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Pharmacology Flashcards

1
Q

What is TIVA

A

Form of anaesthesia utilising only intravenous drugs, commonly a combination of a hypnotic agent such as propofol and a synergistic agent such as remifentanil

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2
Q

Indications of TIVA

A

Patient factors
- History of malignant hyperthermia
- Severe PONV
Surgical factors
- Shared airway surgery
- Smooth emergence required e.g. neurosurgery
- Use of neurophysiological monitoring
Practical
- Non-theatre
- Transfer

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3
Q

Safety considerations

A

General
- Vigilant anaesthetist e.g. drug errors
- pEEG monitoring (particularly if NMBD)
Equipment
- Visible free flowing drip
- Pumps - low / high pressure alarms, near end of syringe alarm
- Anti-syphon and anti-reflux valves
Organisational
- single strength of propofol stocked

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4
Q

Target controlled infusion

A
  • Computer generated relevant pharmcokinetic model
  • Set target concentration (e.g. in effect site) by anaesthetist
  • Uses demographic data to manipulate infusion rate to achieve desired concentration
  • increasing target - pump delivers bolus and increases rate
  • reducing target - pump interrupts delivery then re-starts at lower rate
  • Significant inter-patient variability

User interface
- patient demographic details etc
computer / microprocessor
- implements / calculates the model
infusion device
- up to 1200ml/hr, precision 0.1ml/hr

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5
Q

Three compartment model

A
  • Body in 3 compartment
  • central compartment is plasma where drug is administered and removed from (V1)
  • drug redistributes initially to highly vascular tissue (V2) with rate constant for redistribution between central and V2
  • Also redistributes to less vascular tissue via different rate constants (V3)
  • Eventually all 3 compartments will be in equilibrium
  • Models how infusions of drugs such as propofol behave within the body
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6
Q

Differences between three compartment models

A

Marsh - compartment sizes depend n weight, rate constants are fixed. Plasma target generally
Schnider - V1/V3 fixed, V2 depends on age, some rate constants variable. calculates lean body mass for dosing
Paedfusor / Kataria - paediatrics
Eleveld - new paeds / adults

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7
Q

Marsh vs Schnider

A
  1. size of central compartment
    - Schneider uses fixed central compartment (smaller than marsh) - estimated concentrations will vary
  2. age
    - Schneider better for elderly, allows reduced rate of clearance
  3. dose of propofol
    - differences in infusion rates decreases with time. Schneider uses less
  4. body weight
    - marsh = TBW and can overdose obese unless using IBW
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8
Q

TIVA and obestiy

A

SOBA - recommend adjusted body weight (actual body weight may result in excessive boluses and infusion rates. ABW = IBW + 40%

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9
Q

Propofol and TIVA

A

Physical properties
- cheap
- safe
-stable
- long shelf life
Pharmacokinetic
- Rapid onset and offset
- small Vd
- rapid metabolism
- no excitation or emergence phenomenon
Pharmacodynamic
- antiemetic
- minimal toxicity

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10
Q

Clearance / Vd

A

Clearance = volume of plasma cleared of drug per unit time - accounts for elimination from body. elimination x Vp
Vd = apparent volume that drug is disributed. dose / plasma concentration
Important equations:
1. Loading dose can be calculated from desired plasma concentration and initial Vd (Pc x Vd)
2. Bolus dose to rapidly increase plasma concentration (Cnew - Cactual) x Vd
3. Rate to maintain steady state = Cp x clearance

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11
Q

Context sensitive half time

A

Time for plasma concentration to half when infusion stopped after reaching steady state
comparison between distribution and elimination clearances. drug with high distribution clearance and low elimination clearance will have half a long CSHT
Fentanyl has distribution : elimination ratio of 5:1 propofol 1:1 remifentanil <1 :1

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12
Q

Rate constant

A

coefficient of proportionality relating to rate of chemical reaction and concentration of reactants
half life - time taken to reduce plasma concentration to half it’s original value
time constant - time taken for plasm concentration to reach zero if initial rate of decline continues

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13
Q

Neuropathic pain definition

A

Pain caused by lesion or disease of somatosensory nervous system

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14
Q

Clinical features of neuropathic pain

A

Unprovoked pain - shooting, burning, electric shock, tingling, numbness, painful parasthesia
Allodynia and hyperalgesia

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15
Q

Neuropathic pain syndromes

A

Peripheral nervous system:
Trigeminal neuralgia
Post-herpetic neuralgia
Phantom limb pain
Diabetic neuropathy
Central nervous system:
Spinal cord injury
MS
Post stroke

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16
Q

Drug treatments

A

1st line (Non-TN) = amitriptyline, duloxetine, gabapentin or pregabalin
2nd line = another one
Tramadol rescue
Capsaicin cream for localised symptoms

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17
Q

Pharmacology of neuropathic agents

A

Amitriptyline = TCA, inhibits reuptake of serotonin and noradrenaline. 25-75mg at night
Duloxetine = SNRI. Diabetic neuropathy. 60mg ON
Gabapentin / Pregabalin = anticonvulsant. Inhibts a2d subunit of VGCa channels

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18
Q

What are Antidepressants

A

Drugs whilst alter neurochemistry in such a way as to improve mood. Depression felt to be due to deficiencies in NA, serotonin within CNS and most antidepressants increase their concentration

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19
Q

How are antidepressants classified?

A

SSRI e.g. fluoxetine. Prevent pre-synaptic reuptake of serotonin - increase levels. safer in overdose and more favourable SE profile
SNRI e.g. duloxetine. Prevent reuptake of both serotonin and NA with minimal effects on other NTs
TCA e.g. amitryptilline. prevent presynaptic reuptake of NA and serotonin. Have antimuscarninin, histamine, A1 effects. Sedation, dry mouth, toxic overdose, QTc prolongation
MAOI - Reduce breakdown of neurotransmitters e.g. phenelzine. risk of hypertensive crises, tyramine reaction (cheese, beer)

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20
Q

How do antidepressants interact with anaesthetic agents?

A

TCA - serotonin syndrome with tramadol, pethidine. potentate ephedrine. cholinergic syndromes if withdrawal
SSRIs - serotonin syndrome with tramadol, pethidine. Codeine interference CYP2D6
MAOI - hypertensive crisis indirect sympathomimetics (use direct)

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21
Q

Signs and symptoms of serotonin syndrome

A

Caused by excess serotonin levels, either recreationally or inadvertent overdose
Cognitic / autonomic / somatic
CVS
- Tachycardia, HTN, arrhythmias,
CNS
- Brisk reflexes, clonus, seizures, agitations, confusion, coma, mydriatic pupils
Hyperpyrexia, sweating

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22
Q

Uterotonics - what receptors are on the uterus

A

Contraction
- Oxytocin - Synthesised hypothalamus stored and released from post. pituitary. +ve feedback loop (stimulates uterine contraction, fetal head exerts pressure and causes more release)
- A adrenergic
- Prostaglandin E3
Relaxation
- Beta 2 adrenergic receptors

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23
Q

Drugs causing uterine contraction

A
  1. Syntocinon - 5 unit bolus IM/IV. stimulates oxytocin receptors. SE Tachycardia, vasodilation. ADH-effect (similar structure)
  2. Ergometrine - synthetic ergot derivative. IM. Binds to A adrenoceptors and D2 Can cause vasoconstriction, vomiting, headcache
  3. Haemobate (carboprost) - Prostaglandin agonist, 250mcg IM. cause bronchospasm
  4. Misoprostol - 800mcg PR. Prostaglandin E2 receptors. increase uterine tone. shivering diarrhoea
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24
Q

Drugs causing uterine relaxation

A
  1. Terbutaline - B2 agonist. 5ug/min infusion. Beta agonist SE..
  2. GTN - NO mediated uterine relaxation
  3. Atosiban - competitive oxytocin antagonist. Prevent premature labour
  4. Inhaled anaesthetic agents - direct dose related
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25
Types of calcium channels
Voltage gated - L-type - ventricular myocytes (refractory period) - T-type - cardiac pacemakers Ligand-gated - Ryanodine receptor
26
Calcium channel blockers
Act on L-type Ca channels Class 1 - (cardiac pacemaker cells) phenylalkylamines - verapamil - L-type - slow AP through SA and AV node - Oral / IV preparation Class 2 - (vascular smooth muscle) dihydropyridines - amlodipine - PO only, HTN - nifedipine - PO, SL. coronary and peripheral vasodilator. HTN, angina - nimodipine - oral and IV, crosses BBB, SAH vasospasm Class 3 - benzothiazepines - diltiazem - PO only, coronary and peripheral dilation. HTn and angina
27
Anticonvulsant drugs
Increase GABA activity - Benzodiazepines - BDZ receptor , increase chloride channel opening - Barbiturates - increase chloride channel opening - Gabapentin - A2D subunit of calcium channels Reduce excitatory transmission - Phenytoin - Na channel blocker - Carbamazepine - Na channel blocker - Lamotrigine - Na channel blocker
28
Tell me about a drug
1. Class 2. Uses 3. Mechanism of action 4. Chemical properties 5. Dose 6. Pharmacokinetics ADME 7. Pharmacodynamics by system
29
Suxamethonium
Deplarising muscle relaxant Used in rapid sequence induction of anaesthesia to provide optimal intubating conditions It's MOA is related to structure - essentially 2 ACh molecules joined together. It binds to post-synaptic nACHR at NMJ causing depolarisation. Unlike ACH it does not move away from the receptor so there is sustained activation and influx of cations - uncoordinated muscle contraction (fasciiculations) followed by flaccid paralysis It is presented as vial of clear colourless solution of 100mg/2ml, stored at 4oC The dose is 1-2mg/kg Kinetics - IV 100% bioavailability. Polar and low Vd. Metabolised by plasma cholinesterase's and renal excretion - rapid offset of 5mins Dynamics - Neuro - flaccid paralysis, raised IOP - CVS - binding to muscarinic receptors in heart - bradycardia - raised intragastric pressure - raised serum K+ due to K+ efflux - myalgia - Sux apnoea / MH / anaphylaxis CI - Known MH susceptibility - Previous anaphylaxis - burns or spinal cord injury 24hrs - 18 months - hyperkalaemia
30
Sux apnoea
Autosomal recessive genetically acquired deficiency in plasma cholinesterase's Leads to reduced breakdown of suxamethonium at NMJ and prolonged block 4 alleles - usual - 96% homozygous normal gene - silent - homozygous for silent gene. no enzyme function Dibucaine test - higher number better function Acquired plasma cholinesterase deficiency - pregnancy, liver disease, renal disease, malnutrition, cancer, plasmaphoresis
31
Sux - Phase 1 and 2 blockade
Phase 1 - initial depolarising block - ToF - reduced height, no fade - Tetany - reduced, no fade Further doses --> Phase 2 - features of NDMR - ToF - fade - Tetany - fade
32
Dementia definition
progressive neurocognitive disorder characterised by memory impairment plus other cognitive deficits such as language, complex tasks, reasoning.
33
Types of dementia
Alzheimers - short term memory and word finding. amyloid plaques and neurofibrillary tangles Vascular - 20% - series of minor strokes, stepwise decline Lewy-Body - visual hallucinations and PD Parkinsons dementia Frontotemporal dementia - personality and language changes
34
Dementia drugs (minimal evidence)
Acetylcholinesterase inhibitors (some symptoms felt to be cholinergic deficit) - donepezil - central acting - rivastigmine NMDA receptor blockers - memantine
35
Delirium definition
acute reversible cognitive dysfunction with reduced awareness and inattention. may be associated with hallucinations delusions, memory impairment Hyper/hypo
36
Management of delirium
Non-pharmacological - Orientation - Calm quiet environment - Minimise staff changes, night time disturbances - family - access to hearing aids, glasses - Removing wires and tubes - Mobilisation Pharmacological - Typical antipsychotic e.g. haloperidol - Atypical antipsychotic e.g. olanzapine - Benzodiazepines if contraindicated
37
Vomiting centre
region of the medulla control of vomiting many inputs including - chemoreceptor trigger zone - vagal afferents from GI, outside BBB - nucleus tracts solitarius - vestibular H1 and ACh, cerebral cortex, D2 receptors, muscarinic inputs
38
Classes of antiemetics
5-HT3 antagonists - ondansetron D2 antagonists - Droperidol (act at CTZ) domperidone (act peripherally) metoclopramide (both) H1 antagonists - cyclizine (some anticholinergic properties) works at CTZ Phenothiazines e.g. prochlorperazine - D2 / musc / H1 antagonists in CTZ anti-cholinergic - hyoscine central anti-cholinergic transdermal. Dexamethasone - uncertain mechanism Aprepitant - neurokinin 1 antagonist in GI tract
39
Antiemetic strategy
Risk factors (Apfel score) Risk mitigation (minimise N20, volatile, consider RA, opiate sparing) Risk stratification - 1-2 risks - give 2 antiemetics. 3-4 risks - give 3-4 Rescue antiemesis
40
Neuroleptic malignant syndrome
Idiosyncratic reaction to antipsychotic drugs - fever, rigidity, confusion, autonomic dysfunction - Stop drug, cool, dantrolene, fluid (CK)
41
Principles of chemotherapy
Chemotherapy targets replicating cells and ultimately trigger apoptosis in cancer cells. usually administered in combination to achieve synergy.
42
Regimes
Neoadjuvant - prior to surgical resection, aim to improve chance of curative resection, reduce extent of surgery Adjuvant - given after resection with aim of reducing recurrence Palliative - aim to prolong survival
43
Mechanisms of action of common chemotherapy agents
Alkylating agents - cisplatin, cyclophosphamide - prevent cell replication by cross linking DNA Anti-metabolites - 5-FU, methotrexate. disrupt DNA repair Anti-microtubule agents - paclitaxel - interfere with mitotic processes Cytotoxic antibiotics - bleomycin, doxorubicin - damage DNA
44
Side effects by system
RESP - infection, PE risk - Pneumonitis - methotrexate - Pulmonary fibrosis - bleomycin (aggravated by O2, minimise O2, titrate to 88-92%) CVS - toxicity may cause MI, cardiomyopathy, myopericarditis, cardiac failure - doxorubicin - cardiomyopathy RENAL - platinum based e.g. cisplatin may cause tubular damage HEPATIC - hepatic metabolism, abnormal enzymes common. - methotrexate - fibrosis CNS - peripheral neuropathy, autonomic dysfunction e.g. vincristine GI - vomiting, electrolyte abnormalities HAEM - myelosuppression, neutropenia
45
Radiotherapy
Use of ionising radiation which is toxic to dividing cells, administered directly at cancer cells Generalised side effects - fever, nausea, vomiting Localised fibrosis - head and neck - difficultt airway - thoracic - lung fibrosis
46
Antibiotic classification
mechanism of action - inhibition of nucleic acid synthesis - quinolones - inhibition of cell wall synthesis - inhibition of protein synthesis - aminoglycosides
47
Nucleic acid synthesis inhibitors
Quinolones - ciprofloxacin - inhibit DNA gyrase. Gram +ve and gram -ve Trimethoprim - inhibit enzymes involved in folate synthesis Imidazoles - metronidazole - inhibit DNA synthesis. anaerobic species
48
Cell wall synthesis inhbitors
Penicillins - B-lactam rings inhibit cross linking of peptidoglycan. Gram +ve Cephalosporins - similar mechanism of action Glycopeptides - Teicoplanin, Vancomycin - inhibit peptidoglycan formation, Gram +ve
49
Protein synthesis inhibitors
Aminoglycosides - inhibit RNA binding. gentamicin, narrow therapeutic index macroldies - clarithromycin - inhibit translocation of RNA. narrow spectrum
50
Antibiotics resistance
Innate - some bacteria naturally resistant to certain antibiotics Acquired - genetic mutation by natural selection or horizontal transmission of gene in the form of plasmids Mechanisms - enzyme inhibition - B-lactamase - binding site modification - outer membrane protein channel changes - upregulating cell wall pumps that actively remove antibiotics
51
Plasma proteins
Albumin (60%) A1 globulins A2 globulins B globulins Y globulins
52
Albumin
Large water soluble protein 67kDa, negatively charged at physiological pH synthesised in the liver, 350-50mg/ml hydrophobic core hydrophilic exterior x3 binding sites - responsible for 80% plasma oncotic pressure - Number of substances bind to albumin and transport - hormones -s steroid, thyroxine - unconjugated bilirubin - electrolytes - ca, mg - free fatty acids - drugs - NSAIDs, warfarin, digoxin (compete) - negative acute phase protein (conserve AA for positive APPs) - contributes to anion gap (unmeasured anions in plasma)
53
Human albumin solution
Indications - Burns - Plasma exchange - Paracentesis of ascites - (resuscitation) Presentation - solution of 4.5%, 5%, 20% in 100ml, 250ml, 500ml bottles - Pooled from multiple doors and purified - 3 yr shelf life Kinetics - IV only 100% bioavailability - low Vd (0.07l/kg) - metabolised reticulendothelial system - minimal renal excretion (unless nephrotic) Effects - Increase plasma oncotic pressure - may increase BP - May cause fluid overload - may worsen cerebral oedema following TBI - anaphylactic reactionsA
54
Albumin evidence
Resuscitation - not statistically superior to n/saline (SAFE) - higher mortality in TBI - otherwise safe Septic shock - no evidence of superiority to crystalloid Liver - less circulatory dysfunction with paracentesis - 100ml 20% per 3L expense / transfusion risks Use in SBP Don't use in TBI Don't use to correct low albumin
55
Warfarin
- VKA - inhibits synthesis of II, VII, IX and X - coumarin derivative 99% protein bound to albumin - 3-5d to peak effect interacts with numerous drugs, particularly those that compete with albumin binding sites e.g. antibiotics, NSAIDs teratogenic monitoring
56
NOACs
Rivaroxaban / apixaban Xa inhibitors - Rivaroxaban : 20mg once daily dosing, 3 hours to peak effect, hepatic metabolism - apixaban : BD dosing 3 hours peak, lower dose in renal failure. 2.5 - 5mg BD Dabigatran = thrombin inhibitor BD Dosing, 2 hrs peak 110-150mg BD Dabigatran reversal = idarucizumab Apixaban reversal = Adexanet alpha
57
Heparins
Naturally occurring glycosaminoglycans UFH - antithrombin 3 1000x - inactivates Xa and thrombin. IV bolus infusion. APTTr. 4hrs offset LMWH - antithrombin 3 - augments ability to inactivate Xa. caution renal failure. monitoring xa levels difficult. peak 4 hrs. invasive procedures 12hrs post prophylactic 24hrs post treatment
58
Neuraxial and NOACs
warfarin INR < 1.4 NOACS - 48hrs (apixaban 24-48) (dabigatran 48-96) UFH 4hrs LMWH prophylactic 12 treatment 24
59
Dopamine
Catecholamine neurotransmitter Phenylalinae --> L-tyrosine --> L-DOPA --> DOPA --> NA --> Adr Dopa decarboxylase LDOPA-->DOPA Dopamine broken down by dopamine b hydroxylase to NA / Adr, broken down by COMT and MAO
60
Drugs used to treat parkinsons
1. L-DOPA + Peripheral decarboxylase inhibitor (reduce S/E e.g. carbidopa) 2. Dopamine agonists e.g. ropinerole 3. MAO-B Inhibitors e.g. selegiline - prevents dopamine breakdown 4. COMT inhibitors e.g. entacapone - smooth out off effects
61
Drugs to avoid in parkinsons
1. Antiemetics - metoclopramide, prochlorperazine. (domperidone safe) 2. Antipsychotics - typicals e.g. haloperidol 3. Antihypertensives - pronounced effect 4. central anticholinergics e.g. atropine - cholinergic crisis
62
Blood gas solubility coefficient
The ratio of the amount of anaesthetic in blood and gas when the two phases are of equal volume and pressure at equilibrium at 37oC. Low BGPC = higher partial pressure in blood, higher in brain, faster onset Des 0.42 Sevo 0.68 Iso 1.4 Graph = wash in, time x axis, Fa/Fi y axis
63
Oil:gas partition coefficient
Measure of lipid solubility of anaesthetic agent, correlates to potency. Higher lipid solubility means more drug entering brain and therefore greater potency. Inverse correlation to MAC Meyer-Overton
64
MAC
Measure of potency Concentration of anaesthetic agent at steady state which prevents reaction to surgical stimulus in 50% of subjects at one atmosphere
65
Factors altering MAC
Increase - Hyperthermia - Young age - Chronic alcohol / drug use - Catecholamine Decrease - Pregnancy - Hypotension - Hypothermia - Acute opioid use
66
Ideal volatile
Physical - Stable to heat and light - Inert - Not flammable or explosive - Non-irritant - Atomospherically friendly Biochemical - Low BGPC - quick onset and offset - High OGPC - potent - No toxic metabolites - Only effects CNS
67
Cardiac output and onset of action of volatiles
High cardiac output maintains concentration gradient between alveolus and arterial pressures, slower equilibrium, slower onset of action
68
Serotonin production / metabolism
produced from hydroxylation and decarboxylation of tryptophan (essential amino acid) reuptake and inactivation by MAO. products renally excreted Serotonin found in brain GI (enterochromaffin) platelets
69
Serotonin receptors
5HT1-7 All GPCR apart from 5HT3 (ion channel) 5HT2 = platelet aggreggation 5HT3 = GI tract and area postrema = vomiting 5HT6-7 = limbic function
70
Serotonin syndrome
Excess serotonin in CNS. Triad - autonomic activation --> diaphoresis, HTN, hyperthermia, tachycardia, dilated pupils, diarrhoea - altered mental status --> agitation, delirium, disorientation seizures - neuromuscular excitability --> tremors, rigidity, hypereflexia, nystagmus
71
Hunter criteria for serotonin syndrome
Serotoningeric agent and combination of - spont / inducibe clonus - agitation - diaphoreiss - tremor - hypertonia - hyperreflexia - hyperpyrexia
72
Tricyclics mechanism of action
Complex - H1/H2 blockade - Anticholinergic - Blockade of presynaptic NA / serotonin uptake - Blockade of cardiac fast Na channel
73
TCA kinetics
A - well absorbed 2-4hr peak D - high Vd, low free drug (albumin A1 glycoprotein) M - liver hydroxylation and methylation E - 10% renal excretion
74
TCA cardiac toxicity
Slow phase 0 by Na channel blockade delay depolarisation AV node, prolong QRS, abnormal repolarisation hypotension direct myocardial depression, alpha blockade vasodilation
75
Secondary prevention post MI
ACEi Antiplatelet (DAPT) Beta blocker 12months (indefinite if LVF) Statin (ca channel blocker if beta blocker contraindicated)
76
ACEi indications
secondary prevention post MI Essential hypertension CKD Diabetic nephropathy Heart failure
77
ACEi side effects
- cough - hypotension - electrolyte derangement - hypokalaemia - renal impairment - Angioedema
78
approach to hypotensive agents
BP = CO X SVR Reduce HR - beta blockers Reduce venous return - venodilators - neuraxial blockade Reduce contracility - volatile Reduce SVR - anaesthetic - vasodilators - neuraxial
79
hypotensive drugs
beta blockers - esmolol - selective B1 - labetalol - A1 and B1 (vasodilation, without reflex tachycardia vasodilators - GTN - sodium nitroprusside (arterial and venous) - hydralazine A blocker - phentolamine
80
Sodium nitroprusside
- arterial and venous dilator - hypotensive anaesthesia, management of increased SVR with cross clamp - dose 0.5 - 6mcg/kg/min - presented as brown powder, reconstituted in glucose. covered in aluminium foil as exposure to sunlight cause cyanide ion formation - MOA - prod NO - cGMP - reduce calcium PD - CVS - reduces SVR, preload, causes tachycardia - Resp - inhibit HPVC - CNS - vasodilation and inc ICP Tachypyhlaxis - thiocynaite toxicity (oxygen, chelating, sodium thiosulphate)
81
Three types of anticholinesterases
Easily reversible - edrophonium - tension test - Binds anionic and esteratic sites - ACh will compete Formation of carbamylated-enzyme complex - neostigmine, pyrodistigmine - produced carbamylated enzyme with reacting with ACHE - slower rate of hydrolysis than ACH and ACHE complex - stops ACH hydrolysis Irreversible inactivation - organophosphates - esteratic site of AChE phosphorylated - enzyme inhibition and very stable
82
Organophosphate poisoning
Parasympathetic overload SLUDGE - lacrimation - meiosis - salivation - bradycardia - diarrhoea - urination - bronchospasm - confusion agitatation coma
83
Treatment organophosphate poisoning
- remove clothes, PPE, shower, irrigate eyes, charcoal - ABC - avoid sux - atropine ++ child 20mcg/kg repeat every 20mins - pralidoximine - diazepam - toxbase
84
Warfarin reversal
- Stop warfarin - 2-4 days to reverse - Vit K 4-6 hrs. multiple doses - Prothrombin Complex Concentrate - derived from irradiated plasma, clotting factors II, VII, IX, X. Immediate reversal. - FFP - partial effect, not recommended unless bleeding
85
Anticonvulsant drugs
Increase GABA - Benzodiazepines (BDZ receptor to increase Cl opening frequency - Barbiturates - increase Cl opening duration Antagonise glutamate - Topiramate Reduce excitatory activity - Phenytoin - Carbamazepine - Lamotrigine - Valproate All block Na+ channels Gabapentin - block A2D subunit of Ca channels Keppra - unknown
86
Phenytoin
Antiepileptic drug Action to block Na channels Indicated for status epileptics and treatment of epilepsy Dose 20mg/kg IV or 50-200mg PO Presented clear colourless solution, diluted in N/saline to 10mg/ml or as tablets PK - IV 100% bioavailability PO 90% - Low Vd, 90% PB bound - Liver metabolism, cytochrome P450 inducer Zero order kinetics. small therapeutic range - inactive metabolites renally excreted PD - CNS - reduce seizures - CVS - May have class 1 antiarhythmics. can reduce BP Idiosyncratic - acne - gum hyperplasia - BM depression - peripheral neuropathy - hirsutism -coarsening facial features - teratogenic
87
Leveteracetam
focal / generalised seizures unclear mechanism Oral or IV IV 60mg/kg status epileptics max dose 4.5g 20-30mg/kg maintenance BD IV 500mg/5ml clear colourless PK - PO + IV same 100% bioavailability - < 10% PB, low Vd - Enzymatic hydrolysis - renal excretion, mostly unchanged PD - CNS - antiseizure, somnolescence, mood disturbance - idiosynratic - Steven-Johnson
88
Hepatic enzyme inducers
Increase activity - faster metabolism of drugs PCBRAS - Phenytoin - Carbamazepine - Barbiturates - Rifampicin - Alcohol - Smoking
89
Hepatic enzyme inhibitors
Reduce activity - slower metabolism of drugs OADEVICES - omeprazol - allopurinol - disulfrim - erythromycin - valproate - isoniazid - cimetidine - ethanol (acute) - sulphonamide

Final FRCA SOE (11 decks)

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