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Interaction module: Environment and genes > Week 1 > Flashcards

Week 1 Flashcards

1
Q

bioavailability meaning

A

proportion of an administered drug which reaches the systematic circulation unchanged and is thus available for distribution to the site of action

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2
Q

intravenous injection achieves what 100% bioavailability

A

all the drugs reaches the systemic circulation unchanged

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3
Q

exposure to first pass metabolism

A

can stop 100% bioavailability

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4
Q

state the different types of mucosal routes

A

submingual, buccal
nasal, eye
vaginal and rectal

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5
Q

subcutaneous injection

A

consistent absorption from small volumes

passive diffusion into bloodstream

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6
Q

4 steps of multistep model of tumourgenesis

A

initiation
promotion stage
progression
metastasis

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7
Q

list 10 hallmarks of cancer

A 
Escaping growth suppression
Activating invasion and metastasis
Sustained proliferative signalling 
Avoiding destruction by the immune system
Inflammations that can promote tumours
Genome instability and mutations
Inducing angiogenesis 
Unlimited replication 
Deregulation of cellular energy and
Resisting cell death
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8
Q

what does cancer involve

A

cancer involves activation of oncogenes
drive proliferation
also involved inactivation of tumour suppressor genes
which means the cancer cell can then escape the cell cycle arrest
and apoptosis.

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9
Q

Hypomethylation of repetitive regions causes

A

genome instability (e.g deletion, insertion)

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10
Q

what is the link between epigenetic tags and genetic changes

A

cytosine in CpG sites can be methylated which will form 5-methylcytosine. Now 5-methylcytosine is actually pretty unstable and sometimes in the genome it can undergo a spontaneous deamination. Now the structure you see after deamination is the thymine base. So methylation has given rise to a spontaneous mutation by converting a cytosine to thymine. So what this shows is that epigenetic and genetic changes sometimes do go hand in hand.

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11
Q

if Normal cells progress to hyperplasia to neoplasia and invasive cells then what happens

A

the overall global level of methylation decreases

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12
Q

But if gene specific hypermethylation at CpG islands located within the promoter will increase

A

region of genes increase

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13
Q

the epigenetic progenitor model of tumorigenesis what is it

A

the first trigger is an epigenetic abnormality but the trigger only primes the cells so they now have the potential to become cancer cells

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14
Q

Totipotent stem cells can do what

A

can give rise to any of the 220 cell types found in an embryo as well as extra-embryonic cells (placenta).

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15
Q

Pluripotent stem cells

A

can give rise to all cell types of the body (but not the placenta).

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16
Q

cancer stem cells are

A

drug resistant

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17
Q

what happens during cancer initiation

A

mutated epigenetic regulators lead to wave of epigenetic abnormalities
which trigger oncogenic cellular reprogramming (e.g. dedifferentiation)
promote the acquisition of uncontrolled self-renewal and formation of CSC

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18
Q

3 stages of epigentic management

A

Early Diagonisis
Prognosis
Prediction
Follow-up

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19
Q

are epigentic modifciations reversable

A

yes

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20
Q

DNA methyltransferase inhibitors (DNMTi)

A

prevention of aberrant DNA hypermethylation

lead to activation of these genes

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21
Q

Histone deacetyltransferase inhibitors (HDACi)

A

proven to reverse the transcriptional repression of multiple genes involved in the processes outlined such as cell cycle progression, differentiation, and apoptosis.

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22
Q

agonists

A

bind to rececptor and stimulate it

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23
Q

partial agonist

A

is an agonist that cannot elicit the same levek of biological response as a full agonist

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24
Q

example of agonist

A

salbutomol

for asthma

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25
anatogonist example
Atenolol | used to reduce heart rate
26
partial agonist example
buprenorphine
27
compeitive antagonist is what
they compete for the same binding site as the agonist
28
non competitive agonist definition
the receptor binding site "fit" for the agonist, reducing agonist activity
29
examples of competitive inhibitor and what its used for
Atenolol | Hypertension and cardiac arrhythmia
30
Examples of therapeutic non-competitive antagonist and what its used for
Ketamine | used for an anaesthetic
31
Transporters function
they mediate the movement of specific endogenous signalling molecules and nutrients in and out of cells
32
what happens at the Metbolisim PK phase
where drugs can affect the activity of the liver
33
what can the induction of cytochrome P450 isoenzymes by one drug do
increases the rate of metabolisim resulting in lower plasma concentrations toxicity can occur
34
Example of Pharmcokinetic Drug interactions
Carbamazepine (an antiepileptic drug) is a potent inducer of CYP3A4 Erythromycin (an antibiotic drug) is potent inhibitor of CYP3A4 Midazolam (a sedative drug) is a substrate of CYP3A4.
35
name some drugs that are affected by P450 enzyme induction
Ciclosporin (immunosuppressant), also Citalopram (antidepressant) Oral contraceptive pill (synthetic oestrogen & progestin) Warfarin (anticoagulant) Phenytoin (treatment for epilepsy) Acetylcholinesterase inhibitors (e.g. Donepezil, a treatment for dementia) Theophylline (treatment for severe asthma, Tacrolimus (immunosuppressant) Statins (for cholesterol level control), steroids (broad immunomodulation)
36
How does Opiod Analgesic drugs like codeine work
They work by metabolism to morphine by CPY2D6 8% of the population lack the enzyme so they cant metabolise codeine 1% have extra copies of the enzymes so they are rapid metabolisers
37
Some facts about Adverse drug reactions
4 in 5 older people (≥ 65 years) take at least one medication 36% of older people take ≥4 medicines simultaneously - Polypharmacy Older adults are 3 times more likely to suffer ADRs ADRs account for 5-12% of hospital admissions for older adults Up to 50% of older patients do not take their prescribed medicines as recommended
38
Definition of Adverse Drug reactions
the undesirable effect of a drug beyond it's anticipated therapeutic effects, occurring during clinical use
39
Explain what it means to be "above therapeutic range"
it means a toxic reaction | and is treated by reducing dose
40
Explain what "within therapeutic range" means
Its a collateral reaction | it might be unavoidable
41
Explain what it means to be "below therapeutic range"
its a hypersuceptibility | avoid using foreknowledge of patient susceptibility
42
what happens during the first dose reaction
its a time course related ADR | hypotension
43
What occurs during a time course related ADR
Patients become tolerant to these reactions | Patient can continue with treatment, ADR should wear off
44
What happens during late reactions
Risk of ADR increases with continued or repeated exposure | Implies need for long-term monitoring +/- prevention
45
what occurs during a late reaction
Avoid use of drug in patients who are susceptible
46
Patient Susceptibility ADR includes
``` Genetic suceptibility Advancing age Sex Specific Physiological staates such as pregnancy diseases Exogenous factors ```
47
Normal changes due to ageing | cardiovascular give examples
Cardiac enlargement left ventricular failure Systolic hypertension
48
Normal changes due to ageing | respiratory give examples
FEV1 and increased residual volume susceptibility to respiratory infection susceptibility to aspiration
49
Normal changes due to ageing | endocrine give examples
Insulin sensitivity | Thyroid Hormone production
50
Normal changes due to ageing | gastrointestinal give examples
Gastric acid production | Constipation
51
Normal changes due to ageing | Skin/Hair give examples
Dry skin wrinkles Slower healing (ulcers/sores) Greying hair
52
Examples Drug sensitivity in older adults
``` Receptor responses – e.g. ß-adrenoceptor sensitivity Altered coagulation factor synthesis CNS becomes more sensitive to psychotropics / hypnotics Baroreceptor response less sensitive Renal clearance reduced Thirst response blunted Thermoregulation blunted Altered immune response Slower gastric emptying Reduced plasma albumin Increased ratio of adipose to lean tissue Altered liver metabolism ```
53
Polypharmacy ( taking more than 4 medications) facts
Over 65s make up about 14% of population, but consume 40% of the drug budget 4/5 of over 65s are on regular medication 1/3 of over 75s are on three or more drugs Care home patients take an average of eight medications
54
examples of polypharmacy
Anaemia Depression Glaucoma Osteoarthritis Osteoporosis Rhinitis Stroke Venous eczema
55
Pharmacokinetics can be approached with 4 main phases
Absorption,Distribution, Metabolism, Excretion
56
The lipid solubility of a drug is important
drug molecules pass through the blood more readily | permeate tissues more efficiently before finding their mechanistic targets
57
What is First Pass Metabolism and how does it affect orally ingested drugs?
The Extent of drug metabolism occurring before the drug enters the systemic circulation
58
Which component of blood in particular can significantly affect the rate of drug distribution?
Albumin its an abundant protein in the blood plasma responsible for drug binding
58
Which component of blood in particular can significantly affect the rate of drug distribution?
Albumin its an abundant protein in the blood plasma responsible for protein binding
59
Most important site for drug metabolisim
Liver
60
What types of enzymatic reactions normally occur in Phase II drug metabolism?
They normally drive the conjugation of polar hydrophilic chemical groups acetylation
61
What is a key physiological functional outcome of the Phase II drug metabolic reactions?
Increased drug solubility in water to enhance elimination meaning they are retained better in the bloodstream more effectively and more eliminated.
62
What does First Order Kinetics mean? What key pharmacokinetic parameter can be derived from a drug's pattern of elimination?
a concentration- dependant process such that higher the concentration of drug in the body, the faster the drugs elimination.
63
Why is it important to review medication use regularly in patients over 65?
Chronic kidney disease and decline in renal function is common in over-65s this is because
64
THREE other common and important different types of molecule that can be targeted by drugs and try to give a drug example like in the case of morphine above.
ion channel molecular transporters Enzymes
65
What is precision medicine
it is an approach for disease treatment and prevention that takes into account individual variability in genes environment and lifestyle for each person
66
what are the advantages of precision medicine
Improved ability to predict which treatments will work best for specific patients. Better understanding of the underlying mechanisms by which various diseases occur. Improved approaches to preventing, diagnosing, and treating a wide range of diseases.
67
what are the challenges of precision medicine
where manufacturers can earn more selling these products to a large population, precision medicines do not provide such opportunity.
68
Why is economic evaluation a useful tool
Weighs up both the cost and health outcomes from alternative technologies
69
what are the 3 stages of economic evaluation design
comparator health outcomes costs
70
challenges with economic evaluation
Lack of data with alternatives Uncertainty Costing methodology Constraints and capacity within the NHS More appraisals and the need for bespoke guidance Dramatic pace of technological innovation Equity/ethical concerns
71
differences in outcomes
Treatment effect Bias Chance
72
what is the best way to a create control
Randomisation
73
what are the advantages of Randomised clinical trial
Eliminate selection bias Balance prognostic factors validity of statistical test
74
what is an uncontrolled clinical trial
comparing effects and value of intervention against a control in human subjects
75
what is the definition of a randomised trial
it is a controlled trail where the therapies are allocated by a chance mechanism
76
The zelen method what are its disadvantages
They have not given consent but are still in the study | if they get ethics they don't need to be informed.
77
what is the rationale behind cancer treatment
Destroy/kill ALL cancer cells A possible outcome is achieving complete cure Destroy/Kill MOST cancer cells A possible outcome is prolonging survival time Destroy/Kill SOME cancer cells Outcomes such as eliminating symptoms or preserving quality of life
78
how is treatment efficacy assessed with a tumour response
Complete Response: Disappearance of all signs of disease Partial Response: A reduction of tumour volume by at least 30% Stable Disease :No significant change Disease Progression: An increase of tumour volume by at least 20% or new metastases
79
how is treatment efficacy assessed with a ‘survival’ time
Overall survival: survival time from the start of treatment Disease-free survival: survival time prior to tumour relapse after radical treatment Progression-free survival: survival time prior to tumour progression
80
how do we know that a treatment works
the measures of efficacy | any need treatment needs to be compared to a standard treatment
81
what is a half life
The time it takes for the plasma drug concentration to halve irrespective of the starting dose”

Interaction module: Environment and genes (7 decks)

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