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Semester 1 > Pharm Exam 2 > Flashcards

Pharm Exam 2 Flashcards

1
Q

Chelator

A

“A compound that fosters the formation of a chemical ring by binding the metal that’s in this ring with two or more metallic ions (Tetracycline)
“

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2
Q

Phase 1 reactions

A

Oxidative reactions

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3
Q

Phase 2 reactions

A

Conjugation reactions

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4
Q

Tetracycline Effect

A

Tetracycline is chelated by by Ca++. This inhibits the absorbtion of Tetracycline which reduces it antibacterial effect. More importantly it reduces availability of Ca++ which is needed by the fetus.

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5
Q

Example of chelation therapy

A

It is used in lead poisoning to quickly remove lead from the body

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6
Q

How do drugs Indirectly Reduce Absorbtion

A

Altering gastric pH. Altering Gastric Motility. P- Glycoprotein

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7
Q

What is P-Glycoprotein

A

A member of the Superfamily of eflux transporters which can pump the drug back into the GI tract to keep it from being absorbed.

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8
Q

Displacement

A

When one drug replaces another from a binding site which increases the free drug available. This plays a minimal role in drug interactions. Unbound drug only can cross the plasma membrane

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9
Q

What happens when the drug binds to CYP450?

A

Makes the drug more polar and more reactive which facilitates excretion or biotransformation.

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10
Q

CYP450 accounts for what % of drug oxidation

A

80%

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11
Q

CYP450 is not substrate specific because?

A

One or more drugs can be metabolized by the CYP isoforms. Oxygen of the complex is a powerful oxidizing agent that can react with numerous substrates

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12
Q

Conjugation and hydrolysis enzymes are located where

A

In the cytosol and the ER of hepatocytes

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13
Q

Conjugation occurs in what 2 ways

A

Directly with the drug or with reactive intermediaries generated during phase 1

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14
Q

What happens during phase 2 reactions?

A

A polar group is added which increases H2O solubility and facilitates excretion.
Polar groups; glucuronide, glutathione, acetate, sulfate

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15
Q

Phase 2 reactions are subject to what

A

Polymorphisms such as aceytlation. 40-50% of the population exhibit slow aceytlation and this have a slow metabolism.

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16
Q

Once satration occurs in drug elimination what happens?

A

The clearance rate fails to increase with concentration

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17
Q

How are drugs excreted form the liver into bile?

A

By an ATP family of transporters

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18
Q

What happens to drugs that undergo enterohepatic circulation?

A

They are reabsorbed by the SI and then into the portal and systemic circulation.

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19
Q

What is the role of bacteria in enterohepatic circulation?

A

Hydrolysis of Glucuronides.

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20
Q

What happens if abx kill of the bacteria in the gut?

A

It interferes with enterohepatic circulation.

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21
Q

The ability of one drug to inhibit the excretion of another depends on?

A

Filtration, Tubular Secretion, Reabsorbtion and Urine pH.

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22
Q

An example of a drug interaction with renal filtration.

A

If drug A inhibits the Albumin binding of drug B it increases the free abount of drug B which can then be eliminated by filtration.

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23
Q

An example of a drug interaction with tubular secretion.

A

If drug A limits the secretion of drug B than the amount of B in the body increases. Example Cimetidine decreases the secretion of Metformin which leads to an increased serum level of Metformin.

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24
Q

An example of a drug interaction with renal reabsorbtion.

A

A drug can decrease the kidney’s ability to reabsorb. Example a diuretic can cause more Na to be excreted than is desireable. The body will then stimulate the reabsorbtion of Na. The body can inadvertently reabsob other monovalent ions such as Li which can be toxic.

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25
Q

An example of a drug interaction with changes in urine pH.

A

Changes in either gatric pH or urine pH can cause changes in the absorbtion or secretion of drugs. Example is in alkaline urine renal excretion and clearance may be reduced compared to the same drug in an acidic unine pH.

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26
Q

What are synergistic effects and give an example.

A

Additive effects. Example is Gynco and Warfarin taken at the same time increase the risk of hemorrhage

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27
Q

What can cause drug interactions other than prescriptions drugs.

A

OTC, Illicit drugs, foods and alcohol

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28
Q

Example of a food causing a drug interaction.

A

Warfarin and green leafy vegetables which contain Vitamin K.

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29
Q

Acute ingestion of ETOH does what to drug metabolism?

A

Inhibits the CYP450 system

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30
Q

Chronic ingestion of ETOH does what to metabolism?

A

Stimulates the CYP450 system to try and eliminate ETOH.

31
Q

Strategies for mitigating harm in prescribing medications.

A
  1. Reviewing all of a patient’s medications with them. 2. Examine the rational for each medication prescribed. 3. Consider nonpharmacological interventions (ex. Diet to reduce LDL and increase HDL inisterad of a Statin) 4. Separate the administration of conflictiong drugs. 5. Start low and move slow. 6. Use the resources around you.
32
Q

What are the 4 main stages in life?

A

Fetus, Neonatal, Adult and Elderly

33
Q

What factors determin whether a drug will cross the placenta or not?

A

Size of the drug. Lipid solubility (lipid soluble drugs will cross if the maternal concentration is high enough), and plasma protein binding

34
Q

What do placental drug enzymes do?

A

Detoxify a drug ir increase it’s toxicity.

35
Q

Breakdown of fetal circulation.

A

50% passes through the liver (fetuses do not have sufficient CYP450) and 50% bypasses the libe in the ductus venosa.

36
Q

Category A

A

Controlled studies in women show no harmful effects in the first trimester and later on appears to be low as well.

37
Q

Category B

A

Either animal studies have shown no adverse ffects and there is no controlled study on women OR animal studies have shown adverse effects but a controlled study shown none in women.

38
Q

Category C

A

Either animal studies have shown an adverse affect and there are no controlled studies in women OR there are no studies in women or animals. Only use if the potential beefit outweighs the risk.

39
Q

Category X

A

Studies in animals and humans show a significant risk. The risk clearly outweighs the benefit.

40
Q

What are fetotoxins?

A

Fetotoxins interfere with the functions of the organs themselves.

41
Q

Days 0-14

A

All or nothing effects

42
Q

Days 14-60 (Week 3-9)

A

Exposure to teratogens may lead to death of the fetus or significant malformations (CNS and heart)

43
Q

Days 61 onward

A

Exposure usually does not result in major structural anomolies unless the blood supply has been cut off

44
Q

Affect of ACE inhibitors on the fetus

A

Effects the kidneys resulting in renal failure, can be reversed

45
Q

Factors affecting fetal/ neonatal drug absorbtion.

A

Increased gastric pH (remains high until age 2) and slowed gastric motility.

46
Q

Factors affecting fetal/ neonatal drug distribution

A

TBW of 80% (60% adult), lower plasma protein levels which may cause the displacement of billirubin for albuin (increased billirubin leads to braindamage).

47
Q

Fetal/ Neonatal excretion rate.

A

30% of the normal rate.

48
Q

pH of breast milk compared to plasma

A

BM is more acidic than plasma

49
Q

Category D

A

There is a positive risk in humans. Only used in life threatening situations.

50
Q

What happens to alkaline drugs in breast milk.

A

It becomes ionized and then trapped in the BM leading to toxicity passed onto nursing child. Drugs bound to proteins will also bing in BM

51
Q

Factors determining biological age

A

Lifestyle, Genetics, and medical hx

52
Q

Factors affecting absorption in the elderly

A

Impared GI Motility, Decreased GI blood flow, higher Gastric pH

53
Q

Factors affecting distribution in the elderly

A

Decrease TBW, decrease in plasma

54
Q

Factors affecting metabolism and excretion in elderly

A

Impaired hepatic function and mass along with decreased renal function

55
Q

Pharmacogenetics

A

Focuses on the influence of single genes on drug response

56
Q

Pharmacogenomics

A

Focuses on the influence of the individual’s entire genome on their response to drug therapy

57
Q

Single Nucleotide Polymorphisms (SNP’s)

A

One nucleotide is exchanged for another at a given position

58
Q

Nonsynonymous coding SNP’s

A

Changes the identity of the amino acid which can alter the function of the protein

59
Q

Symonomyous SNP’s

A

Do not change the amino acid and therefor do not change the protein

60
Q

Nonsense SNP’s

A

Create a stop codon

61
Q

Genetic polymorphism

A

The changes that occur in enzyme structure and function due to DNA mutation

62
Q

Drugs metabolized by CYP2D6

A

Antidepressants, Antiarrhythmics, Beta blockers and Analgesics

63
Q

Mutations of CYP2D6

A

SNP’S, Gene deletion and gene duplication. May have up to 13 copies of the gene

64
Q

CYP3A4

A

The isoenzyme that metabolizes most drugs

65
Q

CYP2C9

A

The isoenzyme associated with metabolizing drugs with very low therapeutic indexes such as Warfarin

66
Q

CYP2C19

A

The most common polymorphism. It is more common in Asians than Caucasians or Africans

67
Q

CYP1A2

A

Involved in the biotransformation of nicotine and caffeine

68
Q

Phase 2 polymorphisms

A

Mutations alter the drug response, structure ot presence of target drugs

69
Q

What does acetyl transferase 2 do in phase 2 reactions?

A

Acetyl transferase 2 catalyzes the acetylation of drugs such as Sulfonamides

70
Q

Phase 2 polymorphism example from the book

A

Serotonin Reuptake transporter in chich a mutation causes a reduction in the expression of the transporters themselves

71
Q

Access to therapy as a limitation of pharmacogenetics

A

New drugs may target specific genes, those with a rare phenotype may not receive adequate treatment. Also drugs which are highly specific to one gene are unlikely to be developed due to high cost

72
Q

Complexity of pharmacogenetics

A

Providers will need a number of resources in order to prescribe the appropriate drug for the individual

73
Q

Time and expense as a limitation to pharmacogenetics

A

Patients not responding to an adequate dose may need genetic testing which can be very expensive

Semester 1 (15 decks)

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