Pathophysiological basis of metformin

   

Added on  2023-03-23

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METFORMIN
Pathophysiological basis of metformin
It is a biguanide indicated clinically for treating Diabetes mellitus type 2. Its
mechanism of action is inhibiting the production of hepatic glucose and

increasing the sensitivity of the peripheral tissues to insulin (Rena, Hardie &

Pearson, 2017). Taking note of the physiology of a normal human body,

digestive enzymes and hormones (the insulin and glucagon) are secreted by the

pancreas into the bloodstream where they control the amount of the glucose

circulating. Insulin lowers blood glucose levels by enabling glucose to enter the

body cells. In type 2 diabetes, the beta cell function is altered and less insulin is

released or there is tissue insulin insensitivity whereby the cells ignore the less

insulin produced. The pancreas ability of insulin production is therefore

gradually decreased. When Metformin is administered it decreases the amount

of glucose produced by the liver into the bloodstream, it also decreases the

rate of absorption of glucose by the intestines and lastly it improves insulin

sensitivity by increasing the uptake of peripheral glucose and how it is utilized

(Kahn, Cooper & Del Prato, 2014).

Nursing considerations on Metformin administration.
According to the American Diabetes Association. (2016), Metformin is
considered the drug of choice for patients who are overweight, those

whom dieting has been unable to control diabetes, to patients who are not

overweight and to those whom diabetes cannot be controlled with the

treatment by
sulphonylurea. The advantage of metformin medication is
that it has a lower incidence of weight gain. The gastrointestinal tend to be

more common with higher doses and to avoid them metformin can be

taken with meals (
Karch, 2015). It should not be used with patients who
have renal impairment this is in order to avoid lactic acidosis. Metformin

stored in a cool dry place. Advising the patient to take the drug with food

can help since the side effects are common. Alternatively, slow
-release
tablets can also help.

References
.
American
Diabetes Association. (2017). Standards of medical care in diabetes2017
abridged
for primary care providers. Clinical diabetes: a publication of the American
Diabetes
Association, 35(1), 5.
Kahn,
S. E., Cooper, M. E., & Del Prato, S. (2014). Pathophysiology and treatment of type 2
diabetes
: perspectives on the past, present, and future. The Lancet, 383(9922), 1068-1083
Karch
, A. (2015). Lippincott nursing drug guide. Lippincott Williams & Wilkins
Rena,
G., Hardie, D. G., & Pearson, E. R. (2017). The mechanisms of action of
metformin
. Diabetologia, 60(9), 1577-1585
Caution
.
Creatinine
should be measured before the onset of metformin medication and maintained
twice
a year during the treatment. Metformin is contraindicated to a breastfeeding patient,
pregnant
patient, renal impairment and the one with ketoacidosis (American Diabetes
Association,
2017). Some of the common side effects observed with administration of metformin
include
headache, tinnitus, vertigo, fatigue, feeling of drowsiness, weakness, metallic taste,
rashes,
anorexia, nausea, vomiting, abdominal pain and thrombocytopenia (American Diabetes
Association,
2017). The rare side effects may include erythema, hypoglycemia, lactic acidosis and
a
decrease in vitamin B12 absorption. Metformin is administered orally and it has an increased risk
of
lactic acidosis with alcohol. Monoamine oxidase inhibitors enhance the hypoglycemic effect of
metformin
.
Pathophysiological basis of metformin_1

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