TLRs are cellular receptors for microbial products that induce inflammatory responses through activation of the innate immune system.As with other quinoline antimalarial drugs, the antimalarial mechanism of action of quinine  has not been fully resolved. The most accepted model is based on hydrochloroquinine and involves the inhibition of hemozoin biocrystallization, which facilitates the aggregation of cytotoxic heme. Free cytotoxic heme accumulates in the parasites, causing death.Hydroxychloroquine increases the risk of low blood sugar through several mechanisms. These include decreased clearance of the hormone insulin from the blood, increased insulin sensitivity, and increased release of insulin from the pancreas. History
After World War I, the German government sought alternatives to quinine as an anti-malarial. Chloroquine, a synthetic analogue with the same mechanism of action was discovered in 1934, by Hans Andersag and coworkers at the Bayer laboratories. : 130–131  This was introduced into clinical practice in 1947 for the prophylactic treatment of malaria. Researchers subsequently attempted to discover structural analogs with superior properties and one of these was hydroxychloroquine. Chemical synthesis
The first synthesis of hydroxychloroquine was disclosed in a patent filed by Sterling Drug in 1949. In the final step, 4,7-dichloroquinoline was reacted with a primary amine which in turn had been made from the chloro-ketone shown:

Society and culture
It is frequently sold as a sulfate salt known as hydroxychloroquine sulfate. In the sulfate salt form, 200 mg is equal to 155 mg of the pure form.Brand names of hydroxychloroquine include Plaquenil, Hydroquin, Axemal (in India), Dolquine, Quensyl, and Quinoric. COVID-19
References
External links

"Hydroxychloroquine". Drug Information Portal.
Dobutamine can also be used in hypotensive septic shock to increase cardiac output and correct blood flow to the tissues. Dobutamine is not used as often as epinephrine due to its associated side effects, which include reducing blood flow to the gut. Additionally, dobutamine increases the cardiac output by abnormally increasing the heart rate. Steroids
The use of steroids in sepsis is controversial. Studies do not give a clear picture as to whether and when glucocorticoids should be used. The 2016 Surviving Sepsis Campaign recommends low dose hydrocortisone only if both intravenous fluids and vasopressors are not able to adequately treat septic shock. The 2021 Surviving Sepsis Campaign recommends IV corticosteroids for adults with septic shock who have an ongoing requirement for vasopressor therapy. A 2019 Cochrane review found low-quality evidence of benefit, as did two 2019 reviews.During critical illness, a state of adrenal insufficiency and tissue resistance to corticosteroids may occur. This has been termed critical illness–related corticosteroid insufficiency. Treatment with corticosteroids might be most beneficial in those with septic shock and early severe ARDS, whereas its role in others such as those with pancreatitis or severe pneumonia is unclear. However, the exact way of determining corticosteroid insufficiency remains problematic. It should be suspected in those poorly responding to resuscitation with fluids and vasopressors. Neither ACTH stimulation testing nor random cortisol levels are recommended to confirm the diagnosis. The method of stopping glucocorticoid drugs is variable, and it is unclear whether they should be slowly decreased or simply abruptly stopped.