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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

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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
Necrosis nucleus | Apoptosis nucleus
N : Pyknosis = shrink, Karyorrhexis = fragmentation, Karyolysis = endonuclease degrade and it fades A : Fragmentation to nucleosomes
26
What is seen in reversible cell injury
Lowered cell function | Ultra structural changes (mito, PM, ER, Nuclear changes)
27
What is seen in irreversible cell
1. Biochemical alterations 2 . Ultra structural changes 3. Light microscopic changes 4. Gross morphological changes
28
What is seen in necrotic cell
1. High eosinophilia 2. Glassy looking 3. Myelin figures (phospholipid masses) 4. Calcification
29
Coagulative necrosis
No digestion of cells (only denature proteins) Ischemia due to obstructed vessel = all organs (except brain) - if localized = infarct
30
Liquefaction necrosis
Digests cells - liquid, pus (creamy yellow) Bacteria or fungal infection CNS (brain)
31
Gangrenous Necrosis
Lowe limbs usually from coagulative necrosis, can undergo liquefactive necrosis is bacteria infects it
32
Caseous necrosis
TB ad fungal infection = cheese Iike = Lysed cells, granular debri = granuloma
33
Fat necrosis
Fat destruction, released pancreatic enzymes (lipases) | Calcium deposits
34
Fibrinoid necrosis
Immune reactions in BVs | Fibrinoids (fibrin leaks out)
35
In low ATP levels like from hypoxia
Body depends on anaerobic glycolysis from glycogen stores = lactic acid
36
Irreversible Mitochondrial and lysosomal damage causes
Necrosis
37
3 things that happen when there is mitochondrial damage
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
Increased CA+ 2 into cell causes what 3 things
1. Mitochondrial permeability transition pore 2. Activate ATPase, Protease, Phosphilipases, endonuclease 3. Activate caspases
39
How are ROS (free radicals also removed)
Add to H2O—-> O2 and H2O2 1. Catalase 2. SODs 3. Glutathione peroxidase (makes GSSG)
40
Which VIT are anti oxidants
E and A, C, glutathione
41
What metals can cause ROS
Iron and copper
42
What can you measure in blood to see if there is necrosis in 1. Liver 2. Liver by bile duct epithelium 3. Cardiac myocardium
1. Transaminase 2. Alkaline phosphate 3. Troponin
43
Low ATP due to hypoxia or ischemia =
CA+ into the cell = changes and damage
44
What stimulates new BVs to form
Hypoxia - induce blue factor -1
45
Restoring O2 to ischemic tissues can do what
1. If reversible : repair | 2. If irreversible : make cells die (ischemia- reperfusion injury)
46
ischemia- reperfusion injury how does this happen
Increasing O2 to damaged Mitochondria causes accumulation of ROS Inflammation (from blood coming again) CA+ increases more inside cell due to damaged mito
47
Cyanide
Inhibits cytochrome oxidase = X oxidative phosphorylation
48
What do you see in apoptosis
1. Cell shrinks 2. Chromatin condensation 3. Cytoplasmic blebs + apoptotic bodies 4. M that phagocytose (lysosomes)
49
4 things causing apoptosis
1. DNA damage 2. Protein accumulation 3. Infection like certain viruses 4. Duct obstruction causing atrophy
50
Intrinsic Apoptosis
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
Over-expression of Bcl-2
B- cell lymphoma
52
Extrinsic Apoptosis
1. FAs —> FasL (death receptor on PM, CD95, TNF1) 2. Activates FADD 3. Activates caspase 8 + 10
53
Caspases executing apoptosis
3 and 6 activated by both pathways
54
Necroptosis
NO caspase = like necrosis Programmed cell death = like apoptosis = uses TNF and TNFR1, activating RIP1, RIP3, caspase 8 is not activated
55
Pyroptosis
Programmed cell death with IL1 (fever) released | = IL1 activated inflammasome
56
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
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
3 features of autophagy
1. Double membrane 2. Lysosomes 3. Sequestering vacuoles * *** usually during low nutrition
58
What can caused by uncontrolled autophage
IBS (Crohns) Cancers Neurodegenerative disorders
59
Steatosis
Fatty change : accumulation of TAGs in parenchymal cells due to DM, toxins, low protein diet, obesity, alcohol (LIVER, heart, muscle, kidney)
60
Atherosclerosis
accumulation of cholesterol in M and muscle cells on BVs
61
Xanthomas
accumulation of cholesterol in M on skin and tendons
62
Cholesterolosis
accumulation of cholesterol in GB lamina Propria
63
Niemann- Pick disease , Type C
cholesterol trafficking enzyme mutation = accumulation cholesterol in many organs in lysosomes*
64
Proteinuria and what accumulates
Loss of protein is high and this increases tubules in kidney to reabsorb proteins that go into the tubular epithelium
65
Russell bodies
Are seen when protein is accumulated inside a cell especially immunoglobulins
66
A1-antitrypsin
Is mutated accumulated protein causing either apoptosis(liver) or emphysema (lungs)
67
Neurofibrillary tangles
Cytoskeleton accumulation can be seen in Alzheimer’s
68
Hyaline in DM and HTN
Arteriolar wall in kidney become hyalinized
69
Where can glycogen accumulation in DM
Kidney tubular epithelium, liver cells, B cells of Langerhans, heart muscle cells
70
Coal workers pneumoconiosis
Carbon accumulation in lung M and stay there can cause emphysema
71
Exogenous pigment
Carbon (anthracosis) | Tattoo ink
72
Endogenous pigment
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
Dystrophic Calcification
In necrotic areas | Organ dysfunction
74
Metastatic Calcification
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
What can increase life
Low caloric intake = low IGF-1 and high sirtuins
76
2 types of DAMPs released during necrosis
ATP : from damaged mitochondria | Uric Acid : broken down DNA
77
which receptors have the FasL
T-cells and CTLs
78
Extrinic pathwya inhibited by
FLIP
79
Ferroptosis
Iron dependent pathway for cell death due to lipid peroxidation from Glutathione being overwhelmed
80
increase in ROS and leakage of enzymes and proteins happens in what and lowered ATP
necrosis
81
Lipid peroxidation causes what
membrane damage
82
Protein modification causes what
Breakdown or misfolding of proteins
83
what immune cells make ROS
N and M
84
low O2 does what MILD
lowered ATP from ox phos X NA pump NA and H2O influx swelling (Reversible)
85
low O2 does what SEVERE
influx of Ca and mito swelling | rupture lysosomes and PM
86
which cells can undergo hypreplasia
only cells that can do replication (quiescent cells in G0 state)
87
Amyloid accumulation most likley in
heart
88
Gaucher cells
from in Gaucher Disease in BM M cells that accumulate glucocerebroside (mutated glucocerebrosidase *lysosomal storage disease*
89
Lipofusin accumulates in what cells mostly
heart
90
Asbestos body
Ferruginous body (cell with Fe and Ca)
91
what drug acts to increse sirtuins
Rapamycin
92
Sirituins does what
activate DNA repair enzymes | adaptation to caloric restriction (low caloric intake = lower ROS made)

MOD Midterm (9 decks)

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