Test: General Pharmacology - 6 - NEET PG MCQ

The alpha subunit of the G protein has GTPase activity, which enables it to break down GTP to produce GDP. This leads to the re-association of the α subunit with the β and γ subunits.

It is important to note that guanylyl cyclase functions as an enzyme, while cGMP acts as a secondary messenger.

The three primary categories of secondary messenger molecules are as follows:

• Calcium, in the context of G proteins, is regarded as a third messenger.
• The drug itself is classified as the first messenger.

Competitive inhibitors raise the Km value, while non-competitive inhibitors lower the V_max of an enzyme.

Key medications that lead to hemolysis in individuals with G-6-PD deficiency include:

• Primaquine
• Dapsone
• Sulfonamides
• Nitrofurantoin
• Aspirin
• Menadione
• Chloroquine
• Quinine
• Nalidixic acid

Sulfonamides are known to trigger hemolysis in patients with G-6-PD deficiency, unlike pyrimethamine.

ED₅₀ relates to the potency of a medication rather than its effectiveness. All other claims are accurate.

The Km of an enzyme resembles the potency of a medication. It represents the substrate concentration at which the reaction velocity attains half of the maximum, referred to as V_max (analogous to a drug's efficacy).

A higher Km indicates a slower reaction rate.

• Adrenaline counteracts the bronchoconstrictor effects of histamine (through H₁ receptors) by promoting bronchodilation (via β₂ receptors).
• Thus, these can be classified as physiological antagonists.
• Salbutamol also counteracts the bronchoconstrictor effects of leukotrienes (through cysteinyl leukotriene receptors) by acting on β₂ receptors.
• Consequently, it represents another example of physiological antagonism.
• Isoprenaline (an agonist for β₁ and β₂) and propranolol (an antagonist for β₁ and β₂) serve as pharmacological antagonists because they target the same receptors.
• Therefore, isoprenaline and salbutamol or adrenaline do not function as antagonists.

Primaquine, sulfonamides, and nitrofurantoin have a significant risk of inducing hemolysis in individuals with G-6-PD deficiency.

While chloroquine and quinine may also lead to hemolysis in those with G-6-PD deficiency, the associated risk is relatively low.

Pharmacogenetics relates to the recognition of variations in drug response or metabolism, which are influenced by an individual's genetic makeup.

GPCRs are receptors that have seven transmembrane helices or a serpentine structure. Salbutamol functions by interacting with β₂ receptors, which belong to the GPCR family.

Drugs that generate opposing effects by targeting different receptors are referred to as physiological antagonists.

Steroid hormones possess lipid solubility and interact with cytoplasmic receptors following their passage through the plasma membrane.

Primaquine is a drug that acts as an oxidant. It has the potential to induce hemolytic anaemia in individuals who possess a deficiency of the G-6-PD enzyme. This deficiency is determined by genetic factors.

The considerable divergence between the two curves on the dose-response curve (DRC) indicates that the dose needed to trigger one effect is significantly greater than that required for the other.

• The DRC for salbutamol illustrates its effects on bronchodilation and tachycardia.
• As depicted in the figure, bronchodilation (β₂ action) occurs at lower doses.
• In contrast, tachycardia (β₁ action) is only observed at higher doses.

This indicates that the medication is highly selective for β₂ receptors.

Drugs that operate through ionotropic receptors exhibit the quickest effects, while those that function through nuclear receptors have the slowest actions.