Pharm (Day 6) Flashcards
Benzo Pharmacokinetics
- Pharmacokinetics
a. Absorbed by GI tract and metabolized by liver = dose adjustment if liver disease or older age & interaction with inhibitors of cyp 3A4
b. Accumulation of metabolites = Decreased LOC - Pharmacodynamics
- bind to GABA-A receptor
- Binding tiggers influx of Cl – ions leading to hyperpolarization of membrane
- Reduced firing of neurons = decreased spinal cord activity, cerebral cortex, CSTS Circuit, amygdala circuit.
Propofol indication, dose, conc, metabolism
Indication = induction and maintenance of general anesthesia, sedation
Given IV, Must open vent cap to use it during infusion
Dose: 1-2mg/kg in stable patient, 0.5mg/kg unstable
Maintenance: 25-100 mcg/kg/min
Concentration: 1000mg/ 100mL (1%) ITS BLUE and 2000mg / 100mL its YELLOW and has a RED bar
Metabolism and Excretion = Redistribution, hepatic conjugation/renal clearance
Must increase if the patient uses ETOH heavily as Ethanol downregulation from GABA receptor
Propofol mechanism
- Allosterically increases the binding affinity of inhibitory neurotransmitter GABA for GABAa receptor = Injection site pain
- Prolonged opening of chloride channel
- Hyperpolarization of nerve membrane
- Inhibitory effect on CNS =
CNS = Reduced Cerebral metabolic rate, cerebral oxygen consumption, intracranial pressure
CVS = Reduced systemic vascular resistance, preload and contractility = hypotension
Resp = Reduced hypoxic and hypercapnic respiratory drive = Hypoxia, Hypercapnia, Apnea
Decreased upper airway reflexes - Induction/maintenance of general anesthesia
Succinylcholine mechanisms
Succinylcholine mimics Ach in structure:
Agonist at nicotinic Ach receptors in muscle
2. Generates action potential
3. Not affected by synaptic acetylcholinesterase (unlike Ach)
4. Continuous end-plate depolarization = Fasciculation, Myalgia = Serum K increase (esp in patients with muscle trauma, denervation or immobilization = Hyperkalemia = Cardiac Arrest
5. Inactivation of sodium channels
6. Prevention of repolarization and additional action potentials
7. Skeletal muscle paralysis
Agonist at nicotinic receptors in parasympathetic ganglia, sympathetic ganglia, and muscarinic receptors in SA node of Heart
1. Parasympathetic effect = down HR, down Contractility
2. Sympathetic effects (high dose succinylcholine) = increased HR, Increased Contractility, Catecholamine release
Succinylcholine indications dose excretion
Neuromuscular blockade for endotracheal intubation, surgery, or mechanical ventilation (as adjunct to
general anesthesia):
IM: Up to 3 to 4 mg/kg, maximum total dose: 150 mg.
IV: Intubation: 0.6 mg/kg (range: 0.3 to 1.1 mg/kg).
Rapid-sequence intubation (off-label dosing): 1 to 1.5 mg/kg
Metabolism & Excretion = redistribution and metabolism by pseudocholinesterase in blood plasma and liver
Effect of Substance P in the brain
function is as a neurotransmitter and a modulator of pain perception by altering cellular signaling pathways.
GABA effect in brain
Primarily neural inhibitor
Reduce neuronal excitability by inhibiting nerve transmission.
It causes prolonged opening of chloride channels which causes a Hyperpolarization of nerve membrane, which causes inhibition.
glutamate effect in brain
glutamate is the most abundant excitatory neurotransmitter
Ketamine ind, route, metabolism
Anesthesia
IV/IM
Dose: 0.5-1mg for unstable
Mechanism:
agonist at NMDA receptor
agonist at the opioid receptor
antagonist at the muscarinic receptor
enhance central/peripheral monoaminergic transmission
Metabolism: Hepatic
Elimination: Urine
Opioid receptor agonist peripheral actions
Direct stimulation of mast cells (Histamine release)
Direct stimulation of CTZ (Nausea/vomiting)
u2-receptor agonism in EN5 (Constipation)
Levophed Ind, dose, metabolism
BP in acute hypotensive stare or shock
Cerebral perfusion in patients with cerebral vasospasm
Dose: 2-4mcg/min titrate up every 10-15 minutes to desired pressure
Mechanism : Stimulates Alpha and Beta 1 receptors
Metabolism: Norepinephrine is metabolized in the liver and other tissues by a combination of reactions involving the enzymes catechol-O-methyltransferase (COMT) and MAO
Dopamine
Increase cardiac output for shock due to MI, Sepsis, trauma, cardiac surgery, spinal cord injury and chronic CHF
Mechanism: Alpha and beta
Dose: 1-5 mcg/kg/min increase rate by 1-4 mcg/kg/min every 10-30 minutes
Usual range 20mcg/kg/min
Max 50mcg/kg/min
Dobutamine
INODILATOR
Inotropic agents may be considered in patients with a low cardiac index and low BP, but without hypotension.
Short-term management of patients with cardiogenic decompensation.
Mechanism: Minor alpha, strong beta
Dose: 2-20mcg/kg/min
Metabolism: In tissues and hepatically to inactive metabolites
Phenylephrine
Vasodilatory shock
Mechanism: Pure alpha
50-200mcg IV Direct
100 to 180mcg/min continous IV infusion when stabilized maintain at 40-60mcg/min
Vasopressin
Organ donor: 0.04U/min
Septic shock: 0.01-0.04U/min
Mechanism: V1 and V2
