Pharmacology Flashcards
LA toxicity (RCoA new book)
Mechanism - blocks Na channels from within cells
RFs
- Operator - dose, speed of injection
- Site - vascularity
- Pharmacological - potency, PPB, clearance
Effects - CVS/CNS
Management - Intralipid 20% 1.5ml/kg over 1m, 15ml/kg/hr; max 3 boluses/double rate
Antihypertensives (RCoA old book, Krishnachetty)
By site of action:
Heart: ABs, BBs
Blood vessels: direct (GTN, SNP) and indirect (CCBs), K+ channel activators (nicorandil)
Kidney: ACEi, ARB, diuretics, direct renin inhibitors
CNS: methyldopa, clonidine, dexmedetomidine, ganglion blockers e.g. trimetaphan
Or by part of equation:
MAP = (HR x SV) x SVR
Or by mechanism:
- Drugs that act on RAAS and mainly reduce SVR
- Drugs that increase Na+ and H2O excretion and mainly reduce preload
Causes: primary (essential), secondary (renal, endocrine, vascular).
New agents: direct renin inhibitors (aliskiren). No bradykinin accumulation. <3% bioav. Only for resistant HTN. May cause severe hypotension intraop. Causes diarrhoea.
Age <55: ACEi. Age >55 or black: CCB.
SNP: 0.3-0.5mcg/kg/min. Protect from light - cyanide (antidote hydroxycobalamin).
Flumazenil (RCoA old book, Mendonca)
Competitive BDZ receptor antagonist for iatrogenic BDZ overdose
Rapid distribution, peak effect in 5m, duration <1h
Metabolised by liver
Can increase ICP and lower seizure threshold; N&V, flushing, anaphylaxis
Dose up to 600mcg over 5m, max 1mg; infusion 100-400mcg/h
MAOi (RCoA old book, past Q)
Enzyme present in liver and nervous system; isoenzymes A and B
Part of the inactivation mechanism for naturally occurring vasoactive substances
MAOi: irreversible A and B inhibitors e.g. phenelzine (the problematic type); reversible MAO-A e.g. moclobemide, reversible MAO-B e.g. selegiline.
Reduce breakdown of catecholamines
SEs: sedation, orthostatic hypotension, liver toxicity
Interaction with opioids - problems with postop analgesia
- Type 1 (excitatory): pethidine –> serotonin syndrome
- Type 2 (depressive): enhanced respiratory depression, due to hepatic enzyme inhibition
Indirectly acting vasopressors can cause fatal hypertensive crisis - phenylephrine safe; careful titration of direct agents
Pancuronium can release stored NA
TCAs can cause hyperpyrexia and cerebral irritation
Withdraw at least 2/52 preop (new enzyme has to be formed). Can continue selegiline <10mg/day, just avoid pethidine
D/w psych/MDT, withdrawal risk/benefit, risk of discontinuation syndrome and relapse
If can’t stop, BDZ premed, hydration, cautious titration of phenyl, RA if able (avoid adrenaline), indirect sympathomimetics/pethidine abs CI
Cheese (tyramine) reaction with cheese, yeast, alcohol, chocolate, cream, broad beans
Drugs acting on the uterus (RCoA old book, past Q)
Uterotonics
- PGs (E2, F2a) - abortion, IOL. Latter can cause bronchoconstriction (carboprost)
- Oxytocin - initiation/maintenance of labour, PPH control
- Ergometrine - alpha 1 and 5HT agonist. Can cause severe HTN, vomiting and bronchospasm
Tocolytics
- Beta 2 agonists - salbutamol, terbutaline, ritodrine
- CCBs - nifedipine - headache, nausea
- MgSO4 - competitive calcium antagonist and NM blocker, vasodilator and anticonvulsant
- Volatiles - dose related uterine relaxation
- GTN - NO donor - used in retained placenta, uterine inversion
No effect: IV anaesthetics, analgesics, NDMRs, reversal agents
Drugs used in cancer (Krishnachetty, Dr Barry)
Disease-modifying vs symptom control
Cytotoxics - plantinum-based, antimetabolites, alkaloids, topoisomerase inhibitors, antitumour antibiotics, steroids, monoclonal antibodies.
(Sx - analgesics, antiemetics, anxiolytics, antisialogogues.)
SEs: bleomycin - pul fibrosis and O2 toxicity, doxorubicin - cardiotoxic, platinum agents - nephrotoxic, methotrexate - hepatotoxic and neurotoxic, most agents - myelosuppression, neutropenic sepsis, nausea and vomiting, anorexia, alopecia.
Tumour lysis syn: high K/PO4 (precipitates in kidneys)/uric acid, low Ca. Prevent with hydration, alkalinisation of urine, allopurinol.
Things to avoid in cancer: N2O (?accelerates metastasis), ?volatiles
Antibiotics (past Q, Dr Barry)
NICE prophylaxis of endocarditis
Inhibit synthesis one of three bacterial components: cell wall, protein or DNA
Risk factors for postop infections
Laminar flow
C.diff
When are abx not required? Routine OGD/colonoscopy, dental, genitourinary
High risk of endocarditis: valvular disease, valvular replacement, HCM, previous IE, CHD (excluding lone ASD or repaired VSD/PDA).
Calcium channel blockers (Mendonca)
Ind: HTN, angina, PHTN, arrhythmias, vasospasm prophylaxis in SAH, migraine, Raynaud’s.
Types of Ca channel: L, T, N, P. CCBs block L-type channels. Reduces Ca level in cells, thereby reducing muscle contraction. In heart, reduces HR and contractility. In vessels, relaxes smooth muscle –> vasodilatation. Unlike BBs, CCBs do not reduce the responsiveness of the heart to sympathetic input.
Dihydropyridines: amlod, nifed. Reduce SVR and BP.
Non-DHPs: verapamil (phenylalkylamine) -
more cardioselective. Diltiazem (benzothiapine) - middling class.
PD: vasodilatation, negative inotrope/chronotrope/dromotrope. Can cause heart block/heart failure. Also flushing, HA, palps, pedal oedema.
HTN <55: ACEi. >55/black: CCB.
Interactions: BBs - heart failure/block/severe hypotension. Diuretics - severe hypotension. Digoxin levels may rise.
Dihydropyridines (amlodipine) - reduce SVR
Phenylalkylamine (verapamil) - cardioselective
Benzothiazepine (diltiazem) - middling class
PCA (Mendonca)
Pros: superior analgesia, pt satisfaction, avoids IM injections, reduced nursing workload.
Principle of ‘autoregulation’/negative feedback (no demands if drowsy). Minimum effective analgesic concentration is individual to pt.
PCA pump: computerised, programmable, battery-operated portable pump. Microprocessor stores data. Button and timer.
Safety features: lockout time, max hourly dose, alarms, anti-siphon, keep pump at pt level, lockable cage.
Obs and sedation score monitoring. Rx O2, naloxone, prescription, contact available for advice.
Types of PCA: IV, SC, epidural, peripheral nerve catheter, transdermal.
Neuromuscular blocking drugs (Mendonca, past Q)
Sux - see separate card.
Depolarising agents (sux, decamethonium) - faster onset, fasciculation, reduced single twitch and TOF equal reduced height, no fade, no post-tetanic facilitation. Non-competitive - cannot be overcome. Non-depolarising - slower onset, no fasciculation, reduced single twitch and reducing height in TOF, fade and post-tetanic facilitation. Competitive - can be overcome.
Benzylisoquinolinium esters - trac, cistrac, miv; broken down by non-specific esterases and Hoffman degeneration
Aminosteroids - vec, roc; mainly hepatic excretion, and 40% renal.
Prolongation of NDMRs: hypokalaemia, hypocalcaemia, hypernatraemia, hypermagnesaemia, acidosis, liver/renal failure, hypothermia, aminoglycosides, LAs, volatiles, CCBs, anticholinesterases, lithium.
Reversal
Neostigmine 10mcg/kg - an anticholinesterase. Prevents ACh being broken down and also increases ACh release. XS dosing can cause depolarising type block. SEs: bradycardia (muscarinic effect), hypotension, hypotonia, bronchospasm/constriction, salivation, peristalsis; hence glyco given (similar onset time). Onset 1m, peak 10m, metab by plasma esterases.
Sugammadex: modified gamma cyclodextrin. “Su” = sugar, “gammadex” = structural molecule, gammadextrin. Forms tight 1:1 complexes with aminosteroid MRs. This then creates a conc gradt away from NMJ into plasma. 2/4/16mg/kg for moderate/deep block/immediate reversal.
NSAIDs (Mendonca)
Non-specific vs COX-2 specific e.g. celecoxib (also preferential COX-2 e.g. meloxicam).
COX-1 constitutive, COX-2 inducible (latter only formed when tissues exposed to inflammatory stimuli; made by macrophages). Inhibition of COX-1 causes SEs and anti-plt function. Inhibition of COX-2 gives analgesia and anti-inflammatory
(hence was the target in COX-2i development). COX-2s have reduced GI SEs but increased stroke and MI (VIGOR trial - rofecoxib vs. naproxen). Mechanism = affects PC:TXA2 ratio so latter more abundant, promoting atherosclerosis and thrombosis. Also Na+/H2O retention causing HTN.
SIde effects of NSAIDs
- Increased gastric acid secretion and reduced gastric blood flow - dyspepsia, N&V, GI bleed
- 10-20% asthmatics are sensitive to leukotrienes
- Renal impairment (reduced RBF/GFR)
- Bleeding (plt dysfunction) - even more so with warfarin (displaced)
Arachidonic acid pathway
Paracetamol - sometimes classed as NSAID as may inhibit COX. May also modulate endogenous cannbinoid system. Metabolised mainly to sulphate and glucuronide conjugates, and also to NAPQI by P450 system (normally conjugated with glutathione and renally excreted). In OD, more is shunted down NAPQI pathway and glutathione is depleted. NAPQI causes hepatocellular damage (zone 1). NAC replenishes glutathione.
Remifentanil (Mendonca, past Q)
Synthetic pure mu agonist. Used as adjunct for induction and maintenance (TIVA) of anaesthesia, hypotensive anaesthesia, analgesia e.g. in labour, and ICU sedation. Ultra short-acting. 1, 2 or 5mg hydrochloride salt in glass vial to be made up as solution. 0.05-0.2mcg/kg/min/TCI 3-8ng/ml (8-10ng/ml for intubation without MR). Hydrolysed rapidly by red cell and tissue esterases to caboxylic acid.
Pros: controlled ventilation without NMBs so can nerve monitor, titratable hypotension, stable HR, excellent analgesia, prevents coughing - smooth emergence, context insensitive, reduced PONV, predictable recovery, does not require dose adjustment in hepatic/renal disease, reduces MAC of volatiles
Cons: no postop analgesia, risk of awareness if TIVA (and need dedicated line), remi-induced hyperalgesia, chest wall rigidity, cannot be used as sole agent, bradycardia
pKa 7.1, 80% ionised
Remi PCA in labour:
Unlicensed indication. Not if pethidine within last 4h. Dedicated cannula, nasal O2, naloxone prescribed, BVM in room, midwife 1:1, SpO2 monitoring. 10% incidence of desaturation.
RS: resp depression, apnoea, chest wall rigidity, reduced response to hypoxia/hypercapnoea
CVS: reduces HR, BP, CO
CNS: reduces CBF and ICP, preserves autoregulation
Elderly: increased sensitivity, reduced VD and clearance - therefore bolus and rate need 50% reduction.
Uses: induction/airway control/AFOI, middle ear, neuro, cardiac, ICU, bariatrics.
Alpha-adrenergic blockers (Mendonca)
Non-selective - phenoxybenzamine (long acting, PO preop for phaeo), phenotolamine (short acting, IV intraop for phaeo). Cause vasodilation/reduced SVR, and reflex tachycardia. Phentolamine contains sulphites in the ampoule which can cause bronchospasm in asthmatics.
Selective (alpha-1) - doxazocin, prazocin
Selective (alpha-2) - yohimbine
Post-herpetic neuralgia (Mendonca, past Q)
Varicella zoster. Virus stays dormant for decades in sensory root ganglia.
Age >50
Hyperasthesia, parasthesia, burning pain, pruritis prodrome. Then rash - vesicles take 10/7 to crust over. T5/6 or ophthalmic with eye comps.
Tx
General: cool bath, loose clothes
Topical: capsaicin (exhausts supplies of substance P), LA patches
Pharm: paracetamol, NSAIDs, gabapentin, pregabalin, amitriptyline (TCAs are slower to work and have anticholinergic SEs), antivirals within 72h
Interventional: LA infiltration, sympathetic blockade, nerve blocks, epidural steroids
Other: TENS, behavioural
Gabapentin: NNT 4 (for pain reduction >50%). Has affinity for alpha-2-delta subunit of presynaptic Ca2+ channels. On binding it prevents Ca2+ influx and release of neurotransmitters. Gabapentin may reduce or reverse opioid tolerance and is synergistic with morphine.
Oral hypoglycaemic drugs (Mendonca, past Q)
Increase insulin sensitivity
- Biguanides (metformin)
- Thiazolidinediones (pioglitazone)
Increase insulin secretion
- Sulphonylureas (gliclazide)
- Dipeptidyl peptidase IV inhibitors (sitagliptin)
- Meglitinides (repaglinide)
- Incretin mimetics (exenatide)
Other
- Alpha glucosidase inhibitors (acarbose) - reduce carbohydrate absorption
Drugs for Parkinson’s disease (Krishnachetty, past Q)
Phenylalanine –> L-tyrosine –(tyrosine hydroxylase - rate-limiting step)–> L-dopa –> dopamine –> NA –> A
PD: 1% of >65s
Drugs:
- Dopamine precursors e.g. levodopa (with dopa decarboxylase inhibitor e.g. benserazide)
- Dopamine agonists e.g. apomorphine
- MAO-B inhibitors e.g. selegiline
- COMT inhibitors e.g. entacapone
- Anticholinergics e.g. orphenadrine
- Atypicals e.g. amantidine
Periop: avoid missed doses, can use SC apomorphine
Avoid: atropine (central anticholinergic syn), pethidine, metoclopramide, droperidol, prochlorperazine, classical antipsychotics (all worsen sx)
Caution with antihypertensives (can cause severe hypotension), TCAs (arrhythmias)
Do give: domperidone, glycopyrrolate
Serotonin (Krishnachetty)
Serotonin = 5HT. Made from tryptophan (essential AA). Found in plts, GIT, CNS. Receptors 5HT-1 to 7 exist - most GPCR and act via adenyl cyclase.
Serotonin syndrome - serotonin excess in CNS. Triad: altered mental status, autonomic dysfunction, neuromuscular excitability. Can lead to rhabdo, DIC, AKI. Hunter criteria: pt has taken serotonergic agent (SSRI, TCA, MAOi, pethidine, ondansetron, fentanyl, tramadol, alcohol, cocaine, ecstasy, LSD) and has one or more of: clonus, agitation, diaphoresis, tremor, hyperreflexia, hypertonia, pyrexia. Diagnosis is clinical. Underdiagnosed. May see raised WBC/CK. Tx withdraw agent, supportive. Cyproheptadine is serotonin antagonist.
Tricyclic antidepressants (Krishnachetty, past Q)
OD: CVS (palps, CP, tachy, hypotension, ECG changes, CNS (agitation, visual dist, hyperreflexia, clonus, seizures), anticholinergic (dry mouth/skin, urinary retention)
Mechanisms: anticholinergic, H1/2 antagonism, blockade of presynaptic reuptake of catechols, alpha 1 antagonism, blockade of cardiac fast Na+ and delayed K+ channels (slow phase 0)
Peak levels 2-4h post PO, large Vd, high PPB, liver metab, active metabs.
Rx: charcoal, bicarb (reduces free fraction), BDZ for seizures, treat arrhythmias, ECG monitoring, alkalinise urine. Glucagon?
Drugs used for secondary prevention (Krishnachetty)
To reduce risk of further MI. ACEi, BB, antiplts, statins. ACEi - post MI, HTN (<55 and not Afro-Caribbean), CCF, diabetic nephropathy, CKD. SEs dry cough, refractory hypotension with GA, angio-oedema (more common in Afro-Caribbeans).
Clopidogrel: ADP receptor blocker
Aspirin: COXi
DES: sirolimus (TORi), paclitaxel (alkaloid)
TIVA/TCI (Krishnachetty, past Q)
TIVA ind: when volatiles unavailable, undesirable, or CI.
TIVA desirable drug features: low Vd, rapid metabolism, short CSHL or context insensitive. PC/PK/PD properties of ideal agent.
Components: user interface, microprocessor and infusion device.
3 compartment model: central, vessel-rich and vessel-poor.
CSHT is a comparison between the distribution and elimination clearances. Low Vd and high elimination desirable. After 2h and 4h, ratio of distribution clearance to elimination clearance for fentanyl is 5:1 (48m –> 250m), propofol 1:1 (16m –> 20m), remi <1 (4.5 –> 6m).
Remi model = Minto (weight >30kg, age>12), Davis/Rigby-Jones (not widely available)
Paeds propofol = Paedfusor >5kg, Kataria >15kg
Typical plasma conc: remi 3-8ng/ml (up to 10-15 during stimulating procedures), propofol 5-8mcg/ml
TCI pumps recalculate effect site conc at 10s intervals and either bolus or stop when different desired concs are entered.
Rate of equilibration between blood and effect site depends on rate of drug delivery, cardiac output, cerebral blood flow, lipid solubility and degree of ionisation of drug.
Models for propofol
- Marsh: assumes central compartment volume is directly proportional to weight. Age is entered but not utilised (although pump will not work if age <16 entered). Risk of overdosing obese pts, therefore use ideal body weight rather than total.
- Schnider: newer, 3-compartment. Age, height, weight entered. Lean body mass calculated and used. Central compartment assumed to be same for every pt. Uses less propofol overall. Better for elderly as takes age into account (lower Cl).
Schnider central compartment (4.27L) is a quarter of the size of that of Marsh (15.9L).for a 70kg pt.
In combined propofol/remi, start propofol first as effect site conc slower to rise (also pt may stop breathing before LOC with remi).
Cons of TCI: all TIVA concerns (awareness etc), no postop analgesia, no definitive monitor analogous to EtAA (use BIS; models with BIS feedback under development), models are from healthy volunteers only.
How can you do TIVA without a TCI pump?
- Loading: desired conc x VD
- Maintenance: desired conc x clearance
Which compartment closest resembles brain?
Why does TCI value not match blood sample level?
Would children be over or underdosed on an adult TCI model?
Anticoagulants and bridging (Krishnachetty, past Q)
Antiplatelets: asp, clop (ADP receptor blocker), dipyridamole (PDEi), glycoprotein 2b/3as
Heparins: UFH, LMWH, Xa inhibitors (fonda)
VKAs
NOACs
- DTIs - dabigatran
- Xa i - rivaroxiban
Reversal of warfarin
- Vitamin K - PO/IV works in 4-6h (up to 5mg), 2-4h (5-10mg)
- PCC 50mg/kg (irradiated pooled human plasma) - 30m, lasts 6-12h. Contains CFs 2/7/9/10, + protein C and S and sometimes heparin (to combat prothrombotic tendency)
- FFP (all clotting factors + fibrinogen) - no longer recommended - partial effect, fluid overload
- Stop warfarin - 2-4 days
Warfarin - synthetic coumarin derivative, VKA (2/7/9/10).
Heparin - activates antithrombin 3 (inhibits CFs 2/9/10/11/12). Fractionated = average MW <8kDa. Unfractionated = 3-30kDa.
LMWH pros: less frequent dosing, SC, no monitoring, lower risk of HIT
Heparin pros: quick on/offset - better control and monitoring, can reverse with protamine
Other drugs
- Fondaparinux - synthetic analogue of part of heparin
- Xa inhibitor - rivaroxaban (RECORD study - fewer VTEs in LL arthroplasty and comparable bleeding rates to warfarin)
- Direct thrombin inhibitor - dabigatran
LSCS - 10/7 LMWH standard, 6/52 if high risk
1 unit of activity = the amount required to keep 1ml cat’s blood liquid for 24h at 0C.
Suxamethonium (past Q)
Sux = two ACh molecules bound together. Competes with ACh for post-synaptic nAChR binding sites. Binds to alpha subunit (of the pentameric nAChR). Keeps ion channel open longer than ACh would. Ca2+ and Na+ go in, K+ goes out.
SEs: hyperkalaemia (increases K+ by 0.5mmol/L. Avoid if K+>5.5), myalgia (young muscular ambulatory pts), bradycardia (children, repeated dosing), sux apnoea (cholinesterase deficiency), transient increased IOP/ICP and intragastric pressure (but oesophageal sphincter pressure also rises so no increased risk of regurg), MH trigger, tachyphylaxis and phase 2 block (akin to non-depolarising block), histamine release, anaphylaxis.
Bradycardia is caused by the initial metabolite of sux, succinylmonocholine, which stimulates mAChRs in the heart.
Sux apnoea Plasma cholinesterase deficiency Eu = normal (94% pop EuEu) Ea (atypical i.e. dibucaine-resistant), Es (silent), Ef (fluoride-resistant) Dibucaine testing (dibucaine is a LA that inhibits normal plasma cholinesterase by 80%): - Normal dibucaine number = 80 (94%) - EaEu 60 (4%) - Others rare, number down to 30
Mivacurium is subject to same breakdown pathway.
Options: sedate until wears off; FFP
Acquired sux apnoea: preg, liver/renal/cardiac disease
Opioids (past Q)
Opioids are weak bases - highly ionised in acidic stomach so poorly absorbed, better absorbed from small intestine. High 1st pass metab. High lipid sol and high VDs. Liver metab, excretion in urine/bile.
Classifications: strong/intermediate/weak, naturally occuring/synthetic/semi-synthetic, pure/partial/mixed agonists/antagonists.
Pure agonists - morph/fent/remi/
Partial agonist - buprenorphine, tramadol
Mixed agonist/antagonist - nalbuphine
Antagonists - naloxone - duration 30m; infusion 5-10mcg/kg/h. Naltrexone - longer half life, works for 24h. Used in addiction and compulsive eating.
Oral equivalence ratios: Morphine 1 Oxycodone 2 Tramadol 0.15 Codeine 0.1
Transdermal:
Buprenorphine 5mcg/h patch = 12mg Oramorph over 24h
Fentanyl 50mcg/h patch = 180mg Oramorph over 24h
Many of the SEs of opioids result from peripheral receptor agonism (whereas desirable effects are central) - methylnaltrexone (peripheral antagonist) reduces these.
Receptors - all GPCRs
All reduce neuronal cell excitability and nerve impulse transmission, and inhibit neurotransmitter release.
Activation of opioid receptors causes closing of calcium channels, K+ efflux and hyperpolarisation.
- MOP - throughout CNS; produces resp depression by making chemoreceptors less sensitive to CO2, constipation, meiosis, itch.
- DOP - cerebral cortex; less widespread; resp depression, GI SEs.
- KOP - nucleus raphe magnus; sedation, dysphoria. NO resp depression. Meiosis.
- NOP (non-classical) - role in synaptic plasticity - basis of tolerance and dependence. Does not bind to naloxone. Can be anti-analgesic.
Morphine - peak 30-60m, terminal half life 3.5h. Metab by gut and liver to 70% M3G and 10% M6G (13x more potent).
Fentanyl - metab to norfentanyl (inactive). Peak 3-5m, duration 30m. Terminal half life 3.5h.
Pethidine - metab to norpethidine (active - hallucinations, seizures).
Codeine - CYP2D6. Poor and fast metabolisers.
ACE inhibitors (past Q)
Prodrugs: enalapril, ramipril, perindopril (–> enalaprilat etc). Given as prodrugs because improves gut absorption.
Active drugs: lisinopril, captopril
Ind: HTN <55y, heart failure, post MI, diabetic nephropathy, CKD.
SEs: dry cough (bradykinin), first dose hypotension, refractory hypotension under GA (avoid AM dose), renal impairment, angio-oedema, teratogenicity.
Other prodrugs: codeine, cyclophosphamide, isoniazid, clopidogrel, levodopa.
A prodrug is a compound that has little or no activity on a desired pharmacological target, but is converted to an active, or more active, entity by an endogenous metabolic reaction. Prodrugs can improve pharmacokinetics, reduce toxicity, or facilitate delivery of the drug to specific tissues or cells.
Magnesium
2nd most abundant intracellular cation
25g in adult body, mainly in bone
Antihypertensive
- Calcium antagonism (prevents Ca entry to cells via NMDA channels) - reduces vasospasm
- Direct vasodilator
- Decreases catecholamine release from adrenals
Anti-arrhythmic
- Reduces SAN/AVN conduction
Smooth muscle relaxant
- Reduces presynaptic ACh release
- Reduces sensitivity of postsynaptic membrane
Other roles
- Enzyme cofactor
- Anticonvulsant
Therapeutic 2-4 mmol/L
Loss of reflexes >5
Respiratory depression 6-7
Cardiac arrest >10-12
Thiopentone (past Q)
How did NAP 5 suggest that thio contributes to awareness? Always used with NMB, in RSIs/emergencies
N2 in vial as CO2 in air would react –> precipitates
Intra-arterial injection
Precipitation of acid crystals –> occlusion and spasm of vessel –> critical ischaemia
Stop injecting, keep line in, run in 500ml warm saline, 10ml 1% lidocaine if severe pain, vasodilators e.g. papaverine; then stellate ganglion block or BP block to induce sympathetic blockade, then fully anticoagulate (500-1000u heparin). Vascular opinion. IR1, document, consultant.
Anaphylaxis (past Q)
Incidence of each sign/symptom Specific drug precipitants Anaphylactic vs anaphylactoid Latex is slower reaction as transdermal rather than IV insult Sugammadex for vec/roc anaphylaxis
Drugs for dementia (past Q, Dr Barry)
Donepezil
Memantine
Tranexamic acid
Synthetic lysine derivative
Antifibrinolytic
Prevents conversion of plasminogen to plasmin
CRASH-2
WOMAN April 2017 - reduces death from PPH by 19%
Local anaesthetics (past Q)
Isomers Esters and amides Toxicity - which pts at risk? R-bup - cardiotoxic as binds to myocytes and affects mem potential What preservatives used?
Clinical trials
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