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164 Cards in this Set
- Front
- Back
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What is "Quality use of medicines" defined as?
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- selecting management options wisely
- choosing suitable medications - using medicines safely and effectively |
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Difference between pharmacokinetics and pharmacodynamics?
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Pharmacokinetics = what body does to drug
Pharmacodynamics = what drug does to body |
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Why measure blood concentrations of drugs?
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Because it's a surrogate marker that we know to be ass'd with benefical effect
- Concentration in plasma is analytical method - hard to measure concentration at effect site - pharmacological effect hard to measure |
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What factors affect the rate and extent of drug absorption from GI tract?
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1. Formulation/drug characteristics (i.e. tablet dissolution/disintegration, stability of drug in GI lumen)
2. Pharmacokinetic characteristics (first pass effect - metabolism by bacteria, gut wall, liver) 3. Patient characteristics (gastric/intestinal transit time, disease) 4. Presence of other substances in tract (food, drugs) |
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What is "enteric coating" of a tablet?
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pH dependent coating to allow it to move through the stomach
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Why "enteric coat" a tablet?
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- to prevent irritation of stomach
- to target delivery to intestine (i.e. prevent degradation in stomach) |
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T/F: nicotine has low first pass effect
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FALSE - nicotine has high first pass effect - not active after oral administration
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T/F: food delays gastric emptying
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TRUE - especially a fatty meal which will slow emptying of stomach
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Why co-administer a drug with food?
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To stimulate gastric acid secretion
Incr. absorption by helping solubilise insoluble drugs Slow absorption rate Chelate to form insoluble complexes |
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What are the three steps of renal elimation of a drug?
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1. Filtration --> all unbound drug in plasma is filtered
2. Secretion --> carrier mediated 3. Passive reabsorption --> relatively insoluble/uncharged drugs |
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Renal clearance of drugs is corellated with clearance of ______ ?
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Creatinine.
(a breakdown product of muscle metabolism) Rate of appearance in urine indicates renal function |
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What is "metabolic biotransformation"?
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Enzymatic chemical conversion or conjugation that makes a metabolite MORE SOLUBLE
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T/F: highly bound drugs are more distributed to tissues
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FALSE - while fraction of unbound drugs determines extent of distribution, HIGHLY BOUND DRUGS ARE LESS DISTRIBUTED and UNBOUND SPECIES are pharmacologically active
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What are the 5 pharmacokinetic parameters?
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1. Clearance
2. Volume distribution 3. Bioavailability 4. Half-life 5. Area-under-concentration-time-curve |
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What is "Clearance"
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Efficiency of elimination of drug from body.
[Volume of blood cleared of drug per unit time] |
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What is "volume of distribution"
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apparent volume into which a drug distributes in the body at equilibrium
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What is "Bioavailability"
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Fraction of administered dose that reaches systemic circulation
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What is the bioavailability of a drug after an IV dose?
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1
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What is "Half life"
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time taken for concentration / amount of drug to decrease by 50%
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What is "steady state" and how many half lives does it take to get there?
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Steady state is when:
RATE OF INPUT = RATE OF OUTPUT Takes 4-5 half lives to get there. |
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How do you calculate loading dose?
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Loading dose = V/F x desired concentration
V=volume distribution F=bioavailability |
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How do you calculate maintenance dose rate?
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Maintenance dose rate = Css x CL/F
Css=concentration at steady state CL=clearance F=bioavailability |
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What is "one standard drink"?
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10g alcohol
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Where does absorption of alochol take place?
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Mostly in SMALL INTESTINE.
But also mouth, stomach, large intestine |
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T/F: food "dilutes" alcohol by slowing down gastric emptying.
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TRUE
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Post-absorption, where is the major site of alcohol breakdown?
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90% broken down in liver
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T/F: Alcohol cannot cross BBB
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False - it CAN!
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What is ethanol broken down to?
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1. Ethanol ----(alcohol dehydrogenase)--->
2. Acetaldehyde -----(ALDH)----> 3. Acetic acid ----(Acetyl CoA)----> 4. Citric Acid Cycle |
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Which 3 breakdown pathways promote acetaldehyde formation?
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1. Alcohol dehydrogenase [major]
2. MEOS (microsomal ethanol oxidising system) 3. Catalase |
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Can alcohol dehydrogenase be saturated?
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YES.
At approx 10uM/L |
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Which inducible pathway responds to chronic alcohol exposure?
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Microsomal ethanol oxidising system.
Km=10mM --> kicks in when hig h [ethanol] |
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Which cytochrome P450 enzyme is involved in response to chronic alcohol exposure ?
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Cytochrome P450 2E1
[microsomal ethanol oxidising system] |
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How does acetaldehyde disturb structure of surface proteins?
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forms adducts with proteins.
Binds to SH groups and positively charged lysine side chains |
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T/F: acetaldehyde reduces lipid peroxidation
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FALSE - enhances lipid peroxidation
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Which cancers are associated with acedetaldehyde? What is the mechanism by which they are caused?
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Oral, pharyngeal, esophagus, pancreas, liver, colon
Acetaldehyde induces mutations that deactivate p53 |
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Which is the most important form of ALDH (acetaldehyde dehydrogenase)?
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ALDH2 = major mitochondrial form
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Which ALDH polymorphism promotes flushing syndrome? Why?
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Homozygotes for ALDH2*2.
ALDH2*2 has LOW ACTIVITY --> serum acetaldehyde level markedly increases post-ethanol consumption |
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What is flushing syndrome?
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Increased serum acetaldehyde concentration --> facial flushing, nausea, palpations
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T/F: Heterozygotes [ALDH2*1/ALDH2*2] have "mild flushing syndrome" which can be pleasant
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TRUE
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Where in body is alcohol dehydrogenase?
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Stomach, Liver
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Large ethanol consumption leads to production of lots of ___ ? How?
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ATP.
Acetic acid --> acetyl CoA --> citric acid cycle --> generation of NADH and ATP |
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how does acetaldehyde cause immune responses against liver?
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by making normal proteins immunogenic
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T/F: glycolysis is suppressed following alcohol consumption
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TRUE
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Why do you get decreased fatty acid utilisation after alcohol consumption?
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Don't need fatty acids, because using acetic acid instead to generate acetyl CoA.
Also, need NAD+ (which has been converted to NADH) to convert fatty acids to acetyl CoA |
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Why do you at risk of lactic acidosis after alcohol consumption?
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because you need NAD+ to convert pyruvate to acetyl CoA.
Since NAD+ has been converted to NADH, the pyruvate is converted to lactate instead |
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Thiamine is vitamin ___ ?
How is it activated? |
Thiamine = vitamin B1.
Activated by convertion to thyamine pyrophosphate |
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Thiamine deficiency can lead to _____ in alcoholics.
What are the manifestations of these syndomes? |
Wernecke's encephalopathy or, later, Korsakov's psychosis.
Wernicke's= acute organic brain sydnrome, acute paralysis of extraocular mm. Korsakov's = chronic, persistant STM loss, destructive brain changes (eg mamillary bodies, thalamus) |
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Phospholipase D promotes which uncommon ethanol metabolism pathway?
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Phosphatidycholine OR phosphatidyserine swaps their choline/serine for ETHANOL
i.e. get phosphatidyethanol |
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What are the pathological impacts of phosphatidyethanol ?
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- Intestinal hyperplasia
- Disrupted transcriptional control of cell proliferation |
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What are the acute pharmacological effects of alcohol?
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DEPRESSIVE effects:
- reduced NDMA activity in brain - reduced voltage-gated Ca2+ channel activity - Increased GABA-A activity |
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What are the chronic pharmacological effects of alcohol?
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COMPENSATORY changes.
- increased NMDA receptors - Increased voltage-gated Ca2+ channels - reduced GABA-A |
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T/F: alcohol is a weak drug
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TRUE
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T/F: alcohol withdrawal is a state of hypoexcitability
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FALSE
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T/F: all neurons in brain have glutamate and GABA receptors?
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True.
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What are the two main neurotransmitters in the brain? Are the excitatory or inhibitory?
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GLUTAMATE = excitatory
GABA = inhibitory |
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What are the 2 types of glutamate receptors?
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1. IONOTROPIC (ligand-gated ion channels)
2. METABOTROPIC (G-protein coupled receptors) |
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What are the 3 types of ionotropic glutamate receptors?
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1. NMDA
2. AMPA 3. kainate |
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T/F: AMPA and kainate channels tend to be co-localised
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FALSE.
AMPA and NMDA channels tend to be co-localised |
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T/F: Kainate receptors are often found where AMPA receptors are NOT.
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TRUE
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What percentage of neurons in brain release glutamate?
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50%
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What percentage of neurons in brain release GABA?
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30-40%
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T/F: Neurons can only release one kind of neurotransmitter.
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FALSE
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What are the main differences between AMPA and NMDA receptors?
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AMPA:
- fast onset - rapid desensitisation NMDA: - voltage-dependent activation (due to Mg2+ block) - Slower desensitisation |
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At resting or slightly depolarised post-synaptic membrane potential, glutamate will cause ion flow (and thus an EPSP) through
A) NMDA receptors B) AMPA receptors |
B) AMPA receptors.
NMDA has a Mg2+ block which will prevent conductance of ions. As such the EPSP is caused by ion flow through AMPA receptors |
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How is the Mg2+ block removed from NMDA receptors?
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Sufficient membrane depolarisation (helped along by influx of Na+ through AMPA receptors)
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How does the NMDA channel respond to glutamate?
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If sufficient membrane depolarisation, it will allow influx of Na+ and Ca2+ (which is important second messenger)
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T/F: AMPA receptors can be activated by single glutamate vesicle?
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TRUE
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How does glutamate cause an overal increase in membrane excitability by binding to metabotropic receptors?
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1. glutamate binding causes change in conformation
2. G-protein coupled second messengers --> inhibit K+ channels --> mobilise Ca2+ |
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Which GABA receptors are ionotropic and which are metabotropic?
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Ionotropic = GABA-A and GABA-C
Metabotropic = GABA-B1 + GABA-B2 subunits [i.e. metaBotropic - B] |
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What are the usual subunits of GABA-A
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2 alpha
2 beta 1 gamma |
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What are the usual subunits of GABA-C
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5 subunits of the same type (i.e. its homomeric)
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How does GABA mediate its effects via binding to ionotropic receptors?
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1. GABA binding changes conformation
2. Cl- into cell 3. Reduced membrane excitability |
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How does GABA mediate its effects via binding to metabotropic receptors?
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1. GABA binding causes conformational change
2. G protein coupled 2nd messengers --> activate K+ channels --> inhibit Ca2+ channels 3. Overal reduction in membrane excitability |
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Ethanol reduces
A) excitation in brain B) inhibition in brain |
A) excitation
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Ethanol increases
A) excitation in brain B) inhibition in brain |
B) inhibition
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Ethanol blocks
A)NMDA receptors B)AMPA receptors C)GABA-A receptors D)GABA-C receptors |
A) NMDA receptors (some)
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Ethanol can enhance activation of:
A)NMDA receptors B)AMPA receptors C)GABA-A receptors D)GABA-C receptors |
C) GABA-A receptors (some)
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What does an allosteric modulator do?
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Enchances subsequent binding
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T/F: ethanol is an allosteric modulator of GABA-A receptors
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TRUE
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T/F: ethanol is an allosteric modulator of NMDA receptors
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FALSE - allosteric modulator of GABA-A receptors
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At extremely high ethanol doses (50-400mM) ethanol acts on which GABA-A receptors?
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All of them - i.e. loses selectivity
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At sedative doses of ethanol (0.1 BAC, 20mM) ethanol acts on which GABA-A receptors?
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those containing gamma-2L subunit
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At low doses of ethanol (5mM) ethanol acts on which GABA-A receptors?
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those containing DELTA subunit
(note that most contain alpha, beta and gamma) |
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Many sedative drugs act on which receptor?
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GABA-A
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Barbituates enhance the action of GABA-A receptors by which mechanism?
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Occupancy mechanism
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Benzodiazepines enhance action of GABA-A receptors containing which subunit?
And by what mechanism? |
GABA-A receptors containing gamma-2 subunit
Rate mechanism. |
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What drugs are used to treat alcohol withdrawal ?
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Benzodiazepines
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In NSW, what are the maximal blood alcohol concentrations for the following drivers?
Learner drivers Public vehicle drivers Full license Dangerous goods drivers Provisional drivers Visiting drivers Gross vehicle mass drivers |
Learner drivers - ZERO
Public vehicle drivers - 0.02 Full license - 0.05 Dangerous goods drivers -0.02 Provisional drivers - ZERO Visiting drivers - ZERO Gross vehicle mass drivers - 0.02 |
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Ethanol increases mean opening time of which receptors?
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GABA-A
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What are some behavioural effects of ethanol?
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Muscle relaxation (myorelaxation)
Reduction in anxiety (anxiolysis) Sedation Anticonvulsant At higher doses: motor incoordination, memory loss, sleep induction, respiratory depression |
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Most inhibitory input is on which part of the neuron?
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The axon hillock
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GABA is synthesised from which amino acid?
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Glutamate
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T/F: excitatory input is generally close to the axon hillock
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FALSE.
Excitatory inputs are often further away than inhibitory ones (which are very close to axon hillock) |
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50% of alcohol consumption is consumed by what proportion of the population
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10-20% population
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Given equivalent doses IV and orally - describe the blood concentration curves for each? Is the area the same under each curve?
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IV: early peak, rapid decline
Oral: slower to reach peak, slower decline Area same? YES |
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T/F: time to reach steady state is independent of dosage?
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True
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What is the difference between heroin and methadone in regard to steady states?
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Heroin half life = 3 hrs
Methadone half life = 24 hrs --> Heroin concentration will constantly fluctuate- much harder to reach steady state --> Taking methadone once/day will allow steady state to be reached |
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Donald Goodwin's study of genetic involvement in alcohol dependence came to what conclusion?
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That genetics ARE involved!
Followed adopted children whose biological fathers were alcoholics. 4x Increased risk they would become alcoholics too |
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Cloninger noted two separate modes of inheritance. Identify and describe each.
1. _____ 2. _____ |
1. Patrilineal = adolescent onset, antisocial behaviour and severe drinking problems
2. Milder form affecting both sexes, requires environmental precipitant. (but biological children 2x risk) |
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Different polymorphisms of which gene affects drinking tolerance?
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Serotonin transporter gene
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Which genotype of the serotonin transporter gene confers increased alcohol tolerance?
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The short genotype,
Increased tolerance-->heavier drinking |
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How did ondansetron decrease relapse in alcohol dependence? In which group of people?
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- Serotonin receptor antagonist
- Those with short phenotype responded - Only those with early onset alcohol dependence responded |
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What are the features of alcohol dependence syndrome?
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1. Tolerance
2. Repeated withdrawal symptoms 3. Relief of withdrawal with further drinking 4. Salience of drug seeking behaviour (prioritise it) 5. Subjective awareness of a compulsion to drink (misconstrue compulsion) 6. Narrowing of the drinking repertoire 7. Reinstatement after abstinence |
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Which neurotransmittor is involved in reward pathway?
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Dopamine
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What is an endobiotic? Give an example of one
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chemical substance produced by the body to accomplish a variety of tasks
E.g. steroid hormones, bile acids |
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What are 3 mechanisms by which a cell can cope with toxc molecules?
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Phase I = Oxidative metabolism
Phase II = Conjugative metabolism Phase III = Transport |
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Which group of enzymes are responsible for conjugative metabolism?
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Transferases
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Why make a molecule more water soluble?
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So it can be excreted in bile (-->faeces) or urine
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Which group of enzymes is involved in oxidative metabolism
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Cytochrome P450 family
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Which 2 processes aim to make molecules more water soluble?
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Oxidative (phase I) and conjugative (phase II) metabolism
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Where does metabolism take place?
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Phase I and II predominantly in liver.
Also gut, circulation, other tissues |
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What are some enzymes located in the circulation responsible for metabolism?
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Plasma cholinesterases, proteases
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What is an "inducible enzyme"
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Enzyme that responds in an adaptive fashion by massive up-regulation of expression in response to some xenobiotics
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What is a sinusoid? where are they found?
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specialised, fenestrated capillary that delivers xenobiotics to hepatocytes
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What are the two phases in a biotransformation reaction? What happens in each phase?
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Phase I = Oxidation/reduction
-->Alter a molecules structure/reactivity [mainly cytochrome P450] Phase II = Conjugation to endogenous molecule [mainly transferases] |
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What is "bio-activation". Give an example.
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Bio-activation = metabolism to give a more active compound.
Eg. codeine --> morphine |
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Paracetamol is metabolised via which enzyme? To give which product?
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CYP 2E1
Product = NAPQI (toxic) |
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N-acetyl cisteine is given when? what does it do?
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Given after paracetamol overdose.
Regenerates glutathione stores so that it can be conjugated with NAPQI (-->less toxic) |
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Codeine is conjugated with which molecule to make it less active?
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glucuronide
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Cytochrome P450 enzymes act as what?
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mono-oxidases - the major enzymes of phase I metabolism
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The bioavailability of an orally administered drug depends on:
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1. Fraction absorbed by gut
2. First pass metabolism in liver |
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Which factors determine the rate of liver drug metabolism?
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1. Intrinsic Clearance (liver enzyme affinity)
2. Liver blood flow (determines rate at which drug delivered to liver) 3. Binding to plasma proteins (only free drug can diffuse into liver cells) |
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T/F: only free drug can diffuse into liver cells
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true
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T/F: Induction of enzymes is almost always transcriptional phenomenon
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true
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T/F: enzyme induction is a common source of drug interactions
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True
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Drugs that are rapidly cleared by the liver depend mostly on _____
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Blood flow to liver
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Low clearance drugs depend mostly on ___ and ___
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intrinsic clearance and protein binding.
Blood flow doesn't matter as much |
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What is reversible inhibition of cytochrome P450?
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inhibitor competes with the drug for P450 binding
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How does "Metabolite intermediate complexation" inhibit cytochrome P450?
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Long term de-activation of Cytochrome P450:
- CYP has metabolises the drug - Metabolite binds to CYP molecule and prevents binding of other drugs to it |
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Describe the 2 mechanisms of tolerance
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1. Metabolic
--> induction of degrative enzymes 2. Neuroadapatation --> receptor becomes desensitised or down-regulated |
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Which receptors does nicotine act on? Describe acute tolerance to nicotine.
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Acts on nAChRs to cause influx of Na+.
Acute tolerance = receptors desensitize. Nicotine binds and prevents other substances from binding/prevents other substances from causing a conformational change of the nAChR |
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Describe the effect of prolonged smoking on nAChRs.
How does the brain adapt to this effect? |
nAChRs become irreversibly activated.
Brain counter-adapts i.e. increases expression of nAChRs. |
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T/F: acute nicotine tolerance is reversible?
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True
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T/F: Psychostimulants eg amphetamine or cocaine produce little if any tolerance
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True
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List following in order of potency to cause tolerance:
Psychostimulants Cannibis Opiods Benzodiazepines Nicotine Alcohol |
Opiods >
Benzodiazepines, Cannabis > Nicotine, Alcohol > Psychostimulants |
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What type of receptors are opioid receptors?
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G coupled
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How does tolerance to morphine occur?
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Desensitization of the G protein joined to the mu opioid receptor.
(also get downregulation) |
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Heroin acts on which receptors? and does what?
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Heroin acts on mu opioid receptors to decrease likelihood of neuronal firing:
1. increases K+ efflux (K+ moves out of cell) 2. Inhibits action of adenylate cyclase (--> less cAMP) |
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Repeated use of opioids has what effect on mu opioid receptors?
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1. Morphine binds
2. G protein mobilised within cell (i.e. leaves receptor) 3. Phosphorylation site on receptor exposed 4. G-protein coupled kinases phosphoylate these sites. 5. Receptor now can't interact with intracellular signalling molecules 6. Receptor desensitised. |
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What do Barr (beta arrestins) do?
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After repeated opiod use, opioid receptors have been phosphorylated and thus desensitised. Barr are able to bind to these newly phosphorylated sites and take the receptor to an endosome (where it is degraded or recycled) - i.e. down regulation of the receptor
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Withdrawal from opioids gives which symptoms?
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pain, fever, nausea, diarrhoea, goose-pimples
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T/F: withdrawal symptoms from opioid withdrawal are more life threatening than those from alcohol/benzodiazepine withdrawal
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False.
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T/F: withdrawal symptoms are usually opposite to the symptoms experienced in acute exposure
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True.
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Heroin, nicotine and stimulants excite reward pathway cells that release which neurotransmittor?
|
Dopamine
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Which brain structure is implicated in opioid counter-adaptation?
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The locus coeruleus (in the pons)
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Which transcription factor is up-regulated in chronic opioid users? What does it do? What does this imply for withdrawal?
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CREB.
Increases transcription of gene for adenylate cyclase (--> more cAMP --> increase excitability) Withdrawal - increased excitability because lots of AC and no drug to balance it out |
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What is the mesocortical pathway?
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Connects prefrontal cortex and VTA
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What is the mesolimbic pathway?
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Connects VTA and NAcc
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What is involved in emergency management of seizures?
|
Ensure airway patent
Protect subject from dangerous situations/self-induced injury Anti-convulsants if prolonged |
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What are some specific causes of seizures ?
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Trauma, low O2 content, infections of brain/linings, vascular disorders, pathology in brain, biochemical substances in brain, toxins, hyperthermia
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Grand mal seizures are characterised by:
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Tonic phase: stiffening of body and falling to groun
Clonic phase: gross, non-purposive movements of extremities |
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What is status epilepticus?
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When person does not recover fully from seizure and continues to have successive fits
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What are the proposed underlying mechanisms of a seizure?
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Synchronous neuronal discharges, may be mediated by excessive glutaminergic neurotransmission, or insufficient GABAergic neurotransmission
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In addition to enhancing GABA at GABA-A receptors, acute alcohol exposure also enhances neurotransmission at
1. ____ 2. ____ |
1. nAChRs
2. 5-HT3 receptors |
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T/F: chronic alcohol exposure reduces kainate function
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False
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Memory is often lost at which blood alcohol concentration?
|
0.150g/100mL
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T/F: sensory acuity only becomes impaired at high ethanol concentrations
|
true
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Motor ataxia and slurred speech results from what?
|
loss of descending inhibitory control at motor synapses, and impaired proprioceptor sensation
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What is the difference between the actions barbiturates and benzodiazepines on GABA-A receptors
|
Benzos: increase probability of opening
Baaaaarbiturates: increase mean opening time (think: Barbies are slow) |
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Is tolerance specific for each drug?
|
Tolerance to one sedative tends to generalise (to some extent) to all sedatives
--> CROSS TOLERANCE if have same molecular MOA or act in similular manner on NT system |
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What are the alcohol recommendations for males and females?
|
No more than 4 standard drinks on any one occasion.
No more than 2 standard drinks on any one day. |
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Alcohol accounts for what percentage of deaths in Australia?
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Males: 7%
Females: 4% |
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What is the leading cause of liver cirrhosis?
What can exacerbate it? |
Alcohol.
At lower consumption levels, liver cirrhosis can be exacerbated by Hepatitis B and C |
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What factors can lead to early identification of those at risk of ethanol/sedative withdrawal?
|
Males drinking > 60g alcohol/day
Females drinking >40g alcohol/day Therapeutic or more levels of sedative for 3+ months Pt with Hx of withdrawal Pt with stigmata of harmful consumption (red face, hepatomegaly, Dupuytren's contracture) Pt>60yo with regular ethanol/sedative use |
