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PCL201 Finals review > PCL201TT2 > Flashcards

PCL201TT2 Flashcards

1
Q

How does a drug’s elimination change as time goes on?

A
  1. When enzymes are saturated (such as p450) , drugs can only be removed independent of concentration (no matter how high the conc is, enzymes work at Vmax) 2. As enzymes become less saturated, it becomes conc dependent to first order removal
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2
Q

Half-life formula

A

t(1/2) = 0.693/k

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3
Q

How to find k from slope

A

k = -slope * 2.3

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4
Q

How to calculate 1st order elimination

A

C2 = C1 e^-k(t2-t1)

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5
Q

Total body clearance formula

A

Cl(TB) = k * Vd

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6
Q

What happens to TBW when pregnant?

A

Pregnancy increases TBW

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7
Q

What happens to albumin binding during pregnancy

A

Decreased binding

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8
Q

Factors that contribute to changing renal excretion in pregnant mothers

A

Renal plasma flow increased Increased GFR
Increased drug secretion rate

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9
Q

At what dates is thalidomide causing birth defects?

A

20 ~ 36 days post fertilisation

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10
Q

What is a reactive intermediate mediated toxicity

A

Proteratogens are biotransformed to electrophiles and free radicals that target DNA, proteins and lipids

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11
Q

Cyclophosphamide teratogenic affects

A

CNS malformations and secondary cancers

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12
Q

Warfarin teratogenic effects

A

Growth retardation and chondrodysplasia

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13
Q

Phenytoin teratogenic affects

A

Cleft lip or palate, and fetal Hydantoin syndrome

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14
Q

Carbamazepine and valproic acid teratogenic effects

A

Neural tube defects

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15
Q

Fetal alcohol syndrome affects

A

Smooth philtrum, thin upper lip

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16
Q

Relative infant dose formula

A

RID = Dose in the infant / Dose in the mother * 100%

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17
Q

How to calculate the dose in infant

A

Concentration in milk * 150 ml/kg/day

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18
Q

What factors affect patient compliance

A

Psychological problems Cognitive impairement Social isolation Perception of illness, treatment efficacy

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19
Q

What factors don’t affect patient compliance

A

Demographic factors Age is not a significant factor on its own

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20
Q

How can hyperthyrodism effect the number of B-adrenoreceptors?

A

Increase

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21
Q

How would a monogenic distribution differ from the polygenic ditribution

A

Monogenic - Either Biomodal for polymorphic, or normal for rare variants
Polygenic - Non-normal distribution, wide variety of phenotypes

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22
Q

How did they discover CYP2D6 Polymorphism?

A

Debrisoquine and Sparteine, showed different metabolisms and toxicity

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23
Q

How did they test for CYP2D6 function?

A

Dextromethorphan (DM), safe drug for testing CYP2D6 function

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24
Q

How is tamoxifen affected by CYP2D6?

A

CYP2D6 metabolises Tamoxifen is prodrug to endoxifen. If PM, not enough endoxifen will be made

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25
How does CYP2D6 phenotype effect breast cancer survival rate?
PM will have worse survival rates since not enough tamoxifen will be made
26
How will Omeprazole be effected by CYP2C19 polymorphisms
Poor metabolisers will have increased omeprazole concentration UMs will have decreased therapeutic effects
27
How is 6-mercaptopurine affected by TPMT (Thiopurine methyltransferase) Polymorphisms?
Poor metabolisers of TPMT will have more cytotoxicity
28
What amino acid variance will affect B2-adrenergic receptor for isoproterenol? (AA#, and AA type)
Glutamate @ position 27 will be more effective than glutamine @ position 27
29
What amino acid variance will affect B2-adrenergic receptor for salbutamol? (AA#, and AA type)
Arg/Arg will show more response to salbutamol than Arg/Gly or Gly/Gly
30
Which amino acid genotype will show the best response to opioids in the mu-opioid receptor? (AA and AA#)
Asparagine is better than Aspartic acid at amino acid 40
31
How does Trastuzumab work against breast cancer?
HER2 is overexpressed in some (25%) of breast cancer patients Trastuzumab is a monoclonal antibody against HER2, genetic testing is required to see if HER2 is the cause of breast cancer
32
What is the achievable goal of personalised medicine using pharmacogenomics?
To develop better medications and predictive genetic tests to determine THE RIGHT DOSE, OF THE RIGHT DRUG, IN THE RIGHT PATIENT, AT THE RIGHT TIME
33
How is warfarin effected by CYP2C9 polymorphisms
CYP2C9 PMs will need less dose, and may be subject to bleeding
34
Why might warfarin and CYP2C9 testing NOT be useful
Increased bleeding risk is not solely reliant on CYP2C9 polymorphisms
35
How will 5-FU cause cytotoxicity?
If the person has DPD deficiency, it will form more cytotoxic metabolites increasing the risk of toxicity
36
What's the problem with DPD genetic testing
Only tests 4 variants most common within caucasian populations
37
Why was Vioxx pulled off from the market?
Vioxx had increased rate of myocardial infarctions compared to NSAIDS
38
Why was Valdecoxib pulled off the market?
Severe skin reactions
39
What increases the risk factors of ADRs?
Polypharmacy History of ADRs Impared renal and hepatic functions Age and Gender Genetics
40
Type A vs Type B ADRs
Type A - Dose related Type B - Bizarre unpredictable
41
Warfarin ADR example
Warfarin has a narrow TI, increasing risk of internal bleeding
42
Digoxin ADR example
Digoxin increases force of contraction in the heart But also imparis renal function and disrupts electrolyte balance This triggers arrhthymias
43
B-adrenergic drugs ADR (Dobutamid and Terbutalin)
Dobutamide - Binds to B1 in cardiac myocytes increasing rate of contraction ADR: Hypotention due to other B-receptors found in periphery Terbutaline: Bound to B2 to relax bronchiole smooth muscles ADR: Increased HR, and chest pain
44
What happens to G-6-PD deficient individuals when they take primaquine
Hemolysis
45
Type 1 Immunologic reactions
Anaphylactic -> IgE antibody on mast cells -> Release of histamines
46
Type 2 immunologic reactions
Drug binds to a cell causing it to be "foreign chemical" -> IgG is formed specific for this -> IgG binds to the drug covered cell -> Cell is destroyed
47
Example of Type 2 immunologic
Hemolytic anemia with methyldopa Agranulocytosis with sulfas Thrombocytopenic purpura with ASA or phenytoin
48
Type 3 Immunologic
Drug recognized as foreign -> IgG produced against that drug -> Immune complexes deposit at high blood pressure points -> Complexes are not cleared efficiently, causes inflammation in those areas
49
Type 4 immunologic reactions
T-cell activation, causing cytokine release and causes dermatitis and eczema
50
Which immunologic reactions causes Steven Johnson Syndrome?
Type 3 and Type 4
51
4 ways to study ADRs
Spontaneous reports, Databases, Cohort studies, Case-control studies
52
Disadvantages of spontaneous reporting to find out ADR
1. Underreporting 2. Bias due to only reporting severe events 3. lack of detailed information
53
Disadvantages of Databases for ADR
1. Databases not usually for comparison of drugs
54
Disadvantages of cohort studies
1. Expensive, difficult to perform 2. Selection bias
55
Disadvantages of Case-control studies
Difficult to narrow down the drug if the ADR has a high incidence within the population itself
56
What is toxicology?
the study of adverse effects of chemicals and physical agents on people, animals and other living organisms
57
Poison hemlock vs water hemlock
Poison hemlock acts in PNS to block nicotinic receptors at the NMJ causing paralysis Water hemlock: includes cicutoxin, acts in the CNS to block GABA receptors, seizures Both cause respiratory failures
58
What are the 4 steps of toxicology risk assessment?
1. Hazard identification 2. Dose-Response assessment 3. Exposure assessment 4. Risk characterization
59
How is hazard identification performed?
Sturcture-Activity analyses, In vitro, in vivo tests, Human studies
60
What are the main 2 mechanisms of toxicity?
1. Molecule reversibly binds to a cellular receptor (more similar to Type A ADR) 2. Relative non-toxic chemical, bioactivates to a reactive metabolite that irreversibly binds or oxidised proteins, DNA and lipids
61
How is exposure assessment performed?
1. Looking at route of administration 2. Then looking at duration and frequency of exposure in animal studies (Acute vs Chronic)
62
What are the 4 "times" of exposure?
1. Acute: Exposure for less than 24hours 2. Subacute: Repeated exposure for 1 month or less 3. Subchronic 1 to 3 months 4. Chronic Repeated exposure for more than 3 months
63
How is dose-response assessment performed?
Constructing both graded and quantal dose-response curves
64
What is a quantal dose-response curve
All or none: What freq of population has X effect when exposed to a certain dose
65
Why is threshold response an assumption?
It means that only above a certain threshold of dose will actually show a toxic/harmful response Some chemicals such as carcinogens don't have a threshold -> considered toxic/risky at any concentration or dose
66
Certain safety factor (CSF)
LD1/ED99
67
What does the certain safety factor look at?
It looks at the overlap between the most sensitive individuals (LD1) vs the dose most effective for 99% of population (ED99)
68
Why would a low extraction drug get more affected than high extraction drugs when drug is bound to plasma proteins?
1. Since high extraction drugs will get extracted by the liver no matter what (good affinity for hepatic enzymes) 2. Low extraction has poor affinity for the hepatic enzymes (thus free drug is not readily picked up by them), hence plasma protein binding really alters the extraction
69
What are some high extraction drugs
Lidocaine, Morphine, Propranolol
70
What are some low extraction drugs
Diazepam, Phenytoin, Warfarin
71
How to acidify/alkalinise urine
Acidify - give ammonium chloride Basify - Give sodium bicarb By giving a shit tone of them, it overloads the reabsorption system in the proximal tubule. This then makes them stay in the urine, trapping any drug in the tubule.
72
Infant Dose
Concentration of drug in milk * 150ml/kg/day
73
What are some factors influencing the transfer of drugs into milk?
1. Low MW 2. Generally high lipid solubility 3. Low plasma protein binding 4. pKa of drug, basic drugs are more likely to get trapped in the milk (lower pH)

PCL201 Finals review (7 decks)

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