Pcol 2 Exam 4 Flashcards
Insulin Lispro
Rapid acting insulin
Recombinant DNA by swapping Proline 29 and Lysine30 –> To Lysine 29 and Proline 30 –> giving LysineProline (Enhence LisPro)
Duration of action is 15-20mins
Humalog, admelog, Lyumev
Insulin Aspart
Rapid acting insulin
Novolong, Fiasp
Glulisine
Rapid acting insulin
Apidra
Novalin N
Intermediate insulin
In NPH with phosphate buffer
Insulin + Protamine + Zinc –> has large crystals of Zinc
Humalin N
Intermediate insulin
NPH –> Insulin + Protamine + Zinc –> has large crystals of zinc in phosphate buffer
Glargine
Long acting insulin
Lantus, Basaglar, Joujev
Detemir
leve
Recombinant DNA to produce non crystallized water soluble insulin
Duration of action is 24 hrs and given once a day subcu injection
Levemir
Glargine
Non crystallized recombinat DNA water soluble insulin long acting
Duration is 24 hr
lantus, basaglar, toujeo
Degludec
Long acting insulin
Tresiba
Glargine yfgn
Long ancting insulin
semglee
Glyburide
Micro
Sulfonylureas insulin secretagogues
MOA:
-It will bind to the voltage gates K+ channel in a different spot where the ATP bind and will cause the K+ channels to close so K+ stays inside there is depolarization –> therefore causes the Ca2+ channels to open –> Ca2+ comes in and will bind to the vesicle that has insulin in it and will move it to the membrane and therefore causing the vesicle to open releasing insulin
-Has active metabolites so need to check kidney function –> because if poor kidney function –> the active metabolites will not be excreted and accumulates causing toxicity
Thera:
-For type 2 DM
AE:
-Gain weight
-Hypoglycemia (Hyperinsulemia)
-Fetal abnormalities –> avoid in preg
Micronase, Dibeta
Glipizide
Gluco
Sulfonylureas insulin secretagogues
MOA:
-It will bind to the voltage gates K+ channel in a different spot where the ATP bind and will cause the K+ channels to close so K+ stays inside there is depolarization –> therefore causes the Ca2+ channels to open –> Ca2+ comes in and will bind to the vesicle that has insulin in it and will move it to the membrane and therefore causing the vesicle to open releasing insulin
Thera:
-For type 2 DM
AE:
-Gain weight
-Hypoglycemia (Hyperinsulemia)
-Fetal abnormalities –> avoid in preg
Glucotrol
Glimepride
Ama-
Sulfonylureas insulin secretagogues
MOA:
-It will bind to the voltage gates K+ channel in a different spot where the ATP bind and will cause the K+ channels to close so K+ stays inside there is depolarization –> therefore causes the Ca2+ channels to open –> Ca2+ comes in and will bind to the vesicle that has insulin in it and will move it to the membrane and therefore causing the vesicle to open releasing insulin
Thera:
-For type 2 DM
AE:
-Gain weight
-Hypoglycemia (Hyperinsulemia)
-Fetal abnormalities –> avoid in preg
Amaryl
Repaglinide
pra-
Meglitide - insulin secretagogues
-MOA:
-It will bind to the voltage gates K+ channel in a different spot where the ATP bind and will cause the K+ channels to close so K+ stays inside there is depolarization –> therefore causes the Ca2+ channels to open –> Ca2+ comes in and will bind to the vesicle that has insulin in it and will move it to the membrane and therefore causing the vesicle to open releasing insulin
Thera:
-For type 2 DM
Prandin
Nateglinide
Meglitide - insulin secretagogues
-MOA:
-It will bind to the voltage gates K+ channel in a different spot where the ATP bind and will cause the K+ channels to close so K+ stays inside there is depolarization –> therefore causes the Ca2+ channels to open –> Ca2+ comes in and will bind to the vesicle that has insulin in it and will move it to the membrane and therefore causing the vesicle to open releasing insulin
Thera:
-For type 2 DM
Starlix
Metformin
For type 2 DM
MOA
-Will activate the AMPK enzyme in the liver which results in a change in gene transcription –> Resulting in reduction og gluconeogenesis so less glucose produce
-Decrease gene expression of lipogenic enzymes
-Increase fatty acid oxidation –> So fat breakdown so less fatty acid in the liver which leads to increase insulin sensitivity because decrease fatty acids in liver –> Improve insulin sensitivity
Thera:
-For type 2 dm –> because metformin will make them more sensitive to their own insulin so more glucose transporter inserted to their membrane also improve insulin sensitivity in their muscle
-No risk of hypoglycemia –> because no increase in endogenous insulin release
AE:
-Metallic taste
-Anorexia–> Decrease appetitie
-Diarrhea –> ER formulation is better to use
-High levels of metformin can cause metabolic acidosis–> because metformin is excreted unchange and if the patient has poor renal function (kidney function) they will not be able to excrete the metformin and it builds up in the blood
-Pt should stop metformin if is going to get a GI Scan because is going to be put on constrat media –> and the contrast media will cause the kidney to stop working so cannot excrete the metformin
Glucophage
Rosiglitazone
Ava
-Glitazone
MOA:
Works by activating the PPARy a nuclear hormone receptor and will increase gene transcription and will increase insulin sensitivity
-And cause reduction in free fatty acids in the liver –> so improve insulin sensitivity
-No risk of hypoglycemia
-If administer will insulin need to half the dose of insulin
Thera:
-For type 2 DM
AE:
-Anemia –> Decrease RBC
-Edema–> Weight gain]
-Peripheral edema
-Pulmonary edema
-Can cause HF because of all the fluid acumulation –> CI if pt has HF
-Increase myocardiac infarction
Avandia
Pioglitazone
ac
-Glitazone
MOA:
Works by activating the PPARy a nuclear hormone receptor and will increase gene transcription and will increase insulin sensitivity
-And cause reduction in free fatty acids in the liver –> so improve insulin sensitivity
-No risk of hypoglycemia
-If administer will insulin need to half the dose of insulin
Thera:
-For type 2 DM
AE:
-Anemia –> Decrease RBC
-Edema–> Weight gain]
-Peripheral edema
-Pulmonary edema
-Can cause HF because of all the fluid acumulation –> CI if pt has HF
-Increase myocardiac infarction
Actos
Acarbose
pre-
Alpha glucosidase inhibitor
MOA:
Works only in the GIT and inhibits alpha glucosidase –> therefore slows down the breakdown of the polymers of carbohydrates such as mannitol, dextrin and starch –> prevents the hydrolysis at alpha 1-4 glucosidic bonds so no release of glucose
Thera:
-For type 2 dm
-no risk of hypoglycemia
AE:
-Bloating
-Flatulence
Prelose
Miglitol
gly-
Alpha glucosidase inhibitor
MOA:
Works only in the GIT and inhibits alpha glucosidase –> therefore slows down the breakdown of the polymers of carbohydrates such as mannitol, dextrin and starch –> prevents the hydrolysis at alpha 1-4 glucosidic bonds so no release of glucose
Thera:
-For type 2 dm
-no risk of hypoglycemia
AE:
-Bloating
-Flatulence
Glyset
Exenatide
by-
GLP-1 analog
MOA:
-Glucagon like peptidase –> it is produce by L-type cells in the gastric mucosa –> and it will go to the pancrease and stimulate the release of insulin from the beta cells in response to High blood glucose
-In the N-terminal has His-Gly (replacing Alanine to glycine ) which prevent de activation from DPP-IV
-Suppress glucagon release
-Slow gastric emptying–> so more food stay in the stomach and send info to brain that stomach is full so suppress appetite.
-also suppress apetite by activating GLP-1 receptors in the hypothalamus feeding center
Thera:
-Treat Type 2 DM
-For weight loss
AE:
-Nausea–> because slow GE
-Fetal abnormalities –> avoid if pregnant
Byetta
Liraglutide
Vict-
Sax
GLP-1 analog
MOA:
-Glucagon like peptidase –> it is produce by L-type cells in the gastric mucosa –> and it will go to the pancrease and stimulate the release of insulin from the beta cells in response to High blood glucose
-Has a Palmitic acid conjugated in one of the glutamic acid residues
-Suppress glucagon release
-Slow gastric emptying–> so more food stay in the stomach and send info to brain that stomach is full so suppress appetite.
-also suppress apetite by activating GLP-1 receptors in the hypothalamus feeding center
Thera:
-Treat Type 2 DM
-For weight loss
AE:
-Nausea–> because slow GE
-Fetal abnormalities –> avoid if pregnant
Victoza ,Saxenda
Dulaglutide
tru-
GLP-1 analog
MOA:
-Glucagon like peptidase –> it is produce by L-type cells in the gastric mucosa –> and it will go to the pancrease and stimulate the release of insulin from the beta cells in response to High blood glucose
-In the N-terminal has His-Gly (replacing Alanine to glycine ) which prevent de activation from DPP-IV
-Suppress glucagon release
-Slow gastric emptying–> so more food stay in the stomach and send info to brain that stomach is full so suppress appetite.
-also suppress apetite by activating GLP-1 receptors in the hypothalamus feeding center
Thera:
-Treat Type 2 DM
-For weight loss
AE:
-Nausea–> because slow GE
-Fetal abnormalities –> avoid if pregnant
Trulicity
Ozempic
GLP-1 analog
MOA:
-Glucagon like peptidase –> it is produce by L-type cells in the gastric mucosa –> and it will go to the pancrease and stimulate the release of insulin from the beta cells in response to High blood glucose
-Supress glucagon release
-Slow gastric emptying–> so more food stay in the stomach and send info to brain that stomach is full so suppress appetite.
-also suppress apetite by activating GLP-1 receptors in the hypothalamus feeding center
Thera:
-Treat Type 2 DM
-For weight loss
AE:
-Nausea–> because slow GE
-Fetal abnormalities –> avoid if pregnant
semiglutide
Rybelsus
GLP-1 analog
MOA:
-Glucagon like peptidase –> it is produce by L-type cells in the gastric mucosa –> and it will go to the pancrease and stimulate the release of insulin from the beta cells in response to High blood glucose
-Suppress glucagon release
-Slow gastric emptying–> so more food stay in the stomach and send info to brain that stomach is full so suppress appetite.
-also suppress apetite by activating GLP-1 receptors in the hypothalamus feeding center
Taken PO is a coated tablet that sticks to the gastric mucosa -> so need to take it on a empty stomach, with minimal water and separate from other meds
Thera:
-Treat Type 2 DM
-For weight loss
AE:
-Nausea–> because slow GE
-Fetal abnormalities –> avoid if pregnant
Tirzapetide
Zep-, Moun-
GLP-1/GIP agonist
MOA:
-GIP –> is secreted by K-type cells in the intestine, duodenum and upper intestine .
-GIP –> Gastric-inhibitory peptide –> will cause inhibition of gastric secretion from parietal cells in the stomach –> therefore it causes indigestion
-GIP –> has dual activity and can activate GLP-1 receptors in the pancreas beta cells and cause the release of insulin in response to high levels of blood glucose
Thera:
-Weight loss
-Type 2 DM
AE:
-Fetal abnormalities
-Nausea–>because slow GE and things can back up from the stomach
Zepbound, mounjaro
Sitagliptin
jan-
Inhibits DPP-IV
So prevents deactivation of GLP-1 and GIP –> so now endogenous GLP-1 and GIP can stay longer in the body and cause increase release of insulin in response to high blood glucose levels
Give orally
Less effective because can cause increase release of other endogenous hormones
AE:
-Nausea
Januvia
Vidagliptin
Inhibits DPP-IV
So prevents deactivation of GLP-1 and GIP –> so now endogenous GLP-1 and GIP can stay longer in the body and cause increase release of insulin in response to high blood glucose levels
Give orally
Less effective because can cause increase release of other endogenous hormones
AE:
-Nausea
Galvus
Sixagliptin
Ongly-
Inhibits DPP-IV
So prevents deactivation of GLP-1 and GIP –> so now endogenous GLP-1 and GIP can stay longer in the body and cause increase release of insulin in response to high blood glucose levels
Give orally
Less effective because can cause increase release of other endogenous hormones
AE:
-Nausea
Onglyza
Linagliptin
trad-
Inhibits DPP-IV
So prevents deactivation of GLP-1 and GIP –> so now endogenous GLP-1 and GIP can stay longer in the body and cause increase release of insulin in response to high blood glucose levels
Give orally
Less effective because can cause increase release of other endogenous hormones
AE:
-Nausea
Tradgenta
Pralintide
Exogenous administration of amylin
-Has Proline in position 25,28,29 –> therefore prevents polymerization
MOA:
-Pranlintide exogenous administration of amylin –> amylin receptor contains calcitonin receptor that associate with RAMP and get a GCPR –> can supress the release of glucagon and delay gastric emptying–> therefore slowing the gastric emptying will cause less glucose to be absorb from the GIT
Thera;
-Treat type 1 DM and Type 2 DM
Symlin
Empagliflozin
Jar
-gliflozin -SGLT2 inhibitor
Inhibit Glucose reabsorption
Works in the proximal renal tubule –> inhibits glucose reabsorption now stays in the nephron to be excreted
Thera:
-Treat DM
-have cardiovascular benefits
AE:
-Hyperkalemia –> avoid drugs that can increase K+ levels
-UTI
-Polyuria
Jardiance
Canagliflozin
Inv-
SGLT2 inhibitor
Use PO
MOA:
Inhibits SGLT2 in the proximal renal tubule –> prevent glucose reabsorption –> glucose stay in the nephron to be excreted
Thera:
-Treat DM
-Has cardiovascular benefits
AE:
-UTI
-Polyureia
-Hyperkalemia –> Avoid drugs that can cause hyperkalemia
Invonkana
Dapagliflozin
-gliflozin SGLT2 inhibitor
MOA:
-Inhibits SGLT2 in the proximal renal tubule
-Prevents glucose reabsorption and now is excreted
Thera:
-Treat DM
-Has cardiovascular benefits
AE:
-Polyurea
-UTI
-Hyperkalemia
Farxiga
Sotagliflozin
in-
-gliflozin SGLT2 inhibitor
MOA:
-Inhibits SGLT2 in the proximal renal tubule
-Prevents glucose reabsorption and now is excreted
Thera:
-Treat DM
-Has cardiovascular benefits
AE:
-Polyurea
-UTI
-Hyperkalemia
Inpefa
Bexagliflozin
bren-
-gliflozin SGLT2 inhibitor
MOA:
-Inhibits SGLT2 in the proximal renal tubule
-Prevents glucose reabsorption and now is excreted
Thera:
-Treat DM
-Has cardiovascular benefits
AE:
-Polyurea
-UTI
-Hyperkalemia
Brenzavvy
Ertugliflozin
-gliflozin SGLT2 inhibitor
MOA:
-Inhibits SGLT2 in the proximal renal tubule
-Prevents glucose reabsorption and now is excreted
Thera:
-Treat DM
-Has cardiovascular benefits
AE:
-Polyurea
-UTI
-Hyperkalemia
Steglatro
