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Pathology Midterm > (part 2) Cell injury - lecture1 > Flashcards

(part 2) Cell injury - lecture1 Flashcards

1
Q

what is another word for protein homeostasis

A

proteostasis

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2
Q

what is proteostasis

A

the process that regulates proteins within the cell in order to maintain the health of both the cellular proteosome and the organism itself

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3
Q

give 3 examples of inefficient, ineffective, or harmful proteins

A

-incorrectly folded proteins
-proteins not needed for this time
-damaged by oxygen or other chemicals

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4
Q

what are chaperones?

A

they guide protein folding. if correct folding is impossible, they escort them to their destruction

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5
Q

what do proteosomes do?

A

they execute ubiquitin dependent and ubiquitin independent protein

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6
Q

what is autophagy

A

lysosomes handle the degradative activities that proteosomes cannot

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7
Q

which amino acids participate in ubiquitination

A

mainly lysine (multiple)

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8
Q

what are the types of ubiquitin modifications

A

polyubiquitination at different sites

monoubiquitination at different sites

multiple monoubiquitnation

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9
Q

explain the process of the ubiquitin-proteosome pathway

A

ubiquitin is activated by E1 ubiquitin activating enzyme. Then it is transferred to an E2 ubiquitin-conjugating system. this E2-ubiquitin complex interacts with an E3-ubiquitin ligase to bind to a particular protein

this process may be repeated to attach a chain of ubiquitin

these complexes may be BEUBIQUITINATED by DUBs (deubiquitinating enzymes)

if degradation proceeds, 26s proteosomes recognize the poly-Ub conjugated protein (via 19s subunit) and degrade it into polypeptides (which may have varying fates)

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10
Q

name 4 potential fates of proteins that have been degraded by the ubiquitin-proteasome pathway

A

-further degradation to amino acids
-signaling molecules
-antigens for presentation (immunoproteasomes)
-synthesis of new proteins

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11
Q

name 2 chaperones

A

HSP70 and HSP40

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12
Q

in normal settings (no stress), what are chaperones doing?

A

HSP70 and often HSP 40 situate themselves at ribosomes

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13
Q

if a polypeptide chain is incorrectly folded, what happens?

A

if it cannot be corrected by the chaperones, it becomes part of the ubiquitin-proteosomal system, and is polyubiquitinated and degraded by protesomes

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14
Q

explain the function of HSP70

A

often with the help of HSP40, they assure that proteins have the right configuration.

proteins that are correctly folded are chaperoned from the ribosomes (that produced the protein) to their ultimate destination in the cell

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15
Q

HSPs play a role in preventing and dissasembling….

A

protein aggregates

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16
Q

what does HSP stand for

A

heat shock proteins

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17
Q

an incorrectly folded protein may cause what

A

may form insoluble intracellular aggregates

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18
Q

explain the mechanism of HSPs

A

a misfolded protein is recognized by HSP40 with linker protein Hip

this binds to HSP70 (activated by hydrolyzing ATP)

this complex can be sufficient to put the protein back to its conformation

IF NOT, HSP90 with a linker protein Hop can lead to the proper conformation

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19
Q

Autophagy is part of the cell’s ________

A

homeostasis

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20
Q

type 2 diabetes is a ____ disorder

A

metabolic

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21
Q

what are the types of autophagy

A

macroautophagy
microautophagy
chaperone-mediated autophagy

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22
Q

explain macroautophagy

A

organelles in the cytoplasm are partially sequestered by the phagophore which becomes an autophagosome. this fuses with a lysosome, which degrades the contents to small molecules to be reutilized

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23
Q

explain microautophagy

A

cytosolic organelles are engulfed by the lysosome itself and degraded by lyosomal enzymes

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24
Q

explain chaperone mediated autophagy

A

proteins are conjugated to chaperones and recognized by a lysosomal receptor (LAMP-2A) and the protein is internalized into the lysosome and the chaperone is released.

in the lysosome, the protein is received by another chaperone and then degraded

the original, extra-lysosomal chaperone survives to work further

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25
define xenophagy
a selective autophagy that targets intracellular pathogens
26
what are 2 causes of stimulating autophagy?
starvation and metabolic stress due to LACK OF GROWTH FACTORS
27
what are the activators for autphagy?
kinases AMPK, JNK, ULK1
28
what do the 3 autophagy activators (AMPK, JNK, ULK1) activate?
they activate the Beclin-1 and PI3K-III complex which leads to autophagy -- from the phagophore to the fusion of the phagosome with the lysosome
29
what is the cause of autophagy inhibition?
growth factors binding to the growth factor receptor
30
explain the process of autophagy inhibition
growth factor binds to growth factor receptor. this activates Akt and then mTORC1 mTORC1 INHIBITS THE AUTPHAGY ACTIVATORS (AMPK, JNK, ULK1)
31
when no growth factors are present, what needs to be inhibited? how is it inhibited?
mTORC1 needs to be inhibited because it blocks autophagy from occuring TSC2 inhibits mTORC
32
explain what happens when the mitochondrial membrane is damaged
ROS production is increased, and a parkin protein and Ub-like protein are recruited and form a complex. this complex binds to P62. this complex is now recognized by a specific receptor in the phagophore
33
molecular chaperones are ___ proteins
helper
34
how do proteosomes utilize ATP?
to unfold and translocate the substrate protein into the chamber and catalyze proteolytic reactions
35
chaperones bind what amino acid residues?
HYDROPHOBIC
36
autophagy relies on what organelle in mammals?
LYSOSOMES
37
Define atrophy
decreased size or function of cells or organs
38
define hypertrophy
increase in cell or organ size and functional capacity
39
define hyperplasia
increased number of cells
40
define metaplasia
the conversion of one cell type to another
41
define dysplasia
alteration in size, shape, and organization of the cellular components of a tissue
42
what are 2 methods of intracellular storage
calcification and hyaline
43
name 6 morphological reactions to PERSISTENT STRESS
atrophy hypertrophy metaplasia dysplasia hyperplasia intracellular storage
44
persistent stress leads to.....
ADAPTATION
45
increased functional demand followed by persistent stress will lead to....
hypertrophy and hyperplasia (adaptation)
46
reversible cell injury followed by persistent stress will lead to...
atrophy metaplasia dysplasia storage (adaptation)
47
if reversible cell injury is severe, what will happen
irreversible cell injury and coagulative necrosis
48
what are myocytes adaptation to increased functional demand?
muscle hypertrophy -- increased synthesis of muscle proteins and downregulating the degradation of muscle proteins
49
what are myocytes adaptation to DECREASED functional demand?
muscle atrophy -decreased synthesis of muscle proteins -upregulating muscle proteins degradation
50
true or false within a cell, the signaling pathways that control hypertrophy and atrophy are vastly different
false - closely interconnected
51
atrophy and hypertrophy are a balance between what 2 forces?
anabolic and catabolic
52
true or false the atrophy of an organ differs from cellular atrophy
true
53
the reduction in the size of an organ can be caused by what 2 things?
-reversible cell shrinkage (decrease in physical activity) -irreversible loss of cells (alzhimers = brain atrophy and permanent cell loss)
54
a decrease in physical activity can cause muscle cells to shrink (lose volume) can they ever regain this volume?
yes, by an increase in physical activity
55
hypertrophy of an organ =.....
hypertrophy and/or hyperplasia of cells
56
aging chronic disease insufficient nutrients reduced functional demand increased pressure interruption of trophic signals impaired oxygen supply these are all conditions that can lead to what?
atrophy
57
how can increased pressure lead to atrophy?
localized pressure on the skin can lead to bed sores
58
human skeletal muscle contains what kind of fibers? differentiate between them
slow twitch and fast twitch slow twitch relies on aerobic respiration and used for endurance fast twitch relies on anaerobic respiration and is used for quick contractions
59
in which situation is Akt increased -- hypertrophy or atrophy?
IGF1 (insulin growth factor) causes INCREASED AKT which activates TORC 1 complex and ultimately leads to increased protein synthesis and hypertrophy nutrient deprivation leads to increase in the production of Smads which INHIBIT AKT and leads to the activation of FOXO and ultimately an atrophic fiber
60
Smad increased FOXO increased is this atrophy or hypertrophy
atrophy
61
TOR increased is this hypertrophy or atrophy
hypertrophy. TOR is activated by AKT
62
explain how exercise affects the mitochondria
exercise leads to increased ATP utilization and thus increased AMP and AMP kinase and ultimately leading to increased mitochondrial DNA transcription and increased # of mitochondria
63
what is PGC-1 alpha
a transcription factor coactivator that upregulates energy production and results in an INCREASED NUMBER OF MITOCHONDRIA (due to increased exercise)
64
ubiquitin ligase increased is this atrophy or hypertrophy
atrophy
65
besides nutrient deprivation, what else could lead to atrophy?
chronic inflammation. inflammatory cytokines like IL-1 and TNFa can bind to the cell receptor and increased NFKB and atrophy
66
increased proteosomal protein degradation is this hypertrophy or atrophy
atrophy
67
true or false exercise with small loads does not induce hypertrophy
TRUE increases endurance, numbers of mitochondria, and slow myosin H chain, but the muscle does NOT increase in size (hypertrophy)
68
what causes an increase in AMP kinase? what causes a decrease in AMP kinase?
any sort of exercise, healthy foods, metformin, and aspirin will increase AMPK aging, obesity, overnutrition of unhealthy foods, inactivity, and inflammation will decrease AMPK
69
increased AMPK causes _____ autophagy
increased
70
increased AMPK causes _______ blood glucose
decreased
71
increased AMPK causes _____ lipid levels
decreased
72
increased AMPK _____ insulin sensitivity
increases
73
increased AMPK causes _____ nonessential protein synthesis
decreased
74
increased AMPK ________ antioxidant protection
increases
75
increased AMPK ______ inflammation
decreases
76
what is FAO and FAS? do they increase or decrease with increased AMPK?
FAO = fatty acid oxidation. increases with increased AMPK FAS = fatty acid synthesis. decreases with increased AMPK. important in type 2 diabetes
77
what is HMG coA reductase? does it increases or decrease with increasing AMPK?
the enzyme that synthesizes cholesterol. decreases with increasing AMPK (lipid levels decrease)
78
what is TSC2? does it increase or decrease with increasing ampk?
TSC2 = tuberous sclerosis complex. increases with increasing AMPK causes a decrease in mTORC
79
true or false dysplasia can demonstrate some degree of nuclear atypia
TRUE
80
What is neoplasia
new uncontrolled growth of cells that is not under physiologic control. cells have abnormal architecture, nuclear atypia, loss of cell polarity, nuclear hyperchromasia
81
3 causes of hyperplasia
-increased functional demand -hormonal stimulation -chronic injury
82
hyperplasia increases the risk for ______. explain
neoplasia this is because in hypertrophy mitosis is happening more which increases the risk of mutation and neoplasia
83
name 4 types of hormonal stimulation of hypertrophy. give an example of each
physiologic - increased estrogen in early menstrual cycle increases uterine epithelial cells developmental - increased estrogens at puberty increases uterine epithelial and stromal cells pathologic - renal tumors secrete erythropoeitn stimulates bone marrow erythroid hyperplasia pharmacological - gynecomastia estrogen therapy in prostate cancer
84
how can increased functional demand cause hyperplasia?
bacterial infections increase neutrophils immune response to antigens is lymphoid hyperplasia (lymph node swelling)
85
how can chronic injury cause hyperplasia
long standing irritation like persistent skin rubbing causes calluses (epidermal hyperplasia) chronic physical/chemical injury like psoriasis
86
metaplasia is....
conversion of one differentiated cell type to another
87
is metaplasia reversible?
usually fully reversible if the harmful stimulus is removed
88
metaplasia is usually a ___ response to ___ ___
ADAPTIVE RESPONSE TO PERSISTENT INJURY
89
give a classic example of metaplasia
smoking causes ciliated epithelium of bronchial tree to be replaced with squamous
90
fibrocollagenous metaplasia
due to trauma, leads to bone formation
91
name 5 stimuli that can cause metaplasia
smoking stones trauma gastric acidity vitamin a deficiency
92
dysplasia is ________ cell growth and maturation
disordered
93
true or false in dysplasia, there is no orderly maturation and the nuclei enlarge and become irregular and hyperchromatic
true
94
true or false dysplasia is usually irreversible
FALSE like metaplasia, it is a response to persistent injury and usually regresses when the stressor ceases (person stops smoking, or the immune system eliminates HPV infected cells from cervix)
95
_______ is preneoplastic. what does this mean?
dysplasia it is a precursor morphological phenotype in cancer development
96
severe dysplasia is considered to be a sign of what
aggressive preventative therapy to cure the underlying cause -- like to eliminate a noxious agent
97
"hyaline" is a ___ term
morphological term
98
define calcification
intra or extra cellular deposition of calcium salts in an organ or tissue
99
calcification can be __ or __ calcification
dystrophic or metastatic
100
differentiate between metaplastic calcification and dysplastic calcification
in dystrophic calcification, the deposition occurs in dead/dying tissues in metastatic calcification, deposition occurs in normal tissue (during hypercalinemia) and in metastasizing tissue
101
differentiate between the calcium levels in dysplastic calcification and metastatic calcification
calcium levels are NORMAL in dystrophic. calcium levels are HIGH in metaplastic -- reflects some derangement in calcium metabolism like hypercalcemia and chronic renal failure
102
differentiate between the site of deposition of dystrophic calcification and metaplastic calcification
site of deposition for dystrophic is areas of necrosis site of deposition for metastatic is healthy tissues like the kidney, heart, and lung
103
metastatic calcification is characterized by calcium salt deposition in normal ___ ___
lung parenchyma
104
extensive calcification in the lungs may cause ______. massive deposits in the kidney can cause _____
in the lungs = respiratory deficits in the kidney = renal damage
105

Pathology Midterm (10 decks)

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