12. Antidiabetics Flashcards
(43 cards)
Criteria for OAD
-does not replace the regimen (diet)
-age, weight, blood insulin level
-glycemia - fasting and postprandial
-comorbidities , metabolic syndrome
OAD -general principles
- their ability is bound to the ability of insulin secretion
- most OADs are contraindicated in pregnancy (METFORMIN may be used )
indications for OADs
T2 DM if not properly compensated with diet
T1DM with high insulin resistance -> when insulin does not lead to a decrease in blood glucose
what are the groups of OADS
-biguanides
-sulfonylurea derivatives
-thiazolidindiones
-alpha glucosidase inhibitors
-meglitinides
-Inhibitors of DP IV
-SGLT2 inhibitors
–GLP 1 analogues- insulin alternative that is an injectable antidiabetic
biguanides moa
increase sensitivity of peripheral tissues to insulin
* increase insulin binding to its receptor
* reduce hepatic gluconeogenesis
* decrease glucose absorption from GIT
biguanides and insulin?
-does not affect insulin secretion , b- cell function->NO HYPOGLYCEMIA
what are other benefits of biguanides
-stimulates glycolysis in the periphery
-reduces hep gluconeogenesis
-delays glc absorption from GIT
-decreases plasma glucagon levels
-increases proportion of HDL chol
not metabolised -> low protein binding
excreted non metabolised in kidneys
what are the side effects of biguanides
lactic acidosis
nausea
GIT problems about 20% have diarrhoea
reduced vit b12 absorption
weight loss
disulfuram effect
Metformin contraindications
-kidney disease
-alcoholism, liver disease (higher risk of lactic acidosis )
Indications of metformin
-type 2 DM drug of choice -esp in obese patients
-non obese in combos (with insulin , glitazones, SU , incretins )
what are the off label indications for metformin
PCOS
anticancer effect
SU derivatives -moa
pancreatic - release of insulin from beta cells
extrapancreatic -
potentiation of endogenous I effect on the target tissue
- reduction of hepatal glucose production
- reduction of hepatal Insulin degradation
- reduction of serum glucagon levels
what are the SU derivatives
-glibenclamide
-gliclazide
both 2nd generation
3rd gen-glimepride
-these drugs are 2nd line treatment
adverse effects of su derivatives
-HYPOGLYCEMIA
increased appetite
metal taste in mouth
*headaches, nausea (5 %)
* fluids retention
* allergy, fotosensitivity
what are the CI of SU derivatives
DM Type 1 monotherapy
, hypoglycemia,
ketoacidosis, kidney or liver
failure
pregnancy, hypersensitivity
Thiazolidinones moA
increase the sensitivity of periphery to insulin
- ligands of PPAR gamma (part of the steroid and thyroid superfamily
of nuclar receptors) modulate the expression of the genes
involved in the metabolism of lipids and glucose
what are the thiazolidinones
PIOGLITAZON
effects of thiazolidindiones
- Lowering blood glucose by the primary effect on insulin resistance
- in diabetic and pre-diabetic patients
- NO HYPOGLYCAEMIA
- Increases glycogen synthesis and glycolysis in muscles
- Stimulating glucose oxidation and lipogenesis in adipose tissue and
reducing gluconeogenesis in the liver … optimal metabolic effects
therapeutic use of thiazolidindiones
Sensitizers of insulin receptors
The onset of effect in 4 weeks
what are the side effects of thiazolidindiones ?
Hepatotoxicity
Fluid retention
Increase TAG
what are the CI of thiazolidindiones ?
hypersenisitivity
predisposition of heart failure
liver damage
pregnancy
lactation
what are the inhibitors of intestinal glucosidase ?
Acarbose
what is the moa of intestinal glucosidase inhibitors
-reduce sacharide absorption from GIT
-competitively inhibits a glucosidase -> inhibiting the cleavage of polysaccharide from the meal
what is the effect of intestinal glucosidase inhibitors
- decrease postprandial glycemia
- do not affect monosacharides absorption
- acarbosis do not rech the systemic blood, miglitol does
*
„educative drugs“- consequences in bad compliance
