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1Principles of Biomedicine - MD1 > 95 - Selective Toxicity of Drugs > Flashcards

95 - Selective Toxicity of Drugs Flashcards

1
Q

Examples of selectivity
1
2
3

A

Species-level toxicity
Cell-level selectivity
Organ-level selectivity

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2
Q

Examples of antimicrobials against bacterial ribosomes

A

Tetracyclines, aminoglycosides

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3
Q

Sulfonamides

A

Target bacterial folic acid metabolism.

Resembles para-amino benzoic acid (part of folic acid)

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4
Q

Bacterial folate metabolism
1
2
3

A

PABA (para-amino benzoic acid) converted to folate.
Folate converted to tetrahydrofolate.
Tetrahydrofolate converted to precursors to nucleotides.

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5
Q

Example of syndergy between antimicrobials

A

Sulfonamides (inhibit PABA -> folate), trimethoprim (inhibit folate -> tetrahydrofolate)

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6
Q

Example of synergy between antimicrobials

A

Sulfonamides (inhibit PABA -> folate), trimethoprim (inhibit folate -> tetrahydrofolate)

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7
Q

Enzyme that sulfonamides interfere with

A

Dihyropteroate synthase

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8
Q

Enzyme that trimethoprim interferes with

A

Dihyrofolate reductase

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9
Q

What does methotrexate resemble?

A

Folic acid

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10
Q

Effects of methotrexate

A

Inhibits purine synthesis.
Inhibits DTMP synthesis.
Anti-cancer agent.

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11
Q

Human folic acid metabolism

A

Folate to tetrahydrofolate (through dihydrofolate reductase)

Tetrahydrofolate to precursors of nucleotides (EG: thymidylate).

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12
Q

What does methotrexate inhibit?

A

Dihydrofolate reductase.

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13
Q

Functions of methotrexate
1
2
3

A

✦ Inhibits human dihydrofolate reductase
(inactive in bacteria)
✦ Cytotoxic anticancer agent (large doses)
✦ Cytotoxic immunosuppressant (lower doses,
rheumatoid arthritis)

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14
Q

Functions of methotrexate
1
2
3

A

✦ Inhibits human dihydrofolate reductase
(inactive in bacteria)
✦ Cytotoxic anticancer agent (large doses)
✦ Cytotoxic immunosuppressant (lower doses,
rheumatoid arthritis)

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15
Q

Risk of methotrexate

A

Known teratogen

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16
Q

When is methotrexate prescribed in pregnant women?

A

To terminate an ectopic pregnancy (can abort)

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17
Q

How often is methotrexate taken?

A

Once per week (high risk of overdose, overdose is nasty)

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18
Q

*Kidney ion transfer

A

KIDNEY ION

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19
Q

*Kidney ion transfer

A

KIDNEY ION

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20
Q

Active driver of ion transport in the kidneys

A

Na/K ATPase

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21
Q

Active driver of ion transport in the kidneys

A

Na/K ATPase

22
Q

How is renal architecture unconventional?

A

Transfer of oxygen from arteries to veins via countercurrent exchange

23
Q

Why are the testicular arteries arranged in an unconventional manner?

A

Countercurrent exchange of testosterone.

Reduces the amount of testosterone released into the body, so that it is easier to regulate.

24
Q

How is most testosterone released into the body

A

Through the lymphatics, bound to albumin proteins.
Test released into the venous blood is mostly transferred to the arterial blood, back to the testes (via countercurrent exchange)

25
Q

Outcome of renal unconventional blood supply

A

Relative hypoxia in the kidneys.

Not absolute hypoxia (as kidneys function normally), but is at a risk of hypoxia.

26
Q

Countercurrent exchange of kidneys

A

Arteries of one nephron are beside the veins of an adjacent nephron.

27
Q

What can lead to kidney damage?

A

Conditions leading to low renal perfusion (kidneys already in a state of relative hypoxia)

28
Q

Triple whammy

A

Combination of a diuretic and an ACE
inhibitor (or AT1 receptor antagonist) is
effective treatment for hypertension.

Add in NSAID leads to acute renal failure.

29
Q

Why can NSAID lead to renal failure?

A

Prostaglandin-mediated vasodilation preserves renal blood flow when diuretic and ACE-I are administered.

30
Q

Safe hypertension treatment

A

Diuretic + ACE inhibitor.

31
Q

Safe hypertension treatment

A

Diuretic + ACE inhibitor.

32
Q

Danger with diuretic and ACE inhibitor hypertension treatment

A

Patients can self-prescribe NSAID, which leads to renal failure when co-administered with ACEI and diuretic

33
Q

Example of a nephrotoxic antibiotic

A

Gentamycin

34
Q

Class of antimicrobial that gentamycin is

A

Aminoglycoside

35
Q

Side effects of gentamycin

A

Nephrotoxic, ototoxic (leads to deafness, vertigo)

36
Q

Advised length of gentamycin treatment

A

No more than 48 hours.

Once per day (one bolus)

37
Q

Advised length of gentamycin treatment

A

No more than 48 hours.

Once per day (one bolus)

38
Q

How is gentamycin excreted?

A

Entirely through kidneys

39
Q

Why might gentamycin be ototoxic?

A

Selectively taken up by hair cells in the ear.
Gets into the fluid area of the cochlea (slow clearance area).
Not known how it gets into hair cells

40
Q

Why is gentamycin administered once per day?

A

Equally effective if administered once per day.
Less toxic to ear, kidney.
Need to get through trough period, where gentamycin enters cochlea, leaks out slowly.

41
Q

Patients who are at higher risk of ototoxicity with gentamycin treatment

A

Those exposed to continuous loud sound during treatment, those with tinnitus.

42
Q

Paraquat

A

Herbicide.

43
Q

Paraquat

A

Herbicide.

44
Q

How does paraquat work?
1
2
3

A

Activated into a radical form by getting electrons from electron transport chains.
Radical form oxidises anything it can tough, makes ROS.
Destroys cell membranes, DNA, proteins, etc.

45
Q

What activates paraquat in a plant?

A

e- in chloroplasts

46
Q

How does paraquat get activated in mammalian cells?

A

Accepts electrons from NADPH.

47
Q

Effect of paraquat on mammals

A

Activated by accepting e- from NADPH.

Accumulates in lung epithelial cells via active transport.

48
Q

Effect of paraquat on mammals
1
2

A

Activated by accepting e- from NADPH.

Accumulates in lung epithelial cells via active transport.

49
Q

Effect of paraquat on mammals
1
2

A

Activated by accepting e- from NADPH.
Accumulates in lung epithelial cells via active transport.
Lung epithelium exposed to very high concentrations

50
Q

Dose difference of paraquat for mammals

A

Low dose selectively kills lung epithelial cells.

High doses destroy tissues systemically.

51
Q

Dose difference of paraquat for mammals

A

Low dose selectively kills lung epithelial cells.

High doses destroy tissues systemically.

1Principles of Biomedicine - MD1 (157 decks)

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