Adverse Effects📝

1-Sulfonylureas (glyburide, glipizide ,glimepiride)

💜Hypoglycemia
💜hyperinsulinemia
💜wt gain

2-Glinides (repaglinide and nateglinide)

💛Hypoglycemia
💛 wt gain

3- Biguanide(Metformin)

💙git upset, including NVD
💙due to anaerobic glycolysis lead to lactic acidosis and therefore contraindicated in patients with renal dysfunction
💙vitamin B12 deficiency with long term use

4-Thiazolidinediones
(pioglitazone ,rosiglitazone)

💚liver toxicity
💚wt gain
💚fluid retention
💚associated with osteopenia and increased fracture in women
💚pioglitazone—->may cause bladder cancer
💚rosiglitazone—->increased risk of MI infarction and angina

5- a- Glucosidase inhibitors (Acarbose and miglitol)
🤎flatulence
🤎diarrhea
🤎Abdominal cramping
🤎Patients with inflammatory bowel disease, colonic ulceration, or intestinal obstruction should not use these drugs

6-DPP-4 inhibitors
(Alogliptin, linagliptin,saxagliptin,sitagliptin)
❤️well tolerated
❤️most common adverse effect being nasopharyngitis
❤️Headache
❤️Pancreatitis
❤️disabling joint pain
❤️Alogliptin and sexagliptin increase risk of Heart failure

7- Na- glucose cotransporter 2 inhibitors ( Canagliflozin,dapagliflozin,
empagliflozin,ertugliflozin)

🤍female genital mycotic infection (Vulvovaginal candidiasis)
🤍urinary tract infection
🤍urinary frequency
🤍Hypotension
🤍Ketoacidosis

8-Other agents
(bromocriptine,colesevelam)

🩵 their modest efficacy and adverse effects and pill burden limited use in clinical practice

Mechanisms

🧡Sulfonylureas +Glinides

*they have similar mechanism but Glinides hasn’t sulphonyl group

1- stimulante insulin release from B cell
2-block ATP-sensitive K channels and producing depolarization
3-Ca influx and insulin
4-reduce hepatic glucose production
5-increase peripheral insulin sensitivity
……………………………………………………….
💙Biguanides

1-reduce of hepatic gluconeogenesis
2-slow intestinal absorption of sugar
3-improve peripheral glucose uptake and utilization
……………………………………………………….
💛Thiazolidinediones

1-lower insulin resistance by acting as agonists for the PPAR-Y
2-activation of PPAR-Y regulates the transcription of several insulin responsive genes
3-resulting in increased insulin sensitivity in adipose tissue,liver and skeletal muscle
……………………………………………………….
🩷a-Glucosidase inhibitors
هذا الانزيم يحول starch الى glucose فنثبط هذا الانزيم عن طريق هذا الميكانزم
1- theses drugs reversibly inhibit
a-glucosidase enzyme
2-when taken at the start of a meal ,these drugs delay the digestion of carbohydrates
3-resulting in lower postprandial glucose levels
4-they do not stimulate insulin release or increase insulin sensitivity, therefore theses agents do not cause hypoglycemia
……………………………………………………..
💜Dipeptidyl peptidase-4 inhibitors

1- inhibit the enzyme DPP4, which is responsible for the inactivation of incretin hormones such as GLP-1
2- activation of Incretin hormones act:
-increases release of insulin
-reduce secretion of glucagon
-unlike GLP-1 receptor agonists these drugs don’t cause satiety
……………………………………………………….
💚Na-glucose cotransporter 2 inhibitors

1-inhibit SGLT2 in proximal tubules to decrease reabsorption of glucose,in tubular lumen of the kidney
2-increase urinary glucose excretion
3-lower blood glucose
4-decreases reabsorption of sodium and causes osmotic diuresis.
5-SGLT2 inhibitors may reduce systolic blood pressure
……………………………………………………….
❤️Other agents
Unknown mechanism

الامسكيو شامل لكل شيت السكري + MCQ lippincott+ Katzunge)

تلخيص فوك المواضيع الرئيسية حتى تفرقون بينها ويارب التوفيق