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65 Cards in this Set
- Front
- Back
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AGONIST
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Stimulate the response from the chemical mediaters
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ANTAGONIST
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inhibit the response from the chemical mediaters
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Pharmacology
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A branch of science dealing with the properties and effects of drugs or medication
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Biotechnology
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Based on the DNA of the person
targets a specific enzyme |
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Define drug
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any substance that is used with the intention to provide benefit for the patient
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Pharamacokinetics
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how rapidly it goes through the body, how long it stays in target cells
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Absorption
Barriers: |
: IV IM sub/cut , topical, suppository
Size of molecule, pH of stomach, lipophilic properties |
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Bioavailability
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the amount it’s absorbed. IV is 100%
Some must be taken with food due to bioavailability |
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Distribution how and barriers
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Drugs must be lipophilic in order for absorption to take place solubility in plasma membrane may be limited
If drug binds to protein distribution is improved – once blood has reached the tissue the binding is released Barriers: BBB – capillaries, membrane and astrocyte feet stops some drugs from passing - Placenta barrier doesn’t block as many drugs from crossing over, therefore causing some defects in the baby |
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Metabolised how and why and where
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used to breakdown the chemical properties of the drug to stop it from being lipo-philic and therefore to be excreted faster.
Without metabolism the drugs will build up in the body and become toxic Sites where occur: Placenta, liver, kidneys, membrane, intestines and lungs |
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Phase 1 and 2 of metabolisation
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Phase 1: enzymes effect the structure of the drug
: Oxidisation – adding O2 : Reduction – adding H+ : Hydrolysis – adding H20 Molecules Phase 2: The phase 1 molecule is formed with a another molecule to render the product soluble for excretion |
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First-pass effect what it is and does
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Taken by the hepatic blood system after absorption
Which takes the bolus to the liver for processing The liver is the main metabolic zone and therefore the drug can be extensively metabolised before reaching the body. This is known as the first pass effect - reduces bioavailability |
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Excretionwhere and main
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By kidneys and GI tract
The main excretions are Passive: the glomerular filtration and tubular reabsorption Active: tubular secretion |
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4 Ways excreted
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Drug transported to the liver where it can then be broken down
The drug can be absorped into the GI tract and excreted through faeces The drug can be metabolised in the liver and transported into the kidneys The drug is transported into the kidneys unchanged and excreted in urine |
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Half-life Drugs what and examples
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Used when the periodic re-ingestion of medication is needed through blood concentrations
Long half-life: warfarin Short half-life: adrenaline |
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Pharmacodynamics
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what the body does to the drug
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What drugs act on :
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Receptors – bind perfectly onto the receptors
Enzymes – more specific Chemical action Physical action - osmosis |
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Barriers of pharmacodynamics
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Barriers: Age, liver damage, kidney damage, drug tolerance; the body requires more medication to reach the same effect, heart damage, interaction with other drugs.
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Pharmacoeconomics
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Study of the cost of medication
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Polypharmacy
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Number of medications
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The medication administration cycle DRRDAM
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Decision to dispense – comprehensive, accurate and respond directly to the patients needs
Record - by doctor, legal requirements including contact, doctors name, signiture Review Dispense Administer – Assess the patient, 6 rights Monitor – the effect of the medication if any |
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Human Errors
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Systems approach
All humans are fallible Errors are consequences as opposed to causes |
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Active failures and latent conditions
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Active failures – accidents that have direct effect on the patient
Latent conditions – remain dormant for many years, can be fixed before errors occur. Can include staffing issues, inadequate equipment, alarms etc. |
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Reduction of error techniques:
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Tall Men Lettering
Not putting similar named drugs together Labelling Technology - barcode |
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Adult Learning Principles
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Motivation
Life experiences Application Learning styles including – Visual, auditory and kinaesthetic |
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Sympathetic T1-L2
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Short pre ganglion long post
Nonadrenaline and adrenaline Nerves called adrenergic |
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Adrenergic
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alpha and beta-receptors
Adrenergic agonists – sympathomimetic Adrenergic antagonists – sympatholytic |
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Alpha1 agonists causes
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smooth muscle cellular membrane promoting contraction
Vasoconstriction – increased BP good for decrease blood loss GIT and urinary smooth muscle contraction Sweating and goose bumps |
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Alpha1 antagonist
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vasodilation of blood vessels causing decrease BP
Pupil contriction Increasing GIT and voiding |
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Alpha 2 receptors
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Negative feedback loop, inhibits neurotransmitter release
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Beta 1
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Found in the cardiac muscle cell membrane promoting contraction
Myocardium Smooth muscle GIT sphincters Renal arterioles |
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Beta 1 agonists
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increased heart rate and cardiac output
Reduces digestion and GIT Increased glomular filtration due to heart rate and cardiac output |
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Beta 1 antagonists –
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decreased heart rate and cardiac output
Increased GIT and digestion Decreased renal output, decreased glomular filtration |
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Beta 2
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found in smooth mucle, skeletal muscle, brain, kidney uterus and heart!
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Beta 2 agonist
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bronchodilation
Vasodilation Relaxed uterus |
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Parasympathetic
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Long pre ganglion and short post
Acetacoline Ach Nerves called cholinergic |
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Sympathetic PARASYMPATHETIC
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(adrenaline) (noradrenaline)
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Pharmacology cholingergic
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Cholinergic pharmacology has a greater effect on the para-sympathetic nerve pathway
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CHOLINERGIC MECHANISM OF ACTION
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1. Action potential travels along nerve
2. Depolarisation causes release of Acetylcholine (ACh) into synaptic gap 3. ACh diffuses across synaptic gap and interacts with cholinergic postsynaptic receptors= response enacted 4. The transmitter is removed from the synaptic gap by acetylcholinesterase, an enzyme 5. Choline is returned to the presynaptic terminal to be synthesised into new transmitter |
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Ach receptiors
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nicotinic and muscarinic
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Nicotinic agnoist found and effect
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responds from nicotine
Activated by ach Receptors location in autonomic and CNS divisions Effect: increased skeletal muscle tone – increased muscle spasms and shakes Relaxation and wellbeing Increased adrenaline and noradrenaline from medulla |
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Nicotinic antagonist
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doesn’t respond to nicotine, reduce BP, reduce GIT, reduce urine
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NICOTINIC RECEPTOR ANTAGONIST DRUGS
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Two groups of drugs:
1. Ganglionic blockers a) Act on sympathetic and parasympathetic nerves. b) Decreases cardiac output and HR but now mostly replaced by adrenergic antagonists which are safer 2. Neuromuscular blockers a) Act at the neuromuscular junction b) Ach competitive antagonists c) Depolarizing or Non depolarising |
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Muscarinic agonist
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chemical muscarin
Sympathetic and parasympathetic M1 – CNS; memory, arousal and attention M2 – Heart; electrical signals M3 – smooth muscle; response on bronchioles and bladder |
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neuron secretion
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neurotransmitter
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Endocrine secretion
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local hormone
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Pancreatic secretion
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classic hormone
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autocrine
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Autocoid
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Histamine: Autacoid/autocrine
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Stored in cells – mast, basophils, thrombocytes
Allergic or inflammatory reaction Protective mechanism for the body Stimulates pain receptors and dialates blood vessels – increasing capillary permeability Anaphylactic |
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Histamine receptors:
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H1 and H2 – clinical significance
H3 and H4 - unknown |
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H1 where
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H1 – postcappilary venules
Vascular beds CNS Peripheral nerve endings Resp GIT Heart |
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H2 where
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Stomach
CNS Heart Parietal cells to secrete acid |
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Histamine receptors
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Smooth contract
Dialating blood vessels ( stimulate secretion itching feeling - H1 wakeful ness and sedation |
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Medication on antihistamine
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H1 antagonists - minimise response
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H2 antagonist
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Heart burn (stomach) GORD
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Prostaglandins major effects (think prostate)
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chemical that are distributed widley throughout body
numerous effects Fatty acids needed regulate and control every tissue of the body used when something needs to happen fast |
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Prostaglanins antagonist drugs
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stop anflammatory response
inflammation, swelling, pain |
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Enzyme responsible for prostaglandins product
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COX
if stop this enzyme it will stop prostaglandins from being produced - pain relievers |
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Cox 1 and 2 found
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Cox 1 - stomach, intestine, kidneys, renal, platelets
Cox 2 - pain, inflammation and fever |
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COX 2 inhibiters problem
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blood clot
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Serotonin
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found throughout the body
used as neurotransmitter, increases Ach, neuromodulater, autocoid (locally acting) CNS, smooth muscle, mood |
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Serotonin antagonists
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Depression, anxiety, migraine
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Serotonin syndrome symptoms
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Change in mental
hypertension ataxia |
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nitric oxide
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signalling molecules
airway tone, caridac, inflammation potent vasodialater - endothelial lining of blood vessels |
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Endothelin
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Potent vasoconstrictor
found in endothelial cells |
