break up Flashcards

1
Q

adverse drug reactions

A

can be considered a form of toxicity, can be dose related, can be allergic, can be idiosyncratic.
can be severe, mild, moderate, or fatal

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2
Q

what are drug residues and the importance

A

drugs given to animals can end up in food. however more likely that a microbial contamination occurs. there a residues monitoring program. NOEL
residues can be prevented if simples rules are followed

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3
Q

rules to avoid residues issues

A

don’t use drug off label. identify treated animals, keep excellent tracking/history, accessible records of treatment, store drugs and chemicals correctly. if adding to feed ensure no mixing errors/

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4
Q

what are cytotoxic drugs used for

A

used for the treatment of invading cells, such as pathogenic micro-organisms or invading cancer cells.

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5
Q

what is selective toxicity

A

the use of chemicals indented to be toxic to a pathogenic organism, but harmless for the host.. exploits biochemical differences between the target cell and the host

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6
Q

Pharmacophore

A

Microbial protein = the receptor
antimicrobial moleucule= the ligand
the active chemical moiety of the antimicrobial drug is termed the pharmacophore.

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7
Q

types of selective toxicity mechanims

A

cell wall synthesis in bacteria and fungi, cell membrane synthesis, synthesis of 30s and 50s ribosomal subunits, nucleic acid metabolism, topoisomerase function, viral proteases and integrases

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8
Q

the selective nature of chemotherapeutic agents means..

A

they are usually safe for the host and

associated with few adverse events

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9
Q

antimicrobial drugs

A

assist the host’s defence mechanisms in containing and eliminating the invading micro-organism

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10
Q

how are antimicrobial drugs classified

A
1. Class of micro-organism it kills e.g.
bacteria vs fungus
2. Antibacterial activity
3. Bacteriostatic vs. bactericidal
4. Time or concentration dependent
activity
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11
Q

what is gram-negative and gram-positive

A

gram negative has a thin peptidoglycan layer and gram positive has a thick layer.

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12
Q

what is a narrow spectrum and a broad spectrum

A
narrow= only kills gram negative OR gram positive
broad = kills or inhibits both
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13
Q

MIC ?

MBC?

A
MIC - minimum inhibitory concentration
MBC - minimum bactericidal concentration
MIC= the lowestest concentration of an antibiotic required to prevent growth of an organism
MBC = the lowest concentration of an
antibiotic required to kill the pathogen
MBS is no more than 4x the MIC
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14
Q

Time dependent and concentration dependent

A
time= lenght of time that the serum drug concentration exceeds the MIC determines killing success.
concenctration= the rate of kill increases with the drug concentration above the MIC
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15
Q

Penicillin

A

is a Beta lactam antibiotic, the B lactam ring is essential for the antibacterial activity. it is bactericidal, time-dependent

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16
Q

Penicillin MOA

A

bacteria have a rigid outer cell wall and high internal osmotic pressure, the peptidoglycan component of the cell wall is essential for integrity.
less effective against gram-negative
binding of penicillin binding proteins inhibits peptidoglycan synthesis

17
Q

pencillin resistance

A

the producct of beta lactamases that break the Beta lactam ring. gram -ve postive have inherent resistance, mutation in porin structure

18
Q

overcoming resistance

A

modification of the Beta-lactam nucleus to stabilise the drug in the presence of Beta lactamases. use of beta lactamase inhibitors

19
Q

intrinsic resitance mechanisms include:

A

Low affinity of the drug for the target
◦ Bacteria not permeable to the drug
◦ Efflux transporters
◦ Innate production of inactivating enzymes

20
Q

what is the mutant selection window

A

it is the window betwen MPC and MIC where the bacteria is likely to mutate making the drug ineffective.

21
Q

acquired resistance

A

occurs due to a genetic change in the bacteria, mutation or horizontal gene transfer
Transfer of bacteria between people
◦ Transfer of resistance genes between bacteria
(usually on plasmids)
◦ Transfer of resistance genes between genetic
elements within bacteria (using transposons)

22
Q

benzimidazoles

A

is a anthelmintics, inactive prodrugs, affect the metabolism of the worms by inhibiting Beta-tubulin polymerisation.
the damaged worms are expelled, up to 400x more selective for nematode tubulin.

23
Q

how does benzimidazoles get into the parasite

A

small amounts are ingested, however, majority are by transcuticular diffusion.
lipophilic drugs which aid absorption into the parasite, affected by GIT transit time, the weak base which means ionised in acidic GIT.

24
Q

benzimidazoles efficacy- host fators

A

GIT transit time
Diet type (pH, transit, uptake)
Closure of oesophageal groove intermittently in ruminants – drug bypass
Nutritional status
Liver function – rapid first pass metabolism

25
Q

BZD efficacy Tx factors

A
anthelmintic medications often fail.
◦ Compliance
◦ Inappropriate drug
selected
◦ Wrong dose
◦ Re-infection
◦ Wrong diagnosis
◦ Multi-species
infection
◦ Resistance
26
Q

result of Anthelmintic resistance

A
Becoming a major worldwide issue
Intrinsic modes a minor problem
Inherited
◦ This means populations of worms become R together, rather than individuals
Not reversible
Usually to all drugs in a
class
27
Q

Mechanisms of intrinsic resistance

A

Parasites go through different stages of a life cycle – some stages may be protected from the drug (and go on to mature)
Different species of parasites in geographical regions may have different susceptibilities
Action of parasite may differ
between hosts

28
Q

Mechanisms of true resistance

A

Loss of high affinity binding sites i.e. mutation of β-tubulin
Increased efflux of drug by parasite
◦ Increased number of pumps
Modified enzyme activity by parasites