Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
31 Cards in this Set
- Front
- Back
|
List the (5) major modes of action (targets) of antimicrobial drugs.
|
1. Inhibition of cell wall synthesis.
2. Inhibition of protein synthesis. 3. Inhibition of Nucleic acid synthesis. 4. Injury to plasma membrane. 5. Inhibit the synthesis of Essential Metabolites. |
|
|
Describe: Inhibition of cell wall synthesis.
|
-Peptidoglycan (PGC) is found only in bacterial cell walls (animals do not have PGC/cell walls).
-Penicillin (PCN)prevents the synthesis of PGC, weakening the walls and the cell undergoes lysis. |
|
|
Describe: Inhibition of protein synthesis.
|
This affects the ribosomes b/c antibiotics (ABX) target the 70S ribosomes. We (eukaryotes) have 80S ribosomes, so it does not affect our cells.
|
|
|
Describe: Inhibition of Nucleic acid synthesis.
|
No DNA replication.
|
|
|
Describe: Injury to plasma membrane.
|
Antibacterial & anti-fungal drugs.
Polymyxin B and bacitracin cause damage to plasma membranes. |
|
|
Describe: Inhibit the synthesis of Essential Metabolites(any chemical involved in metabolism).
|
Sulfonamides competitively inhibit folic acid synthesis.
Sulfa drugs prevent the production of folic acid by combining with the drug instead of PABA. We (humans) don't produce folic acid, we ingest/eat it. |
|
|
Why are there so few chemotherapeutic agents to treat viral, fungal, protozoal, and helminthic infections?
|
We don't have many drugs for viral infections b/c these medications have to target our own host cells in order to kill the virus.
There are a few anti-fungal medications for athlete's foot and helminthic (ringworm) infections. |
|
|
What is a "Magic Bullet"?
|
A magic bullet kills the pathogen without harming the host.
|
|
|
Explain the selective toxicity of sulfa drugs, PCN, protein synthesis inhibitors, and Isoniazid.
|
Toxicity of the following drugs:
-Sulfa: prevents the production of folic acid -PNC: prevent the production of PGC in cell walls -Protein synthesis inhibitors: targets the 70S ribosomes. -Isoniazid: inhibits the synthesis of mycolic acids (Mycobacteria causes TB) |
|
|
What is a natural ABX?
|
PNC-G is a naturally made ABX. However, PNC-G cannot be taken orally b/c the stomach acids break it down; it is given by injection only.
|
|
|
What are semisynthetic ABXs?
|
Semisynthetic ABX means that there is some sort of alteration made. Semisynthetic PCNs are made in the laboratory by adding different side chains onto the B-lactam ring made by the fungus. These types are resistant to penicillinases and have a broader spectrum of activity than natural PCNs.
|
|
|
Why use semisynthetic ABXs?
|
Semisynthetic ABXs are used b/c:
-Are effective against more strains of bacteria(broad-spectrum) -Resistant to ABX resistance. -Administered orally instead of through an injection. -When taken orally, the medication flushes out through the urine and helps to treat UTIs. |
|
|
Explain the advantages and disadvantages of broad-spectrum ABXs.
|
-Advantages of broad-spectrum ABX: effective against more bacteria strains.
-Disadvantages: Upsets the normal flora; doesn't target exact bacteria. |
|
|
What is an opportunistic pathogen?
|
An opportunistic pathogen is a pathogen that usually takes advantage of a compromised system, i.e., had a prior illness/weakened immune system.
|
|
|
What is a primary pathogen?
|
Primary pathogen: will cause disease in an otherwise healthy individual.
|
|
|
Why does superinfection by Candida albicans(underlined) often occur after treatment with ABXs?
|
This occurs b/c ABX take out the bacteria and upsets the normal flora; all that is left is the yeast (there is no competition) and it grows inhibited.
|
|
|
Compare the terms bacteriocidal and bacteriostatic.
|
-Bactericidal: kills the bacteria.
-Bacteriostatic: inhibits the growth of the bacteria. |
|
|
How can bacteriostatic drugs result in the elimination of a bacterial infection?
|
Bacteriostatic drugs inhibit the new bacteria to grow and slows down the process, allowing the Immune System to catch-up and takeover.
|
|
|
List the (4) major mechanisms of resistance to antimicrobial drugs.
|
1. Inactivation of ABX: example- breaks up the B-lactam ring and the bacteria is no longer toxic.
2. Exclusion: example- keeps it out of the cell walls, doesn't let it in (porins). 3. Alter (the target: example- protein inhibitor synthesis; ribosome mutation occurs and protein is not going to fit in. 4. Ejection: get it out before it can take effect (where?) In the plasma membrane; ATP/protein transports. |
|
|
Who becomes resistant to the ABX: the patient or the bacterium?
|
The microbe developed the resistance, not the patient.
|
|
|
Compare PCN resistance and PCN allergy.
|
-PCN resistance is when the microbe develops a resistance to it.
-Whereas, PCN allergy happens once an antibody against the hapten has been formed. This drug is not antigenic by itself, but some people will develop an allergic rxn to it. Allergic rxns are a type of immune response. |
|
|
If someone is allergic to PCN what other ABXs are they likely to be allergic to?
|
If allergic to PCN, will also be allergic to Ampicillin, Amoxycillin, and Keflex (Cephalosporin).
|
|
|
How does natural selction explai the increase in ABX resistance in recent decades?
|
-Populations are composed of diverse individuals.
-Organisms that are better adapted to local conditions leave more offspring. -Some of these will inherit these better favorable characteristics. -Thus, these favorable traits increase in the population. |
|
|
Antibiotic (ABX)
|
An antimicrobial agent, usually produced naturally by a bacterium or fungus.
|
|
|
Broad-spectrum ABX
|
An ABX that is effective against a wide range of both gram (+) and gram (-) bacteria.
|
|
|
Chemotherapeutic agent
|
A chemical (drug) used in the treatment of disease.
|
|
|
MRSA
|
Strains of S. aureus(underlined) developed resistance to methicillin.
-MRSA: methicillin resistant Staphylococcus aureus(underlined) |
|
|
superinfection
|
The growth of a pathogen that has developed resistance to an antimicrobial drug being used; the growth of a opportunistic pathogen.
|
|
|
VRE
|
Vancomycin-resistant Enterococcus spp.(underlined)
|
|
|
Who discovered the first chemotherapeutic agent?
|
Ehrlich discovered Salvarsan, which was used to treat syphilis.
|
|
|
Selective toxicity
|
The property of some antimicrobial agents to be toxic for a microorganism and non-toxic for the host.
|
