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Foundations of Medicine > FOM Week 5 > Flashcards

FOM Week 5 Flashcards

1
Q

Why is DNA used to store information

A

It is stable
It is easy to copy/access
It can store ‘infinite’ amount of information

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2
Q

DNA Methylation

A

A long term covalent modification used to silent DNA from being transcribed
Very common in heterochromatin and repetitive DNA

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3
Q

DNA Acetylation

A

A short term modification used to open up DNA from the nucleosome
Occurs on lysine residues
Done by the enzymes HAT and HDAC

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4
Q

What makes up the Human Genome

A

Half is repetitive (LINEs, SINEs, Retroviral)

Half is unique (Introns, Exons, Non repititive DNA that is not involved in transcription)

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5
Q

Active Metabolite to Treat Actinic Keratosis

A

Actinic Keratosis is a pre malignant skin cancer

The drug gets incorporated into the DNA and causes strand breaks leading to cell death

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6
Q

What happens in FSHD

A

Their repeats in repetitive DNA get lost and therefore are no longer recognized as repetitive DNA. This leads to their transcription which causes the pathogenesis

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7
Q

Compare LINEs vs SINEs

A

LINEs are about 20% of genome. SINEs are 13%
LINEs have transposon capability
LINEs are around 6000 nt long. SINEs are around 280

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8
Q

Explain the Effects of Low Methylation in LINEs

A

People who have low methylations have a higher risk of dying early and getting some forms of cancer
Some LINEs are oncogenes if they become expressed

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9
Q

Mosaicism/Chimerism

A

Occurs during development and gives you multiple copies of genes
Occurs in about 20% of people

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10
Q

What can happen if DNA replication goes wrong

A

Cell catches it and repairs itself
Apoptosis
Cancerous

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11
Q

Rules of DNA Replication

A

It must only occur once per cell cycle
It must be regulated
It must be accurate
It is semi-conservative

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12
Q

Basic Steps to DNA Replication

A

Locate the origin and unwind from there
Initiate replication using a RNA primer
Elongate while preventing supercoils from forming
Reassemble into chromatin once done

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13
Q

Origins in Eukaryotes vs Prokaryotes

A

Prokaryotes only have one-two origins and are conserved

Eurkaryotes have 30k-50k origins and are not as conserved but still AT rich

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14
Q

Explain the Formation of the Pre-Replicative Complex

A

ORC binds to the origin

CDC6 binds to the ORC and recruits CDT1 which carries the MCM helicase along with it

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15
Q

Regulation of CDC6 and CDT1 in the Cell Cycle

A

CDC6 is only active during the G1 phase
CDT1 is only present during the G1 phase and then gets degraded
Geminin is a protein inhibitor of CDT1 as well and is highly present in the S and G2 phase

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16
Q

Enzymes Involved in DNA Replication

A 
MCM Helicase
DNA Primase
DNA Polymerase (delta/epsilon)
PCNA
Topoisomerase
DNA Ligase
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17
Q

Explain the Role of RPA during Replication

A

It is involved in binding the SSB’s to prevent reannealation of the DNA strands

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18
Q

Lagging Strand vs Leading Strand

A

Lagging stand goes away from the replication fork and requires discontinous replication
Leading strand goes towards the fork and is synthesized as one long fragment

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19
Q

Quinolone/Etoposide

A

Quinolone is an antibiotic that inhibits topoisomerase

Etoposide in an anti tumor drug that inhibits topoisomerase

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20
Q

Explain the Role of Chaperones in DNA Replication

A

They work to rearrange the nucleosomes so the DNA is accessible by the machinery and then reposition them once it is complete

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21
Q

Explain the Role of Telomerase

A

In the lagging strand, replication can never copy all of the DNA because of its need for lots of primers
Telomerases add nucleotides to the end of the chromosomes to prevent them from shortening after each replication
Cancer Cells have lots of them

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22
Q

Role of Blood

A

Transport O2 and nutrients to tissues
Transport CO2 and waste away from tissue
Works to maintain homeostasis

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23
Q

Composition of Blood

A

55% Plasma (90% water, lots of albumin)
Buffer region which contains WBCs
45% RBCS

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24
Q

Hematopoiesis During Development

A

Originally occurs in the yolk sac, then the liver/spleen
Once we are born it occurs in the bone marrow
At about age 20 it stops in long bone because the BM gets replaced by adipose

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25
Q

Erythrocytes

A

About 7 micros in diameter
Have no organelles
Are bioconcave in shape

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26
Q

EPO

A

A hormone produced by the kidneys

Gets released during times of hypoxia to stimulate more production of RBCs

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27
Q

HbA1C

A

A measurement used for the long term measure of glucose levels in the blood (2-3 months)
Glucose naturally binds to the n terminus of Hb and causes problems to the RBC

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28
Q

Neutrophils

A

12-15 micros in diameter
Multi lobed nuclei
60% of all the leukocytes
They are very short lived once they enter tissue

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29
Q

Eosinophils

A

12-15 micros in diameter
Bi lobed nuclei
The granules have two shades of staining in the EM
Involved in parasitic infection/modulation of inflammation

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30
Q

Basophils

A

12-15 micros in diameter
Bi lobed nuclei
The granules are large and stain very densely
Involved in releasing histamine

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31
Q

Lymphocytes

A

6-8 micros in diameter
Include B, T, and NK cells
30% of circulating leukocytes
Lifespan is hours to years

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32
Q

Monocytes

A

12-20 micros in diameter
Differentiate into macrophages in the tissue
Involved in APC process

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33
Q

How does diapedesis occur

A

Macrophages in the tissue relase ILs that bind to the endothelial
The endothelial will begin to express selectin receptors
Neutrophils have selctin ligands and will interact with the receptors causing slow rolling
Neutrophils begin to express ICAM and integrin which leads to a tight bind
Neutrophils will then exit into the tissue

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34
Q

What is a mutation

A

It is when the DNA has been damage and unrepaired. They are permanent
Can be somatic or germline

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35
Q

What type of damage does UV light cause in DNA

A

It forms thymidine dimers. Also causes ROS

Around 4000 per hour in sunlight

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36
Q

What type of damage does smoking cause in DNA

A

It forms aromatic DNA adducts

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37
Q

What type of damage does medical imaging cause to the DNA

A

It forms DSBs

At a very low rate though

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38
Q

Effects of DNA Adducts

A

They chemically modify the DNA

This leads to improper base pairing or DSBs

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39
Q

Cisplatin

A

A cancer drug that forms intrastrand cross links in DNA making them inseperable
This means not replication or transcription can happen

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40
Q

Steps to Repairing Simple Lesions

A

Recognize the mutation
Remove the mutation by nuclease
Replace with DNA pol
Ligate the nicks

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41
Q

Steps to Repairing Thymidine Dimers and Cross Links

A

Nucelotide Excision Repair

Same as the simple lesions except more base pairs are removed (more complex)

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42
Q

Fanconis Anemia

A

A genetic disease when the ICL repair does not work

Leads to a build up of genetic mutations

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43
Q

Two Ways to Repair DSBs

A

Homologous Recombination:

  • Error free
  • Can only occur during S or G2 phase

Non Homologous End Joining

  • Occurs when homologous recombination cannot
  • Two ends of the chromosomes are joined together without properly filling in the break
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44
Q

What happens in cells with a buildup of mutations

A

Cell death

Neoplasia

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45
Q

PARP1

A

An enzyme that recognizes mutations and flags down the machinery needed to repair
In cancer cells we inhibit this and it prevents DNA repair leading to so many mutations that eventually the cell will die

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46
Q

Importance of Regulating Gene Transcription

A

It leads to the differentiation of cell lineages

Determine the morphology and function of cells

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47
Q

Promoter

A

A region of DNA next to the gene and is where RNA pol 2 binds
Defines the transcription start site

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48
Q

Enhancers and Silencers

A

Can be located all throughout the genome and be even be in between genes
They are specific to a certain gene
This is where the transcription factors bind

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49
Q

Effects of Mutations in TFs

A

It will lead to improper expression of the gene leading to malfunction of the cell

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50
Q

Lineage TFs for Cardiocytes

A

GATA4
TBX2
TBX5

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51
Q

3 Domains of TF

A

DNA binding domain
Transcriptional Activation Domain
Dimerization domain

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52
Q

How do domains bind to the DNA

A

They recognize specific bases based on bonding and also shape of the DNA based on major/minor groove

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53
Q

How do TFs alter transcription

A
  1. They recruit proteins to alter chromatin structure (CRC/HAT/HDAC)
  2. They recruit other TFs
  3. They recruit kinases to activate RNA pol
54
Q

Lineage TFs for pluripotent induced stem cells

A

Oct3
Oct4
Sox2
Expose fibroblasts to these

55
Q

How does environment influence transcription

A

They environment of cells determine which TFs are present

Ex is infection, inflammation, cell cycle stage, etc

56
Q

NF-kB

A

Inhibits production of inflammatory genes by blocking the receptor from binding glucocorticoids

57
Q

Null Hypothesis

A

There is difference/association between exposure and disease

RR=1

58
Q

Alternative Hypothesis

A

There is a difference/association between exposure and disease
RR does not equal 1

59
Q

What do each of these tests compare
Chi Square
T Test
ANOVA

A

Chi square compares categorical data
T test compare numerical/mean data
ANOVA compares numerical/mean data as well but is better

60
Q

What does a high and low p value mean

A

A high p value means that your data is consistent with the null hypothesis
A very low p value means that your data is inconsistent with the null hypothesis

61
Q

Type 1 Error vs Type 2 Error

A

Type 1 error is false positive
Alpha is the probability of committing a type 1 error (want less than .05)
Type 2 error is a false negative
Beta is the probability of committing a type 2 error (want less than .20)

62
Q

What is the most reliable test to base data off

A

Confidence Interval

You want these to be small and narrow

63
Q

Informed Consent

A

The process of communication between a physician and patient that results in the patients authorization to undergo a specific medical intervention

64
Q

Negligence

A

Deviation of the standard of care

Leads to malpractice

65
Q

Battery

A

When consent was not given from the patient but you went ahead with the intervention anyways

66
Q

What came from the patient self determination act

A

Patients have the right to:

  • participate in their healthcare decisions
  • accept or refuse treatment
  • prepare an advance directive
  • receive clear information
67
Q

Implied Consent

A

In times of emergency where they patient cannot respond and has no one to speak on his behalf

68
Q

3 Elements of Informed Consent

A

Preconditions
Information
Consent

69
Q

How much information needs to be given to a patient

A

Enough information that a typical physician would give and enough information that the average patient would need to know in order to make an informed decision

70
Q

Trends of US Health Care

A

We spend the most on medical treatment and research yet do not have the best outcomes
Ranked 30th in infant mortality
Of all developed countries, we have the lowest percentage of people without insurance

71
Q

How do health disparities/inequalities arise

A

Differences in quality of care
Differences in access to care
Differences in lifestyles

72
Q

Barriers to Access of Care

A 
Number of PCPs
Financial
Geographical
Cultural
Language barriers
73
Q

What is the Gap

A

The gap is people who do not have health insurance. They live in states where medicaid was not expanded after the ACA was signed and do not make enough to apply for insurance through the exchange

74
Q

Which group of people are most likely to not have health insurance

A

Young working people

75
Q

4 Rules to Equity Based Care

A

Make SDH number 1 priority
Ensure a respectful, empowering clinic
Tailor care to the population served
Deal with cultural competence

76
Q

Apoptosis

A

Programmed cell death that involves a series of biochemical rxns leading to chromatin condensation and blebbing

77
Q

Things that cause apoptosis

A

Natural causes
Mutation in DNA
Loss of organelle function

78
Q

Necrosis

A

Cell death that is less orderly and due to stress from infection/pathogens
The cell leaks and causes inflammation

79
Q

Examples of irreversible cell injury

A 
Pathogens
Membrane defects
Calcification of mitochondria
ROS
Lots of DNA mutations
80
Q

Examples of reversible cell injury

A 
All the -trophy's
hydropic swelling
Mitochondria swelling
Lack of ATP
Etc
81
Q

Eosinophila

A

Common in necrotic cells

They stain very red because of their denatured proteins

82
Q

Karyorrhexis vs Karyolysis

A

Destruction of the nucleus

Dissolution of the DNA

83
Q

Coagulative Necrosis

A

The most common

Occurs from hypoxia

84
Q

Liquefactive Necrosis

A

When the rate of destruction is higher than the rate of repair
Forms abscesses which are balls of puss/bacteria

85
Q

Caseous (Cheesy) Necrosis

A

Necrosis associated with mycobacterium (Tb)

Can spread very rapidly if left untreated

86
Q

Fat Necrosis

A

Occurs in adipose tissue and is often associated with pancreatitis
Forms calcium deposits from saponification of the lipids

87
Q

3 Steps to RNA Processing

A

5’ Cap
3’ Poly A Tail
Splicing

88
Q

What function does the 7 methyl Guanosine cap have

A

It helps to stabilize
It is the binding side of the ribosome
It helps recognize mRNA as self

89
Q

What function does the poly A tail have

A

It helps to stabilize

It helps to increase translation efficiency

90
Q

What contributes to the reason that 1 gene can produce many different forms of a protein

A

Alternative splicing

Produces multiple forms of the same protein but they each have a particular function

91
Q

How does mutated SMN1 lead to SMA in infants

A

SMN1 interacts with snRNPs and is needed for their assembly

This leads to lower snRNP levels so splicing gets all messed up leading to malfunctioning proteins

92
Q

snRNPs

A

Critical for splicing
Have 5 parts to them:
-U1 and U2 bind to the splicing sites
-U4, U5, and U6 then join to form the spliceosome

93
Q

KLF6 Splice Variant

A

KLF is a tumor supressor gene
This SV binds to the same DNA region as normal KLF but does not carry out any function. It just blocks KLF from binding. Called a dominant negative SV

94
Q

List the Types of RNA

A 
mRNA- used to create proteins
rRNA- used to make up the ribosomes
tRNA- used to bring aa to ribosomes
snRNA- used to assemble the snRNP
miRNA- used to regulate translation
95
Q

What is the cap binding complex

A

eIF4F. Has three different parts to it
It recruits the ribosomes and make sure only mRNA is translated
It gets elevated in cancers

96
Q

eIF4F

A

eIF4E- The limiting factor. Actually binds to the cap
eIF4A- has helicase activity to straighten the RNA
eIF4G- a large scaffold protein that interact with poly A tail

97
Q

Strong vs Weak mRNAs

A

Strong mRNAs do not need a high level of eIF4E to be translated (housekeeping proteins)
Weak mRNAs do need high levels of eIF4E to be translated (sensitive proteins)
Most mRNAs are strong

98
Q

Steps to the Initiation of Translation

A
  1. eIF4F binds to the cap
  2. eIF2 loads met-tRNA onto the small sub unit
  3. eIF1 and 3 interact with cap binding complex to bring in the ribosome
  4. Small ribosome scans until it locates AUG
  5. Large subunit binds and elongation occurs
99
Q

PAPB

A

Binds to the poly A tail and interacts with eIF4G to improve translation

100
Q

eIF2 Role in Elongation

A

It is responsible for translocating the ribosome
Requires GTP
Diptheria toxin inhibits this process

101
Q

eIF1 Role in Elongation

A

It is responsible for bringing the tRNA to the ribosome

Requires GTP

102
Q

PERK Kinase

A

Becomes activated when there are lots of unfolded proteins present
It phosphorylates eIF2 making it inactive which means the ribosome cannot move

103
Q

Walcott Rallison Syndrome

A

A mutation in the PERK gene. Leads to lots of unfolded proteins causing cell death
Diabetes arises very early in these patients

104
Q

miRNAs

A

Short nucelotide fragments (20-22) that bind to specific mRNAs preventing their translation

105
Q

Changes to the Nuclear Envelope During Mitosis

A

At interphase the lamins and linker proteins are present
At prophase they begin to collapse
At telophase they begin to reform around daughter DNA

106
Q

How do small and large molecules get into the Nucleus

A

Through the nuclear pores
Small ones can diffuse. Large ones require active transport using RAN proteins
In the cytosol there is lots of GDP. In the nucleus there is lots of GTP
It uses this gradient to transport cargo into and out

107
Q

Ran GEF and Ran GAP

A

Ran GEF is in the nucleus and swaps out a GDP for GTP

Ran GAP is in the nucleus and hydrolizes the GTP to GDP

108
Q

How are proteins shuttled into the ER

A 
Co Translationally (most common)
Post Translationally
Both are done by the proteins having signal sequences
109
Q

What modification to the proteins occur in the ER and Golgi

A

In the ER glycosylation first begins and there are also chaperones to help with folding
In the Golgi glycosylation continues along with sulfation

110
Q

Clathrin Process

A

Used for endocytosis
When a ligand on the outside binds to its receptor the inside part binds AP2. This pulls down the area and recruits clathrin which surrounds and forms the vesicle

111
Q

COPI and COPII Process

A

When a ligand binds its receptor a GEF protein called Sec12 places a GTP on Sar1 which activates it. This then recruits COPI or COPII which will form the vesicle

112
Q

Explain How a Vesicle Gets to Its Right Location

A

The routing is controlled by a specific Rab protein. Has to have a GTP on it
On the vesicle there a V snares that interact with the t snares to form fusion
Tethering–> Docking–> Fusion

113
Q

Where is clathrin, COPI, and COPII used in the cell

A

Clathrin is used for endocytosis of plasma membrane
COPI is used by golgi
COPII is used by the ER

114
Q

Explain How a Protein Gets Into Mitochondrial Outer Membrane

A

Cytosolic chaperones present it to TOM

It then goes to SAM where it will get incorporated

115
Q

Explain How a Protein Gets Into Mitochondrial Inner Membrane

A

Cytosolic chaperones present it to TOM

It then goes to TIM22 and then TIM23 where it will get incorporated

116
Q

Explain How a Protein Gets Into Mitochondrial Matrix

A

Cytosolic chaperones present it to TOM

It then goes to TIM22 and then PAM where it will get incorporated into the matrix

117
Q

What causes the release of the ligand from the receptor in the endosomes

A

Endosomes have lower pH so this lowers the affinity

118
Q

Salmonella Endocytosis

A

They have evolved a surface protein that will bind to one of our receptors and become endocytosed by the cell where it can live/replicate/avoid the immune system

119
Q

Listeria (monocytogenes) Endocytosis

A

They have evolved a surface protein that will bind to one of our receptors and become endocytosed by the cell where it can live/replicate/avoid the immune system
They also have tails that can hydrolize actin and use this to move from cell to cell

120
Q

Anitgen Presentation

A

An Ag that has been bound by Abs will bind to macrophages. This will then get endocytosed and the Ag protein will get degraded
After this it will then move to the membrane where it will be presented to other immune cells

121
Q

Exonucleases vs Endonucleases

A

Exonucleases attack from either the 5’ or 3’ and degrade one by one
Endonucleases attack at a specific sequence and and create two shorter fragments

122
Q

Exosome

A

Exonuclease that degrades from the 3’ end
Scleroderma is an autoimmune disease that attacks them. It is lethal
5-fluorouracil is a drug that inhibits them

123
Q

XRN1

A

Exonuclease that degrades from the 5’ end

124
Q

How Cells Fix Stalled Translation

A

There is a hairpin that is blocking the ribosome from moving forward
An endonuclease cuts at the area creating two mRNAs and then XRN1 and exosomes degrade it

125
Q

How Cells Fix Early Stop Codons

A

An endonuclease cuts at the area creating two mRNAs and then XRN1 and exosomes degrade it
This is common in T cell Receptors

126
Q

How Cells Fix if There is No Stop Codon

A

The problem is at the 3’ end so only the exosome is used to degrade this mRNA

127
Q

Explain How miRNA can be Used for Degradation of mRNA

A

A protein recognizes when miRNA binds to mRNA and this can lead to two things
It can be place in a p body or it can be degraded

128
Q

How Cells Degrade Normal mRNAs

A

They first remove the poly a tail and 5’ cap

Then an XRN1 degrades from the 5’ end

129
Q

How are short lived proteins degraded

How are long lived proteins degraded

A

Short are done by proteasome (have to be tagged with ubiquitin and requires ATP)
Long are done by lysosome (can be autophagy or chaperone guided)

130
Q

How Cells Degrade Oligosaccharides

A

They are done in the lysosome

They first get taken off the protein and are degraded by glycosidases

131
Q

How Cells Degrade Lipids

A

They get sent to the lysosome where there are lipases

The FAs can then be used for fuel/signaling/inflammation

Foundations of Medicine (5 decks)

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