Drugs Flashcards
(215 cards)
1
Q
Describe a wash in curve
A
X axis time
Y axis FA/FI
Negative exponential
Related to BGPC where lowest reach FA/FI first
2
Q
Factors which increase speed of onset of volatiles
A
Equipment - FiVO, FGF
Patient - high MV, low FRC (large FRC dilutes volatile), low CO, CBF
3
Q
What is the blood gas partition coefficient?
A
Solubility of agent in the blood compared to the pp it exerts in its gaseous phase at same T and vol at equilibrium
4
Q
What is the oil gas partition coefficient
A
Measure of lipid solubility, inversely related to MAC (high O:GPC = low MAC = more potent)
5
Q
How does the blood gas coefficient effect offset of volatiles
A
Low BGPC have faster offset
6
Q
Describe wash out curve for volatiles
A
X axis time
Y axis FA/FAE (pp in alveoli when gas turned off)
Lowest BGPC washed out first
7
Q
What is the context sensitive half time
A
Time taken for plasma concentration to fall by 1/2 of its value after stopping administration at steady state
8
Q
MAC definition
A
Dose required at steady state to prevent 50% of subjects reacting to standard surgical stimulus
9
Q
Factors which increase MAC
A
Young
Chronic alcohol
Hyperthermia
Hyperthyroid
10
Q
Factors which decrease MAC
A
Neonate/ old
Acute intoxication
Sedatives
Hypothermia
Hypothyroid
11
Q
Why is halothane more lipid soluble
OGPC? MAC?
A
Smaller molecule than ether volatiles. Most potent
OG:PC 224 MAC 0.75
12
Q
Why is halothane more blood soluble than ether volatiles
A
Can form stronger hydrogen bonds
BGPC 2.4
13
Q
What is the difference between isoflurane and enflurane
BGPC of each
A
Structural isomer
Due to positions of flouride atoms iso is less blood soluble therefore has a quicker onset
Isoflurane BGPC 1.4
Enflurane BGPC 1.8
14
Q
Why is desflurane least blood soluble
A
Has 6x fluoride atoms therefore more electronegative.
15
Q
What is the unique metabolite of sevoflurane
A
Hexa-flouro-iso-propanolol
16
Q
Which volatile is metabolised the most
A
Halothane
17
Q
Which CYP450 enzyme Mx volatiles and is the same enzyme which is induced by chronic alcohol use
A
CYP2E1
18
Q
Pharmacodynamics of volatiles
A
Brain - increase ICP?
Excitatory phenomenon
Decrease GCS
Resp - Decrease TV, increase RR
Bronchodilator
Cardiac - Decrease MAP/ SVR
Des/ sevo - increase heart rate
Sevo - increase QTc
GU - relaxes uterus (sevo)
19
Q
Ideal phsyical properties of vapour
A
Stable liquid at room temp
Inert
Cheap
Non flammable
High SVP, low latent heat of vaporisation
20
Q
Ideal pharmacological properties of vapour
A
Pleasant non irritating smell
Low BGPC
High OGPC
Cardiovascularly stable
No toxic metabolites
21
Q
Pathophysiology of MH
A
Uncontrolled release of calcium from SR in skeletal muscle due to RYR1 receptor mutation
22
Q
Symptoms of MH
A
Tachycardia
High O2 requirement
Hypercapnia
Hyperthermia (late)
Rigidity
23
Q
Mx of MH
A
Dantrolene 2.5mg/kg bolus, repeat 1mg/kg up to 10mg/kg
24
Q
How is nitrous oxide made
A
Heating ammonium nitrate to 250 degrees
25
What colour cylinders is N2O stored in
Blue
26
How does N2O work
Inhibits glutamate at NMDA receptor
27
Negative effects of N2O
Increase CBF/ CMRO2
Decreases TV, increases RR
B12/ bone marrow suppression
28
What is the concentration effect
Disproportionate rise of FA/FI when high concentrations of N20 used. Due to large concentration gradient large amount diffused into pulmonary vessels leads to concentration of remaining gases
29
What is diffusion hypoxia
N2O more soluble than N2
N2O leaves the blood into the alveoli quicker than N2 can travel in the opposite direction which dilutes gases to a hypoxic mixture in the alveoli
29
What is the second gas effect
Concentration of volatiles increases quicker in the presence of N20
30
Pharmacological properties of xenon
BGPC
OGPC/ MAC
CT
0.1
1.9/ 71
16.6
31
Pharmacodyanmics of xenon
Brain - neuroprotective
Lungs - apnoea at high concentrations
CVS - no effect
32
Describe the inhibitory pathways in the CNS
Glycine
GABA
33
How does GABA receptor work
5 subunits
Ligand gated ion channel to chloride
Influx of chloride hyper polarises membrane therefore harder to generate AP
34
Excitatory pathways in CNS
nACh (ionotropic receptor)
5HT
Glutamate (metabotropic GPCR)
35
Proposed mechanism of induction agents
Enhance GABA/ glycine
Inhibit glutamate
36
Structure of propofol
Phenol derivative
Aromatic group with 1x OH and 4x CH3 attached
37
Mechanism of propofol
Increases GABA A
Also works at NMDA rec
38
pKa of propofol
11
39
Vd of propofol
4L
40
Pharmacodynamics of propofol
Brain - Sedative/ anticonvulsant
Decrease ICP and CMRO
Eyes - decrease IOP
Airway - obtunds laryngeal reflexes
Resp - Bronchodilates
Cardiac - decrease BP/ SVR
GI - antiemetic
41
pKa of thiopentone
7.6
Weak acid
42
Pharmacokinetics of propofol
A - rapid lipid soluble
D - large Vd (4L), 98% protein bound
M - Liver 60% quinol (repsonsible for green urine)
40% gluconoride
E- renal
Elimination 1/2 life 5-12 hours
43
Formulation of thiopenton
Racemic mixture of keto and enol form
Yellow powder
Dissolved in water pH 10-11 in more soluble enol form
At body pH is becomes more unionised
44
Vd of thio
2.2
45
Mechanism of thiopentone
Mimics chloride at GABA rececptor
Also works at NMDA receptor
46
What kinetics does thio display at repeat doses
Zero order
47
Pharmacodynamics of thiopentone
Brain - decrease ICP/ CBF
Anticonvulsant
Airway - DOES NOT suppress airway reflexes
CVS - decreases BP/ CO
48
Pharmacokinetics of thio
A - highly lipid soluble
D - Vd 2.2L, highly protein bound
M - P450
49
pKa and acid/base status of ketamine
Weak base
pKa 7.5
50
What is ketamine a derivative of
Phencyclidine
51
Mechanism of action of ketamine
Non competitive antagonist at NMDA receptor
Agonist at opiate receptor
Also acts on both ACh receptors and adrenergic receptor
52
Sedative dose of ketamine
0.2-0.75 mg/kg IV
2-4 mg/kg IM
53
Induction dose of ketamine
1-2 mg/kg IV
5-10 mg/kg IM
54
Pharmacodynamics of ketamine
Brain - dissociation, increase CMRO
Eyes - increases IOP
Airway - DOES NOT affect laryngeal reflex, increases secretions
Resp - increases RR, bronchodilates
CVS - Increases HR, increase BP (direct negative inotropy counteracted by catecholamine release)
GI - N+V
Renal - fibrosis, ketamine bladder syndrome
55
Pharmacokinetics of ketamine
A - poor oral BF
D - Vd 3L
20-50% protein bound
M - CYP450 to norketamine
E - Renal
Elimination 1/2 life 2-3 hours
56
Phases of peripheral nerve action potential
Phase 1 - Na/K/ATPase pump maintains resting potential of -80mv
Phase 2 - -60mV is threshold for AP generation. Na influx to +30mV
Phase 3 - K efflux through voltage gated channel restores potential
57
LA are weak acids or bases?
Weak bases
58
Mechanism of action of LA
Block Na channel intracellularly to stop AP
59
Factors which affect quicker speed of onset of LA
Smaller and myelinated fibres
Vasodilated area
60
Structure of LA
Lipophilic ring (responsible for lipid solubility)
Hydrophilic tertiary amine
Ester or amide linkage
61
Which LA are esters
What is their risk
Procaine
Cocaine
Mx to PABA which carries risk of anaphylaxis
62
Pharmacokinetics of LA
A - Depends on blood flow
intercostal> caudal> epidural > brachial plexus > sc in order of risk
D - More protein bound - longer duration of action
M - Esters - pseudocholinesterase (rapid)
Amides - liver
E - 5% unchanged really
63
pKa of bupivicane and ropivicane
8.1
64
Order of LA protein binding
Bupivicine/ ropivicane
Lidocaine
Prilocaine
Procaine
65
Why does lidocaine/ prilocaine have the quickest onset
pKa is 7.7 / 7.9 respectively
Therefore less ionised drug as closer to physiological pH
66
Which LA has the slowest onset, what is its pKa
Procaine
pkA 8.9
67
Mx of LA toxicity
Intralipid
1.5ml/kg over 1 min
15ml/kg/hr infusion
Repeat dose at 5 mins if no improvement and increase infusion to 30ml/kg/hr
Cumulative dose 12ml/kg
68
Mechanism of paracetamol
COX3 inhibitor
Possibly increases cannabinoid receptor
69
Pharmacokinetics of paracetamol
A - PO 80%
D - 1/2 half 2 hours
M - 90% glucuronidation
10% CYP450 to NAPQI
NAPQI conjugated to glutathione which is non toxic
E - Renal
70
Mechanism of NAC
Stimulates glutathione production
Directly binds to NAPQI
Reduces NAPQI back to paracetamol
71
Describe the arachidonic acid pathway
Membrane phosophilds metabolised to Arachidonic acid by phospholipase A2
Arachidonic acid Mx to
1) Leukotrienes by lipoxygenase
2) Prostaglandins and thromboxane A2 by COX 1
3) Prostaglandin (PGE2) and prostacyclin by COX 2
72
Function of prostaglandins made by COX 1
Function of TXA2
GI protection
Renal blood flow
Uterine contraction
Platelet aggregation
73
Function of induced prostaglandins made by COX 2
Pain/ inflammation
Vasodilation
Prostacyclin - platelet relaxatiob
74
Mechanism of aspirin
Irreversible non selective COX inhibitor
75
Formulation of aspirin
Aromatic ester of acetic acid
76
Mechanism of aspirin overdose
Uncouples oxidative phosphorylation
77
Pharmacodynamics of aspirin
Brain - stimulates CTZ --> n+V
Resp - respiratory alkalosis
GI - irritation
Renal - metabolic acidosis, hypoglycaemia.
Decrease renal blood flow
78
Pharmacokinetics of aspirin
A - BF 70%
D - Lasts 7/7 (life of pet)
M - Esterases to salicylate
E - Renal
79
Pharmacokinetics of NSAIDs
A - Rapid
D - Highly protein bound (can displace other highly protein bound drugs to increase their effect ie warfarin)
M - Limited first pass Mx, liver
E - Renal
80
Are opiates weak acids or bases
Weak bases
81
Opiate receptors and ligands
Mu - endorphins
Delta - enkephalins
Kappa - dynorphins
82
Describe how a GPCR works for opiates
Ligand attaches to receptor
G alpha inhibits adenyl cyclase to prevent ATP conversion to cAMP
G beta blocks calcium channel to prevent influx to presynaptic membrane
G gamma stimulates potassium efflux to hyperpolarise post synaptic membrane
83
pKa of
Morphine
Fentanyl
Alfentanyl
Remifentanyl
8
8.4
6.5
7.1
84
Why does alfentanyl have a quicker action of onset than fentanyl
Fentanyl is more lipid soluble however alfentanyls pKa means that it is 90% unionised at a pH of 7.4
85
Which opiates have no active Mx
Fent and alf
86
Vd of morphine and fentanyl
3-5L
87
Metabolism of codeine
60% Codeine 6 gluconorate
20% CYP3A4 to norcodeine
10% CYP2D6 to morphine
88
Features of dihydrocodeine
Semi synthetic derivative of codeine, more potent
89
Mechanism of buprenorphine
Partial agonist of mu receptor
Antagonist at D/K receptor
Higher affinity to receptor > morphine therefore can precipitate acute withdrawal
90
Pharmacokinetics of buprenorphine
A - variable
D - 10 hour duration
M - CYP3A4
E - biliary
91
Pharmacokinetics of morphine
A - PO BF 25%
D - Low lipid solubility
Vd 3-5L
M - 70% M3G (inactive
M6G (active, more potent)
Normorphine
E - Urine and bile
92
Features of diamorphine
Prodrug
More lipid soluble therefore able to cross BBB
Mx by esterases to 6MAM which is mx to morphine
93
Pharmacodynamics of opiates
Brain - analgesia, euphoria, sedation
Eyes - miosis
Airway - suppresses cough reflex
Resp - decreased RR, wooden chest at high doses, histamine release
CVS - decreases HR and BP
GI - N+V/ constipation/ Oddi spasm
Renal - retention
Other - itch, tolerance, dependance
94
Physiology of neuromuscular junction
AP propagates to pre synaptic terminal
Stimulates Ca2+ influx through N type channels
Ca2+ stimulates Act release from vesicles in cytoplasm and attached to membrane
ACh binds to NAChR at 2x alpha subunits on post synaptic membrane
Stimulates conformational change of ligand gated sodium channel to allow Na influx to continue propagation of AP
AChE in clefts of post synaptic membrane Mx ACh to acetyl coA and choline
95
Structure of ACh
Single ester linkage
Ammonium ion
96
Structure of AChE
Anionic site cleaves choline
Esteratic site Mx ester linkage
97
Why does neostigmine require glycopyrolate
Acetylcholinesterase inhibitors are non selective therefore also block muscarinic receptors
98
Structure and dose of suxamethonium
Water of lipid sol?
2x Ach molecules
1mg/kg
Water sol due to ammonium ion
99
Metabolism of suxamethonium
PLASMA cholinesterase (therefore neostigmine will prolong block by inhibiting theses enzymes)
100
Phases of depolarising NMB block
Phase 1 - NAchR agonist and depolarises membrane then renders inactive
Phase 2 - Characteristics of NDNMB
101
Side effects of suxamethonium
Increase ICP
Increase IOP
Decrease HR
Myalgia
Hyperkalaemia
102
Mechanism of ND NMBs
Competitive antagonist of NAChr
103
Which drugs are benzylisoquinoloniums
Atracurium
Cisatracurium
Mivacurium
104
How is atracurium/ cisatracurium Mx
1) Non specific esterases
2) Hoffman degradation
105
How is mivacurium Mx - what is the implication
Mx by plasma cholinesterase therefore can't give to someone with sux apnoea
106
Pharmacokinetics of NMBD
A - highly ionised and polar therefore water over lipid soluble
D - Small Vd
Limited crossing of BBB and placenta
M - see separate
E - Urine and biliary (mono quaternary compounds (vec/roc) more biliary)
107
Factors that will prolong NMB
Pt - hypothermia, acidotic
Mg, hypoK
Anaesthetic - TCA/ aminoglycoside
108
Which NMBD are aminosteroids
Pancuronium (most potent)
Vecuronium
Rocuronium
109
Methods of monitoring NMB
Mechanomyography - tension of contraction
Acceleromyography - acceleration of thumb twitch
Electromyography - current of AP
110
Describe reversal of NMBD
Drug is cleared from the plasma which creates a concentration gradient so that drug dissociates from NAChR.
111
Mechanism of AChi
Non selective binding of AChE at nicotinic and muscarinic.
Binds to ACh enzyme at same sites of ACh so it can't bind, thereby increasing concentration of ACh over drug at membrane
112
Organophosphates mechanism
Irreversible binding to enzyme
113
Mechanism of suggamadex
Cyclodextrin ring, lipophilic centre and hydrophilic outer ring. Attracted to ammonium ion on NMBD to encapsulate drug. Excreted as whole complex renally.
114
Patient risk factors for PONV
Female
Non smoker
Previous
Prolonged fast
115
Surgical risk factors for PONV
ENT
Eye
Gynae
Neuro
Laparoscopic
116
Anaesthetic factors for PONV
Volatiles
Opiates
Neostigmine
N2O
117
Inputs to the vomiting centre
1) Higher centre
2) GI - 5HT3 and ACh rec
3) Vestibular - ACh and H1 rec
4) CTZ - 5HT3 and D2 rec
118
Where is the CTZ
Dorsal surface of medulla on floor of 4th ventricle
119
Structure of ondansetron and receptor
Synthetic carbazole
Serotonin rec in GI and CTZ
120
Pharmacodynamics of ondansetron
constipation, prolonged QTc
121
Pharmacokinetics of ondansetron
A - 60% BO
B - 75% protein bound
M - liver to inactive Mx
E - renal
122
Structure of cyclizine and receptor
Piperazine derivative
H1 antagonism, some antimuscarinic
123
SE's of cyclizine
Woozy, dry mouth, tachycardia
124
Prochlorperazine receptor
D2 antagonist in CTZ
Some H1
Some antimuscarinic
125
SE's of prochlorperazine
Decrease seizure threshold
Exacerbate PD
NMS
126
Metoclopramide receptor
D2 antagonist in CTZ
Some 5HT3 antagonism
127
SE's metoclopramide
Oculogyric crisis
EPSE/ dystonia
Prokinetic
128
Which antiemetic works on antimuscarinic receptors in vestibular system
Hyoscine
129
SE's of hyoscine
Sedation, dry mouth, anticholinergic syndrome
130
Action of oxytocin (syntocinon)
Acts on GPCR to stimulate uterine contraction and breast milk ejection
131
Pharmacokinetics of synt
A - immediate
D - 30% protein bound, crosses placenta
M - hepatic
E - bile/ urine
132
What conditions require cautious use of oxytocin
Cardiomyopathies
Decreases BP/ increases HR
133
What is the second line uterotonic? What is its action
Ergometrine
Alpha adrenergic receptor antagonist
134
SE's of ergometrine
Increases BP
Reflex Brady
Headache
N+V
135
What is the action of carboprost
When is it contraindicated
Prostaglandin rec
CI - asthmatics
136
Dose of carboprost
250 mcg IM
Repeat every 15 mins to 2mg
137
What is the most important factor dictating IOP
CVP via episcleral vessels - if increased causes decreased drainage of aqueous humour
138
Which drugs decrease production of aqueous humour
Timolol
Alpha agonists
Acetozolamide
139
Which drugs increase drainage of aqueous humour
Musc. agonists - pilocarpine
Latanoprost
140
Which drugs can increase IOP
Ketamine, N2O, Sux
141
Which drugs affect cell wall of bacteria (5)
Penicillins
Cephalosporins
Carbapenems
Monobactams
- inhibit cross linking of chains
Vancomycin - inhibits NAG/NAM binding
142
Which drug prevents 50S ribosome to move along mRNA
Is it bacteriostatic or bactericidal?
Erythromycin
Bacteriostatic
143
Which drugs acts on 30S ribosome to misread mRNA
Is it bacteriostatic or bactericidal?
Gentamicin
Bacteriocidal
144
Which drugs acts on 30S ribosome to inhibit tRNA?
Tetracyclines
145
Which drug inhibits dihydrofolate reducates
Trimethoprim
146
Which class of drug inhibits DNA gyrase in bacteria with examples
Quinolones
Ciprofloxacin
Levofloxacin
147
How does increasing generation of cephalosporin affect cover of organisms
Decreasing G positive
Increasing G negative
148
Examples of gram positive cocci and appropriate Abx
Staph/ strep
Pencillins, cephalosporins, linezolid
149
Examples of gram positive rods
Clostridium
Listeria
150
Poor staining bacteria
Mycoplasma
Listeria
151
Gram negative cocci?
Example of appropriate Abx
Neisseria
Higher generation cephalosporins
152
Gram negative rods?
Examples of appropriate Abx
E. coli
Klebsiella
Pseudomonas
Co-amox/ Taz
Cipro
Gent
153
How do azole drugs work? Give examples
Inhibit enzyme that makes ergosterol
Fluconazole
154
How do polyene drugs work
Give an example
Binds to ergosterol in cell wall and makes holes
Amphotericin
155
How do echinocandins work
Give an example
Inhibit Beta gluten synthesis
Caspofungin
156
Which receptors does salbutamol work on
B2 agonist
Some B1 agonist activity
157
SE's of salbutamol
Arrythmias/ Tachycardia
Hypokalaemia
Increased lactate
Uterus relaxation
158
How does ipratropium work
What is its structure
Antimuscarinic therefore blocks parasympathetic driven bronchoconstriction
Quaternary structure --> doesn't cross BBB
159
Mechanism of aminophyline (3)?
Non selective PPD inhibitor
(PPD is responsible for breakdown of cAMP)
Increased cAMP levels decrease Ca2+ release to cause muscle contraction --> bronchodilator smooth muscle
NA release
Stabilises mast cells
160
How is aminophyline metabolised
CYP450 - narrow therapeutic index
Zero order kinetics
161
SE's of aminophyline
Decrease seizure threshold
Positive ionotropy/ chronotropy
Arrythmias
Hypokalaemia
162
Site of action of loop diuretics
Binds of Cl binding site of NKCC2 carrier in thick ascending limb to inhibit reabsorption of filtrate
163
Structure of furosemide
Sulphonamide derivative
164
Pharmacokinetics of furosmide
Highly protein bound
Hepatic Mx
Really excreted unchanged
165
SE's of furosemide
Electrolye disturbance
Increase uric acid --> gout
Hearing loss
166
Structure and mechanism of thiazide diuretics
Sulphonamide
Acts on Na/Cl co transporter in early DCT preventing passage into tubular cell
167
SE's of thiazide diuretics
Hypokalaemia, hypochloraemic metabolic alkalosis
Hyperglycaemia
Gout
Impotence
168
Site of action of potassium sparing diuretics
Competitive antagonist for aldosterone at MR in late DCT and collecting duct
169
SE's of MRA
Metabolic acidosis
Gynaecomastia
170
Pharmacokinetics of MRA
A - slow onset - max 3-4 days
D - highly protein bound
M - Mx in gut and liver to active Mx
E - Urine and bile
171
Classes of antiepileptics
Na channel blockers - phenytoin/ carbamazepine/ lamotrigine
GABA enhancers - Keppra, SoVal, Benzos
Glutamate blockers - Topiramate
172
Pharmacokinetics of benzodiazepines
A - Good PO bioavailability
D - Strongly protein bound, lipid soluble --> crosses BBB
M - Active Mx, some with long half lives
E - urine
173
Pharmacodynamics of benzodiazepines
CNS - Anxiolytics, sedation, anti convulsant
Resp - Obtunds laryngoscopy response, resp depression
CVS - Decreases CO
Renal - decreases blood flow
174
Possible adverse effects of vancomycin
Red man syndrome (histamine release)
175
SE's of quinolones (cipro/ levo)
C.diff
Tendonitis
Seizures
176
Difference between tertiary and quaternary antimuscarinic
Tertiary crosses BBB
177
Examples of tertiary antimuscarinic
Atropine, hyoscine
178
PD of atropine/ glyco
CNS - agitation/ confusion (atropine)
Eyes - increases IOP
Resp - bronchodilates
CVS - increases HR
GI - increases secretions, lower LOS tone
179
Pd of noradrenaline
Cardiac - increased SVR ++
Reflex Brady, increased O2 consumption
Resp - increased PVR
GI - decreased blood flow
Uterus - fetal Brady
Other - necrosis
180
Pk of noradrenaline
A - 1/2 life 2 mins
M - COMT - inactive Mx
E - Urine
181
Receptor site of dobutamine
B1 >B2
182
Cardiac effect of dobutamine
Increased HR and contractility
B2 usually decreases SVR however BP usually maintained
183
CI of dobutamine
Fixed CO - AS, tamponade
184
Pd of adrenaline
Resp - bronchodilator
CVS - Increased CO and O2 consumption
decreased SVR at low doses, increased at high doses
Renal - decreased flow
Metabolic - glucose and lactate rise
185
Pk of adrenaline
A - IM > SC
M - MAO/ COMT to inactive Mx
E - Urine 1/2 life mins
186
Which volatile interacts with adrenaline
Halothane
187
Effect of ephedrine
Direct - alpha and beta
Indirect - NA release from sympathetic nerves
188
Pk of ephidrine
A - 100%
D - Rapid
M - Hepatic therefore half life
E - 65% excreted unchanged in urine
189
Class 1a antiarrythmics
Quinidine
Procainamide
190
Class 1b antiarrythmics
Lidocaine/ phenytoin
191
Class 1c antiarrythmics
Flecainide
192
Class 2 anti arrythmics
B blockers
Propanolol
Metoprolol
193
Class 3 antiarrythmics
Amiodarine
194
Class 4 antiarrythmics
Verapamil
Diltiazem
195
Action of clopidogrel
Irreversible ADP P2Y12 antagonist
Prevents fibrinogen binding
196
Mx of clopidogrel
Prodrug, hepatically Mx to active form
197
Ticagrelor action
Reversible allosteric inhibition of ADP receptor
198
Dipyradimole action
PDE receptor - inhibits platelet adhesion
199
G1b/G3a rec action and examples
Inhibits adhesion of fibrinogen binding
Tirofiban
Eptifbatide
200
Action of heparin/LMWH
Wraps around anti-thrombin-thrombin complex so can't act
LMWH is smaller molecule (<8000 daltons) which wraps around X10
201
Time frame of HIT vs non immune thrombocytopenia
4-14 vs <4
202
Do heparins cross placenta/ BBB
No
203
Pk of DOACs
A - 60-80%
M - CYP3A4
E - Renal (apixaban least therefore better in renal failure)
204
Action of dabigatran
Mx of dabigatran
Prodrug, 2a antagonist
Hepatic and plasma esterase
205
Pd Sodium nitroprusside
CVS - Aterio and veno dilator by producing NO
Decreases SVR --> BP
Decreases preload
Reflex tachycardia
RS - Increased shunt
CNS - cerebral vasodilation increases ICP
206
Pk of sodium nitroprusside
A - No PO BF, duration 10 mins
M - RBCs, hepatic, renal, creates cyanide
E - Urine
207
Action of GTN
Ventilator by producing NO
Activates granulate cyclase to increase cGMP. Decreases cytoplasmic Ca --> vasodilation
208
Pd GTN
CVS - Decreases preload, O2 demand
Increase flow to subendocardial tissues
Decreases SVR and tachy in high dose
CNS - headache
209
Pk GTN
A - dependent
D - not protein bound
M - 1st pass Mx (nicorandil), denitration
E - 20% of metabolite excreted in urine
210
pKa of lidocaine
7.8
211
Calculate max dose of bupivicaine
0.5% = 0.4 x wt
0.25% = 0.8 x wt
212
Which LA's can ppt metHb
EMLA and prilocaine
213
Which LA need to be avoided in sux apnoea
Procaine
214
Which LA can be motor sparing
Ropivicaine
