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Unit 1 > Unit I Deck 3 > Flashcards

Unit I Deck 3 Flashcards

1
Q

What is the major obstacle in eradicating tuberculosis?

A

AIDS.

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2
Q

Why does M. tuberculosis gram stain poorly?

A

Mycolic acid in its cell wall

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3
Q

Mycobacteria are gram __1__ and acid-fast __2__.

A
  1. Negative

2. Positive

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4
Q

What is the process by which M. tuberculosis infects?

A

It gets eaten by naive macrophages to use them as a trojan horse. Then the CD8 cells kill the macrophages creating granulomas, where the TB is hidden. TB then travels to the lymph nodes and attacks.

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5
Q

In what places can you get extrapulmonary TB?

A
  1. Neck - scrofula
  2. GI (rare)
  3. CNS - abscesses
  4. Genitourinary
  5. Skeletal
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6
Q

What is miliary?

A

Millet-like non-calcified foci of infection of liver, lung and spleen, evidence of hematogenous spread of TB throughout body, fatal if untreated

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7
Q

What are two main hallmarks of TB tx?

A
  1. Observed dosing

2. Isoniazid

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8
Q

What vaccine is used for TB abroad, but not here in the US?

A

BCG vaccine, live attenuated M. Bovis, effective against about 70% of TB

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9
Q

True or False: Latent cases of TB remain contagious.

A

False. Latent TB is not contagious.

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10
Q

What are atypical mycobacteria?

A

Neither M. TB nor M. leprae. Live in environment, cause infections in humans rarely, usually a cutaneous infection.

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11
Q

What kind of infection could be respinsible for scrofula in children?

A

Most likely an atypical mycobacteria, M. scrofulaceum. Scrofula is usually evidence of s re-infection, so the likelihood of a reinfection of TB in a child is low. But it could still be TB.

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12
Q

True or False: M. Leprae has no in vitro culture system.

A

True! A few labs keep armadillos as reservoirs.

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13
Q

What is another term for Hansen’s disease?

A

Leprosy

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14
Q

What are the treatments of choice for Hansen’s disease?

A
  1. Dapsone

2. Rifampin

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15
Q

What does the Lepromin PPD test for?

A

The Lepromin PPD tests for anti-leprosy response and position on the TB-lepro spectrum. It cannot determine exposure.

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16
Q

What is the most common atypical mycobacterial infection? How is it treated?

A

M. Marinum, found in fresh and salt water, creates lesions where it came into contact with previously broken skin. Treat with tetracycline.

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17
Q

What is the difference between the M. Leprae PPD and the M. tubercolosis PPD?

A

M. Leprae is a hypersensitivity test, while M. TB is an antibody test.

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18
Q

Name 2 instances of normal apoptosis.

A
  1. Normal development (adult or embryonic)

2. In response to an error found at a cell growth checkpoint

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19
Q

What is the source of syndactyly?

A

Syndactyly occurs when, during development, cells that should have apoptosed to produce fingers/toes, do not.

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20
Q

Give an example of apoptosis in an adult.

A

In mammary glands post-lactation

Lining of gut

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21
Q

What are trophic factors?

A

Trophic factors are “survival factors,” without which a cell will initiate apoptosis, ie at birth, when there are many more neurons than target cells, the lack of trophic factors to certain neuronal cells prunes them out

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22
Q

Why does apoptosis not initiate an immune response? How is this different from necrotic cells?

A

Intracellular contents are not released, controlled waste disposal, whereas necrotic cells swell and burst, initialting an immune response to the foreign contents.

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23
Q

What are the steps leading up to apoptosis, beginning with the lack of trophic factors?

A

Trophic factors normally phosphorylate Bad and inactivate it.

  1. Without trophic factos, Bad is free to to interact with apoptotic proteins Bcl2 and Bcixi in the mitochondrial membrane
  2. Bcl2 and Bcixi are now not doing their job of inhibiting the Bax ion channel in the mitochondrial membrane.
  3. Bax opens and releases cytochrome c into the cytosol
  4. Cytochrome c initiates a caspase cascade (a series of cytosine proteases) that go around cleaving and being bad
  5. Result is a proteolytic amplification cascade
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24
Q

Name 2 types of cells that have reached terminal differentiaion.

A
  1. Neuronal cells

2. Cardiac cells

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25
Q

What stage do cells enter when they run out of telomerase?

A

Senescence

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26
Q

What is telomerase made of?

A

Telomerase is a ribozyme, part protein, part RNA

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27
Q

Where does telomerase add its GGGTTA?

A

To the parental strand, so that during replication, no terminal genes are lost AND the chromosomes don’t anneal

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28
Q

True or False: Most adult tissues lack telomerase.

A

True.

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29
Q

When telomeres get too short, what is activated, leading to senescence?

A

p53, which blocks cells in G1. p53 is an important tumor suppressor gene.

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30
Q

What are the 2 main goals of senescence?

A
  1. To limit unwanted proliferation

2. To protect cells from replicating incomplete or unstable chromosomes.

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31
Q

Name a locally-acting growth factor and its function.

A

PDGF - platelet-derived growth factor, stimulates would repair and epidermal/epithelial cell migration.

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32
Q

Name a systemically-acting growth factor.

A

EPO - erythropoietin, made in kidney, stimulated RBC synthesis

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33
Q

What is anoikis?

A

Anoikis, from the Greek for “without a home,” refers to anchorage-dependent regulation of cell growth and describes how a cell floating in a medium, with nowhere to adhere, or call home, will apoptose.

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34
Q

Anchorage-dependent cell growth refers to what specific tissue?

A

Epidermal tissue, where only the cells in contact with the basal lamina will proliferate.

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35
Q

Describe a situation influences by contact inhibition of cell proliferation.

A

Wound repair. When cells meet each other, they exert contact inhibition one another and normally do not proliferate. When a wound occurs, the cells regrow to fill the gap.

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36
Q

What does GEF stand for?

A

Guanine-nucleotide exchange factor

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37
Q

What does GAP stand for?

A

GTPase activing protein

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38
Q

What is the normal proliferation of skin epidermis?

A
  1. As long as stem cells are attached to the basal lamina, they will continue to proliferate.
  2. When cells detach, they stop proliferating and start differentiating
  3. Increase in cadherins and keratins –> increase in desmosomes
  4. After 2-4 weeks, skin is sloughed off and replaced
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39
Q

Name 4 situations that cause cancerous activity of cells.

A
  1. Upregulation of telomerase, or downregulation of p53
  2. Stop needing growth factors to initiate replication
  3. No cell-cell contact inhibition –> form foci when cells pile up on top of each other
  4. No more anchorage-dependence for growth
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40
Q

What is an oncogene?

A

An oncogene is a disregulated (mutated or overexpressed) version of a gene normally found in the cellular genome.

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41
Q

Conversion of a proto-oncogene to an oncogene is usually the result of:

A

A somatic mutation, not inherited

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42
Q

What are the functions of p53?

A

Induces synthesis of inhibitor cdk21
Blocks Rb phosphorylation
May induce apoptosis or senescence

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43
Q

DNA viruses carry genes within their normal genome that encode proteins that block ___1___ and ___2___ function, thereby leading to hyperproliferation and transformation of infected cells.

A
  1. Rb

2. p53

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44
Q

Name 2 viruses known to cause cancer.

A
  1. SV40

2. HPV virus

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45
Q

True or False: Mutation of a single proto-oncogene cannot alone cause cancer.

A

False. It only takes one!

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46
Q

Name 2 notable tumor suppressor genes.

A
  1. Rb - Retinoblastoma

2. p53

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47
Q

Can a heterozygote with 1 mutant tumor suppressor gene produce adequate function to inhibit genes?

A

Yes

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48
Q

Mutations in tumor suppressor genes tend to be ___1___ while mutations in proto-oncogenes tend to be ___2___.

A
  1. inherited (ie retinoblastoma)

2. acquired somatic mutations

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49
Q

Give an example or a proto-oncogene where 1 small mutation in the gene creates a hyperactive protein.

A

pp60Src - tyrosine kinase protein in Rat sarcoma (Ras)

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50
Q

Give an example of a proto-oncogene that is the result of the fusion of two proteins that turns monsterous

A

Brc-cbl, the fusion protein responsible for chronic myeloid leukemia (CML)

51
Q

Penillins, cephalosporins, monobactam (aztreoname and carbapenems all do what to bacteria?

A

Poke holes in the peptidoglycan cell wall, so when the bacteria divides, Pop!
Doesn’t work with TB bc the bacteria grow too slowly.

52
Q

Even though both vancomysin and penicillin classes use the bacterial cell wall to act on, what is the difference between them?

A

Vancomysin is a bacterial-static, not a bacterial-cidal, so that it stops the growth of bacteria.

53
Q

As you increase the generations of cephalosporins, how does the bacterial target change?

A

As you increase the generations, you become more effective against gram (-) bacteria and less effective against gram (+) bacteria.

54
Q

What classes of drugs are susceptible to B-lactamase?

A

All the beta-latams (penicillin, aztreonam, cephalosporins) except *carbopenems.

55
Q

An example of a carbopenem is:

A

Imipenem

56
Q

An example of a cephalosporin is:

A

Ceftriaxone. Everything begins with “cef”

57
Q

An example of penicillin is:

A

Amoxicillin, ampicillin

58
Q

An example of a synthetic penicillin:

A

Pipericillin

59
Q

What is Zosyn?

A

Pipericillin-tazobactam

60
Q

What is tazobactam?

A

It is the beta-lactamase inhibitor that helps penicillins function.

61
Q

What the the function of trimethoprim?

A

Folate inhibitor, packaged with a sulfa-drug to make Bactrim, and together they are synergistic to be a broad-spectrum antibiotic bc they inhibit separate paths of the folic acid biosynthesis of the bacteria

62
Q

Give an example of a tetracycline.

A

Doxycycline

63
Q

What is the mechanism of the tetracyclines?

A

Ribosome inhibitor (30s) - a bacteriostatic

64
Q

What is the function of aminoglycosides?

A

Ribosome inhibitor (30s) - but unlike the tetracyclines, is a potent bacteriocidal.

65
Q

Name an example of an aminoglycoside.

A

Gentomysin, IV only - all aminoglycosides are IV only

66
Q

Give an example of a glycopeptide.

A

Vancomycin

67
Q

Why is vancomycin inappropriate for gram (-)’s?

A

The molecule is too big to fit into the cell wall

68
Q

All the “mycins” are:

A

Protein/ribosome inhbitors

69
Q

What is an example of a lincosamide?

A

Clindamycin, good broad-spectrum antibiotic, can treat community-acquired MRSA, good for cellulitis

70
Q

What are two major drawbacks of the aminoglycosides?

A
  1. Hearing loss, permanent

2. Kidney failure

71
Q

Give an example of a fluoroquinolone.

A

Gyrase inhibitor, ciprofloxacin, bateria-static

72
Q

In what class is ceftriaxone?

A

Cephalosprin, for gonorrhea

73
Q

In what class is azithromycin?

A

Macrolide class, also a ribosome inhibitor

74
Q

When would you use chloramphenicol?

A

To treat rocky mountain spotted fever

75
Q

When might you use linazolid?

A

TO treat VRSA

76
Q

Name two classes of antibiotics that are highly toxic:

A

Polymyxins

Phenicols

77
Q

What antibiotics are in neosporin?

A

Polymyxins
Neomycin
Bacitracin
–highly toxic is absorbed systemically

78
Q

Most proteins imported into the ER lumen or ER membrane (including those destined to other organelles) are converted to:

A

Glycoproteins

79
Q

What is the most common kind of glycosylation, found on 90% of glycoproteins?

A

N-linked glycolsylation

80
Q

What is N-linked glycosylation?

A

Adding of sugars to the NH2 group of an asparagine residue.

81
Q

What enzyme is responsible for the co-translational modification of proteins to proteoglycans in the ER?

A

Oligosaccharyl transferase

82
Q

Why must disulfide bonds be created in the ER lumen?

A

Because the cytosol is too reducing an environment. Catalyzed by **protein disulfide isomerase

83
Q

What will happen to a protein if misfolds numerous times in the ER lumen?

A

They will be degraded by proteasomes in the lumen of the ER.

84
Q

When is the URP, unfolded protein response triggered?

A

If the quality control system becomes overwhelmed and misfolded proteins accumulate in the ER, the UPR signals the ER to expand in size and increase the number of chaperones to help. **If the UPR fails, the cell will be directed to apoptose.

85
Q

___1___ move ____2____ phospholipids from one half of the ER bilayer to the other, thereby redistributing the phospholipids evenly along the bilayer.

A
  1. Scramblases

2. Random

86
Q

Where do flippases act? What is their function?

A

Flippases act in the Golgi membrane. They flip specific phospholipids from one side of the bilayer to another to design any necessary asymmetry for vesicle formation.

87
Q

True or False: The smooth ER is continuous with the rough ER, despite their differing function.

A

True

88
Q

Give an example of a kind of cell that has abundant smooth ER.

A

Leydig cells of the testes that produce testosterone.

Liver cells, because of their role in lipid metabolism.

89
Q

The endoplasmic reticulum serves as the major cellular storage site for:

A

Ca2+

90
Q

Name the two directions in which the clathrin coat is useful in vesicular protection.

A

Outward from the Golgi to the pm, and inward endocytically.

91
Q

Clathrin coats are made up of what 2 major proteins?

A

Clathrin and adaptin, **the adaptins vary from one coat to another, depending in the cargo being moved.

92
Q

What is the function of adaptins?

A

As part of the clathrin coat, they cind the clathrin coat to the vesicle membrane and help to pick out the kind of cargo.

93
Q

What is dynamin and what is its function?

A

Dynamin is a small monomeric G-protein active in the formation of clathrin-coated vesicles. It sits at the neck of the vesicle, and when GTP is hydrolyzed, itpiches the vesicle off of the membrane.

94
Q

When is the clathrin coat dissassembled?

A

As soon as the dynamin effects the pinching off of the vesicle.

95
Q

Transport vesicles display surface markers that identify their origin and cargo, and these markers much be recognized by receptors on the target membranes. The major proteins involved in this recognition step are:

A
  1. Rabs
  2. Tethering proteins
  3. snares
96
Q

Name this protein: A very large subfamily of monomeric GTPases that serve as the molecular markers identifying each membrane type.

A

Rabs

97
Q

Name this protein: They capture transport vesicles for fusion by their interaction with Rabs.

A

Tethering proteins

98
Q

Name this protein: proteins on the vesicular membrane that interact with complementary proteins at the destination membrane.

A

V-snares

99
Q

Name this protein: Interacts with complementary protein on the vesicle to help an incoming vesicle dock.

A

T-snares (for “t”arget membrane)

100
Q

Where are Rabs found?

A

On vesicles

101
Q

Why is vesicular fusion energetically unfavorable?

A

Because it involves the displacement of water by the bilayers.

102
Q

What protein plays the main catalytic role in vesicular docking and fusion?

A

The snares, by wrapping around one another and pulling the vesicle in for it to fuse.

103
Q

The virulence factors for spirochetes are generally intended to achieve:

A

Immune evasion

104
Q

What is a gumma?

A

In tertiary syphilis, you get nodules of collections of spirochetes, like lumps. Can be anywhere in the body

105
Q

Jarisch-Herxheimer reaction may be helpful in diagnosing:

A

Lyme disease or Syphilis (spirochetes)

106
Q

H. Pylori is a __1__ bacteria, however most of these bacteria live __2__ and are __3__.

A
  1. vibrio
  2. in the ocean
  3. halophiles
107
Q

In general cholera lives in ___1___ and is not harmful to humans. If it becomes pathogenic, most pathogenic strains have an O1 ___2___ transmitter by a ___3___

A
  1. plankton
  2. genetic marker that carries virulence factor
  3. lysogenic bacteriophage
108
Q

What is Campylobacter jejunum?

A

Most common source of gastroenteritis/GI upset/foodborne illness

109
Q

What is the virulence factor of note for C. jejunum?

A

Attachment pilus

110
Q

What is the virulence factor in cholera?

A

Mucinase allows cholera to attach directly to the wall of the small intestine

111
Q

Erlichia and Babesiosa are different from Burgdorferi in that:

A

They are worse at hiding from the immune system, and cause high fever.

112
Q

What is erythema migrans?

A

Bulls-eye rash (B. Burdorferi)

113
Q

Syphilisis caused by:

A

Triponema Palladium

114
Q

Treat syphilis with:

A

Penicillin-G.

115
Q

In 2/3 of cases, syphilytic patients will

A

Achieve a latent stage and the disease will not progress. They will remain intermittently infectious for the rest of their life.

116
Q

Of the sexually transmitted infections, which two are professional first-exposure infectors?

A

T. Palladium (syphilis) and N. gonhorrheae

117
Q

What is the promiscuity difference between spirochetes and rods?

A

Spirochetes are LESS promiscuous. They tend not to pick up antibiotic resistance, hence why Penicillin is still effective.

118
Q

What is an unusual but recurring theme regarding the spreading of spirochetes?

A

They cross easily into the bloodstream from Day 1.

119
Q

Name 3 spirochetes:

A

Leptospirosis (environmental)
B. Berdorferi
T. Palladium

120
Q

Why can’t you gram stain T. palladium?

A

Too narrow; use darkfield

121
Q

Lyme disease is famously hard to test for. What follow-up tests to your ELISA would you order for confirmation?

A

Western Blot or PCR.

122
Q

Stage 3 Lyme disease requires treatment with:

A

Ceftriazone, a 3rd generation cephalosporin

123
Q

Name the disease associated with “Can’t see can’t pee can’t climb a tree”

A

Reactive arthritis

124
Q

True or False: The V. Cholera vaccine is effective for 3 to 6 months.

A

True

Unit 1 (5 decks)

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