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Unit 3: LGS > Week 5 > Flashcards

Week 5 Flashcards

1
Q

Etiology

A

cause of disease; can be unknown

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2
Q

Pathogenesis

A
  • How etiology caused disease; and sometimes why?
  • Mechanism with a process
  • How did HPV cause cancer
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3
Q

Morphological changes

A
  • Changes that occur in form (of tissue or cell);

- Cellular changes at microscopic or gross level

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4
Q

Clinical manifestations

A

-Incorporates progression of disease, signs and symptoms, and progression or outcome of disease

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5
Q

Cellular response to stress

A
  • homeostasis
  • adapted cell
  • injured cell
  • cell death
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6
Q

Cellular homeostasis

A
  • Balanced, maintaining stable internal conditions
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7
Q

Adapted cell

A

-Cell will make changes but will continue to survive

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8
Q

Injured cell

A
  • Stimulus will cause injury
  • The cell must adapt and regenerate in order to continue living
  • Reversible/irreversible: depends on time, nature, severity of injury
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9
Q

Cell death

A
  • apoptosis or necrosis

- caused by irreversible damage

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10
Q

Adaptations to stress

A
  • hypertrophy

- hyperplasia

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11
Q

Hypertrophy

A

increase in size of cells

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12
Q

Hyperplasia

A

an increase in number of cells

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13
Q

Kind of adaptation with exercise

A

-Physiologic adaptation
- Increased stress load–causes hypertrophy
○ Increase in size of muscle cell–will increase work
Why not make more muscle cells? Muscle cells do not proliferate, only increase in size

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14
Q

Kind of adaptation with pregnancy

A
  • Uterine hypertrophy (physiologic adaptation)
  • Organ and components undergoes hypertophhy to stretch; Myometrium makes up bulk of uterus and is where most hypertrophy occurs
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15
Q

Kind of adaptation with lactation

A

-Hyperplasia and Hypertrophy during breast feeding (physiologic adaptation) of epithelial duct cells

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16
Q

Kind of adaptation with chronic elevated blood pressure

A
  • Pathologic cardiac hypertrophy
  • Heart will undergo hypertrophy because there is increased resistance to outflow ad heart will have to work harder to pump out blood
  • If heart works too hard; will have thickened walls, which will lead to ischemia and this can lead to cell death
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17
Q

Kind of adaptation with liver

A
  • Hyperplasia of liver (physiologic adaptation)

- Any defect in liver or part of liver is removed it has capacity to regenerate itself

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18
Q

How does hyperplasia occur?

A

Increased mitotic activity of stem cells which is caused by hormones or growth factors

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19
Q

Kind of adaptation with BPH

A

Pathologic hyperplasia and hypertrophy (physiologic) of stromal cells which is obstructing the part of the urethra that runs through the prostate

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20
Q

Atrophy

A

smaller in size

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21
Q

Causes of atrophy

A
  • disuse (cast)
  • de-innervation (nerves no longer sending signals to contract)
  • decreased nutrients (can be caused with collapsed vessel)
  • ischemia (does not have oxygen to make ATP to carry out cellular functions and therefor cannot work)
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22
Q

Etiology and pathogenesis of patient with 30 pack-year history cough

A
  • etiology: smoking
  • patho: Smoking causes paralysis of cilia of epithelium in throat; cannot clean air coming in; have to cough to void all the toxins
  • cells will go through metaplasia (columnar to squamous; tougher due to tight junctions)
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23
Q

Metaplasia

A

change in cell type (phenotype)

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24
Q

How does metaplasia occur?

A

Stem cells will change phenotype in response to injury

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25
Q

Barrets esophagus

A

epithelium will go from squamous to columnar; which will allow for goblet cells from columnar cells to produce mucus as protective mechanism for acid reflux

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26
Q

Risk with metaplasia

A

can turn into neoplasia

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27
Q

Reversible cell injury

A
  • cellular swelling

- fatty changes

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28
Q

cellular swelling

  • other names
  • how is it caused
  • histo
A
  • hydropic change, hydropic swelling)
  • Ion changes, result in swelling of cell
  • Histo: tend to see vacuoles in cytoplasm; difficult to see in cell but easy to see in organ because organ will be swollen, pale, and have increase turgor
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29
Q

Necrosis

  • occurence
  • how?
  • inflammation?
  • group or individual?
  • where
A
  • Most common type of cell death
  • Pathologic
  • Occurs due to membrane damage due to denaturation of proteins in membrane
  • Will cause inflammation to get rid of organelles that are released from faulty membrane
  • Enzyme from necrotic cell: derived from neutrophils and lyosomes
  • Occurs in zone
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30
Q

Apoptosis

  • occurence
  • how?
  • inflammation?
  • group or individual?
  • where
A
  • less common
  • Not usually due to pathology
  • Individual cell death
  • Cells shrinking
  • Structure of membrane is changing but not releasing intracellular components to environment
  • Will be broken down by macrophages; will not cause inflammatory response
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31
Q

Coagulative necrosis

A
  • architecture of dead tissue is retained for several hours; will have denaturation of structural proteins and enzymes;
  • enzymes are denaturing and do not have immediate phagocytosis of dead tissue
  • tissue will eventually be degraded with inflammatory response
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32
Q

Fibrinoid necrosis:

A
  • fibrin like; caused by fibrin; sometimes has dead platelets
  • Caused by autoimmune injury
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33
Q

At what point does injury become irreversible?

A
  • Apoptosis: Activation of caspases (proteases that will kill the cell)
  • Necrosis: No specific event; Proteases will be released from lysosome
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34
Q

Damage to which organelle is most associated with cell death?

A

mitochondria; will cause decrease in ATP and increase in ROS

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35
Q

Why does decreased ATP lead to cell death instead of cell stasis?

A

Cell cannot meet metabolic demand; homeostasis requires energy

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36
Q

What does the increased ROS typically damage in the cell?

A

Damage to lipids, proteins, DNA

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37
Q

How is ROS normally handled?

A

glutathione

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38
Q

Entry of which ion is most associated with cell death?

A

Ca; increases permeability and activates multiple cellular enzymes

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39
Q

Activation of which enzymes are most associated with cell death?

A

-proteases, capases, lipases

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40
Q

What are consequences of membrane damage that are most associated with cell death?

A

-loss of cellular components to extracellular space (damage to plasma membrane) and enzymatic digestion of cellular components (lysosomal membrane)

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41
Q

What is the consequence of protein misfolding/ DNA damage?

A

activation of pro-apoptotic proteins (BAX)

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42
Q

BCL-2

A
  • Anti-apoptotic
  • Activated by cellular survival signals (growth factor)
  • Will suppress action of BAX channel in mito membrane
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43
Q

BAX

A
  • Pro-apoptotic
  • DNA damage and lack of survival signal will created BH3 proteins which will antagonize BCL2 and allow for activation of BAX channel
  • BAX channel allows for cytochrome C to leak out of mito; this will cause activation of capases and lead to apoptosis
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44
Q

How does cancer avoid apoptosis?

A

Down regulate BAX, upregulate BCL2 to decrease chance that cancer cell kills itself

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45
Q

What if capases are inhibited?

A
  • Necroptosis: cell can still kill itself even if capases are inhibited
46
Q

3 interrelated factors critical to immortality of cancer cells

A
  1. Evasion of senescence
  2. Evasion of mitotic crisis
  3. The capacity for self renewal
47
Q

Development of cancer through step-wise acquisition

A
  • normal cell: initiating mutation
  • initiated precursor w/ stem cell-like properties: acquisition of genomic instability
  • precursor with mutator phenotype: acquisition of cancer hallmarks
  • founding cancer cell: further genetic evolution
48
Q

accumulation of mutations

A

-typical pathogenic process of cancer

49
Q

etiology of cancer

A
  • UV rays damage DNA causing dimers
  • carcinogens inc. the rate of mutations more than what can be repaired
  • environment might trigger response from tissue causing metaplasia which is a normal cell being replaced by another cell that shouldn’t be there and then this could cause dysplasia
50
Q

carcinogen

A

-increase the rate of mutations

51
Q

Typical pathogenic process of cancer

A
  • Inactivation of APC; cell seems normal but is pre-disposed to proliferate excessively
  • mutational activation of K-ras; cell begins to proliferate too much but is otherwise normal
  • Loss of DCC, over-expression of COX-2; cell proliferates more rapidly, undergoes structural changes
  • Loss of TP53, activation of telomerase; cell grows uncontrollably and looks obviously abnormal
52
Q

How can cancer cells avoid apoptotic fate?

A

• p53 mutation: Dec. effectiveness of BAX
• Mutation that inc. expression of BCL2: Blocks apoptotic factors like BAX
• Interaction b/w BCL2 and BAX: Creates a channel in the mitochondrial membrane allowing cytochrome c to leave which activates initiating factors
-Downregulate cytochrome C and other pro-apoptotic proteins

53
Q

Significance of cancer cells avoiding apoptosis

A
  • The cell has accumulated mutations that enable it to change and proliferate in the environment
  • Tumor can become heterogenic - evolution of tumor cells; become alost like a different species, it expresses diff. proteins and acquire new properties and have diff genes turned on and off
  • This will affect treatment b/c might need combination therapy; also makes it harder for the treatment to work b/c they start to become drug resistant
  • With time, worried about metastasis to over parts of the body
54
Q

Why are different repair mechanisms needed?

A
  • Type of damage that happens to the DNA determines which one of these will be used
  • Repair rate and rate of succession are competing w/ each other over time
55
Q

Nucleotide Excision repair

A
  • removes DNA damage induced by ultraviolet light (UV).
  • results in thymine dimers and 6,4-photoproducts.
  • Recognition of the damage leads to removal of a short single-stranded DNA segment that contains the lesion.
  • The undamaged single-stranded DNA remains and DNA polymerase uses it as a template to synthesize a short complementary sequence. Final ligation to complete NER and form a double stranded DNA is carried out by DNA ligase.
56
Q

Base excision repair

A
  • DNA glycosylases recognize small distortions in DNA involving lesions caused by damage to a single base.
  • A glycosylase cleaves the N-glycosidic bond that joins the damaged base to deoxyribose; leaves sugar-phosphate backbone without base (apurinic)
  • apurinic/apyrimidinic endonuclease cleaves sugar-phosphate strand at this site
  • same enzymes involved in other types of repair mechanisms restore this region to normal
57
Q

Mismatch repair

A
  • mismatched bases recognized by enzymes of mismatched repair systems
  • since neither of the bases are damaged this repair mechanism must recognize which base to correct
58
Q

Transcription-coupled repair

A
  • genes that are actively transcribed to produce mRNA are preferentially repaired
  • RNA polymerase that is transcribing a gene stalls when it encounters a damaged region of the DNA template
  • Excision-repair proteins are attached to the site and repair the damaged region similar to NER so that RNA polymerase can resume transcription
59
Q

Oncogenes

A

Ras, Raf, PI3K, MYC, cyclins

60
Q

Tumor suppressor genes

A

p10, GAP (GTPase activating protein) which activates RAS,

61
Q

Proto-oncogenes

A

normal gene that promotes self proliferation; mutation causes it to lose regulation and then it becomes an oncogene

62
Q

Cyclins

A
  • involved in cell cycle progression
  • Interact w/ cyclin dependent kinases (CDKs)
  • CDK can’t make cell progress until bound w/ cyclin
63
Q

P53

A
  • activation by DNA damaging agents or hypoxia leads to cell arresting in G1 and induction of DNA repair
  • Have two alleles, can have one that doesn’t work as long as its normal but if yo have two that don’t work then its gonna be a sad cell
  • Transcription factor that can activate several different proteins
64
Q

How does RB work?

A
  • It binds to E2F (elongation factor) to make it inactive so it won’t transcribe
  • RB gets hyperphosphorylated to release E2F and allow for transcription
  • Even if growth factors are present, RB must be phosphorylated in order for transcription to occur
65
Q

Pathogenesis of retinoblastoma

A
  • two mutations of the RB locus on chromosome 13q which leads to neoplastic proliferation of the retinal cells
  • sporadic mutation: both mutations are acquired
  • familial mutation: one mutated copy of RB gene from carrier parent, so only one additional RB mutation is needed to complete loss of RB function
66
Q

mitochondrial intrinsic pathway

A

cell injur occurs–BCL2 senses damage–BCL2 family effectors activated (BAX and BAK)–Mitchindrial membrane is affected–cytochrome C and other apoptotic proteins leak out of mitochondria–activates initiator capases–activate executioner capases–endonuclease activation occurs (leads to nuclear fragmentation) and breakdown of cytoskeleton—cytoplasmic blebs are created and released making an apoptotic body with ligands for phagocytic cell receptors–apoptotic body is phagocytized

67
Q

death receptor extrinsic pathway

A

Fas binds to TNF receptor–adaptor proteins activated– activates initiator capases–activate executioner capases–endonuclease activation occurs (leads to nuclear fragmentation) and breakdown of cytoskeleton—cytoplasmic blebs are created and released making an apoptotic body with ligands for phagocytic cell receptors–apoptotic body is phagocytized

68
Q

Darwins finches

A
  • Evolutionary tree of cancer
  • how cancer collects mutations
  • cell has accumulated mutations that enable it to change and proliferate in the environment
  • Tumor can become heterogenic
69
Q

heterogenic tumor

  • what is it
  • how does it affect treatment
  • what are we worried about over time?
A
  • evolution of tumor cells; become almost like a different species, it expresses diff. proteins and acquire new properties and have diff genes turned on and off
  • This will affect treatment b/c might need combination therapy; also makes it harder for the treatment to work b/c they start to become drug resistant
  • With time, worried about metastasis to over parts of the body
70
Q

APC

A
  • major mutation in cancer
  • APC leads to the destruction of Beta catenin when WNT is not bound
  • Once WNT binds, thenbeta catenin can bind to TCF to start transcription of genes involved in cell cycle progression
  • When APC is mutated or absent, beta catenin is not destroyed, intracelular levels remain high which allows for cell cycle progression genes to always be transcribed, pushing the cell to move into next stage of cell cycle
71
Q

Why do cancer cells have the capacity to continue to replicate

A

-telomerase is continually expressed so telomeres are not shortened allowing for cell to be “immortal”

72
Q

Escape of cells from senescence and mitotic catastrophe caused by telomerase shortening

A
  • Replication of somatic cells that do not express telomerase leads to shortening of telomeres. When telomeres reach certain length the cell will stop replicating and start to die.
  • In cells with mutations on their check point genes will cause cells with shortened telomeres to enter nonhomologus end-joining pathway to be inappropriately activated leading to formation of dicentric chromosomes
  • when the dicentric chromosomes are pulled apart during mitosis will cause double-stranded breaks, which will then cause NHEJ pathway to be activated again
  • Cells will undergo multiple rounds of bridge-fusion-break cycle which will generte massive chromosomal instability and numerous mutations
  • If cells fail to reproduce telomerase they will undergo mitotic catastrophe and death; but if it is re-expressed it will break the cycle, creating a cancer cell
73
Q

cachexia

A
  • loss of body mass by malnutrition
  • 80% of cancer patients suffer from this by the time they die
  • includes anorexia, early satiety, anemia, altered metabolism
74
Q

hallmarks of cancer

A
  • sustaining proliferative signaling, enabling replicative immortality, tumor promoting inflammation, activating invasion and metastasis, genomic instability, inducing angiogenesis, resisting cell death, de-regulating cellular energetics
  • avoiding immune destruction, evading growth suppressors
75
Q

p53 characteristics

  • what does it cause?
  • what does it act through
  • what does it induce?
  • what is it a main component of?
  • negatively regulated by
  • what alters it
A
  • causes cell cycle arrest and apoptosis
  • acts mainly through p21
  • transcription of pro-apoptotic genes such as BAX
  • G2/ M checkpoint
  • MDM2
  • tumor suppressor gene altered by cancer
76
Q

RB characteristics

  • what does it bind?
  • what controls its action?
  • What does it prevent?
A
  • E2F transcription factors
  • being hyperphosphorylated
  • G1/S transition
77
Q

APC characteristics

  • what does it inhibit?
  • what is it common in?
  • what does it hold in check?
A
  • WNT signaling
  • colonic polyps and carcinomas
  • Beta catenin activity
78
Q

PTEN

-what does it inhibit?

A

-PI3K/ AKT signaling

79
Q

BCR-ABL

  • what is it?
  • what does it cause?
A
  • chimeric tyrosine kinase

- CML

80
Q

NMYC

-amplified in?

A

-neuroblastomas

81
Q

MYC

  • causes?
  • what does it do?
  • induced by?
A
  • cause upregulation of telomerase
  • factor in reprogramming somatic cells into pluripotent stem cells
  • gene induced y RAS/MAPK signaling to promote proliferation
82
Q

Chronic Lymphocytic Lymphoma symptoms

A
  • Fatigue
  • Loose stool
  • Pleural effusion
  • Low blood sugar
83
Q

Why do endocrine evaluation on patient with low blood sugar?

A

-cortisol causes increase in blood glucose which will stimulate glucagon release; which will induce glycogenolysis and gluconeogenesis

84
Q

Why would patient remain hypoglycemic and have high lactic acid if given dextrose?

A

Warburg effect

85
Q

Warburg effect

A

cancer cells alter metabolic pathway they use so they start to use anaerobic respiration

86
Q

Aerobic glycolysis

A

using glycolysis even in the presence of oxygen–creating high level of pyruvate to lactic acid

87
Q

Normal cells vs cancer cells

A
  • cancer cells have glucose hunger and so they take up more glucose
  • cancer cells use aerobic glycolysis while normal cells use aerobic respiration
88
Q

Why do cancer cells use less efficient way to produce ATP?

A

Cancer cells will need cellular components (lipids, proteins, nucleic acids) to proliferate, so by switching to less efficient they have enough ATP to proliferate and the other end products go to build up cellular components to make daughter cells at faster rate

89
Q

Cancer cells use of PPP

A
  • Oxidative: Allows for G6p to be made into Ribose 5 phosphate which will be used as a precursor in DNA and RNA to make nucleotides; Rate limiting enzyme of PPP is G6PD– will take G6P down oxidative pathway
  • Non-oxidative (Hexose monophosphate shunt): Ribulose 5 phosphate to G6P; Not needed because there is enough ATP being made
  • Transketylase and transadelyase converts excess ribose 5 phosphate to G6P to go back to PPP
90
Q

Use of NADPH from PPP

A
  • will reduce ribose to deoxyribose with Ribonucleotidereductase
  • Also used for lipid synthesis
  • Keep glutathione reduced which keeps oxidative stress low in cell
91
Q

How would oxidative phosphorylation be utilized in cancer cells?

A
  • Intermediates of TCA will make more biomolecules; Amino acids and lipids
  • Acetyl CoA will join with oxaloacetate in TCA which is made into citrate which then goes outside mito, back into acetyl CoA to be used in lipid synthesis
  • Malate used to make pyruvate (made into alanine) and aspartate
92
Q

RAS-MAPK pathway

A
  • Regulates cell growth; Makes D cyclins helping cell cycle continue
  • Function: upregulates telomerase which increases longevity of the cell allowing for continued replication
  • Makes ribosomes: Will transcribe rRNA genes, making rRNA which will make ribosomes which helps with making proteins
93
Q

effect of oncogenic form of mTOR

A
  • Results in increased protein synthesis

- Assesses nutritional access in the cell

94
Q

effect of oncogenic form of PI3K/AKT

A

High expression will support warburg effect by upregulating the synthesis of glycolytic enzymes, which supports aerobic synthesis
Support glucose hunger

95
Q

effect of oncogenic form of P53

A

Tumor suppressor gene; turned off; supports warburg effect by allowing for continued expression of glut receptors (glut 1 and glut 4) and helps with overexpression of glycolytic enzymes

96
Q

effect of oncogenic form of receptor tyrosine kinase

A

Will stop pyruvate kinase which prevents PEP from going to pyruvate; allows for PEP build up

97
Q

MEK

A
  • supports gluatmine metabolism
98
Q

Function of glutamine

A
  • carries extra amine groups that are produced during AA production to kidneys to be excreted via uria
  • Can go to glutamate which goes to alpha ketogluterate and then be used in different routes
99
Q

How does Warburg effect help in cancer detection

A
  • Used in basic principles of FDG PET CT
  • Flourodeoxy glucose: derivative of glucose
  • Cancer cells will absorb FDG because they think it is glucose and it will be phosphorylated to keep it in the cell but cannot be used in metabolism
100
Q

How can H pylori cause cancer?

A

-causes mutations in cells

101
Q

mutation TP53

A

Allows for cell to continue to go through cell cycle with DNA mutations and allows for aerobic glycolysis; works through P21 to repress

102
Q

APC

A

binds to beta catenin to stop WNT pathway; cancer will turn it off allowing for continued transcription

103
Q

RAS

A

continued transcription

104
Q

E-cadherin

A

keeps tumor cells together which will stop cancer growth because only can grow so much in a certain area; decreased amount allows for metastasis; cetuximab

105
Q

Her2

A

growth factor receptor (tyrosine kinase); ERBB genes are EGF receptors; tratuzamab targets her2 speifically and does not allow for EGF to bind

106
Q

VEGF

A

allows for angiogenesis

107
Q

Telomerase

A

aids in cell immortality by elongating telomeres; bevacizumab

108
Q

what happens to cancer cells with hypoxia

A

Hypoxia of any cells will trigger hypoxia inducible factors which will allow for excretion of VEGF and induce angiogenesis

109
Q

Four steps of invasion

A
  • loosening of intercellular junctions
  • degredation of the ECM (collagenase and other proteases break down ECM)
  • develop novel ways to attach to ECM
  • Migrate through ECM (by making proteins to migrate–new genes must be expressed to do this)
110
Q

Steps of metastasis

A
  • clonal expansion, growth, diversification, angiogenesis
  • metastatic subclone
  • adhesion to and invasion of basement membrane
  • passage through extracellular matrix
  • intravasation
  • interaction with host lymphoid cells
  • tumor cell embolus
  • adhesion to basement membrane
  • extravasation
  • metastatic deposit
  • angiogenesis
  • growth

Unit 3: LGS (7 decks)

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