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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
Q

define xenophagy

A

a selective autophagy that targets intracellular pathogens

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26
Q

what are 2 causes of stimulating autophagy?

A

starvation and metabolic stress due to LACK OF GROWTH FACTORS

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27
Q

what are the activators for autphagy?

A

kinases
AMPK, JNK, ULK1

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28
Q

what do the 3 autophagy activators (AMPK, JNK, ULK1) activate?

A

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

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29
Q

what is the cause of autophagy inhibition?

A

growth factors binding to the growth factor receptor

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30
Q

explain the process of autophagy inhibition

A

growth factor binds to growth factor receptor. this activates Akt and then mTORC1

mTORC1 INHIBITS THE AUTPHAGY ACTIVATORS (AMPK, JNK, ULK1)

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31
Q

when no growth factors are present, what needs to be inhibited? how is it inhibited?

A

mTORC1 needs to be inhibited because it blocks autophagy from occuring

TSC2 inhibits mTORC

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32
Q

explain what happens when the mitochondrial membrane is damaged

A

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

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33
Q

molecular chaperones are ___ proteins

A

helper

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34
Q

how do proteosomes utilize ATP?

A

to unfold and translocate the substrate protein into the chamber and catalyze proteolytic reactions

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35
Q

chaperones bind what amino acid residues?

A

HYDROPHOBIC

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36
Q

autophagy relies on what organelle in mammals?

A

LYSOSOMES

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37
Q

Define atrophy

A

decreased size or function of cells or organs

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38
Q

define hypertrophy

A

increase in cell or organ size and functional capacity

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39
Q

define hyperplasia

A

increased number of cells

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40
Q

define metaplasia

A

the conversion of one cell type to another

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41
Q

define dysplasia

A

alteration in size, shape, and organization of the cellular components of a tissue

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42
Q

what are 2 methods of intracellular storage

A

calcification and hyaline

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43
Q

name 6 morphological reactions to PERSISTENT STRESS

A

atrophy
hypertrophy
metaplasia
dysplasia
hyperplasia
intracellular storage

44
Q

persistent stress leads to…..

A

ADAPTATION

45
Q

increased functional demand followed by persistent stress will lead to….

A

hypertrophy and hyperplasia (adaptation)

46
Q

reversible cell injury followed by persistent stress will lead to…

A

atrophy
metaplasia
dysplasia
storage
(adaptation)

47
Q

if reversible cell injury is severe, what will happen

A

irreversible cell injury and coagulative necrosis

48
Q

what are myocytes adaptation to increased functional demand?

A

muscle hypertrophy – increased synthesis of muscle proteins and downregulating the degradation of muscle proteins

49
Q

what are myocytes adaptation to DECREASED functional demand?

A

muscle atrophy

-decreased synthesis of muscle proteins
-upregulating muscle proteins degradation

50
Q

true or false

within a cell, the signaling pathways that control hypertrophy and atrophy are vastly different

A

false - closely interconnected

51
Q

atrophy and hypertrophy are a balance between what 2 forces?

A

anabolic and catabolic

52
Q

true or false

the atrophy of an organ differs from cellular atrophy

A

true

53
Q

the reduction in the size of an organ can be caused by what 2 things?

A

-reversible cell shrinkage (decrease in physical activity)

-irreversible loss of cells (alzhimers = brain atrophy and permanent cell loss)

54
Q

a decrease in physical activity can cause muscle cells to shrink (lose volume)

can they ever regain this volume?

A

yes, by an increase in physical activity

55
Q

hypertrophy of an organ =…..

A

hypertrophy and/or hyperplasia of cells

56
Q

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?

A

atrophy

57
Q

how can increased pressure lead to atrophy?

A

localized pressure on the skin can lead to bed sores

58
Q

human skeletal muscle contains what kind of fibers? differentiate between them

A

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
Q

in which situation is Akt increased – hypertrophy or atrophy?

A

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
Q

Smad increased
FOXO increased

is this atrophy or hypertrophy

A

atrophy

61
Q

TOR increased

is this hypertrophy or atrophy

A

hypertrophy. TOR is activated by AKT

62
Q

explain how exercise affects the mitochondria

A

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
Q

what is PGC-1 alpha

A

a transcription factor coactivator that upregulates energy production and results in an INCREASED NUMBER OF MITOCHONDRIA (due to increased exercise)

64
Q

ubiquitin ligase increased

is this atrophy or hypertrophy

A

atrophy

65
Q

besides nutrient deprivation, what else could lead to atrophy?

A

chronic inflammation. inflammatory cytokines like IL-1 and TNFa can bind to the cell receptor and increased NFKB and atrophy

66
Q

increased proteosomal protein degradation

is this hypertrophy or atrophy

A

atrophy

67
Q

true or false

exercise with small loads does not induce hypertrophy

A

TRUE

increases endurance, numbers of mitochondria, and slow myosin H chain, but the muscle does NOT increase in size (hypertrophy)

68
Q

what causes an increase in AMP kinase?
what causes a decrease in AMP kinase?

A

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
Q

increased AMPK causes _____ autophagy

A

increased

70
Q

increased AMPK causes _______ blood glucose

A

decreased

71
Q

increased AMPK causes _____ lipid levels

A

decreased

72
Q

increased AMPK _____ insulin sensitivity

A

increases

73
Q

increased AMPK causes _____ nonessential protein synthesis

A

decreased

74
Q

increased AMPK ________ antioxidant protection

A

increases

75
Q

increased AMPK ______ inflammation

A

decreases

76
Q

what is FAO and FAS? do they increase or decrease with increased AMPK?

A

FAO = fatty acid oxidation. increases with increased AMPK

FAS = fatty acid synthesis. decreases with increased AMPK.

important in type 2 diabetes

77
Q

what is HMG coA reductase? does it increases or decrease with increasing AMPK?

A

the enzyme that synthesizes cholesterol. decreases with increasing AMPK (lipid levels decrease)

78
Q

what is TSC2? does it increase or decrease with increasing ampk?

A

TSC2 = tuberous sclerosis complex. increases with increasing AMPK
causes a decrease in mTORC

79
Q

true or false

dysplasia can demonstrate some degree of nuclear atypia

A

TRUE

80
Q

What is neoplasia

A

new uncontrolled growth of cells that is not under physiologic control. cells have abnormal architecture, nuclear atypia, loss of cell polarity, nuclear hyperchromasia

81
Q

3 causes of hyperplasia

A

-increased functional demand
-hormonal stimulation
-chronic injury

82
Q

hyperplasia increases the risk for ______. explain

A

neoplasia

this is because in hypertrophy mitosis is happening more which increases the risk of mutation and neoplasia

83
Q

name 4 types of hormonal stimulation of hypertrophy. give an example of each

A

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
Q

how can increased functional demand cause hyperplasia?

A

bacterial infections increase neutrophils
immune response to antigens is lymphoid hyperplasia (lymph node swelling)

85
Q

how can chronic injury cause hyperplasia

A

long standing irritation like persistent skin rubbing causes calluses (epidermal hyperplasia)

chronic physical/chemical injury like psoriasis

86
Q

metaplasia is….

A

conversion of one differentiated cell type to another

87
Q

is metaplasia reversible?

A

usually fully reversible if the harmful stimulus is removed

88
Q

metaplasia is usually a ___ response to ___ ___

A

ADAPTIVE RESPONSE TO PERSISTENT INJURY

89
Q

give a classic example of metaplasia

A

smoking causes ciliated epithelium of bronchial tree to be replaced with squamous

90
Q

fibrocollagenous metaplasia

A

due to trauma, leads to bone formation

91
Q

name 5 stimuli that can cause metaplasia

A

smoking
stones
trauma
gastric acidity
vitamin a deficiency

92
Q

dysplasia is ________ cell growth and maturation

A

disordered

93
Q

true or false

in dysplasia, there is no orderly maturation and the nuclei enlarge and become irregular and hyperchromatic

A

true

94
Q

true or false

dysplasia is usually irreversible

A

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
Q

_______ is preneoplastic. what does this mean?

A

dysplasia

it is a precursor morphological phenotype in cancer development

96
Q

severe dysplasia is considered to be a sign of what

A

aggressive preventative therapy to cure the underlying cause – like to eliminate a noxious agent

97
Q

“hyaline” is a ___ term

A

morphological term

98
Q

define calcification

A

intra or extra cellular deposition of calcium salts in an organ or tissue

99
Q

calcification can be __ or __ calcification

A

dystrophic or metastatic

100
Q

differentiate between metaplastic calcification and dysplastic calcification

A

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
Q

differentiate between the calcium levels in dysplastic calcification and metastatic calcification

A

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
Q

differentiate between the site of deposition of dystrophic calcification and metaplastic calcification

A

site of deposition for dystrophic is areas of necrosis

site of deposition for metastatic is healthy tissues like the kidney, heart, and lung

103
Q

metastatic calcification is characterized by calcium salt deposition in normal ___ ___

A

lung parenchyma

104
Q

extensive calcification in the lungs may cause ______. massive deposits in the kidney can cause _____

A

in the lungs = respiratory deficits

in the kidney = renal damage

105
Q
A

Pathology Midterm (10 decks)

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