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Clinical Pharmacology - Coggle Diagram

- - - - Promotes NA release
- - - - 9-12L VoD
    - - Excreted unchanged in urine, 90% in first 24h
    - - 3h after oral dose, rapid after IV injection
  - - - 1.5% mortality benefit with 1g given within 3h of injury
    - - 1g for PPH 0.4% mortality benefit from haemorrhage
    - - Reduced blood loss in cardiac surgery
- - - - Previous PONV
      - Motion sickness
      - Female
      - Non smoker
      - Anxiety/migraine/age (>3)
    - - Laparoscopic
      - Gynae
      - Middle ear
      - Eye
    - - N2O use
      - Intra or postoperative opioid use
      - Volatile use
      - Increased duration
  - - - Accupuncture
      - Aromatherapy
      - Avoid GA
      - Avoid dehydration
    - - H1R antags (cyclizine)
      - D2R antags (metoclopramide)
      - 5HT3 antagonists (ondansetron)
      - Anti muscarinics (scopolamine)
  - - - Neuronal pathways from vestibular
      - Reflex afferents from cerebral cortex
      - Vagal mucosal pathway from GIT
      - Midbrain afferents
      - Chemoreceptor trigger zone
  - - - 4 factors
        
        Hx of PONV or motion sickness
        
        Non smoker
        
        Female
        
        Post op opioids
      - Score & risk
        
        2 = 40%
        
        3 = 60%
        
        1 = 20%
        
        4 = 80%
        
        0 = 10%
- - - - Irreversible inhibition of P2Y12 ADP R
    - - Prevent crosslinking of platelets of vWF to subendothelium
    - - Irreversible nonselective COX inhibition
        
        Reduced thromboxane A2 production
    - - Phosphodiesterase inhibitor - increases cAMP
    - - Binds Gprotein coupled R -> increasing cAMP by adenylate cyclas to keep platelets inactive
    - - ADP analogue - alters the P2Y12R and inhbitis ADP binding - reversible
- - - - Tachycardia, arrhythmias, orthostatic hypotension
    - - Bloating after meals, constipation, diarrhoea
    - - Impotence, loss of bladder control
  - - - Nephropathy
      - Neuropathy (motor & sensory -> glove & stocking, autonomic neuropathy)
      - Retinopathy
      - Microvascular cardiac disease
    - - Cerebrovascular disease
      - HTN
      - Coronary artery disease
      - PVD
  - - - Stimulate insulin release
    - - Stimulate insulin release
    - - Increased peripheral insulin sensitivity, increased peripheral glucose uptake
    - - Slow carbohydrate digestion in gut
    - - Decrease hepatic gluconeogenesis & improves peripheral insulin sensitivity
    - - Inhibit glucose reabsorption in kidney
    - - Stimulate insulin secretion and inhibit glucagon release from meals via GLP-1 effect
    - - Via incretin pathway
- - - - Drug leaves to go to vessel rich compartment V2 then poor blood supply compartment V3
        
        Two superimposed reducing infusion rates to maintain V1 conc
      - Once equilibrium is achieved, only loss is via metabolism & elimination
        
        Steady state achieved
      - Bolus given to achieve drug conc x Vd
      - Size of compartments and rates vary between drugs, model and pts (height, weight, age)
      - V1 is plasma or where drug is injected - calculated by pt parameters
- - - - Redistribution occurs down its conc gradient into plasma from NMJ as plasma level decreases
      - Reduction in plasma level due to metabolism by liver and excretion in bile
      - After administration there is dynamic association and dissociation of rocuronium with nicotinic Rs
    - - Reversible acetylcholinesterase inhibitors (Neostigmine)
        
        Neostigmine hydrolyses acetylcholinesterase forming a carbamylated enzyme complex leading to increased ACh @ NMJ, competeing with rocuronium
        
        Advantages
        
        Cheap, familiar
        
        Disadvantages
        
        Muscarinic R action causing bradycardia (so given with glyco but causes tachy), no use in CICO, requires specific ToF before use
      - Cyclodextrins (Sugammadex)
        
        Ring like structure with hydrophilic outer surface & lipophilic inner that encapsulates rocuronium
        
        Advantages
        
        Full paralysis-full reversal, no risk of re-blockade, no significant CVS effects, facilitates rapid case turnover, use in myotonic dystrophy
        
        Disadvantages
        
        Flucloxacillin & fusidic acid can displace rocuronium from suggamadex, reduces OCP effectiveness, cost, allergy
  - - - Flouride resistant
        
        BChE 1600-4100, DN 79-81%, 1 in 150k
      - Silent
        
        BChE 0-650, DN 0, 1 in 40k
      - Atypical
        
        BChE 1600-4100, DN 24-31%, 1 in 3000
      - AS
        
        BChE 540-1800, DN 24-31%, 1 in 8000
      - Usual
        
        Normal BChE, DN 83-88%, About 96% population
      - FS
        
        BChE 1000-3800, DN 78-84%, v rare
- - - - Synthetic pentasaccharide
      - Xa inhibitor
    - - Unfractionated
        
        Mucopolysaccharide 15k-18k daltons
        
        Binds reversibly to AT 3 - increases removal of factors 9, 10, 11 & 12
        
        Reversed by protamine
        
        SEs - thrombocytopenia & osteoporosis
      - LMWH
        
        Average weight 2k-10k daltons
        
        Inhibit factor 10a
        
        Longer half life so given as OD or BD dose
    - - Reversible inhibitor of thrombin
      - Half life 14-17h, daily dosing BD
    - - Inhibits Vit K synthesis and so reduces Vit K dependent factors (2, 7, 9 & 10) and proteins C&S
      - Highly protein bound, so easily displaced
      - Effects PT (normally recorded as INR)
    - - Direct Xa inhibitor
      - OD dosing
      - Half life 7-9h
      - Dose reduction with low eGFR (<50)
      - Higly protein bound and removed by liver (p450), renally exceted
    - - Xa inhibitor
- - - - Chronic exposure (steroid and Cushing's)
    - - Delayed effects (increased Ca risk with childhood chemo)
    - - Bizzare idiosynchratic reactions (agranulocytosis with carbimazole)
    - - End of Rx effects (withdrawal from long term benzos)
    - - Augmented or dose dependent effects (eg coagulopathy wit warfarin)