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Anaesthesia > Pharmacology in anaesthesia > Flashcards

Pharmacology in anaesthesia Flashcards

1
Q

Definition of Volume of Distribution (Vd)

A

Volume of Distribution (Vd) is the apparent volume into which a drug has mixed or distributed throughout the body.

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2
Q

Factors that affect Volume of Distribution (Vd)

A

Lipid Solubility: Drugs with higher lipid solubility tend to have a higher Vd because they can easily cross cell membranes.
Protein Binding: Drugs that bind strongly to plasma proteins have a lower Vd, as more of the drug remains in the blood.
Ion Binding: Electrical charge affects drug distribution, with ionized drugs being less likely to cross membranes.
Molecular Weight: Smaller drugs can cross membranes more easily, leading to a higher Vd.

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3
Q

Formula for Volume of Distribution (Vd)

A

Vd = Total quantity of drug / Plasma concentration at steady state

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4
Q

Definition of Vc (Central Volume)

A

Vc represents the central volume, which includes plasma and highly perfused organs (organs with a high blood supply).

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5
Q

Definition of Vp (Peripheral Volum

A

Vp represents the peripheral volume, which includes peripheral tissues and poorly perfused organs (organs with a lower blood supply).

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6
Q

Definition of Bioavailability

A

Fractional dose of a drug that is actually able to reach the systemic circulation.

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7
Q

Definition of Volume of Distribution

A

Relationship between the dose of a drug and the resulting serum concentration based on the theoretical volume of fluid

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8
Q

Definition of Phase I Metabolism

A

Metabolism that results in the loss of pharmacologic activity through cleavage or formation of a new or modified functional group (oxidation, reduction, and/or hydrolysis).

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9
Q

Definition of Phase II Metabolism

A

Metabolism that involves conjugation of the parent drug or Phase I metabolite with endogenous compounds (glucuronidation, sulfation, or acetylation).

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10
Q

Definition of Hepatic Clearance

A

Volume of blood or plasma that is completely cleared of a drug by the liver per unit of time (Hepatic blood flow × hepatic extraction ratio).

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11
Q

Definition of Clearance (CL

A

Clearance (CL) represents the volume of blood or plasma from which the drug is completely eliminated in a unit of time (ml/min).

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12
Q

Formula for Clearance (CL)

A

CL = CLR + CLH + CLx, where:

CLR = Renal clearance
CLH = Hepatic clearance
CLx = Other routes of clearanc

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13
Q

Rate of Drug Elimination

A

The rate of drug elimination is the amount of drug eliminated (mg/min) per unit of blood or plasma concentration (mg/ml).

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14
Q

Organs responsible for drug clearance

A

The liver and kidneys are the primary organs responsible for drug clearance.

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15
Q

Definition of Total Body Clearance

A

Total body clearance is the sum of different ways of drug elimination from the body.

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16
Q

Definition of the One-Compartment Model

A

In the one-compartment model, the rate of drug elimination is proportional to the amount of drug in the body (X) at any time (t), following first-order kinetics.

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17
Q

One-Compartment Model: Rate of Drug Elimination

A

The rate of drug elimination decreases exponentially with time and is represented by the equation:
dX/dt = kX
(where k is the elimination rate constant and X is the amount of drug in the body at time t).

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18
Q

Definition of Agonism

A

Agonism refers to the stimulation of a receptor, activating it to produce a biological response.

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19
Q

Definition of Antagonism

A

Antagonism involves the inhibition of a receptor, blocking it from producing a biological response

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20
Q

Definition of Synergism

A

Synergism refers to an enhanced effect when two or more drugs work together to produce a greater effect than the sum of their individual effects.

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21
Q

Definition of Additivity

A

Additivity is the combined effect of two drugs, where their total effect is equal to the sum of their individual effects.

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22
Q

Definition of Partial Agonism

A

Partial agonism refers to the partial stimulation of a receptor, producing a less than maximal biological response.

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23
Q

Definition of Inverse Agonism

A

Inverse agonism refers to the reversal of receptor activity, producing an effect opposite to that of an agonist.

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24
Q

what is the MOA of thiopental

A

Thiopental is a barbiturate that enhances the activity of the GABA-A receptor by increasing chloride ion influx, leading to hyperpolarization of neuronal membranes and CNS depression. This results in sedation, hypnosis, and anesthesia.

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25
Q

Why is Thiopental considered ultrashort-acting?

A

Thiopental is ultrashort-acting primarily due to its rapid redistribution from the brain to other tissues (muscle and fat) after administration. Its high lipid solubility allows it to quickly reach the brain, inducing anesthesia, but it also causes the concentration in the brain to drop quickly as it redistributes, leading to a short duration of action. Metabolism plays a minor role compared to redistribution.

26
Q

side effects of thiopental

A

reduced icp
reduced cerrebral flow
hypotention

27
Q

Mechanism of Action (MOA) of Ketamine

A

Ketamine primarily acts as an N-methyl-D-aspartate (NMDA) receptor antagonist, inhibiting glutamate, which is a major excitatory neurotransmitter. This action results in dissociative anesthesia, characterized by analgesia, sedation, and amnesia. Ketamine also affects opioid receptors and may have a role in increasing synaptic plasticity and neuroprotection.

28
Q

side effects of ketamine

A

increased sympathetic tone
maintains laryngeal tone
increase icp
bronchodilation

29
Q

which agent is coadministered with ketamine to reduce halluciantions

A

Benzodiazepines

30
Q

What is the MOA of propofol

A

ropofol acts primarily as a positive allosteric modulator of the GABA-A receptor, enhancing the inhibitory effects of gamma-aminobutyric acid (GABA). This leads to increased chloride ion influx, resulting in neuronal hyperpolarization and CNS depression, producing sedation and anesthesia. Propofol also has some effects on sodium channels and may have antioxidant properties.

31
Q

Why is propofol ideal for LMA

A

Reduces laryngeal reflexes

32
Q

Side effects of propofol

A

Venous irritation can be administered with lidocaine

33
Q

Properties of Halothane

A

Halothane is a colorless liquid with a pleasant smell, making it easy to breathe. It decomposes when exposed to light and contains thymol as a preservative.

34
Q

Cardiac Effects of Halothane

A

Halothane can cause cardiac dysrhythmias, reduced myocardial contractility, heart rate (HR), cardiac output (CO), and blood pressure (BP).

35
Q

Halothanes Effects on Cerebral Blood Flow

A

Halothane increases cerebral blood flow and intracranial pressure (ICP).

36
Q

Respiratory Effects of Halothane

A

It reduces tidal volume (VT), increases respiratory rate (RR) and partial pressure of carbon dioxide (PaCO2), and decreases laryngeal reflexes and airway resistance.

37
Q

What are the Obstetric Considerations with use of Halothane

A

Halothane causes uterine relaxation, which is a critical consideration in obstetrics.

38
Q

Properties of Isoflurane

A

Isoflurane is a halogenated methyl ethyl ether, a colorless volatile liquid with an irritant smell. It is expensive and not widely used in Malawi.

39
Q

Onset and Recovery of Isoflurane

A

Isoflurane has a lower blood/gas solubility than halothane, allowing for a rapid onset and recovery from anesthesia.

40
Q

Toxicity of Isoflurane

A

Isoflurane has low toxicity to the liver and kidneys.

41
Q

Cerebral Effects of Isoflurane

A

Isoflurane increases cerebral blood flow and intracranial pressure (ICP), but to a lesser extent than halothane.

42
Q

Cardiovascular Effects of Isoflurane

A

Isoflurane does not cause arrhythmias and does not increase myocardial sensitivity to adrenaline. It causes a dose-dependent decrease in blood pressure due to reduced systemic vascular resistance (SVR) with little effect on myocardial contractility.

43
Q

Respiratory Effects of Isoflurane

A

Isoflurane reduces tidal volume (VT) and increases respiratory rate (RR).

44
Q

Structure of Suxamethonium

A

Suxamethonium consists of 2 molecules of acetylcholine joined together.

45
Q

Onset and Duration of Action of Suxamethonium

A

Suxamethonium has a rapid onset of action (1 minute) and is short-acting (4-6 minutes) after observable muscle fasciculations.

46
Q

Mechanism of Action of Suxamethonium

A

Suxamethonium leads to persistent depolarization of the motor endplate, causing muscle paralysis.

47
Q

Undesirable Effects of Suxamethonium

A

Can cause mild to severe muscle fasciculations, leading to increased cardiac output (CO), blood pressure (BP), and intracranial pressure (ICP).

48
Q

Myalgia and Hyperkalemia Risks-suxa

A

Suxamethonium may cause myalgia and hyperkalemia, particularly in patients with burns, neurological conditions, peripheral nerve injuries, renal failure, or acidosis, which can lead to cardiac arrest.

49
Q

Other Side Effects of Suxamethonium

A

Includes dual block, increased intraocular pressure, malignant hyperpyrexia, parasympathetic effects, and prolonged activity due to reduced plasma cholinesterase or genetic variants.

50
Q

What type of drug is Vecuronium?

A

Vecuronium is a steroid-based, non-depolarizing neuromuscular blocking agent.

51
Q

Why is Vecuronium widely used?

A

Vecuronium is widely used due to its low cost and minimal cardiovascular effects.

52
Q

Onset and Duration of Action of Vecuronium

A

Vecuronium has a moderately short onset of action (2 minutes) and a moderate duration of action (20 minutes).

53
Q

Vecuronium and Histamine Release

A

Vecuronium rarely causes histamine release, reducing the risk of allergic reactions or hypotension.

54
Q

What type of drug is Rocuronium?

A

Rocuronium is a steroid-based, non-depolarizing neuromuscular blocking agent, and a cousin of vecuronium.

55
Q

Onset and Duration of Rocuronium

A

Rocuronium has a fast onset of action (60 seconds), similar to suxamethonium, but has a longer duration of action compared to vecuronium.

56
Q

Potency and Usage of Rocuronium

A

Rocuronium is less potent than vecuronium but otherwise has similar effects. Due to a reduction in price, it is increasingly being used as a replacement for vecuronium.

57
Q

What type of drug is Atracurium?

A

Atracurium is an ester-based, non-depolarizing neuromuscular blocking agent

58
Q

How is Atracurium metabolized?

A

Atracurium is metabolized by Hofmann degradation into laudanosine and through ester hydrolysis. This makes it independent of liver and kidney function for metabolism.

59
Q

Why is Atracurium the drug of choice in renal and hepatic failure?

A

Atracurium does not rely on the liver or kidneys for metabolism, making it ideal for use in patients with renal or hepatic failure.

60
Q

Side Effects of Atracurium

A

Atracurium can cause severe histamine release, which may lead to profound hypotension.

Anaesthesia (18 decks)

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