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MSK Midterm > Pharmocology > Flashcards

Pharmocology Flashcards

0
Q

Define antibiotics.

A

an antimicrobial agent of microbial orgin

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1
Q

Define chemotherapy.

A

the treatment of disease with antibiotics and other chemical agents (chemotherapeutic agents).

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2
Q

Antibiotic characteristics (4)

A
  1. microbial origin
  2. low molecular weight (bc microbes are also small)
  3. specific spectrum of activity (broad or narrow)
  4. specific mechanism of action (determines spectrum)
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3
Q

What is meant by the generation of an antibiotic?

A

Generations group antibiotics by antimicrobial properties. Successive generations have increasingly broad spectra due to chemical modification of the drug to increase the spectrum of activity and/or resistance patterns.

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4
Q

How can turbidity illustrate drug effectiveness?

A

Turbidity is a measure of the cloudiness. A drop off in the presence of an antimicrobial agent would indicate the agent had lysed the bac cell. Not as informative a measure as viability (any drop off indicates death of microbes).

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5
Q

What are the tenants of selective toxicity? (3)

A
  1. Absence of target from the host (drug meant to kill microbe won’t also kill host)
  2. Permeability differences (drug can be taken up much more by microbe than host cells)
  3. Structural differences in the target: allows for specificity, or variation may challenge the spectrum of activity
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6
Q

Identify the methods of susceptibility testing, and what info they give.

A
  1. Plate dilution method: determine min. inhibitory concentration of a drug.
  2. Tube dilution method: determine the MIC of a bactericidal drug
  3. Broth microdilution method: determine MICs of multiple drugs, and sensitivities of particular concentrations
  4. Disc diffusion method: determine the MIC of a drug against a given bacterial isolate; can test multiple antibiotics on a single plate; can’t tell you if the drug is bactericidal or bacteriostatic
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7
Q

Bacteriostatic agents vs bactericidal agents?

A

Bacteriostatic: reversibly inhibit bacterial growth; often resemble metabolite analogs and act as competitive inhibitors

Bactericidal: lethal; may or may not cause cell lysis; generally only effective against growing cells

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8
Q

What are the factors which can limit the success of chemotherapy? (3)

A
  1. Location of bacteria (can’t get to it, or the environment where the bac is adversely affects the drug)
  2. Abcess formation and necrosis (limits access of the drug, and natural immune response
  3. the presence of foreign bodies and obstructions
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9
Q

Define the 4 possible types of drug interaction.

A
  1. Indifference: combined effect is not greater than the more effective drug alone.
  2. Additive response: combined effect is only slightly better than the more effective drug
  3. Synergism: the combined effect is significantly more effective than either of the drugs alone (2 bactericidal drugs)
  4. Antagonism: the presence of the second drug actually inhibits the more effective drug (a bactericidal and a bacteriostatic)
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10
Q

What are the mechanisms of antibiotic resistance? (3)

A
  1. Intrinsic: the target on which the antibiotic works is missing
  2. Acquired: spontaneous mutation, horizontal gene transfer
  3. Selective pressure: treatment with an antibiotic selects for those bac which have acquired resistance
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11
Q

Major modes of action for antibiotics (3)

A
  1. target an essential metabolic pathway
  2. target nucleic acid synthesis (transcription/DNA replication)
  3. disrupt bacterial membranes
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12
Q

Contrast eukaryotic and prokaryotic ribosomes.

A

Eukaryotic are larger, originate in the 80S protein that split into the 60S and 40S large and small subunits. Prokaryotes have a 70S that divides into a 50S and 30S large and small subunits.

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13
Q

What are the inhibitors of amino acid activation in proteins?

A

There are none that are clinically significant.

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14
Q

What drugs inhibit the formation of initiation complexes (protein synthesis) in bacteria?

A

Linezoid (Zyvox) of the oxazolidinone class of antibiotics. It binds to the 30S complex and prevents formation of the N-formylmethionyl-tRNA-mRNA-70S ribosomal ternary complex. Only approved for treatment of Gram positive bacteria.

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15
Q

What drugs inhibit the recognition step of peptide chain synthesis in bacteria? (3)

A
  1. Aminoglycosides (esp. Streptomycin)
  2. Spectinomycin
  3. Tetracyclines
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16
Q

What is Spectinomycin?

A
  • inhibitor of recognition
  • bacteriostatic
  • causes unstable 70S initiation complexes
  • exclusively treat gonorrhea in patients allergic to penicillin
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17
Q

What are the mechanisms of action of streptomycin? (3)

A
  1. Misreading (insertion of incorrect amino acid)
  2. Cyclic polysomal blockade (binds to 30S, makes the 70S unstable so that it falls apart –> bacterial cell death)
  3. Faulty outer membranes (translational misreading –> mutant outer membrane proteins weaken the membrane –> makes opportunity for more drug to attack the 30S subunit).
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18
Q

What is one of the drawbacks of using Aminoglycoside antibiotics?

A

they induce bacterial biofilm formation; makes bacterial much more resistant and difficult to kill.
- they can also cause balance or hearing problems, especially when combined with Furosemide

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19
Q

The steps of bacterial protein synthesis

A
  1. Amino acid activation: AA side chains bind to tRNA
  2. Formation of initiation complexes (30S and 70S)
  3. Polypeptide chain synthesis (4 steps: recognition, peptidyl tranfer, translocation, and release)
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20
Q

What are Tetracyclines?

A
  • broad spectrum antibiotic
  • bacteriostatic
  • inhibitor of recognition
  • hydrophobic
  • used for the treatment of Chlamydia, Mycoplasma, Rickettsia, G+, G-
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21
Q

What are the inhibitors of peptidyl transfer in bacteria? (2)

A
  1. Chloramphenicol

2. Lincomycin and Clindamycin

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23
Q

What drugs inhibit translocation in bacteria? (3)

A
  1. Macrolides
  2. Ketolides (esp. Telithromycin)
  3. Streptogramins (Dalfopristin, Quinupristin, & Synercid)
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24
Q

What is another name for penicillin?

A

Beta-lactam antibiotics

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25
Q

Explain the mechanism of synergism between sulfa drugs and trimethoprim.

A

Sulfa drugs inhibit the synthesis of folic acid by acting as a competitior with p-aminobenzoic acid for co-enzymes such as tetrahydroformyl folic acid. Trimethoprim blocks the utilization of folic acid (e.g., by inhibiting dihydrofolate reductase).

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26
Q

What is the mechanism of beta-lactam antibiotics?

A
  • broad spectrum; bactericidal
  • interacts with penicillin-binding proteins once it has penetrated the outer membrane and activates autolysin that degrades the cell wall murein
  • humans have no comparable structure (completely insensitive to the drug)
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27
Q

What are some general concerns about intolerance of certain drugs?

A
  • allergies
  • creating selective pressure and resistant bac
  • broad sprectrum; can kill normal flora –> colitis, infection by an opportunistic bac/fungi
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28
Q

What are 3 general steps in antimicrobial drug action?

A
  1. Associate w bacteria and penetrate the envelope
  2. Transported to an intracellular site of action
  3. Bind to specific biochemical target
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29
Q

What are some of the major beta-lactams to know by name? (3)

A
  • penicillin
  • cephalosporin
  • carbepenem
30
Q

What are the characteristics of sulfa drugs?

A

AKA sulfonamides

  • broad spectrum
  • bacteriostatic drugs
  • block folic acid synthesis (humans don’t make it, get it preformed in diet); but bac can still use any stored folic acid
  • specifically inhibit dihydropteroate synthetase (competes w p-aminobenzoic acid)
  • often used w trimethoprim (blocks utilization of folic acid)
31
Q

What are the characteristics and typical use of p-aminosaliclic acid

A
  • mechanism similar to sulfonamides

- effective against Mycobacterium tuberculosis (sulfa drugs are not)

32
Q

Discuss selective toxicity of sulfa drugs and trimethoprim.

A
  • Sulfa drugs: humans do not make folic acid, get it pre-formed in diet
  • trimethoprim: there are sufficient structural differences between bacterial and host dihydrofolate reductatses
33
Q

What are the characteristics of Rifampin and Rifabutin?

A
  • bactericidal antibiotic
  • inhibit initiation of transcription in bacteria
  • narrow spectrum: G+ bac (Staph and Strep), Neisseria, and Mycobacteria
  • Mech: binds to beta subunit of RNA polymerase, inhibits transcriptional initiation but not transcription already in progress
34
Q

What are the characteristics of Quinolones?

A
  • bactericidal antibiotics
  • inhibit DNA replication via bacterial DNA gyrases and/or topoisomerase IV
  • some are narrow spectrum (e.g., Nalidixic acid); used for UTIs from G- bac
  • Many more broad spectrum (against Pseudomonas)
35
Q

What are the characteristics of Metronidazole?

A

AKA Flagyl

  • bactericidal antibiotic
  • disrupts DNA structure; causes secondary mutations
  • given inactive form, metabolized into active form by bacterial enzymes
  • narrow spectrum: anaerobic infections (H. pylori)
36
Q

Which antibiotics affect bacterial nucleic acid synthesis? (3)

A
  1. Rifampin and Rifabutin
  2. Quinolones
  3. Metronidazole (Flagyl)
37
Q

What are the characteristics of Polymyxins Colistin?

A

AKA Polymyxin E

  • bactericidal antibiotic
  • affects bacterial cell membranes
  • narrow spectrum: primarily for Pseudomonas infections
  • Mech: hydrophobic tail inserts into cell membrane, hydrophilic head binds to PE and LPS (which we don’t have) –> disrupts membrane
38
Q

What does Vancomycin inhibit?

A
  • It prevents transglycosylation (disaccharide linking) by steric hindrance
  • impt for multi-resistant Staph and Enterococcus infections
  • serious side effects
  • resistance: the target (D-ala-D-ala) is altered
39
Q

What inhibits transpeptidation?

A

Beta-lactam molecules inhibit the enzymes (transpeptidase & carboxypeptidase, AKA penicillin binding proteins) that cross-link peptides in the peptidoglycan layers, which halts cell wall synthesis

40
Q

Distinguish eukaryotic and prokaryotic ribosomes, and identify the exception.

A
  • Prokaryotic is designated 70S, made up of 50S and 30S.
  • Eukaryotic is 80S, made up of 60S and 40S.
  • eukaryotic mitochondrial ribosomes more like prokaryotic
41
Q

What are the components of prokaryotic ribosomes?

A
  • large subunit (50S) is made up of 2 rRNA molecules (5S and 23S) and 31 diff proteins (L1-L31)
  • small subunit (30S) is made up of 1 rRNA molecule (16S) and 21 diff proteins (S1-S21)
42
Q

What are the steps of protein synthesis in prokaryotes/bacteria? (3)

A
  1. amino acid activation
  2. formation of initiation complexes (30S & &70S)
  3. polypeptide chain synthesis
43
Q

Identify Chloramphenicol and its mechanism of action.

A
  • inhibits peptidyl transfer (protein synthesis) in bacteria
  • Mech: binds refersibly to 50S and alters tRNA structure, blocking the peptide bind formation
  • broad spectrum bacteriostatic
  • not used clinically in the US
44
Q

Identify Lincomycin and Clindamycin and their mechanism of action.

A
  • inhibits peptidyl transfer (bacterial protein synthesis)
  • Mech (probably): binds refersibly to 50S and alters tRNA structure, blocking the peptide bind formation; similar to Chloramphenicol
  • narrow spectrum bacteriostatic
  • Clindamycin v. effective for staph and anaerobic (Bacteroides) infections
45
Q

Identify Macrolides and their mechanism of action.

A
  • includes erythromycin
  • inhibits translocation (bacterial protein synthesis)
  • mech: unclear, but likely prevents elongation, release of empty tRNA, or blocks transpeptidation
  • has a characteristic 12-22 carbon lactone rings
  • medium spectrum bacteriostatic
  • used w penicillin allergy or beta-lactamase producing bac
46
Q

Identify Ketolides, the most common example, and the mechanism of action.

A
  • inhibits translocation in bacterial protein synthesis
  • binds within the exit tunnel of the 50S and prevents the peptide from leaving
  • can be bactericidal or bacteriostatic depending on bacterium
47
Q

Identify Streptogramins, the 3 examples, and the mechanism of action for each.

A
  • all inhibitors of translocation (bacterial peptide synthesis
  • Dalfopristin: binds to 50S, prevents elongation, & facilitates binding of Quinupristin to 50S; bacteriostatic
  • Quinupristin: binds to 50S; causes premature release of peptide chains from ribosomes; bacteriostatic
  • Synercid: Dalfopristin and uinupristin combined; combo is bacteriocidal
48
Q

Identify the antibiotics which inhibit the release of empty tRNA during bacterial protein synthesis.

A

There are none for this step specifically.

49
Q

What are the mechanisms of antibiotic resistance for aminoglycosides? (3)

A
  • altered target in 30S
  • decreased uptake into cell
  • enzymatic modifications of the drug (acetylation, adenylation, or phosphorylation)
50
Q

What are the mechanisms of antibiotic resistance for tetracyclines? (3)

A
  • decreased uptake (often due to mutations in the OmpF porin)
  • efflux from bac cell
  • elongation factor-like proteins that protect the 30S
51
Q

What is the main mechanism of antibiotic resistance for chloramphenicol?

A

a plasmid-encoded acetyl transferase that causes acetylation of -OH groups; prevents 50S binding

52
Q

What is the main mechanism of antibiotic resistance for Lincomycin and Clindamycin?

A

methylation of 23S (rRNA molecule on 50S) which prevents drug binding to 50S

53
Q

What are the mechanisms of antibiotic resistance for macrolide resistance? (3)

A
  • methylation of 23S on 50S which prevents binding of the drug
  • hydrolysis of the lactone ring by an esterase
  • efflux of the drug
54
Q

Acetylcholine is the main neurotransmitter for which nerves?

A
  • all preganglionic autonomic fibers
  • most postganglionic parasympathetic fibers
  • a few postganglionic sympathetic fibers (the neurotransmitter for most of these is norepinephrine)
55
Q

What is the action of acetylcholinesterase?

A

Terminates the activity of acetylcholine within the synapse.

56
Q

AChE (Acetylcholinesterase) is a member of what class of enzymes and why?

A

It is a serine hydrolase, so named because the reaction intermediate is bound to the serine, then released when water attacks serine, releasing the product and regenerating the Ser side chain.

57
Q

What is the limiting factor on the rate of AChE reactions?

A

They react so fast that they are diffusion-limited, meaning they use up substrate as soon as it can enter the system.

58
Q

What are the two cholinesterases relevant to humans?

A

Acetylcholinesterase (AChE) and plasma cholinesterase (AKA butyrylcholinesterase, pseudocholinesterase)

59
Q

The sympathetic and parasympathetic nervous systems are classified under what larger heading, and what is the shorthand for differentiating them?

A

Both fall under the autonomic (involuntary) nervous system of the PNS. The sympathetic causes the body’s flight/fight reaction (e.g., increasing heart rate, decreasing blood flow to GI tract), and parasympathetic returns the body to its resting state (e.g., lowering heart rate and resuming normal digestion).

60
Q

What does Linezolid inhibit and what is its mechanism?

A
  • AKA Zyvox

- inhibits the formation of initiation complex (bacterial protein synthesis)

61
Q

Daptomycin

A
  • Disrupts cell membrane
  • Inserts lipophilic tail into cell membrane and binds PE & LPS.
  • Forms pore for ions (leads to osmotic death; bactericidal)
  • Not toxic to us; we don’t have LPS, PE
  • Treatment for G+ and MRSA
62
Q

What are 2 major mechanisms of resistance against beta-lactams?

A
  1. Beta-lactamase (penicillinase); presence of an enzyme to render drug inactive.
  2. Gene MecA (PBP2’); alters the transpeptidase so it can’t bind
63
Q

What does bacitracin inhibit and what is its mechanism?

A
  • Inhibits cell wall synthesis (just like vancomycin)

- stops export of PG components across the cell membrane

64
Q

What makes up augmentin, and how are bacteria becoming resistant to it?

A
  • Aumentin: amoxicillin + claulanic acid

- resistance: alter 30S target, decrease uptake, modify drug (inactivation)

65
Q

Coagulase is another name for what?

A

Metronidazole

66
Q

Triazoles

A
  • more broad spectrum
  • infection is more systemic
  • taken orally
  • liver toxicity concerns
  • inhibits urgosterol
67
Q

Imidazoles

A
  • superficial or system anti-fungal
  • given topically
  • inhibits urgosterol
68
Q

What are the symptoms for a cholinergic crisis?

A

SLUDGEM:

  • Salivation
  • Lacrimation
  • Urination
  • Defication
  • GI upset
  • Emesis
  • Miosis
69
Q

What will cause a cholinergic crisis?

A
  • organophophate poisons: pesticides/insects (malathion), nerve gas (sarin)
70
Q

When would anti-cholinesterases be given?

A

After someone has overdosed with an anti- (e.g., anti-histamines), or when waking them up from anesthesia

MSK Midterm (9 decks)

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