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Foundations of Medicine > FOM: week 3 > Flashcards

FOM: week 3 Flashcards

1
Q

What are the three shapes of bacteria?

A

Rod (bacillus), circular (cocci), corkscrew (spirochete [flexible], spirillum [rigid])

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2
Q

What are the prefixes for bacterial names and what do they mean?

A

strepto – long chains
staphlo – clumps
palisades – side-by-side, ‘X’, ‘V’, or ‘Y’ figures

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3
Q

What are some of the differences between eukaryotic and prokaryotic cells?

A

Chromosome: single circular (P) vs. paired linear (E)
Extrachromosomal DNA: plasmid (P) vs. Mito/Chloroplast (E)
Site of cellular respiration: cell membrane (P) vs. mitochondria (E)
Ribosomes: 70S (P) vs. 80S (E)

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4
Q

Compare cell envelopes of gram-positive and gram-negative bacteria.

A

Gram-positive: cell membrane with 250 angstoms of peptidoglycan
Gram-negative: cell membrane, 30 angstroms of peptidoglycan, periplasmic space, outer envelope with porins

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5
Q

What is the process of gram-staining?

A
  1. Bacteria are heat fixed to a slide
  2. Crystal violet is added - all cells stain blue
  3. Iodine fixes the stain into the bacterial cell
  4. Alcohol decolorizes gram-neg bacteria (white) while gram-positive remains blue/purple.
  5. Safranin stains the gram-neg bacteria pink in color
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6
Q

What are some unique features of gram-positive envelopes?

A
  1. teichoic/teichuronic acids: polymer of ribitol or glycerol joined by phosphodiester linkages
  2. lipteichoic acid (LTA): lipid attached to teichoic acid – adhesin
  3. polysaccharides: most likely composities of sugars released from teichoic/teichuronic acid
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7
Q

What are some unique features of gram-negative envelopes?

A
  1. lipoproteins: corss-link outer membrane to peptidoglycan
  2. periplasmic space: gel-like matrix that contains enzymes and binding proteins
  3. outer membrane: bilayer containing liposaccharides (LPS) and porins – protect from hydrolytic enzymes
    LPS are made of lipid A (aka endotoxin)
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8
Q

What are some unique features of mycoplasma?

A
  1. have NO CELL WALL – no peptidoglycan

2. cell membrane contains sterols which are required for growth (not synthesized by bacteria)

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9
Q

What are some unique features of acid fast bacteria?

A
  1. have a small amount of peptidoglycan (not able to be detected by gram stain)
  2. contain large amounts of glycolipids – make cell walls impermeable
    - some common glycolipids = liparabinomannan (LAM) and mycolic acids
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10
Q

What is the process of gram-staining?

A
  1. Bacteria are heat fixed to a slide
  2. Crystal violet is added - all cells stain blue
  3. Iodine fixes the stain into the bacterial cell
  4. Alcohol decolorizes gram-neg bacteria (white) while gram-positive remains blue/purple.
  5. Safranin stains the gram-neg bacteria pink in color
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11
Q

What are some unique features of gram-positive envelopes?

A
  1. teichoic/teichuronic acids: polymer of ribitol or glycerol joined by phosphodiester linkages
  2. lipteichoic acid (LTA): lipid attached to teichoic acid – adhesin
  3. polysaccharides: most likely composities of sugars released from teichoic/teichuronic acid
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12
Q

What are some unique features of gram-negative envelopes?

A
  1. lipoproteins: corss-link outer membrane to peptidoglycan
  2. periplasmic space: gel-like matrix that contains enzymes and binding proteins
  3. outer membrane: bilayer containing liposaccharides (LPS) and porins – protect from hydrolytic enzymes
    LPS are made of lipid A (aka endotoxin)
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13
Q

What are some unique features of mycoplasma?

A
  1. have NO CELL WALL – no peptidoglycan

2. cell membrane contains sterols which are required for growth (not synthesized by bacteria)

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14
Q

What are some unique features of acid fast bacteria?

A
  1. have a small amount of peptidoglycan (not able to be detected by gram stain)
  2. contain large amounts of glycolipids – make cell walls impermeable
    -
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15
Q

Bacterial secretion systems play an important role in the function of bacteria. Describe the structure and function of these secretion systems.

A

Protein secretion systems are involved in bacteria interacting with their environment through transporting proteins or nucleic acid outside of the cell, periplasm, or inside host cells. These proteins can be adhesins or toxins that modify host physiology which causes pathology.

Some systems are more complex and have an injectosome which is a transmembrane structure that injects bacterial products.

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16
Q

What are endospores and why/how do they form?

A

In nutrient-limiting conditions (starvation), increased heat, desiccation, and chemical damage endospores result to allow a bacterium to live in harsh conditions. The structure of an endospore is as follows (from inside out): nucleoid, protective cortex, spore coat, and spore wall.
Note: calcium dipicolinate is responsible for endospore’s ability to resist heat.

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17
Q

What are some characteristics of viruses?

A

Viruses are:

  • obligate intracellular parasites (need a host)
  • have either DNA or RNA as viral particle
  • outer coat protects genetic material (protein coat)
  • contains no enzymes, organelles, or other biosynthetic machinery
  • nucleic acids code for proteins needed in viral replication
  • can either be naked (nucleic material + coat/capsid) or enveloped (acquire host membrane)
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18
Q

What are some characteristics of viroids?

A

Viroids are:

  • very small SS circles of RNA
  • cause disease in plants
  • replication strategy is unknown (probably through host)
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19
Q

Dimorphic fungi are?

A

Dimorphic fungi exist as yeast/yeast-like and filamentous forms that are controlled by environmental conditions such as temperature and nutrient supply.
-Yeast form found in body, filamentous form found in the environment

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20
Q

What are some characteristics of fungi?

A

Fungi characterized by:
-eukaryotic organisms
-have cell wall for protection
-ergosterol is dominant membrane sterol
-require preformed organic compounds for growth
-three main types: yeast, mold, mushrooms
Note: yeast and mold cause disease

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21
Q

Yeast, it raises bread but also causes disease. What are some features of yeast?

A

yeast are single celled fungi that reproduce by budding. Some strains produce pseudohyphae.

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22
Q

What are hyphae?

A

Hyphae are long, filamentous structures and are the main mode of vegetative growth. Collectively, hyphae are called mycelium.

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23
Q

Moldy, moldy, mold. What are some features of mold?

A

mold grows in forms called hyphae. Many molds produce cross walls of hyphae called septae.

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24
Q

Dimorphic fungi are?

A

Dimorphic fungi exist as yeast/yeast-like and filamentous forms that are controlled by environmental conditions such as temperature and nutrient supply.

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25
Q

What are spores and why are they important in regards to fungi?

A

Spores are similar to endospores in bacteria in that they form to protect the fungi during adverse conditions. Spores are important in identifying the source of fungi. Some examples include:

  1. Conidia (asexual spores of mold)
  2. Arthroconidia (formed from joints in hyphae then fragementation)
  3. Blastoconidia (yeast cell buds)
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26
Q

Parasites are also sources of disease. What are the two main categories of parasites?

A

Protozoa and Worms

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27
Q

Protozoa are?

A

Protozoa are single cells that exist as trophozoites (mobile) and cysts (static). Some move by flagella and some move by cilia.

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28
Q

Worms cause disease by?

A

Worms usually cause infection upon ingestion or larval or cyst forms. Examples include: trematodes (flukes), cestodes (tapeworms), and nematodes (roundworms).

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29
Q

What are some growth requirements for bacteria?

A

All the elements for organic matter (especially carbon), ions for energy generation, catalysis, and osmotic maintenance. Some species do not require some of the elements.

Anything required by bacterium that is not synthesized by bacterium must be provided/obtained from the host.

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30
Q

Bacteria are classified based on nutritional requirements. What are heterotrophs?

A

Heterotrophs require pre-formed organic compounds like sugars, amino acids, and vitamins.

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31
Q

What are autotrophs?

A

Autotrophs can synthesize everything it needs from inorganic compounds like carbon dioxide.

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32
Q

What are hypotrophs?

A

Hypotrophs are obligate intracellular pathogen requiring the host to provide organic compounds.

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33
Q

How do bacteria multiply?

A

Binary fission

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34
Q

What are the steps of binary fission?

A
  1. replication of DNA
  2. separation of daughter chromosomes
  3. generation of cross-wall
  4. separation
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35
Q

How do bacteria take up nutrients?

A

permeases that are in the cell membrane take up nutrients from the media

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36
Q

What are the three basic permeases in bacteria?

A
  1. Carrier mediated diffusion (facilitated)
  2. Phosphorylation-linked transport
  3. Active transport
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37
Q

Describe the process occurring in a bacterial growth culture.

A
  1. Saturated broth culture used to inoculate fresh media

2. Bacterial counts are taken at different time points and plotted as cell number vs. time

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38
Q

How does phosphorylation-linked transport work?

A

It is an energy-dependent process which requires the generation of a proton-motive force. Protons are pumped out of the cell – requires a symport.

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39
Q

What is doubling time?

A

It is the amount of time that binary fission requires for one cell to become two. It is also called generation time. DOUBLING TIME = GENERATION TIME

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40
Q

What is a bacterial colony?

A

A bacterial colony is tens of millions of individual bacteria from a single organism.

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41
Q

How does a liquid sample bacterial colony count work?

A

A given culture = one colony.

Process:

  1. Make a 10-fold dilution of a culture
  2. Spread a known volume on an agar plate
  3. Allow colonies to grow
  4. Count the number of colonies
  5. Calculate original concentration (at time of sampling)
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42
Q

Describe the process occurring in a bacterial growth culture.

A
  1. Saturated broth culture used to inoculate fresh media

2. Bacterial counts are taken at different time points and plotted as cell number vs. time

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43
Q

How is energy made during fermentation?

A

formation of ATP not coupled to electron transfer

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44
Q

How is energy made during respiration?

A

formation of ATP via oxidative phosphorylation (normal)

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45
Q

How is energy made during photosynthesis?

A

ATP is formed via the reduction of an oxidant via light energy - similar to respiration.

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46
Q

Bacteria metabolize pyruvic acid in different ways but during fermentation they form different end products which indicates which bacterium caused the infection. What do streptococcus, lactobacillus, and bacillus form after fermentation?

A

Lactic acid

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47
Q

Bacteria metabolize pyruvic acid in different ways but during fermentation they form different end products which indicates which bacterium caused the infection. What does saccaromyces form after fermentation?

A

Ethanol and carbon dioxide

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48
Q

Fermentation products from propionibacterium?

A

propoinic acid, acetic acid, carbon dioxide, and H2

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49
Q

Fermentation products from clostridium?

A

Butyric acid, butanol, acetone, isopropyl alcohol, and carbon dioxide

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50
Q

Fermentation product from escherichia, salmonella?

A

ethanol, lactic acid, succinic acid, acetic acid, carbon dioxide, and H2

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51
Q

Fermentation product from enterobacter?

A

ethanol, lactic acid, formic acid, butanediol, acetone, carbon dioxide, and H2

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52
Q

There are 5 basic types of bacteria classified by oxygen requirements. What are obligate aerobes?

A

Obligate aerobes must have oxygen for growth.

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53
Q

What are obligate anaerobes?

A

Obligate anaerobes do not require oxygen and are killed by oxygen radicals generated during metabolism of oxygen.

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54
Q

What are facultative anaerobes?

A

Facultative anaerobes can grow with or without oxygen.

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55
Q

What are microaerophilic bacteria?

A

Microaerophilic bacteria must grow at low concentrations of oxygen (less than 20%)

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56
Q

What are aerotolerant anaerobes?

A

Aerotolerant anaerobes are similar to facultative anaerobes, but prefer anaerobic (fermentative) growth

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57
Q

Can there be a media that is both differential and selective?

A

Yes, MacConkey agar - example: bile salts and crystal violet inhibit gram positive growth and has lactose plus a pH indicator to indicate fermentation of lactose.

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58
Q

What are mesophiles?

A

Mesophiles grow best in the range of 20-40 C

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59
Q

What are thermophiles?

A

Thermophiles grow best in the range of 45-90 C

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60
Q

What is differential growth media?

A

Differential growth media supplies nutrients and indicators (i.e. pH) for visual determination of organisms present

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61
Q

What is selective growth media?

A

Selective media selects AGAINST growth of particular bacteria by the additions of dyes, acid/base, salts, or antibiotics

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62
Q

Can there be a media that is both differential and selective?

A

Yes

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63
Q

Draw the reaction of folate to dihydrofolate to tetrahydrofolate.

A

DHFR used in both reactions and requires the oxidation of NADPH

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64
Q

Draw the reaction of tetrahydrofolate down to methylcobalamin with other supplying reactions.

A

remember that His –> FIGLU –> 5,10-methenyl THF and that Ser–> 5,10-methylene THF

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65
Q

What is the vitamin precursor of THF and cobalamin?

A

THF –> folate

Cobalamin –> vitamin B12

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66
Q

Where is folate found in the diet?

A

Folate is abundant in green leafy vegetables, liver, legumes, yeast, and fortified flour.

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67
Q

Where is vitamin B12 obtained in the diet?

A

Vitamin B12 is found in meat, eggs, and dairy.
Note: Cobalamin has a cobalt group which can either bind a methyl group or adenine nucleotide. It is often involved in methyl transfers.

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68
Q

What is the pathway of vitamin B12 digestion? Draw it out :)

A

What a beautiful drawing!!!

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69
Q

What other reactions are cobalamin involved in? Draw out the reactions please :)

A

methylmalonyl CoA –> succinyl CoA

homocysteine –> methionine

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70
Q

What form of cobalamin is found in circulation and in storage?

A

Circulation: cobalamin complexed with transcobalamin II
Storage: cobalamin complexed with cubillin

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71
Q

Within the conversion of methionine to homocysteine makes S-adenosylmethionine (SAM). SAM then reacts with other substrates. What are some of those?

A 
Norepinephrine --> epinephrine
Guanidinoacetate --> creatine
Nucleotides --> methylated nucleotides
Phosphatidylethanolamine --> phosphatidylcholine
Acetylserotonin --> melatonin
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72
Q

The reaction of Serine to Glycine uses THF and dUMP as substrates. dUMP the is converted to dTMP by thymidylate synthase. Why is this reaction important?

A

dTMP is used as a nucleotide structure for a substrate for DNA synthase.

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73
Q

What is the molecular pathophysiology of spina bifida?

A

Spina bifida is caused by a folate deficiency in pregnancy and is associated with neural tube defects.

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74
Q

How is hyperhomocysteinemia caused?

A

Hyperhomocysteinemia can be caused by either a mutation in methionine synthase, a deficiency in vitamin B12 or a deficiency in vitamin B6. The vitamin B6 comes from PLP - which is involved in making tetrahydrofolate (THF). Due to this defect/deficiency it will result in a build up of homocysteine in the blood.

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75
Q

What is the molecular pathophysiology of pernicious anemia?

A

Pernicious anemia is due to a vitamin B12 deficiency. This is not necessarily a dietary deficiency, but because intrinsic factor is not produced from the parietal cells in the stomach. It can also result because there is a loss of function of transcobalamin II or cubillin. Many cases are caused by autoimmune destruction of parietal cells.

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76
Q

What causes megaloblastic anemia?

A

Megaloblastic anemia is caused by a dietary deficiency of folate because blood cells cannot synthesize enough DNA to replicate their own chromosomes. This causes the cells to grow very large since they cannot divide until their genomes replicate. This disease is characterized by a high turnover rate of RBCs.

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77
Q

What is the cause of hereditary folate malabsorption?

A

Hereditary folate malabsorption is caused by an inherited mutation in the proton coupled folate transporter (PCFT, gene SCL46A1) which causes a functional folate deficiency despite adequate folate in the diet.

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78
Q

How can folate metabolism be a target for cancer treatments?

A

By inhibiting the ability of dihydrofolate reductase (DHFR) to produce THF this causes DNA synthesis to stop and protein translation to halt, thus blocking ways in which cancer cells can replicate and survive. The three main drugs are methotrexate (folate analog), 5-fluorouracil (uracil analog that inhibits thymidylate synthase), and pyrimethamine (used as an antimalarial drug).

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79
Q

What is referred to as the ‘methyl trap’?

A

In the reduction of THF to 5-methyl THF, the only reaction that can be performed once in the 5-methyl THF form is with cobalamin which makes methylcobalamin. When there is a dietary of functional deficiency of cobalamin, the folate becomes “trapped” as 5-methyl THF and is unable to undergo any other reactions. This last step is irreversible.

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80
Q

What are some features of glycogen?

A

Glycogen is a polymer of glucose that has either 1,4 or 1,6 alpha linkages.

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81
Q

How does glycogen function as an organismal glucose buffer in hepatocytes?

A

Hepatocytes degrade glycogen to glucose which is then able to be transported to other tissues for energy.

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82
Q

Draw out the steps of glycogenogenesis.

A

Nice job!

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83
Q

Draw out glycogenolysis degradation.

A

sweet drawing picaso!

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84
Q

What are the key enzymes in glycogen degradation and why?

A
  1. Glycogen phosphorylase - cleaves glucose from glycogen chains and adds inorganic phosphate to G1P. Cannot cleave glucose when it gets within four units of a branch point.
  2. Debranching enzyme - 4:4 transferase (cleaves 1,4 glycosidic bonds), a-1,6 glucosidase (cleaves 1,6 glycosidic bonds)
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85
Q

How is glycogen metabolism regulated?

A

Glycogen metabolism is regulated by phosphorylation of glycogen phosphorylase.
Fed: glycogen phosphorylase (inactive), glycogen synthase (active)
Fasting: glycogen phosphorylase - P (active), glycogen synthase -P (inactive)

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86
Q

How is glycogenolysis and glycogenogenesis regulated in the fasting state in hepatocytes? Draw pathway.

A

:D Yep, epinephrine and glucagon phosphorylate glycogen synthase, glycogen phosphorylase kinase, and glycogen phosphorylase which allows glycogenolysis to occur and shuts down glycogenogenesis.

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87
Q

How is glycogenolysis and glycogenogenesis regulated in the fed state in hepatocytes and skeletal muscle? Draw pathway.

A

Insulin phosphorylates protein phosphatase-1 (active) and glycogen synthase kinase-3 (inactive) which promotes glycogenogenesis. Super job there!

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88
Q

What is the difference between hepatocyte and skeletal muscle in the fasting state?

A

Skeletal muscle does not have glucagon receptors and glycogenolysis can only be activated by epinephrine, nerve impulses, or work done by muscles.

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89
Q

Draw out skeletal muscle’s response in the fasting state to stimulate glycogenolysis.

A

:)

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90
Q

In the glycogen phosphorylase reaction there are two different forms of GP, a and b. What is the difference between these two forms?

A

Glycogen phosphorylase a is phosphorylated by phosphorylase kinase (uses ATP) and glycogen phosphorylase b is dephosphorylated and loses the phosphate as inorganic phosphate. This is an energy loser for the cell!

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91
Q

Draw out glycogenolysis and glycogenogenesis. And show where the GSD mutations occur.

A

good work

92
Q

What is the cause of GSD 0?

A

There’s a defect in glycogen synthase (glycogenogenesis). Results in normal glucose tolerance with variable clinical presentations of exercise intolerance, cardiac and muscle hypertrophy.

93
Q

What is the cause of GSD I?

A

There is a deficiency in glucose-6-phosphatase (only found in hepatocytes in glycogenolysis). This results in a whole body glucose homeostasis problem, fasting hypoglycemia, lactic acidosis, hetpatomegaly (due to glycogen accumulation), hyperuricemia, and hyperlipidemia.

94
Q

What is the cause of GSD III?

A

There is a deficiency in 1,6-glucosidase activity (branching enzyme - glycogenogenesis). Results in fasting hypoglycemia and ketoacidosis, hyperlipidemia, hepatomegaly (elevated levels of AST/ALT).

There are two different isoforms of the disease: GSD IIIa - affects liver and muscle
GSD IIIb - affects only liver

95
Q

What causes GSD IV?

A

GSD IV results in a deficiency of branching enzyme (4:6 transferase - glycogenogenesis). Results in FTT, hepatomegaly, liver failure. This disease is fatal!

96
Q

What causes GSD V?

A

GSD V results in a deficiency of muscle glycogen phosphorylase – glycogenolysis. The physiological effects are late childhood onset of exercise intolerance, myoglobinuria after exercise, increased creatine kinase, exaggerated increase of creatine kinase, and ammonia after exercise.

97
Q

Viruses are …?

A

obligate intracellular parasites – need a host to replicate and cause disease

98
Q

How are viral pathogens classified?

A

They are classified based on their virion structure, nucleic acid material, and replication strategy.

99
Q

What is a virion?

A

it is the infectious virus particle

100
Q

What are the components of a virion?

A

Composed of nucleic acid material (DNA or RNA), has a capsid, and some have envelopes. The capsid can be helical or icosahedral in shape.

101
Q

ssRNA can be either have a positive or negative polarity. What does this mean?

A

Positive polarity = is mRNA that can be directly translated into protein
Negative polarity = mRNA that needs to be transcribed to create a complimentary strand before translation can occur.

102
Q

Genomes can be linear, circular, or segmented. What property does a segmented genome have?

A

Segmented genomes often code for one or more polypeptides necessary for replication.

103
Q

Viral genomes are ________ and retrovirus genomes are ________.

A

haploid, diploid

104
Q

What are the six steps of viral replication?

A
  1. Attachment
  2. Penetration
  3. Uncoating
  4. Virus component synthesis
  5. Assembly
  6. Release
105
Q

Upon release, naked capsids ______ cells and enveloped viruses leave cells _______.

A

lyse, intact (although these cells can be killed due to foreign glycoproteins and VAPs)

106
Q

What is a productive virus infection?

A

This is where cells yield new infectious viruses.

107
Q

What is a non-productive virus infection?

A

This type of infection occurs when viral genetic material persists in a cell (latent state), but no infectious virus is formed.

108
Q

The viral one step growth cycle …?

A

indicates how long it takes an individual virus to infect and replicate within its host cell.

109
Q

What constitutes early proteins?

A

Early proteins are involved in replication of RNA or DNA material and is shut off by regulatory system

110
Q

What constitutes late proteins?

A

Late proteins are the structural proteins of viruses.

111
Q

What are viroporins?

A

Viroporins are small, hydrophobis virus-encoded proteins that oligomerize at host cell membranes where they are involved in enveloped virus budding and non=enveloped virus cellular lysis.

112
Q

What are the cytopathogenic effects of viroporins?

A

Viroporins cause the formation of hydrophilic pores and alterations of calcium and hydrogen gradients.

113
Q

DNA containing viruses are typically replicated in the _________.

A

nucleus

114
Q

What is the class of DNA virus that is replicated in the cytoplasm?

A

poxvirus

115
Q

In order for DNA viruses to replicate, the host cell needs to be in ________. If it isn’t, the virus will form a ___________ ___________ and become latent.

A

S phase; non-productive infection

116
Q

What are some features of Hepadnavirus?

A

Hepadnavirus has a partially ddDNA genome which replicates its DNA in the nucleus via an RNA intermediate. This involves reverse transcription via an RNA-dependent DNA polymerase. This action can transform cells.

117
Q

What kind of disease does Hepadnavirus cause?

A

Hepatitis B

118
Q

How is pregenomic RNA used in Hepadnavirus?

A

Pregenomic RNA is used to make specific signals for production of nucleocapsid proteins, etc.

119
Q

The class of cytoplasmic DNA virus, poxvirus, replicates how?

A

Poxvirus provides its own mRNA and DNA synthetic machinery and codes for viral DNA and is dependent on RNA polymerase. Poxvirus synthesizes its own envelope.

120
Q

RNA viruses replicate typically in the ___________.

A

Cytoplasm

121
Q

ssRNA viruses have either negative, positive or ambisense polarity to their RNA. What unique feature does negative polarity RNA have?

A

All negative sense RNA viruses are enveloped!

122
Q

All ssRNA replicate via __________ intermediate.

A

dsDNA

123
Q

More mutations occur in RNA viruses than DNA viruses because why?

A

Because RNA polymerase is not as accurate in synthesizing genetic material as DNA polymerase.

124
Q

RNA viruses can produce individual peptides because their RNA is ________________.

A

polycistronic

125
Q

Papvavirididae causes ___________________ due to ________________.

A

genital tumors (cervical, vulvar, penile cancers), squamous cell carcinoma; Human papillomaviruses

126
Q

Herpesviridae causes ____________________ due to ________________.

A

Nasopharyngeal carcinoma, African Burkitt’s lymphoma, B-cell lymphoma/cervical carcinoma; EBV virus/herpes simplex type 2

127
Q

Hepadnaviridae causes _________________ due to ________________.

A

hepatocellular carcinoma; Hep B virus

128
Q

Retroviridae causes __________________ due to __________________.

A

adult T-cell leukemia; HTL virus

129
Q

__________ tumor viruses have oncogenic potential for permissive cells. What components are essential for this transformation?

A

RNA –> retroviruses

positive sense RNA and reversetranscriptase

130
Q

How do retroviruses cause transformation?

A
  1. introduction of oncogenes
  2. insertional activation or promoter insertion
  3. transcriptional activation
131
Q

What does virogene mean?

A

A virogene is the combination of genes that a virus needs to replicate.

i.e. HIV virogenes = gag, pol, env, and int

132
Q

What does replication involve in retroviruses?

A

Reserve transcription and integration into DNA of host cell

133
Q

What happens if a virogene is integrated next to an oncogene or a tumor suppressor?

A

The virogene would activate the oncogene and inactivate the tumor suppressor (allow the gene to be expressed). Both of these actions are ways cancer can originate.

134
Q

What are the types of viruses involved in replication for retroviruses?

A
  1. viral oncogenes
  2. non-defective viruses
  3. defective viruses
135
Q

What pathways are viral-oncogenes involved in?

A

v-oncs are involved with cellular division or differentiation pathways

136
Q

What is a non-defective virus?

A

A non-defective virus has all of its virogenes and oncogenes and forms infectious viral progeny. These types of viruses are often implicated in leukemia and Rous sarcoma viruses.

137
Q

What is a defective virus?

A

A defective virus has lost part or an entire virogene which has been replaced by an oncogene. This virus requires a helper virus for replication.

138
Q

Both non-defective and defective viruses are ________ _________________ _______ because they introduce oncogenes which can be turned on in other host cells spreading cancer.

A

acute transforming viruses

139
Q

What are the two mechanisms of oncogenicity?

A
  1. insertional activation or promoter insertion

2. transcriptional activation

140
Q

What does insertional activation entail?

A

This process of oncogenicity occurs randomly, thus is chronic, and involves a viral promoter and transcriptional enhancer in LTRs of cellular oncogenes.

141
Q

What does transcriptional activation entail?

A

Transcriptional activation is a type of oncogenicity that involves a transactivator protein to activate cellular oncogenes. The transactivator protein acts as a transcription factor to encourage gene transcription.
ex. Tax protein of HLTV-1 enhances transcription of IL-2, IL-3, GMCSG, and IL-2 receptor

142
Q

What are bactericidal drugs?

A

Bactericidal drugs result in 99.9% reduction in bacterial inoculums within a 24 hour period of exposure.

143
Q

What are bacteriostatic drugs?

A

Bacteriostatic drugs limit growth and if removed the organism can grow again. These drugs usually are successful because they allow the immune system to catch up and kill the remaining bacteria.

144
Q

What is the better drug to use if a patient is immunocompromised?

A

Since the patient has a compromised immune system, the best drugs to use are bactericidal drugs because the patient’s immune system can’t kill the remaining bacteria.

145
Q

Many bactericidal drugs do not work well if cell are not _________ ___________.

A

actively dividing

146
Q

absorption

A

movement of drug into the vascular system

147
Q

distribution

A

transfer of drug from intravascular to extravascular, blood-brain barrier presents a challenge

148
Q

metabolism

A

irreversible transformation of parent compound into daughter metabolites often in the liver

149
Q

excretion

A

elimination of the drug from the body through urine or feces

150
Q

It is important to treat the patient with the right _______, right ________, and right ________ to kill enough bacteria to eliminate the infection.

A

drug, dose, duration

151
Q

prophylatic

A

treat an infection that has not yet developed in individuals at a high risk of developing an infection

152
Q

pre-emptive

A

have lab test indicating infection but no symptoms. Advantage decreases amount of antibiotics being used.

153
Q

empiric

A

take cultures, patients have an infection with serious potential consequences but the organism has not been identified (broad spectrum)

154
Q

definitive

A

pathogen identified (monotherapy, narrow spectrum drug)

155
Q

suppressive

A

after initial disease is controlled, therapy is continued at a lower dose

156
Q

Antibiotics need to injure the invading organism while causing minimal adverse effects to the host. This means that an organism the is _______ like the host will be better.

A

less

157
Q

therapeutic index

A

high therapeutic index means fewer adverse effects

158
Q

Drugs are classified based on the spectrum of their activity. What are the three types?

A

narrow, extended, and broad

159
Q

What are the forms of resistance that a bacterium can take?

A
  1. increased elimination (efflux pumps - pump antibiotic out of bacteria)
  2. decreased uptake
  3. drug-inactivating enzyme - protein that inhibits enzyme function
  4. alteration in target molecule - resistance plasmid
160
Q

intrinsic resistance

A

an absence or inaccessibility of the target for the drug action to affect that bacteria

161
Q

acquired drug resistance

A

bacteria change their DNA (mutation) or acquire new DNA resulting in resistance

162
Q

One way bacteria can achieve acquired drug resistance is through DNA mediated transformation. What is DNA mediated transformation?

A

It is when bacteria take up neighboring bacterial DNA and integrate it into their genome

163
Q

How do bacteria achieve DNA mediated transformation?

A
  1. bacteriophages use transduction - insert “needle”
  2. conjugation of sex pili - transfer plasmid resistance
  3. transposition - movement of genetic material within genome
164
Q

How does one minimize/prevent drug resistance? What are some strategies?

A
  1. Perform antibiotic susceptibility test - look for minimum inhibitory concentration (MIC)
  2. ask about past/present medications
  3. ensure full regimen on antibiotics is taken
  4. take actions to restore indigenous microbiota through prebiotics and probiotics – boost immune system!!!
165
Q

Draw out purine synthesis pathway.

A

Pathway utilizes folate derivatives and PRPP synthase makes PRPP and is allosterically inhibited by GDP and ADP

166
Q

At what phosphorylation level are nucleotides converted from RNA precursors to DNA precursors?

A

ADP –> dADP; at the diphosphate level

167
Q

What is the important intermediate in purine synthesis?

A

IMP - inosine monophosphate

168
Q

What is the mechanism for conversion from NDP to dNDP?

A

involves a thioredoxin and loss of energy through NADH oxidation (thioredoxin reductase)

169
Q

What are some highlights of purine degradation?

A
  1. only adenosine can be directly phosphorylated to AMP by adenosine kinase
  2. other purine nucleosides must have ribose sugars removed, then added back from PRPP to make monophosphate nucleotides
  3. this process is an energy loser!!!
170
Q

How are pyrimidines synthesized? Draw it out my friend!!

A

remember connection to urea cycle; uses CPS II to convert glutamine, CO2, and 2ATP to carbamoyl phosphate
+ PRPP
- UTP (an end-product)

171
Q

Draw out how UMP becomes UTP, CTP, dCTP, and dTTP. Thanks!

A

Sweet drawing! Remember 5-FU inhibits 5,10-methylene THF in the conversion of dUMP to dTMP

172
Q

Pyrimidine degradation results in what two end products?

A

Cytosine –> uracil –> CO2, NH4, and b-Ala

Thymine –> CO2, NH4, and b-aminoisobutyrate

173
Q

Accumulation of pyrimidine metabolites results in pathology, T or F?

A

False, only accumulation of purine degradation metabolites results in disease

174
Q

Draw out purine synthesis pathway and indicate which enzymes, when defunct, cause disease.

A

Nice, nice

175
Q

What enzyme is deficient in CID? And what are the symptoms of this disease?

A

Enzyme: purine nucleoside phosphoylase (PNP) –> there are two of these enzymes!
Symptoms = low but not absent T-cells, chronic infections, FTT, neurologic symptoms

176
Q

What enzyme is deficient in SCID? And what are the symptoms of this disease?

A

Enzyme: adenosine deaminase (ADA) –> leads to accumulation of 2-deoxyadenosine which is toxic to lymphocytes
Symptoms = low lymphocyte count, costrochondral junction dysplasia

177
Q

What enzyme is deficient in Lesch-Nyhan Disease (LND)? And what are the symptoms of this disease?

A

Enzyme: hypoxanthine-guanine phosphoribosyltransferase (HGPRT- He’s got purine recycling trouble)
This is an X-linked syndrome.
Symptoms = elevated uric acid, mental retardation, dystonia, recurring vomiting, self-inflicted injuries
Treatment = allopurinol

178
Q

What enzyme is targeted in gout treatment? And what are the symptoms of this disease?

A

Enzyme: xanthine oxidase, treated with allopurinol

Symptoms = accumulation of uric acid in distal joints

179
Q

What enzyme is deficient in hereditary orotic aciduria? And what are the symptoms of this disease?

A

Enzyme: UMP synthetase
Symptoms = megaloblastic anemia, delays in physical and intellectual development
Treatment = uridine supplements

180
Q

What are the stages of bacterial pathogenesis?

A
  1. Transmission from an external source into the body
  2. Evasion of initial host defenses (immune system)
  3. Attachment to mucous membranes
  4. Colonization at attachment site
  5. Sometimes spread and reattachment
  6. Disease symptoms caused by toxins or tissue invasion followed by inflammation
  7. Non-specific and specific immune host responses
  8. Progression or resolution of the disease
181
Q

What three bacterial mechanisms cause disease?

A
  1. tissue invasion followed by inflammation
  2. toxins (exotoxins and endotoxins)
  3. immunopathogenesis
182
Q

What is a virulence factor?

A

A virulence factor consist of the properties of a bacterium which assist in causing disease

183
Q

What are some examples of virulence factors in bacteria?

A
  1. Bacterial Structures: pili, biofilms, glycocalyx, bacterial secretion systems, exotoxins/endotoxins
  2. Secreted enzymes: collagenase and hyaluronidase, coagulase, IgA protease
  3. Other bacterial factors: A protein, pathogenicity islands (PAIs)
184
Q

What is the structure of an exotoxin?

A

Exotoxins have an A and B subunit structure.
A = toxic activity
B = binding to receptor/cells

185
Q

What are toxoids?

A

Toxoids are made when exotoxins are treated with formaldehyde and/or heat –> made into vaccines

186
Q

What are the five biological effects of exotoxins?

A
  1. alter cellular components
  2. superantigens
  3. inhibit protein synthesis
  4. increase synthesis of cAMP
  5. alter nerve impulse transmissions
187
Q

What two mechanisms to exotoxins take to administer their toxin to host cell?

A
  1. exotoxin is released from endosome due to low pH and B subunit generating a hole for the A subunit to leave
  2. exotoxin is delivered via an injectosome
188
Q

What is the mechanism of Diphtheria toxin infection?

A

A and B subunits are enclosed in an endosome. When B subunit binds it releases the A subunit into cytoplasm which inactivates eF2 which is used in translation in eukaryotes. This action blocks ADP ribosylation of eF2.

189
Q

What is an endotoxin?

A

An endotoxin is considered to be a toxin kept “within” the bacterial cell until the bacterial cell wall is destroyed. Endotoxin is usually synonymous with lipopolysaccharides (LPS).

190
Q

What are some biological effects of endotoxins?

A

Fever, shock, hypotension, disseminated intracellular coagulation, release of endogenous pyogenes, increased vascular permeability

191
Q

innate immunity

A

immunity achieved from the immune system through the work of macrophages and complements – these assist the host immune cells and utilize antibodies to lyse bacteria and virus-infected cells

192
Q

acquired immunity

A

antibodies and cytotoxic cells that result as products from a previous infection – kill antibody-coated bacteria and virus-infected cells

193
Q

passive immunity

A

administration of preformed antigen-specific antibodies to protect against disease

194
Q

active immunity

A

administration of specific antigens to stimulate an individual to develop immunity to protect against disease ex. vaccines

195
Q

What two obstacles do bacteria have to evade in the immune system?

A

Bacteria have to evade both the innate immunity and acquired immunity of the host.

196
Q

How do bacteria evade innate immunity?

A
  1. avoid contact with phagocytes
  2. inhibition of engulfment
  3. survival within the phagocyte
197
Q

How do bacteria evade acquired immunity?

A
  1. Antigenic variation - bacteria spontaneously change surface protein profile –delay in immune response (have to make anitbodies)
  2. immunological disguise - bacteria coat themselves with host proteins (disguise as ‘self’)
198
Q

What are the most common symptoms associated with C. difficile?

A

Diarrhea, colitis, pseudomembranous colitis, nausea, abdominal pain, fever (inflammatory response), loss of appetite

199
Q

What other infections present with similar symptoms as C. diff?

A

Cholera and E. coli present with diarrhea, viruses, lactose intolerance

200
Q

What tests are used to diagnose C. diff infection?

A
  1. gram- stain (should be positive)
  2. PCR for toxins A+B
  3. GDH tesing
  4. Toxin A immunoassay
  5. Toxigenic culture
  6. stool culture
  7. molecular test to detect B toxin
  8. ELISA
  9. C. diff cytotoxin neutralization assay
201
Q

What is the pathophysiology of C. diff?

A

C. diff vegetative cells and spores are ingested, most vegetative cells are killed in stomach (acidic), spores go into small intestine where bile acids allow the spore to become vegetative cells again. These cells adhere to the colon epithelial cells and then toxin A and B are produced which cause opening of epithelial cell junctions, inflammation, and epithelial cell apoptosis. Hydrolytic enzymes are produced and result in colitis and pseudomembranous colitis and watery diarrhea.

202
Q

What are potential treatments of C. diff?

A

Metronizadole - causes free radicals to kill bacterial cells
Vancomycin - cell wall inhibitor and targets D-alanyl-D-alanine
Fidaxomicin - used for recurrent infections of C. diff
Fecal transplant - restore native microflora

203
Q

What are the four ways bacteria can transfer genes to other bacteria?

A
  1. Transduction
  2. Transformation
  3. Transposition
  4. Conjugation
204
Q

What does transduction mean?

A

It involves the transfer of bacterial chromosomal DNA in a bacterial virus (phage) from a dead host cell to a live host cell

205
Q

What does generalized transduction do?

A

Generalized transduction is involved in transferring random genes from bacteria to bacteria via a phage virion that integrates in the first bacteria’s DNA at random.

206
Q

What does specialized transduction do?

A

Specialized transduction is involved in transferring a specific gene to a second bacteria. This is done because the phage integrates in the first bacteria’s DNA at a specific site.

207
Q

Transduction involves the use of phages. What is a virulent phage?

A

A virulent phage infects bacterium and replicates, killing the bacterium in the process.

208
Q

Transduction involves the use of phages. What is a temperate phage?

A

A temperate phage infects a bacterium and can either replicate, killing the bacterium or integrate into the bacterial chromosome and become replicated with the bacterial genome.

209
Q

Temperate phages are allowed to remain dormant due to a ___________ __________ that can be degraded by _____-_______ or ________.

A

phage protein; UV-light, heat

210
Q

Temperate phages, once out of repression undergo induction. What is induction?

A

Induction is when the phage cuts itself out of the host DNA. Following this, replication occurs and the bacterium is lysed (killed).

211
Q

What does transformation mean?

A

Transformation involves the transfer of naked bacterial chromosomal DNA from a dead cell to a living cell.

212
Q

How does transformation occur?

A

A bacterium dies and releases its DNA and another bacterium is able to take up the other bacterial DNA for incorporation into its genome. This requires a competence factor to take up new DNA.

213
Q

What does conjugation mean?

A

Conjugation involves the transfer of bacterial chromosomal DNA through a pilus from a living cell to a living cell.

214
Q

How does this transfer via conjugation occur?

A

F factors are transferred between bacteria via conjugation through sex pili.

215
Q

What is an Hfr bacterium?

A

Hfr bacterium have an F factor that is integrated into the host chromosome and can be transferred upon replication if lasts longer than 90 minutes (F factor replicated last).

216
Q

What is an F+ bacterium?

A

An F+ bacterium is when the F factor is free within the cytoplasm.

217
Q

What is an F- bacterium?

A

F- bacterium is a bacterium without an F factor.

218
Q

What is an F’ bacterium?

A

F’ bacterium is a bacterium that has an F factor that carries a piece of host chromosomal DNA.

219
Q

An F factor acts similarly to a _____________ and ___________ and it can integrate into host DNA at ____________ sites.

A

transposon, resistance transfer factors (RTFs); specific

220
Q

What does transposition mean?

A

Transposition involves the transfer of DNA sequences from one DNA site to another. Plasmids can be involved in this DNA transfer too.

221
Q

What is a transposon?

A

A transposon is the mobile genetic element involved in transposition. It can carry genes that confer antibiotic resistance in addition to may others. It has sequences of DNA that recognize complementary sequences in other DNA and hop from one complementary sequence to another.

222
Q

What are transposons called when they collect antibiotic resistance genes?

A

resistance transfer factors (RTFs)

223
Q

What other types of transposons are common in bacteria besides RTFs?

A

Integrons and pathogenicity islands

224
Q

What are some features of integrons?

A

They consist of insertion sequences, transposase, and antibiotic resistance genes (can have other virulence factors though too).

225
Q

What are some features of pathogenicity islands (PAIs)?

A

PAIs can have different virulence factors and are usually found adjacent to tRNA genes. They also are commonly found in gram-negative bacteria.

Foundations of Medicine (8 decks)

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