Anti-diabetic medications

this is a video on anti-diabetic medications we're going to be talking about drugs used to treat diabetes mellitus by lowering blood glucose levels before we begin we're going to break down the list of drug classes that we have on the left here we have the insulin sensitizers the insulin-secreting Oggs the anti alpha-glucosidase is which allow for slow absorption of carbohydrates we have peptide analogs that serve a couple functions that we'll talk about we have the glycol so your X which block reabsorption of glucose in the kidneys and then we have two random grab-bag drugs that are approved for anti-diabetic purposes but really have other primary purposes that's a bile acid sequestrants colas civilian and bromocriptine a dopamine agonist when I start off by talking about insulin which is of course a protein that decreases blood glucose levels insulin comes in many formulations all of them break down to find the insulin receptor and the insulin receptor activates a tyrosine kinase receptor pathway that does the many effects oklets of insulin these insulin variants can be used for diabetes type 1 type 2 as well as gestational diabetes we're start with a rapid acting insulins these are lists Pro s part and glue the seen these are monomeric insulin analogs they are monomers in solution they break down pretty quickly and that's why the rapid acting so the peak time here is one hour and there's really no lag before these rapid acting insulins start to take effect so that lag is a mnemonic that can help you remember Lisp Pro s parts and glue the scene these are used for postprandial glucose control that means controlling your glucose after a meal you might pop these in right after a meal or right before meal or during a meal to help control the postprandial glucose spike next we have short-acting insulin this is just called regular insulin it's the same insulin found in the human body it's a dimer or hexamer in solution breaks down a little more slowly the rapid-acting insulin so it reaches its peak in two to four hours this is administered intravenously for people who come in in diabetic ketoacidosis next up is the intermediate acting insulin this is called NPH it Peaks in four to ten hours so intermediate amount of time before it reaches its maximum potential but it's not quite as long acting as the long-acting insulin which is glargine and debt Amir which don't really peak at all they kind of go in your body and they and they even precipitate at body pH depending on the pH s some of them might might not even be in solution so these don't really peak as I said earlier the relatively flat and because they're relatively flat they're good for mimicking the basal glucose levels that your pancreas usually secretes so in people with type one diabetes they might be given a long-acting insulin that kind of keeps up that basal insulin release next is the Bhagwad eyes big one here is metformin very commonly used drug for diabetes metformin mechanism of action is to sensitize to insulin it does this by stimulating the liver enzyme amp K the exact mechanism of action is unclear but it's definitely through that enzyme ampk this does not require functioning beta cells so it means it does work in DM type 1 as well as DM type 2 it's more effective in the liver than the muscle at sensitizing to insulin and that's in contrast to another drug that we'll talk about later metformin is an is administered orally it decreases hemoglobin a1c by about one to two percent which is a pretty good decrease compared to some of the other drugs on this list we also see mild weight loss with metformin use some side effects include diarrhea nausea vitamin b12 deficiency and the commonly tested one is lactic acidosis so it's important to to associate metformin with the risk of lactic acidosis metformin is contraindicated in liver kidney and heart failure so somebody's kidneys aren't working don't give a metformin metformin is first-line for diabetes type 2 in addition to or sometimes slightly after weight loss and exercise next is the style addenda dones these are also called T CDs or the glitter zones to drugs that are worth knowing or Pio glitter zone and Rosie glitter zone these like metformin sensitized to insulin they increase the number and sensitivity of insulin receptors they specifically bind to the PPAR gamma receptor that's the peroxisome proliferator activated receptor gamma receptor they are more effective in the periphery this is the muscle or the fat tissues than the liver unlike metformin and they do not require functional beta cells again so this could be used in type 1 and type 2 these glitter zones are also administered orally and they decrease hba1c by 1 to 1.5 percent also a pretty good decrease these are uncommon these are unpopular because they cause mild weight gain which is usually the opposite in what we're trying to do in diem patients they can also increase a LDL which can put you at risk for coronary problems they're also pretty expensive and slow onset so it's easy understand why these are less popular than metformin side effects here as we said earlier our weight gain we see some edema we also see heart failure liver toxicity and fractures of the bones but these are safe with renal failures if you have a patient with dm2 has some renal failure you might not be able to give them at Foreman but you can give them one of the Glitter zones next up are these two categories which are the insulin-secreting dogs they increase the secretion of insulin directly they both tend to decrease hba1c by about one to two percent also pretty effective suffix here o that they cause weight gain and they put you at risk for hypoglycemia which kind of makes sense if you're May forcing the body to release its stores of insulin it's possible that too much insulin would be released and you can become hypovolemic so people also have allergies specifically to the sulfonylureas people who have sulfa allergies might not want to give them the Silvano ureas and they're administered orally so let's talk about the two groups cell phone to your wheels these are broken down into first generation and second generation the first generation sulfonylureas are told beautified and chloro provide and the second generation sulfonylureas are glipizide Colibri ride and glimepiride these last three second generation I'll start with GL and end with IDE that's how I remember I'm second generation so funnel yuri is these bind to the cell phone or your cell phone or your real receptor on the ATP activated potassium channel of beta cells and they do require functional beta cells so they bind to a fatass iam receptor they block it forcing the those beta cells to depolarize which makes the calcium channel on those cells open up calcium rushes in and it releases insulin it's worth looking into the release mechanism of insulin to understand this so they block that potassium channel calcium influx into the cell and it activates insulin release similar mechanism of action in McGlinn ID so these are rapidly died and the tag line ID so they end in england ID these bind to another receptor to block the potassium channel so it's this it's a different receptor on the same potassium channel they have the same mechanism of action after that so they block the potassium channel which leads to calcium influx and that again activates insulin release the second group the militant IDEs have faster onset and a slower duration and they're also more expensive compared to the sulfonyl ureas next drug is anti alpha-glucosidase these two drugs are acarbose and mcglue tal mechanism here is at the slow absorption of carbohydrates in the proximal gut alpha-glucosidase is an enzyme that hydrolyzes carbohydrates in the brush border of the gut so if you inhibit this enzyme they're going to slow the absorption and slow the breakdown and slow the absorption of carbohydrates in the gut so you're going to delay car break down and thus delay carb absorption you're also going to decrease post post prandial hyperglycemic spikes using these drugs they're getting administered orally you want to get them into the GI tract they increased the they decrease the hba1c percentage by a modest amount point five to one percent and one of the big cons of using these drugs are the severe flatulence and other GI disturbances that you get by using this which kind of makes sense you're kind of feeding your gut bacteria a bunch of glucose that you're failing to absorb so people tend to have gas and that causes poor adherence to these drugs they're also pretty expensive next group of drugs is the in critten mimetics it's worth reviewing that the inc Returns which are glp-1 and GIP our gut derived hormones have a couple functions they stimulate insulin release they inhibit glucagon secretion and they slow gastric emptying they also promote satiety so we can stimulate inc return release and by eating by stretching the stomach in the gut and it's secreted by the gut there are a couple analogs to these in cretons or in critten mimetics that we can administer as medicine to get these same four effects these glp-1 receptor analogs are eggs and tied low reglue tied and dual a glue tied so that again they mimic that ink return and they produce the same in critten effects which can result in weight loss which can be desirable to patients next we're going to talk about an enzyme called dipeptidyl peptidase-4 which is the enzyme that breaks down these in cretons so you can imagine that if you inhibit dpp-4 you're going to have your endogenous in cretons around for a longer amount of time and that's exactly what dpp-4 inhibitors do they increase the blood concentration of your in cretons so the drugs that do this the drugs that inhibit dpp-4 are the egg Lipton's so we have sittig lipton we have sexy GLIP 10 and linagliptin these are the dpp-4 inhibitors that break that block the breakdown of in cretons and these are also administered orally next group of drugs is the emmalin analogs so there's a synthetic Emaline analog called pram lin tide now Emlyn is usually a molecule that's co secreted with insulin in the body some people call it the second blood glucose decreasing drug so it has the following effects inhibits glucagon secretion it slows gastric emptying and it promotes satiety so these emmalin analogues act like the endogenous molecule emmalin and it has these three effects the synthetic version is called pram land tide and they decrease hba1c by modest amount again point five to one percent side effects here are nausea and hypoglycemia these can also promote moderate weight loss which can be desirable and these are also administered orally or subcutaneously next is a group of drugs called the glycosyl Eurex these promote renal secretion of glucose renal excretion they are excreted glucose is excreted through the kidneys so there's a transporter in the distal convoluted tubules called excuse me there's a transporter in the proximal tubules called the sodium-glucose cotransport ER – and if you kind of promote this channels activity you're going to absorb more glucose if you inhibit this transporters activity they're going to be dumping more glucose into the urine you're going to be wasting glucose and that's one method of lowering your blood glucose level so if you inhibit the sglt2 co-transporter you're going to have an effect of decreasing blood glucose and that's what these drugs do so we have connect the flows in Depok glyph losen and impact LIF flows in now I remember these in that they all have flow in them they all ended flows in and that's because they allow for the free flow of glucose through the renal tubules and out in the urine these also decrease hba1c by a modest amount point five to one percent and there's a whole list of side effects that are related to peeing out excess glucose here but your risk UT is especially in women you can get vulva vaginal candidiasis which is yeast infections in the vagina you can get glycosuria which is kind of the point you want to be peeing out glucose you can get renal failure and this can also decrease your blood pressure cause dehydration and cause hyperkalemia so all kinds of other kidney affects that you get from purposely peeing out the glucose these also promote substantial weight loss because you're essentially ridding your body of sugar through your urine next is a drug that's not primarily used for diabetes but it is approved for use in diabetes mellitus this is colas 7 a.m. it's a bile acid sequestrants and its exact mechanism is unknown it decreases hba1c by a very modest amount point 32.4% so not the best on this list at all some side effects for this drug are constipation dyspepsia nausea and hypertriglyceridemia next is bromocriptine which is a dopamine analog this again is not primarily used for diabetes but it has been approved the exact mechanism of action is unknown but it also decreases hba1c by very modest amount point 4 2.5% side effects here are headache dizziness nausea and vomiting this has been a overview of drugs used to treat diabetes mellitus I hope this was helpful and thank you for listening


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