q

Lipid peroxidation causes what

A

membrane damage

82
Q

Protein modification causes what

A

Breakdown or misfolding of proteins

83
Q

what immune cells make ROS

A

N and M

84
Q

low O2 does what MILD

A

lowered ATP from ox phos
X NA pump
NA and H2O influx
swelling (Reversible)

85
Q

low O2 does what SEVERE

A

influx of Ca and mito swelling

rupture lysosomes and PM

86
Q

which cells can undergo hypreplasia

A

only cells that can do replication (quiescent cells in G0 state)

87
Q

Amyloid accumulation most likley in

A

heart

88
Q

Gaucher cells

A

from in Gaucher Disease in BM
M cells that accumulate glucocerebroside (mutated glucocerebrosidase
lysosomal storage disease

89
Q

Lipofusin accumulates in what cells mostly

A

heart

90
Q

Asbestos body

A

Ferruginous body (cell with Fe and Ca)

91
Q

what drug acts to increse sirtuins

A

Rapamycin

92
Q

Sirituins does what

A

activate DNA repair enzymes

adaptation to caloric restriction (low caloric intake = lower ROS made)

MOD Midterm (9 decks)

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