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MD2002 > Week 8 content > Flashcards

Week 8 content Flashcards

1
Q

Define pharmacology

A

Origin , nature, effects and uses of drugs

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2
Q

Define toxicology

A

Study of the side effects of chemical, biological and physical agents

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3
Q

Define pharmacodynamics

A

What drug does to body: drug-receptor interactions, effects, concentrations

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4
Q

Define pharmacokinetics

A

What body does to drug: metabolism and excretion.

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5
Q

List the reasons why pharmacokinetics is important.

A

-TDM- Therapeutic dose monitoring
-Drug recommendations
-Predict drug interactions
-influence of disease on drugs
-Safely administer drugs in urgency cases.

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6
Q

List the steps of pharmacokinetics.

A

Liberation
Absorption
Distribution
Metabolism
Excretion

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7
Q

Discuss advantages and disadvantages of different routes of administration

A

-Oral
-Sublingual
-Rectal
-Transdermal
-IV
-Intramuscular
-Topical
-Inhalation

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8
Q

What is bioavailability and which is the most bioavailable method

A

Bioavailability- is the fraction of unchanged drug that reaches the systemic circulation.

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9
Q

Factors affecting drug absorption

A

-Lipophobicity of drug
-pH of compartment
-routes of administration
-Barriers to absorption

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10
Q

Explain the compartment model

A

Explains the rate of drug absorption from plasma to other compartments dependant on factors like cardiac output and capillary permeability.

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11
Q

What factors influence distribution between fluid compartments.

A

-pH of fluid compartments
-Lipophobicity of drug
-Cardiac output
-capillary permeability
-drug ionisation
-Plasma protein binding

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12
Q

Describe structure and properties of bethanechol

A

Quaternary amine, very highly charged
-Can’t be absorbed into the GI but can have contact with it, treating hypotonia of GI tract.

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13
Q

Describe structure and properties of pilocarpine

A

Tertiary amine, slighly less charged than bethanechol.
-Used in small concentrations in the eye

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14
Q

Describe protein binding

A

Hydrophobic drugs must bind to plasma proteins to be able to be transported in the blood to the target tissue.
They bind to albumin(mostly), globulin, lipoprotein and 1-alpha-glycoprotein.

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15
Q

Describe epigenetics and epigenetic tags

A

Epigenetics- process of modifying DNA to monitor gene expression without changing the main gene sequence.

Epigenetic tags are said modifications.

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16
Q

Describe genomic imprinting

A

-Over 200 imprinted genes.
-Only one allele used, the other remains naturally silent.
-Depends on parental origin.
-Imprinting resets when passed through the germline in gametes that escape DNA de-methylation.

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17
Q

Describe DNA methylation and its function

A

-Methyl group added to carbon 5 of cytosine( by enzyme de novo methylase) forming 5-methylcytosine.

-This happens mostly in CpG islands( areas rich in CG).
-Inhibits gene transcription by preventing transcription factors binding to promoter.
-MeCpG binding proteins recruit more proteins that helps in further compacting of DNA after methylation.

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18
Q

Describe Prader-Wili syndrome: causes, symptoms,etc.

A

-Caused by epigenetic paternal deficiency of genes in chromosome 15.
-Symptoms: behavioural problems, obesity, neurological defects.

-This is because lack of expression of those genes affect the hypothalamus.

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19
Q

Describe Angelman syndrome:causes, symptoms,etc.

A

-Caused by epigenetic maternal deficiency leading to absence or malfunction of Angelman gene in chromosome 15.

-Symptoms: neurological deficiencies, behavioural effects, jerky movements, inappopiate laughs, “happy puppet” face ,…

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20
Q

Warfarin vs Aspirin

A

98% of warfarin binds to albumin.
-But aspirin has a greater affinity to albumin than warfarin causing it to displace warfarin.
-Higher percentage of unbound warfarin present in plasma
-This is dangerous as warfarin has a very narrow therapeutic window.

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21
Q

Differences between heterochromatin and euchromatin

A

-Heterochromatin is highly compact in interphase, is transcriptionally inactive, contains few genes and is replicated late in S phase

-Euchromatin forms 30 nm strands in interphase, is transcriptionally active and contains loads of genes. It is replicated early in S phase.

22
Q

What is Position Effect

A

Heterochromatin spreads into euchromatin spaces, altering its gene expression. Leads to gene silencing.

23
Q

What is X chromosome inactivation

A

-Women have 2 X chromosomes that both have disease genes while males only have 1.
-To make it fair, 1 X chromosome is silenced in females by X ist which codes for 17 kilo bases RNA that will remain in nucleus

24
Q

Describe uniparental disomy

A

Child inherits both copies of chromosome from the same parent. Expression of imprinted genes altered.
Example in Prader-Willis and Angelman’s syndromes.

25
Q

Describe the terms locus and allele

A

-Locus: position of a gene in the chromosome
Allele- different variations of a gene.

26
Q

Possible causes of genetic disease

A

-Chromosome aneuploidies: extra or missing chromosomes
-Change in gene sequence
-Chromosome abnormalities.

27
Q

Describe the different type of mutations that can occur

A

-Stop mutation: sequence stops prematurely, no more sequence after that.
-Insertion mutation: base pair addition, shifts the frame
-Deletion mutation(out of frame); shifts frame
-Deletion mutation (in frame): whole chunks of baes deleted but doesn’t change the frame
-Substitution mutation: doesn’t change the frame
-Triplet expansion: abnormal codon repetition.

28
Q

What criteria must diseases with Mendelian inheritance have

A

Change in a single gene causes a clinical disease, is inherited in a pattern predicted by Mendelian Laws

29
Q

Describe Autosomal Dominant inheritance: percentage of offspring and example

A

-1 copy needed for the person to be affected
-Present in all generations
-50% of offspring affected
- Marfan’s syndrome: causes arachnodactylyl, pectus excavatum and heart problems like aorta dilation.

30
Q

Describe Allelic heterogeneity and explain an example.

A

Different mutations in the same gene can cause the same disease

32
Q

Describe Autosomal Recessive and explain example

A

-2 copies of the faulty gene needed to cause disease
Example sickle cell anaemia.

32
Q

Describe locus heterogeneity

A

-Different mutations in different genes cause the same disease.
-Example:Hereditary Haemorrhagic Telangiectasia.
HHT1- mutation in Enolgin gene. Affects inner mouth
HHT2- mutation in ALK1 gene. Affects tongue.

33
Q

Describe X linked recessive inheritance

A

-Gene fault lies on X chromosomes
-Affects more men than women because the women have X another X chromosome with the correct gene but males don’t.

-If Affected male has children- all his male offspring unaffected but his female offspring all carriera.
-If affected female has children, all her male offspring affected and her female offspring carriers.

34
Q

Describe Epidemiology

A

Study of distributions and determinants of health events in a population in a specific area with the intention of using the study to control the health problems.

35
Q

List the different study designs

A

-Case Series
-Cohort Study
-Cross Sectional studies
-Case-control study
-Ecological studies

36
Q

Describe standardisation

A

Set of tecniques to remove the effect of a confounding factor influence on the variables when comparing 2 or more populations

37
Q

Explain the 2 types of standardisation

A

-Direct: Happens directly on population you want to measure

-Indirect: done on reference population and then SMR of reference and interest population.

38
Q

Describe SMR factors affecting it

A

SMR= number of deaths/number of expected deaths.
Expected deaths depends on age-specific mortality rates and age and sex of the population you are working on.

39
Q

Difference between confounding and bias

A

Confounding is the distortion of measure of effect of exposure on outcome due to a third factor that also influence both variables

40
Q

Causes of bias or systematic error

A

Data collection
Data analysis
Data interpretation
Data report

41
Q

List the criteria for causality

A

-Reproducibility/Consistency
-Temporality
-Specificity
-Coherence
-Analogy
-Plausibility
-Biological Gradient
-Experimental

42
Q

Describe the 2 phases of drug metabolism

A

Phase 1: Adding a reactive group or exposing the drug’s reactive group by oxidation, reduction and hydrolysis.

Phase 2: Conjugative and synthetic reactions resulting in hydrophilic compounds or conjugates.

43
Q

Properties of CYP450 enzyme

A

-Monooxygenase
-Involved in metabolism of endogenous and exogenous compounds.
-Involved in biosynthesis of steroids, fatty acids and bile acids.
-There are 57 genes that code for CYP450 enzymes

44
Q

Metabolism of paracetamol in presence and absence of glutathione

A

Paracetamol broken down into sulphuric, glucoronide and a third conjugate.
This third compound is broken down by binds to gluthatione in the presence of glutathione leading to conjugation and excretion

45
Q

Examples of drug interactions

A

-Simvastatin and grape fruit juice: Grape fruit juice inhibits CYP3A4 Which is in charge of breakdown of simvastatin

-Warfarin and phenobarbital: Phenobarbital increases expression of CYP450s involved in breaking down warfarin

-Warfarin and Aspirin: Aspirin displaces warfarin in binding to albumin so more unbound warfarin available to act.

46
Q

List sources of drug excretion

A

-Breath
-Milk
-Sweat(perspiration)
-Saliva
-Urine
-Faeces
-Bile
-Hair

47
Q

How do you calculate onset and duration of action

A

-Onset of duration: time until drug plasma concentration reaches minimum therapeutic concentration.

-Duration of action: Time drug plasma concentration stays at minimum therapeutic dose or above.

48
Q

How do you calculate peak plasma and time taken to reach peak plasma concentration

A
  • C max.= concentration at peak of curve
    -T max.= time taken to reach C max.
49
Q

How do you calculate absorption half life?

What are the effects of an increased absorption half life

A

-Time between onset of action and T max.
Increasing absorption half life means lower onset, higher duration of drug but lower C max.

50
Q

How do you calculate the plasma clearance half life

A

Time taken betweeen peak plasma concentration and reaching minimum effective dose concentration after C max.

51
Q

What are the factors affecting pharmacokinetics?

A

-Age
-Sex
-Pregnancy
-Body weight
-Ethnicity
-Disease
-other medication
-Genetic variability

MD2002 (10 decks)

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