MOA

Question 1

Normal inflammatory response
desired effects
MOA

Answer 1

Inflammation is triggered by damage to mast cells which release histamine which cause vasodilation of blood vessels and increased permeability of capillaries, this increased blood flow causes an accumulation of phagocytes and lymphocytes. During a COPD exacerbation, injury to these cells amplifies the inflammatory response.
The desired short-term effects of prednisolone are anti-inflammatory in the lungs to relieve breathlessness, wheeze and mucus.
Prednisolone is a glucocorticoid receptor agonist
once prednisolone activates the glucocorticoid receptor it binds to Glucoccorticoid Response Elements in the nucleus.
Triggering changes in gene expression that result in various downstream effects over a period of hours to days;
Decreases vasodilation, reduces capillary permeability which improves airway oedema and breathlessness.
inhibiting pro-inflammatory signals, and promoting anti-inflammatory signals.

Inhibits leukocyte migration to inflammation sites, inhibits neutrophil apoptosis and demargination, upregulates anti-inflammatory lipocortin-1 which inhibits phospholipase A2, to decrease arachidonic acid derivatives; suppresses NF-Kappa B, reducing cytokines (e.g., TNF-α, IL-1- IL-6) and other inflammatory transcription factors; they promote anti-inflammatory genes like interleukin-10. this process prevents excessive inflammation and tissue damage.
Immunosuppressive: Decreases the activity of neutrophilss, T-cells and lymphocytes, reducing antibody production.

Question 2

CNS effects

Answer 2

Prednisolone can cause central nervous system effects, including euphoria, mania, insomnia, poor concentration, memory issues, and psychosis, especially at high doses or with prolonged use. These effects are believed to result from the steroids’ impact on brain chemical pathways, altering mood regulation and neurotransmitter balance.

Question 3

infection risk

Answer 3

Prednisolone suppresses the immune system, increasing infection risk. It causes neutrophil demargination, suppresses T-cell activity, and reduces inflammatory mediators, weakening both innate and adaptive immunity.

Question 4

Hyperglycemia

Answer 4

Prednisolone reduces insulin sensitivity and stimulates gluconeogenesis, it also impairs glucose uptake in peripheral tissues, leading to increased blood sugar levels.

Question 5

Myopathy

Answer 5

Prednisolone causes catabolism, breaking down muscle proteins over time, which can lead to myopathy

Question 6

suppression of HPA axis

Answer 6

Prednisolone suppresses the HPA axis by mimicking cortisol, reducing natural cortisol production. Prolonged use, high doses, or frequent dosing can lead to adrenal insufficiency, impairing the body’s stress response.

Question 7

Fat Metabolism (redistribution)

Answer 7

Prednisolone increases fat metabolism, releasing free fatty acids that may contribute to fatty liver disease. Chronic use can cause fat redistribution (central obesity, moon face, buffalo hump), features of Cushing syndrome.

Question 8

Osteoporosis

Answer 8

prednisolone reduces osteoblast activity and activates osteoclasts, which leads to osteoporosis.

Question 9

Impaired wound healing

Answer 9

prednisolone impairs wound healing by disrupting fibroblast activity, and collagen deposition.

Answer 10

Prednisolone can irritate the stomach lining by inhibiting protective prostaglandins. To prevent irritation, it is recommended to take prednisolone with food and a proton pump inhibitor (PPI).

Prednisolone reduces insulin sensitivity and stimulates gluconeogenesis, it also impairs glucose uptake in peripheral tissues, leading to increased blood sugar levels.

Prednisolone suppresses the immune system, increasing infection risk. It causes neutrophil demargination, suppresses T-cell activity, and reduces inflammatory mediators, weakening both innate and adaptive immunity.

Prednisolone suppresses the HPA axis by mimicking cortisol, reducing natural cortisol production. Prolonged use, high doses, or frequent dosing can lead to adrenal insufficiency, impairing the body’s stress response.

Prednisolone can cause central nervous system effects, including euphoria, mania, insomnia, poor concentration, memory issues, and psychosis, especially at high doses or with prolonged use. These effects are believed to result from the steroids’ impact on brain chemical pathways, altering mood regulation and neurotransmitter balance.

prednisolone impairs wound healing by disrupting fibroblast activity, and collagen deposition.
Prednisolone causes catabolism, breaking down muscle proteins over time, which can lead to myopathy

prednisolone reduces osteoblast activity and activates osteoclasts, which leads to osteoporosis.

Prednisolone increases fat metabolism, releasing free fatty acids that may contribute to fatty liver disease. Chronic use can cause fat redistribution (central obesity, moon face, buffalo hump), features of Cushing syndrome.