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Final FRCA SOE > Pharmacology > Flashcards

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
Q

Types of calcium channels

A

Voltage gated
- L-type - ventricular myocytes (refractory period)
- T-type - cardiac pacemakers
Ligand-gated
- Ryanodine receptor

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26
Q

Calcium channel blockers

A

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

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27
Q

Anticonvulsant drugs

A

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

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28
Q

Tell me about a drug

A
  1. Class
  2. Uses
  3. Mechanism of action
  4. Chemical properties
  5. Dose
  6. Pharmacokinetics ADME
  7. Pharmacodynamics by system
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29
Q

Suxamethonium

A

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

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30
Q

Sux apnoea

A

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

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31
Q

Sux - Phase 1 and 2 blockade

A

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

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32
Q

Dementia definition

A

progressive neurocognitive disorder characterised by memory impairment plus other cognitive deficits such as language, complex tasks, reasoning.

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33
Q

Types of dementia

A

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

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34
Q

Dementia drugs (minimal evidence)

A

Acetylcholinesterase inhibitors (some symptoms felt to be cholinergic deficit)
- donepezil - central acting
- rivastigmine
NMDA receptor blockers
- memantine

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35
Q

Delirium definition

A

acute reversible cognitive dysfunction with reduced awareness and inattention. may be associated with hallucinations delusions, memory impairment
Hyper/hypo

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36
Q

Management of delirium

A

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
Q

Vomiting centre

A

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
Q

Classes of antiemetics

A

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
Q

Antiemetic strategy

A

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
Q

Neuroleptic malignant syndrome

A

Idiosyncratic reaction to antipsychotic drugs
- fever, rigidity, confusion, autonomic dysfunction
- Stop drug, cool, dantrolene, fluid (CK)

41
Q

Principles of chemotherapy

A

Chemotherapy targets replicating cells and ultimately trigger apoptosis in cancer cells. usually administered in combination to achieve synergy.

42
Q

Regimes

A

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
Q

Mechanisms of action of common chemotherapy agents

A

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
Q

Side effects by system

A

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
Q

Radiotherapy

A

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
Q

Antibiotic classification

A

mechanism of action
- inhibition of nucleic acid synthesis - quinolones
- inhibition of cell wall synthesis
- inhibition of protein synthesis - aminoglycosides

47
Q

Nucleic acid synthesis inhibitors

A

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
Q

Cell wall synthesis inhbitors

A

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
Q

Protein synthesis inhibitors

A

Aminoglycosides - inhibit RNA binding. gentamicin, narrow therapeutic index
macroldies - clarithromycin - inhibit translocation of RNA. narrow spectrum

50
Q

Antibiotics resistance

A

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
Q

Plasma proteins

A

Albumin (60%)
A1 globulins
A2 globulins
B globulins
Y globulins

52
Q

Albumin

A

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
Q

Human albumin solution

A

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
Q

Albumin evidence

A

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
Q

Warfarin

A
  • 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
Q

NOACs

A

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
Q

Heparins

A

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
Q

Neuraxial and NOACs

A

warfarin INR < 1.4
NOACS - 48hrs (apixaban 24-48) (dabigatran 48-96)
UFH 4hrs
LMWH prophylactic 12 treatment 24

59
Q

Dopamine

A

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
Q

Drugs used to treat parkinsons

A
  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
Q

Drugs to avoid in parkinsons

A
  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
Q

Blood gas solubility coefficient

A

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
Q

Oil:gas partition coefficient

A

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
Q

MAC

A

Measure of potency
Concentration of anaesthetic agent at steady state which prevents reaction to surgical stimulus in 50% of subjects at one atmosphere

65
Q

Factors altering MAC

A

Increase
- Hyperthermia
- Young age
- Chronic alcohol / drug use
- Catecholamine
Decrease
- Pregnancy
- Hypotension
- Hypothermia
- Acute opioid use

66
Q

Ideal volatile

A

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
Q

Cardiac output and onset of action of volatiles

A

High cardiac output maintains concentration gradient between alveolus and arterial pressures, slower equilibrium, slower onset of action

68
Q

Serotonin production / metabolism

A

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
Q

Serotonin receptors

A

5HT1-7
All GPCR apart from 5HT3 (ion channel)
5HT2 = platelet aggreggation
5HT3 = GI tract and area postrema = vomiting
5HT6-7 = limbic function

70
Q

Serotonin syndrome

A

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
Q

Hunter criteria for serotonin syndrome

A

Serotoningeric agent and combination of
- spont / inducibe clonus
- agitation
- diaphoreiss
- tremor
- hypertonia
- hyperreflexia
- hyperpyrexia

72
Q

Tricyclics mechanism of action

A

Complex
- H1/H2 blockade
- Anticholinergic
- Blockade of presynaptic NA / serotonin uptake
- Blockade of cardiac fast Na channel

73
Q

TCA kinetics

A

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
Q

TCA cardiac toxicity

A

Slow phase 0 by Na channel blockade
delay depolarisation AV node, prolong QRS, abnormal repolarisation
hypotension direct myocardial depression, alpha blockade vasodilation

75
Q

Secondary prevention post MI

A

ACEi
Antiplatelet (DAPT)
Beta blocker 12months (indefinite if LVF)
Statin
(ca channel blocker if beta blocker contraindicated)

76
Q

ACEi indications

A

secondary prevention post MI
Essential hypertension
CKD
Diabetic nephropathy
Heart failure

77
Q

ACEi side effects

A
  • cough
  • hypotension
  • electrolyte derangement - hypokalaemia
  • renal impairment
  • Angioedema
78
Q

approach to hypotensive agents

A

BP = CO X SVR
Reduce HR
- beta blockers
Reduce venous return
- venodilators
- neuraxial blockade
Reduce contracility
- volatile
Reduce SVR
- anaesthetic
- vasodilators
- neuraxial

79
Q

hypotensive drugs

A

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
Q

Sodium nitroprusside

A
  • 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
Q

Three types of anticholinesterases

A

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
Q

Organophosphate poisoning

A

Parasympathetic overload SLUDGE
- lacrimation
- meiosis
- salivation
- bradycardia
- diarrhoea
- urination
- bronchospasm
- confusion agitatation coma

83
Q

Treatment organophosphate poisoning

A
  • remove clothes, PPE, shower, irrigate eyes, charcoal
  • ABC
  • avoid sux
  • atropine ++ child 20mcg/kg repeat every 20mins
  • pralidoximine
  • diazepam
  • toxbase
84
Q

Warfarin reversal

A
  • 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
Q

Anticonvulsant drugs

A

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
Q

Phenytoin

A

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
Q

Leveteracetam

A

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
Q

Hepatic enzyme inducers

A

Increase activity - faster metabolism of drugs
PCBRAS
- Phenytoin
- Carbamazepine
- Barbiturates
- Rifampicin
- Alcohol
- Smoking

89
Q

Hepatic enzyme inhibitors

A

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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