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MSI Unit I > extra info from Review Sessions > Flashcards

extra info from Review Sessions Flashcards

1
Q

what do CDC6 and CDT1 do?

A

both essential for DNA replication and formation of pre-RC. they act as vehicles to assemble the pre-rc. Once loaded, you can assembly primase, helicase, etc..

cdc6 - loads MCM (helicase) proteins onto the DNA. regulates cell cycle checkpoints. activity regulated by cyclinA

cdt1 - knockouts for cdt1 are lethal - cells undergo mitosis but not dna replciation

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2
Q

what enzymes are needed to unite the lagging strand?

A

Fen-1, DNA pol delta, ligase

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3
Q

error in helicase?

A

meier-garlin

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4
Q

error in clamp loader (r-27)

A

autoimmune disease, chronic inflammation, cancer

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5
Q

why does replicative DNA poly have high fidelity

A

it’s 3-5 exonuclease activity

enzyme has low kM for strand when mismatch occurs. it slows down rate that DNA unravels, allows the mismatch to be sequestered far away and be repaired

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6
Q

what encourages tight binding of DNA polymerase?

A

the narrow channel. More error prone DNA polymerases have larger crevice

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7
Q

describe nucleotide pool imbalance

A

as a result of accumulation of a particular nucleotide, a mistake if quickly skipped over because of the annealing of high concentration nucleotides occurs so quickly

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8
Q

what can stall the fork?

A

anything that gets in the way
centromeres - lots of protein
telomeres - lots of capping proteins
dna lesions or bulky adducts

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9
Q

premature activation/misregulation of the pre-RC can lead to

A

nucleotide pool stress

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10
Q

environmental factors that can mess up replication

A

sunlight casuing DNA damage (TT dimers)

massive amounts of damage - cell undergoes apoptosis. triggered by ATM stimulating p53 via the DDR

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11
Q

describe the error prone response

A

trasnlesion DNA polymerase uses non-template double strand.

when you have massive damage, sometimes you can’t repair it. translesion polymerases skip the damage by including any random nucleotide. If it can keep the replication fork from moving without being stalled, that is one way to deal with massive DNA damage

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12
Q

repetitive elements can cause..

A

loops out of DNA sequences. another type of error in DNA replication.

-Error that occurs when Polymerase slips

once the stable hairpin structure forms, it becomes an impediemnt to replication

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13
Q

errors in XPA-G? what pathway?

A

errors in the NER pathway. Xeroderma pigmentosum

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14
Q

what is the common set of steps of repairing DNA damage

A
  1. damage recognition by an enzyme specific to that damage type
  2. enzyme will remove damage (just base, entire nucleotide, large segment) and leave a gap
  3. DNA poly syntehsizes DNA to fill in
  4. Ligase ligates
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15
Q

what causes HNPCC?

A

mismatch repair errors

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16
Q

what causes aicardi gouteries?

A

error in RER Excision repair, RNAse

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17
Q

in BER, the lesion is removed by?

A

DNA glycosylase = cuts sugar/ cuts base/ cuts bond between sugar and base, cuts glyosidic bond

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18
Q

In NER, gap is filled by?

A

DNA polymerase. Dna poly does make the phosphodiester bond with previous nucleotide, but need ligase for next one to seal

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19
Q

what is the biochemical mechanism that can be used to regulate actin assembly into microfilaments?

A

energy output and input involved. By using ATP as energy, can control rates of assembly.

fast growing end can do work through the assembly process

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20
Q

fillapodia

A

fast gorwing ends towards the membrane

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21
Q

stress fibers

A

bundles where each + end is against membrane. in middle you get overlapping - filaments

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22
Q

lammelapodia

A

broad edge of cell being pushed out. You have branched filaments. ART binds to ends to existing filaments and creatse a place to nucleate and assemble

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23
Q

contractile ring

A

similar to stress fibers - lots of filaments go around cell and overlap with each other. Can have myosin between filaments pulling them, involved in cytokinesis.

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24
Q

myosin I

A

Myosin 1- monomeric, standalone vesicular motor. Sngle ATP binding site. Tail associates with membrane, does not have long tail, has short tail. Vesicular transport if free, or binding of mysoin to plasma membrane to move the filaments relative to the PM.

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25
Q

myosin II

where in non-muscle?

A

Myson I I - contracile arrays. In muscle and non muscle.

  • where in non muscle? Epithelial sheet that has to change shape during a process.
  • bipolar arrays cause contraction
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26
Q

assembly of microtubules is…

rate limiting step?

A

more complicated than filaments, Uses GTP not ATP.

the slow GTPase activity of bound subunits

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27
Q

meier garlin syndrome

A

helicase error

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28
Q

clamp loader mutation

A

autoimmune, chronic inflammation, cancer

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29
Q

mechanism that controls DNA replication to once oer cycle

A

cyclinA/CDK kinase - degrade CDC6 and CDt1 by phosphorylation and removing

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30
Q

microfilaments can form

A

microvilli
filipodium/lammelapodium - fast growing ends push membrane out

stress fibers - each + end against membrane, overlapping filaments in center to get contraction

lamellapodium - broad edge fo cell fushed out, branched filaments, actin related protein (ART) binds to ends, allows nucleation.

contractile ring - lots of filaments go around cell and overlap. can have myson between filaments pulling, involved in cytokinesis

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31
Q

extending nerve terminus

A

assembly of actin. get actin subunits to the end, vesciles get transportered to end and “hop off”

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32
Q

secretory and actin

A

vesicles get close to membrane, actin filamnets bring them up to membrane, allow secretion

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33
Q

mysosin walking across actin filaments

A

same cycle of ATP bidning, myosin release, ATP hydrolysis, change in confirmation, reattatch, release energy and pull along filament

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34
Q

how is mysoin regulated?

A

depends where you are

in skeletal/cardiac muscle - directly involves calcium assocation with proteins on thin filament

or phosphorylation of proteins associated with myosin like chains

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35
Q

general contraction/relaxation cycle

A

Thin filament (actin), mysoin tries to move toward plus ends at Z disk, trying to move in 2 direction at once. The contractile unit (Sarcomere) shortens. This happens when calcium bins to the proteins on actin filaments, moving the tropomysin out of way so myosin can interact with actin. Regulated through sequestration of CA in membrane vesicles of SR that get released and pumped back in.

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36
Q

intermediate filaments

A

family of proteins that provide structural support, NOT tracks for motility

keratins, vimentin/related, neurofilaments, nuclear lamins (all cells)

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37
Q

microtubules vs microfilaments

A

microtubules - hollow, more complicated assembly, uses GTP and slow GTPase of beta subunits

microfilaments - use ATP and actin

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38
Q

microtubules involved in

A

nucleic and cell division, organization of intracellular structure, and intracellular transport, as well as ciliary and flagellar motility

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39
Q

where are microtubules found in cells?

A

nucleating sites (where - are togheter and cant assemble) associated with gamma tubulin rings to rapid assembly

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40
Q

what moves along microtubules?

A

membrane associated things

ER and golgi comparments move to different parts of cell

Dynein - pulls things closer to centrosome (-). keeps golgi next to nucleus. nuclear membrane and golgi have dynein associated

ER - spreads throughout microtubule network using kinesin

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41
Q

motile vs non motile cilia

A

motile - have dyneins

non-motile - lots of sensory receptors on membrane, no dynein

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42
Q

primary places where you see defects with cilia?

A

not having receptors on non motil cilia - causes polycistic kidney disease where the kidney cilia dont assemble or receptors are mutated

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43
Q

ramachandran plot

glycine?

A

certain regions are compatible with secondary structures due to bonding angles

glycine has large area in plot suggsting flexibility

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44
Q

can the C-N bond rotate?

A

no, all four atoms connected are in a plane and rotate together, C-N bond has partial double bond character

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45
Q

Phi Angle?

PSi angle?

A

Phi - Con

Psi - CC

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46
Q

phi and psi in beta sheets?

alpha helicies?

A

beta sheets - close to 180

minus 60 - alpha helix

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47
Q

if NH3+? pH must be..

if histidine is protonated?

if carboxyl is deprotonated?

A

below 8

must be below 6.5

must be above 4

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48
Q

Alpha-1-antitrypsin

A

serine protease, example of disease cuased by protein misfolding

leading to aggregation or loss of function

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49
Q

Correct function of alpha1-antitrysin

A

reactive center loop where neutrophil elastasce likes to cleave (cheese in mousetrap).

Bites the loop, forms covalent bond to loop. Loop cleaves and now inserts into central beta sheet (it is complementary)

  • Loop drags neutrophil elastase down to lower section of alpha-1-at, and the interaction cuases neutorphil elastase to misfold
  • other proteases now degrade neutrophil elastase
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50
Q

what can do wrong with alpha-1-antitrypsin?

2 things

A

-suggested by lock of similar antithrombin enzyme

when reactive loop inserted into beta sheet, it sprung all by itself (more stable, cant go back). Can no longer inhibit. Happens too much due to mutation - can no longer inhibit neutrophil elastase

second thing that can go wrong - insertion happens without cleavage, it mis inserts into neighboring molecule. Abundant in liver, causes a cascade of polymerization that builds up in liver

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51
Q

alpha helix amino acids

A

helix formers - mainly alanine, but also arginine and leucine

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52
Q

if the N-terminal is in the internal lumen of the ER…

A

, then when it is sent to the plasma membrane, the N-term will be on the external face.

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53
Q

Biosynthesis of glycosaminoglycan chains on proteoglycans occurs primarily in

A

golgi

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54
Q

When a protein destined for the plasma membrane is synthesized, it is inserted into the ER membrane with its extracellular domain on

A

the lumenal side of the ER membrane.

to be facing out of the cell, must be facing inside of the ER

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55
Q

lyosome, endosome, peroxisome

A

lyososome - degradation/recycling

endosome - sorting from endocytosis

peroxisomes - creates h202

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56
Q

2 organelles that do not communicate with other organelles via vesicles

A

mitochondria and peroxisomes are not a part of the vesicular trafficking pathways

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57
Q

when LDL receptor iis synthesized in the ER..

A

the LDL binding domain faces the ER lumin, but will face the cytosol once it reaches the PM

the adaptin domain starts off facing the cyotosol, will end up pointing inward

When we put proteins into the ER, we put them in the same way in correct orientation every time. Something that needs to face outward and inward
-something initially faces lumen then faces outside

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58
Q

mitochondrial receptor VS ER receptor

A

the receptor for the mito signal sequence is on the mito membrane

the receptor for the ER directing signal is in the lumen (Soluble)

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59
Q

scanning EM of golgi vs rough ER

A

rough ER will have visible studded ribosomes

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60
Q

golgi Vs SMOOTH ER?

A

golgi- tight pancake stack

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61
Q

lysosome scanning image

A

very dark, black

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62
Q

peroxisome scan

A

uniform gray, smooth, very dark spot in center (Crystallization of enzymes)

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63
Q

Phospholipids and Sphingolipids

A

Phospholipid
ex) phosphoglyeride - 2 fa, glycerol backbone, phosphate alcohol head

Sphingolipid
ex) Glycolipid- sphingosine backbone/fa, carbohydrate

shingomyelin -is a sphingolipid and a phospholipid (sphingosine, fatty, acid, phosphate choline

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64
Q

mito genome is in the

A

mito matrix

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65
Q

proteins required for Mito genome (RNA poly, DNA poly) come from the…encoded where?

A

cytosol, in the nucleus

transcribed in nucleus, translated in cytosol, transported into mitochondria

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66
Q

x-linked adenoleukodystrophy

A

cant import long fatty acids, beta oxidation doesnt occur, they accumulate

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67
Q

familial hypercholesterolemia

A

LDL can’t get taken up by endocytosis. LDL receptor suffers a loss of function mutation, accumulated in blood

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68
Q

where are the ABO antigens synthesized?

A

in golgi

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69
Q

3 functions of golgi

A

n-linked sugars modified

o-linked sugars added to proteins and lipids

GAGS built on proteoglycan core proteins

ABO blood group antigens

degrade glycoproteins and proteoglycans

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70
Q

mucopolysaccharidoses

A

-defects in the degradtion of GAGS

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71
Q

oligosaccharidosis

A

defend in degredation of oligosaccharides

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72
Q

sphingolipidosis

A

defects in degredation of sphingolipids

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73
Q

inclusion-cell disease

A

defect in generating M6P tag on lyososomal enzymes. lysosomes fill with substrate with nothing to degrade them. the enzymes are sent throguh default pathway which is harmless because they only act at low pH

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74
Q

why don’t the proteases in lysosomes self digest the other enzymes?

A

the other enzymes are protected by sugars, proteins are heavily glycosylated

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75
Q

all nuclear pores are ______, what determines the direction taken?

A

equivalent, direction is based on the carrier intermediate

76
Q

there are vanishing amounts of GTP in the

A

cytoplasm

77
Q

Role of Ran GTPase?

A

provides energy for transport in form of energy stored as chemical gradient

helps form export compleex and accompanies these complexes out of nucleus

78
Q

homologous recombination mixes up…

A

parent and grandparent alleles by exhanging arms of chromosomes

79
Q

we all inheret ______ loss of function alleles

A

250-300

80
Q

half of our genome are ________

A

transposable element sequences

81
Q

retrotranspons

A

in humans, move via RNA intermediate with RNA reverse transcriptase

82
Q

retrotranspons and exon shuffling

A

Rretrotranspons have unique transposon ends. The enzymes recongize these tranposable ends. Make RNA out of this, reverse transcriptase can recognize the other two, and move entire
Normally the RT would transcribe and transport the small pink, instead it mistakenly cuts out and tranports the larger green gene between the two similar transposons

-this can cause misalignment

83
Q

creation of unequal gene families by crossing over

A

an entire gene can get duplicated, or the same thing can occur WITHIN a gene causing a single exon duplication or deletion

84
Q

multiplex PCR

A

many PCR in single tube, get multiple products. You’ve got 9 reactions at same time, done diagnostically, how you look for deletions in dystropin

85
Q

RT-PCR

A

You can PCR and amplify when template is RNA - use RT enzyme to do first early rounds to turn RNA into DNA, then it’s a normal PCR. It’s a PCR where the first round is

86
Q

Microarrays

A

lung cancer example but lots of things. Different kinds of tumors in cancers, how they might respond to different chemo treatments. Microarrays give you a readout of all the genes being expressed in that tumor. Gives you a very detailed view of what that cell is doing and how its doing it. Much more so then under a microscope (Stain, shape) very high res.

- tells subtype of cancer
- what mutations might be present
- what pathways elevated - will tell you what chemo will or wont work
87
Q

FISH vs Microarray

A

fish - looking at whole chromosome, you see large changes in chrosomomes. Cancer cell karyotype. Shows approximate lesions of chromosome and how its been moved

typical microarray - analyzes mrna to determine expression (what and how much) of a gene. Tells more than fish, lets you get to see exactly where translocation is

88
Q

spirochetes under a microscope can appear

A

either spiral or invisible (pallidum). need darkfield

89
Q

What do we do antibiotics resistance testing on?

A

the enterobacteriaecae - they are so abx resistant due to horizontal gene transfers that we need to do agar plate + abx disks

90
Q

what would a culture of rickettsia on agar look like?

A

rickettsia is intracellular, plane of agar would be blank. must culture in tissue

91
Q

we do not do antibiotic resistance testing on…

A

environmental microbes, such as clostridium

92
Q

to establish intracellular infection (4)

A

need type 3SS - important for host cell takeover/living inside of them

93
Q

why don’t we use the TB vaccine (bcg)?

A

our incidence of TB is low, and we primarily screen people as necessary with PPD. Giving people the vaccine would cause all PPD to come back positive, new way to screen would require chest xray

94
Q

Childhood infection due to bacteriophage, has been declining ever since

A

scarlet fever

95
Q

N.meningitidis

A

gram negative diplococcus that oxidizes maltose and has a a capsule

96
Q

N.Gonorrhea

A

gram - diplococcus that does not oxidize maltose, has pili

97
Q

most common disinfectant used for living tissue?

A

alcohol, is also a crossover agent used for countertops/objects

98
Q

quaternary ammonium compounds

A

most common use of sterilization and disinfecting and detergent in hospital of surfaces. Quats have residual activity even after wiped off.

99
Q

Augmentin, ceft, vancomycin all…

A

inhibit peptidoglycan synthesis

the beta lactams act as PBP substrate analog

vancomycin (glycoproteins) - bind to the terminal d-ala strands to block PBP

100
Q

penicillinase/beta lactamase resistant penicillins

A

used against organisms that product beta lactamase

101
Q

MRSA

A

has found a way to become resistant to all beta lactams and beta lactamse inhibitors

MRSA changed its PBP2 to PBP2a

102
Q

cephalosporin generations

A

move up food chain, become more and more resistant to beta lactamase

103
Q

carbepenams

A

the most powerful beta lactams, resistant to ALL beta lactamases, sensitive to carbepenemases

104
Q

CRE

A

carbepenam resistant enterobacteriaca - stared off as just kleb, produces carbepenamases

105
Q

why might a patient not respond to cephalosprin treatment?

A

the organism is producing beta lactamase to “break the floor of the garage”

106
Q

treatment of simple betalactamases expressing organisms?

A

can use antibiotic + b lactam inhibitor (augmentin_

107
Q

treatment of sophisticated beta lactamase expressing organisms?

A

produced by the ESBLS, can no longer use 3rd and 4th gen cephalosporins. use carbepenam

108
Q

CRE’s are ____

A

plasma encoded superbugs. plasmids contain genes for all mechanisms of resistance. we only have colistin left

109
Q

treatment of CRE’s?

A

colistin

110
Q

most common immunodeficiency?

A

lack of IgA - get more colds and gi infections

111
Q

why doesnt cholera have a high infant death rate?

A

IgA are present in breast milk

112
Q

why is IL1B in a prophase?

A

so it is already made, and can quickly be cleaved by the inflammasome to be realeased to begin inflammation

113
Q

enzyme for immunoglobulin class witching and somatic hypermutation?

A

AID

114
Q

RAG1 and RAG 2 are needed to

A

recombine the b cell chain DNA

115
Q

TDT

A

adds n-regions during splicing to give random diversity

116
Q

N regions exist primarily in

A

heavy chains, leading to more diversity

117
Q

someone without TDT

A

has antibody and t-cell receptors, but doesnt make as high affinity antibody because they dont have the same amount of diversity to start with

118
Q

_______ is never present in T-CElls

A

AID

119
Q

what stimulates AID in b-cells?

A

t-cells

120
Q

t-independant antigen wil not

A

class switch or do hypermutation

121
Q

western blot and elisa both show….

difference?

A

how much antigen there is

western blot takes longer and limits how much can be run at once

Western blot does let us know the molecular weight of the antigen

122
Q

advantage of western blot?

A

lets us know molecular weigth of the antigen

-sometimes there is a mixture of things that are reactive, but we want to know the particular protein that is causing the reaction

123
Q

_____ provides better info about size

______ is much more quantitative

A

western blot - size

elisa - quantitiative, shows amount

124
Q

which can tell concentration of antibody, western of elisa?

A

both can, simply titrate until you don’t have reaction anymore

125
Q

Fc receptor on macrophage binds the

A

IgG constant region

126
Q

what is an allergen?

A

an antigen that binds IgE

127
Q

epitope

A

part of antigen that single monoclonal antibody binds to

128
Q

the is no Fc receptor for…

A

IgM

129
Q

complement can enhance phagocytosis due to

A

prescence of receptors for c3b on macrophages and neutrophils

130
Q

____ is the main target of major complement receptors

A

c3b, used to opsonize a target to be cleared out of the body

131
Q

b-cell differentiation timeline

A

heavy chain, then light chain. Heavy chain gets made first and each chromsome gets only one chance to rearrange its VDJ successfully.

Light chains get multiple cahnces to rearrange their DJ regions.

132
Q

hapten experiment

A

carrier coated with hapens

t-cells respond to carrier
b-cells respond to hapten and carrier

switching the carrier - no secondary response by the B cells against the hapten

-B cells and T-cells need to be on the same page to have a secondary response

133
Q

toxoids are similar to hapten molecules. TF

A

True

134
Q

we get less crossreactivity with a monoclonal because

A

this is a laboratory artifact, we screen for crossreactives and they are not used

135
Q

mito matrix contains

A

mito genome, beta-oxidation enzymes, TCA cycle enzymes

136
Q

mito inner membrane contains

A

components of oxidative phosphorylation, ETC proteins

137
Q

mito outer membrane contains

A

porin molecules

138
Q

intermembrane space contains

A

cytochrome c - important for cell death signaling

139
Q

all bacteria have…

A

internal plasma membrane

140
Q

describe exotoxins

A

polypeptides secreted from pathogen or injected into host cell via t3ss

  • superantigenicity
  • actin depolarization
  • interference with signal transduction
141
Q

unknown anaerobes can be identified by

A

gram stain, biochemical tests, gas chromatography analysis of waste products

142
Q

major pathogenic anaerobes

A

Clostridium, GNAB, and actinomyces

Gnab are gram -
clostridum and actinomyces are gram +

GNAB, actinomyces, and C.diff are normal flora

remainer of clostridum are soil organsism (tetani, botulinum) that depend on spore forming ability

143
Q

anaerobic virulence depends on

A

exotoxin expression and tissue degrading enzymes to create abscesses

144
Q

metabolism of staph?

A

facultative anaerobes - wall themselves off

145
Q

treatment of anearobic infections?

A

antibiotics against the bacteria, antitoxin against the toxin, and wound draining/debridement

146
Q

spirochetal trasmission

A

sexual, vector, environmental

147
Q

common spirochete themes

A

cross into bloodstream quickly/easily

virulence primarily due to immune evasion (not antigenic but also immunomodule the host) - no vaccines

diagnosis challening - treponema are too small to see, cause various odd symptoms. Lyme tests are difficult

treatment easy

often get herx reaction

148
Q

vaccines against spirochetes effective?

A

no vaccine, spirochetes are not immunogenic enough

149
Q

syphilis

A

3 stages
painless chancre to variable rash/flu

to either early or late latency

to dangerous cardiac or CNS involvment. “Gummas”

150
Q

lyme stages

A

early localized - rash
early disseminated - meningitis, facial paralysis, rashes, cardiac symtpoms

late disseminated - arthritis, encephalitis

151
Q

treatment of lyme

A

doxycycline

152
Q

appearance of vibrios

reservoir?

A

curved, gram - rods.

ocean dwelling, infected humans, halophiles (thrive in high salt concentrations)

153
Q

most vibrios can cause

A

fecal oral gastroenteris primarily

may infect wounds exposed to ocean water

H.pylori causes peptic ulcurs

154
Q

v.cholera

A

complex planktonic lifecyle outside of human host

pathogenic strains have O1 antigenic marker of colonization by lyosgenic phage that carries virulence factors

trasmission is fecal oral, usually killed in stomach via acid

155
Q

virulence of v.cholera

A

encoded by lysogenic phage (has O1 marker)

  • secretes mucinase to attatch/colonize intestine
  • secretes choleragen - AB enterotoxin that interferes with signal transduction = massive watery diarreah
156
Q

treatment of v.cholera

A

antibiotics may not be necessary, self limiting in otherwise healthy host

provide hydration and electrolytes

157
Q

intracellular bacteria may be facultative-

A

facultative - enter has part of life cycle, can replicate outside on agar
-neisseria, enterics, mycobacter, bacilli, legionalla

or obligate, must be grown on tissue
-rickettsial, chlamydia

158
Q

how do they get around?

A

pathogens use infected macrophages for transport around body, avoid humoral

159
Q

treatment of intracellular bacteria?

A

tetracyclines except pregnant

160
Q

Reactive arthritis may be caused by

A

chlamidia, shigella, or eneterohemmogenic e.coli

161
Q

listeria

A

causes gentroententeritis, escapes endosome after endocytosis and uses actin based motility to spread between cells (ActA)

162
Q

chlamyida

A

use t3ss to enter and create paranuclear inclusion body for the larger reticulate bodies to multiple in

163
Q

enterobacteriaca

A

two groups

foodborne - shigella, e.coli, salmnella, yersinia

oppotunistic ICU bugs - kleb, enterobacter, proteus, providencia, serrata, morganella

164
Q

describe the testing results of enterbacteraicace

A

gram -, non spore forming, straight rods, facultative anaerobes

catalase +, oxidase -, glucose fermenters

165
Q

problem with the enterobacteriaceae

A

promiscuous with DNA, extreme abx resisitance is common. must do sensitivity testing

166
Q

virulence factors of enterbacteriaceae?

A

pili for attatchment, t3ss for injecting enterotoxins and subverting gut macrophage.

allow themselves to be sampled by M-cells in peyers patches

167
Q

Y.enterocolicita and macrophages

A

use subverted macrophages as trojan horse to local lyph nodes (false apendicitis)

168
Q

s.typhi

A

system wide entry using macrophages

169
Q

HUS

A

hemolytic uremic syndrome - pediatric complication caused by release of shiga toxin into bloodstream by either shigella or eneterhemmogenic e.coli

170
Q

patients with human antigen b27 infected with enterobacteriaceae

A

may develope reactive arthritis (conjunctivitis, urethritis, and arthritis) after infection from Shigella, salmonella, yersinia, campylobacter, or chalomydia

171
Q

the 6 ICU bugs

defense?

A

kleb, enterobacter, morganella, proteus, serratus, providencia

172
Q

growth rate of M.tuberculosis

A

slow, difficult to culture and defeats some antibiotics

173
Q

gram stain of M.Tuberculosis?

A

poorly due to mycolic cell wall

174
Q

spread of M.Tuberculosis

A

inhalation of infectious particles, spreads to lymph nodes, long bones, kindney, and CNS by hematogenous spread (trojan horse macrophages)

175
Q

immunocompetent reaction to TB?

A

creates strong CMI, can hold latent

176
Q

cd8 cells respond to tb by

A

killing infected macrophages and forming granulomas to wall off infection

177
Q

classic TB

A

cough, weight loss, fever, bright pink chains of rods in sputum

178
Q

extrapulmonary TB

A

ussually reactivations - scrofulas, genitourinary, CNA, skeletal

179
Q

in pediatrics, TB can cause

A

miliary and meningitis

180
Q

main treatment of TB

A

4 drug coctail with isoniazid, 2 week isolation

181
Q

aytipical mycobacteria?

infection symptoms?

A

environmentally acquired, don’t cause TB or leprosy

ussually cutaneous - scrofulas.
in compromised - may mimic TB, especially M.Kansasii

182
Q

two forms of leprosy

treatmetn?

A

tuberculoid - strong cmi that causes nerve damage, paucibacillary, ppd +

leproid - weak CMI, causes extreme cutaneous damage, multibaccilarry, PPD -

2 years dapsone/rifampin

183
Q

TF can be a…

A

an activator, repressor, or recuitor of chromatin modifier

184
Q

what can result from enhancer translocation?

A

t-cell acute lymphocytic ademia - make tons of T-cells, way more than needed

185
Q

Transcription factors use different motifs to..

A

contact DNA and provide specificity

typically have an alpha helix that inserts into major groove. multiple contacts gives specificity, does not need to unwind DNA helix

186
Q

Transcription factors stimulate the general transcription machinery via a

A

mediator
-bridges RNA pol activators to RNA pol II and general factors

-required for transcription activation

187
Q

what do chromatin modifiers do?

A

adds covalent modifications to histone N-terminal tails

acetylation - activation
deacteylation - deactivation
methylation - activation or repression
phsophorlyation - coupold to acetylation

MSI Unit I (52 decks)

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