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Pharmacokinetics of the gays Flashcards

1
Q

(1) Process of administraction

A

1) Absorption
2) Distribution
3) Metabolism
4) Elimination

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2
Q

(1) Bioavailability

A

Proportion of dose that reaches the site of action

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3
Q

(1) Intravenous injection

A 
PROS
100% Bioavailbility 
CONS
-Sterile equipment 
-Trained personnel 
-Expensive 
-Potentially painful
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4
Q

(1) Oral route

A

PROS
Safest, most convenient and economical route
CONS
-Less than 100% Bioavailablility (due to enzymes and pH
-Complex with good
-Requires patient compliance

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5
Q

(1) Fick’s law of passive diffusion

A

Rate = Permeability x surface area x conc diff / thickness of membrane

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6
Q

(1) Other methods of absorption (not including passive diffusion)

A
  • Active transport
  • Ion-pair absorption
  • Pinocytosis
  • Solvent drag
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7
Q

(1) Sites of drug absorption

A

MAIN: Small intestine with large surface area

LITTLE AB: Stomach and colon due to small surface area

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8
Q

(1) Examples of orally administered drugs with problems

A

Aspirin: Irritate stomach and nausea
Tetracyclines: Chelate metals so absorption reduced by milk and iron preparations

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9
Q

(1) WAT is first-pass metabolism

A

After absorption, drugs enter portal system (some drugs rapidly metabolised by liver and gut wall)

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10
Q

(1) Inhalation

A

Lipid soluble anaethetics: rapid absorption

Avoids first pass

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11
Q

(1) Transdermal

A

Outer layer (stratum corneum) rate limiting step
-Low input rate
E.g. Nicotine patches

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12
Q

(1) Buccal/sublingual

A 
Passive absorption (saliva may wash away)
(e.g. GTN for angina)
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13
Q

(1) Intranasal

A

Epithelial metabolism, passive diffusion

e.g. GTN for angina

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14
Q

(1) Rectal

A

Only middle and lower rectum avoid FPM

- Passive diffusion
e. g. Diazepam rectal tubes for status epilepticus

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15
Q

(1) Subcutaneous (under dermis)

A

Only small volumes, passive diffusion, dependent on blood flow
(e.g. vaccines and insluin/GH)

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16
Q

(1) Intramuscular injection

A

LARGE blood flow
-Quick uptake into body

CONS

  • No self administration
  • Can be painful

(e.g. vaccines, antipsychotic drugs)

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17
Q

(1) Only free drug is active and eliminated

A

COURAGE

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18
Q

(1) Factors in tissue distribution

A

1) Lipid solubility
2) Plasma protein binding
3) Molecular weight

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19
Q

(1) WAT is blood-brain barrier

A
  • Layer of tightly joined endothelial cells
  • Prevents many drugs entering brain
  • Lipid soluble drugs pass by passive diff
  • Water soluble drugs only pass via carrier mechanisms
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20
Q

(1) WAT happens to drugs in metabolism

A

1) Converted to inactive metabolties
2) Converted to active metabolites
3) Some drugs are excreted unchanged

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21
Q

(1) Phases of drug metabolism

A

Phase 1: Transforms molecular structure of drug
(Example: Oxidation, hydrolysis, reduction)
Induce polar group/increase water solubility

Phase 2: Conjugation

  • Attaches an endogenous substance (e.g. sulphate) to parent drug or phase 1 metabolite
  • Increases water solubility so it can be elminated in urine
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22
Q

(1) Main excretion route

A

Renal: Only unbound drug is excreted

Lipid soluble drugs can be reabsorbed in renal tubules

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23
Q

(2) What defines estimated volume of distribution

A

Warfarin
-Low lipid solubility + low tissue binding

Amitriptyline
-High lipid solubility + tissue binding

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24
Q

(2) VAS IS DAS Clearance

A

Rate of elimination/conc of input

-Represents virual volume of blood cleared of drug per unit time

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25
(2) Creatinine clearance
Renal clearance of drugs varies linearly with creatinine clearance (Creatinine is break down product of creatine phosphate in muscle)
26
(2) First order elimination kinetics
Rate of elimination of proportional to drug concentration
27
(2) Half-life
This is the time taken for the drug conc to fall by half
28
(2) DISTRIBUTION and ABSORPTION IS A FIRST ORDER PROCESS BRO
Retard
29
(2) Zero order kinetics
Rate of elimination is not proportional to drug conc but is constant (e.g. High dose aspirin) Half-life is not constant but depends on starting concentration
30
(2) Therapeutic drug monitoring
Measuring drugs conc in body to determine most effective dose/avoid toxicity
31
(2) Drugs via therapeutic drug monitoring
- Cardiac drugs: (digoxin due to narrow theraputic) | - Immunosuppressants: Cyclosporin (prevent rejection)
32
(2) Use of urine sampling
- No blood sample needed | - Good for drugs that are eliminted in urine
33
(3) 4 types of receptors`
1) Ligand gated ion channels (ionotropic) 2) GPCR (metabotropic) 3) Kinase-linked R 4) Receptors linked to gene transcription (Nuclear receptors)
34
(3) Responses due to agonists
- Muscle contraction - Change in membrane potential - Production of 2nd messenger - Inhibition of transmitter release
35
(3) Maximum response
1) Finite number of receptors: all occupied 2) Property of tissue/cell (e. g. maximum muscle contraction)
36
(3) Affinity
How well a drug binds to the receptor
37
(3) Efficacy
Measure of the response of the receptor once drug is bound
38
(3) Potency
Combination of both affinity and efficacy
39
(3) How to measure ligand affinity
Ligand binding assay using radio-labelled ligand (must account for non-specific binding)
40
(3) Desensitisation/Tachyphylaxis
1) Receptor modification (phosphoylation) 2) Loss of receptors (internalisation) 3) Exhaustion of mediators 4) Physiological adaptation (homeostatic response)
41
(3) Clinical use of agonists
Adrenaline (Heart: Increase heart rate) Salbutamol (asthma) Dopamine (heart, increase rate and force contraction)
42
(3) Partial agonists
Cannot product a maximal response
43
(3) Clinical use of partial agonists
Buprenorphine (Temgesic) | -Less abuse liability
44
(3) Inverse agonists
Reduce activity of GPCRs that are active in absence of ligand (activity too low to be important in physiological states) (e.g. IA decrease opening of GABA-A receptor)
45
(3) Competitive antagonists
Increase EC50 - Have zero efficacy - Shift to the ring
46
(3) Use of competitive receptor antagonists
- B-blockers (heart hypertension) | - Tubocurarine: nicotinic R antagonist (muscle relaxant)
47
(3) Non-competitive R antagonists
Cannot reach maximum response
48
(3) Spare receptors
Not all 100% of receptors are needed to get full response - Don't need to occupy all R for full response - Kd doesnt equal EC50.
49
(3) Use dependency
The greater a receptro/ion channel is activated the greater the block (Mech: Open channel block or binding to inactivated state)
50
(4) Changes by Anaesthesia
1) Unconsciousness 2) Loss of response to pain (analgesia) 3) Loss of reflexes
51
(4) Local aneasthetics
Act locally to block nerve conduction
52
(4) General anaesthetics
Act in the brain to cause loss of consciousness (Used for operations)
53
(4) stages of anaesthesia
STAGE 1 - Still awake but drowsy - Distorted perception ``` STAGE 2 -Loss of conscinousness -Stimulation of CNS (uncontrolled movements) -Irregular breathing Dangerous phase: Move through as fast ``` STAGE 3 (surgical) - Regular breathing - Cough + vomit reflex depressed - Large skeletal muscles relax STAGE 4 - Breathing becomes shallow and feeble pulse - No ventilation due to depression of medulla oblongata
54
(4) How can depth of anaesthesia be measured?
Using EEG
55
(4) Lipid theory
GA agents dissolve in mem: -Changes bilayer thickness, order parameters, curvature elasticity EVIDENCE 1) Pressure reversal 2) No defined chemcial structure of GAs 3) Meyer-Overton correlation
56
(4) Problems with lipid theory
1) Stereoisomers 2) New compounds don't fit Meyer-Overton correlation 3) Increase carbon chain length (cut off effect) 4) Non-immobilisers 5) Small increases in temperature produce similar changes than GA 6) Similar correlation with partition of GAs into protein
57
(4) Protein theory
GA bind specific mem proteins 1) GABAa R (inhibit) 2) 2 pore K+ channels (control resting potential) 3) NMDA R (excitatory)
58
(4) Criteria for identifying relevant anaesthetic protein targets
1) Reversibly alters target function at clinically relevant conc 2) Target expressed in appropriate anatomical location in brain/spinal cord 3) Stereo selective effects in-vivo parallel actions on target in vitro 4) Target exhibits appropriate sensitivity/insensitivity to model and non-anaesthetic compounds
59
(4) Properties of ideal anaesthetic
1) Rapid action +recovery 2) Minimal irritant properties 3) Miscidble with air/oxygen (doesnt explode) 4) analgesic 5) Muscle relaxant
60
(4) Minimum alveolar concentration (MAC)
Alveolar partial pressure of an inhaled anesthetic, which prevents movement in response to a standard noxious stimulus in 50% of patients
61
(4) Pharmacokinetics of inhaled agents
1) Greater solubility in blood (determined by blood/gas co-efficent) 2) Reduced rate of rise of alveolar partial pressure 3) Reduced rate of rise of brain partial pressure 4) Slower rate of anaesthesia onset
62
(4) Recovery from anaesthesia
Elimination of inhaled anaesethetics mainly by ventilation through lungs
63
(4) Factors decreasing length of recovery
1) Reduction of inspired concentration 2) High alveolar ventilation 3) Low blood gas solubility 4) Short duration of anaesthesia
64
(4) Intravenous anaesthetics
Propofol - GABAa receptor responses - Used as induction agent - Metabolised in liver Thiopental - GABAa receptors - Highly lipid soluble - Poor analgesic and muscle relaxant Etomidate - Induction of anaethesia - Rapid recovery Ketamine - Abuse potential and dependance - Paediatric anaethesia
65
(4) Inhalation anaesthetics
Halothane - potent and smooth induction - moderate muscle relaxation Isoflurane - Less potent - Fall in BP - Depress relaxation - Muscle relaxation - Less risk of hepatotoxicity but less than halothane Nitrous oxide - Maintainance of anaesthesia - used in obstetrics
66
(5) Pain
An unpleasant sensory and emotional experience assocaited with real or potential tissue damage or described in terms of tissue damage
67
(5) Peripheral pain pathways
1) Fast pain (sharp, short duration, well locailised) A (delta) fibres: myelinated with large diameter 2) Slower pain (dull, diffuse, long lasting, poorly localised) C fibres: Unmyelinated Small diameter
68
(5) A pain pathway
Spinothalamic tract
69
(5) Analgesics (pain killers)
- Local anaesthetics (block nerve conduction) - General anaesthetics - Opioids (morphine)
70
(5) CNS effects of Opioids
1) Profound analgesia (without loss of consciousness) 2) Respiratory depression (reduces PCO2 sensitivity of respiratory centre in medulla) 3) Nausea and vomiting 4) Euphoria 5) Dry mouth 6) Drowsiness 7) Depression of cough reflex Pinpoint pupils are diagnostic feature of opiate overdose
71
(5) Other effects of opioids
1) GI tract - Increases tone and reduced motility of gut 2) Direct release of histamine (mast cells) - Bronchocontriction
72
(5) Endogenous ligands for opioid receptors
Endorphins and enkephalins HOW FOUND 1) Made brain extracts 2) Tested extracts on contractions in guinea pig ileum with actions blocked by naloxone
73
(5) Distribution of Opioid receptors
Found in areas like PAG, rostral ventral medulla, substantia gelantose)
74
(5) Types of Opioid receptors
1) MOP (CNS/periphery) - Analgesia, respiratory depression 2) DOP (Pontine nuclei) - Analgesia, key in periphery 3) KOP (Hypothalamus, PAG) - Analgesia, sediation
75
(5) Central actions on nociceptive pathways
1) Inhibition of pain transmission through dorsal horn | 2) Inhibit transmitter release from primary afferents
76
(5) Effects of injecting morphine into PAG
- Analgesia - MOP R in PAG - Removes GABA inhibition in PAG to enhance descending inhibition of pain transmission in spinal cord
77
(5) Tolerance
Increase in dose required to produce a pharmacological effect
78
(5) Dependence
Compulsive craving that develops as a result of repeated administration of drug.
79
(5) Morphine
Used for acute and chronic pain | -3-4 hour half life
80
(5) Other examples of opioids
Codeine Pethidine Methadone
81
(5) Opioid antagonists
Naloxone | Used to treat overdose
82
(5) Partial agonists
Buprenophine (Temgesic) | Partial agonist at MOP receptors

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