Diabetes Flashcards
Aspart
- ) What class?
- )
1.)Rapid-Acting Insulin
Amylin Analog
- ) Drug class?
- ) MOA?
- )ADR
- ) Amylin Analog
- ) slows gastric emptying→ increased fullness
- )
- Nausea
Sitagliptin
- ) Drug Class
- ) MOA?
- ) C/I?
- ) DDP-4 inhibitors
- ) Inhibits DDP-4 enzyme → REDUCE breakdown of GLP-1
- ) HF
Glulisine
- ) What class?
- )
1.)Rapid-Acting Insulin
Nateglinide
- ) Drug class?
- ) MOA?
- ) DDI’s?
- ) Indication?
- ) Glinides
- ) Binds to 140-kDA SU receptor → blocks K+ channel in beta cells → increased insulin release
- ) Don’t combine with sulfonylureas
- ) Better for post prandial glucose lowering (take b4 each meal)
Glargine U-300
- ) Drug class?
- ) MOA?
- ) Ultra long acting
2. ) Injected as acidic solution→ neutralization of it leads to micro-precipitates for slower absorption
Dulaglitide
- ) Drug Class
- ) MOA?
- ) GLP-1 Receptor Agonists-“Incretin Mimetics”
- )
- slow gastric emptying
- ↓’s appetite
- activates beta cells
- suppresses glucagon release
Repaglinide
- ) Drug class?
- ) MOA?
- ) DDI’s?
- ) Indication?
- ) Glinides
- ) Binds to 140-kDA SU receptor → blocks K+ channel in beta cells → increased insulin release
- ) Don’t combine with sulfonylureas
- ) Better for post prandial glucose lowering (take b4 each meal)
Linagliptin
- ) Drug Class
- ) MOA?
- ) C/I?
- ) DDP-4 inhibitors
- ) Inhibits DDP-4 enzyme → REDUCE breakdown of GLP-1
- ) HF
Empagliflozin
- ) Drug class?
- ) MOA?
- )ADR?→ can lead to?
- ) Sodium glucose transport -2 inhibitors (SGLT-2 inhibitors)
- ) Inhibits SGLT-2 → increased urinary glucose excretion
- ) Polyuria→ dehydration
Lixisenatide
- ) Drug Class
- ) MOA?
- ) GLP-1 Receptor Agonists-“Incretin Mimetics”
- )
- slow gastric emptying
- ↓’s appetite
- activates beta cells
- suppresses glucagon release
Glargine U-100
- ) Drug class?
- ) MOA?
- ) Long acting
2. ) Injected as acidic solution→ neutralization of it leads to micro-precipitates for slower absorption
Semaglutide
- ) Drug Class
- ) MOA?
- ) GLP-1 Receptor Agonists-“Incretin Mimetics”
- )
- slow gastric emptying
- ↓’s appetite (causes weight loss)
- activates beta cells
- suppresses glucagon release
What are Incretin Hormones What are their purpose?
What inactivates them?
-GI Tract releases Incretin Hormones (GLP-1, GIP)
o Role: Amplify insulin secretion by sensitizing Beta cells
Compliments insulin
Inactivated by DPP-4 enzyme
→ → Rapidly degrades Incretin hormones, reducing their duration of action
Liraglutide
- ) Drug Class
- ) MOA?
- ) GLP-1 Receptor Agonists-“Incretin Mimetics”
- )
- slow gastric emptying
- ↓’s appetite
- activates beta cells
- suppresses glucagon release
What is the purpose of protamine added to regular insulin?
Slow absorption
Major ADR’s of Insulin?
- ) Lipoatrophy
- ) Lipohypertrophy→ accumulation of fat deposit (rotate where you inject the insulin each time)
- )Weight gain
Basal vs. Bolus
https://quizlet.com/349076863/basal-vs-bolus-insulin-flash-cards/
Alogliptin
- ) Drug Class
- ) MOA?
- ) C/I?
- ) DDP-4 inhibitors
- ) Inhibits DDP-4 enzyme → REDUCE breakdown of GLP-1
- ) HF
Glimeperide
- ) Drug class?
- ) MOA?
- ) Caution with what pt’s?
- ) 2nd gen sulfonylureas
- ) Binds to 140-kDA SU receptor → blocks K+ channel in beta cells → increased insulin release
- ) Caution with pts with ↓ renal function→ accumulation of active metabolite
Canagliflozin
- ) Drug class?
- ) MOA?
- )ADR?→ can lead to?
- ) Sodium glucose transport -2 inhibitors (SGLT-2 inhibitors)
- ) Inhibits SGLT-2 → increased urinary glucose excretion
- ) Polyuria→ dehydration
Exenatide
- ) Drug Class
- ) MOA?
- ) GLP-1 Receptor Agonists-“Incretin Mimetics”
- )
- slow gastric emptying
- ↓’s appetite
- activates beta cells
- suppresses glucagon release
Glipizide
- ) Drug class?
- ) MOA?
- ) Caution with what pt’s?
- ) 2nd gen sulfonylureas
- ) Binds to 140-kDA SU receptor → blocks K+ channel in beta cells → increased insulin release
- ) Caution with pts with ↓ renal function→ accumulation of active metabolite
Rosiglitazone
- ) Drug Class?
- )MOA?
- ) ADR?
- ) How long does it take to see clinical effect?
- ) Thiazolidinedions (TZD’s)
- ) Activate PPAR-gamma → increases GLUT-4 transporter expression
- )
- Weight gain/edema - ) 4.) How long does it take to see clinical effect?
Regular Insulin
- ) Class?
- ) Indication?
1.) Short-acting (regular) insulin
2.)Commonly used IV for inpatient use in setting of Diabetic Ketoacidosis
o Hyperglycemic crisis
Neutral Protamine Hagedorn (NPH)
- ) What class?
- ) Is this drug use often? Why?
- ) Intermediate-acting
2. )No there is 50% variable absorption → drug is difficult to dose
Pioglitazone
- ) Drug Class?
- )MOA?
- ) ADR?
- ) How long does it take to see clinical effect?
- ) Thiazolidinedions (TZD’s)
- ) Activate PPAR-gamma → increases GLUT-4 transporter expression
- )
- Weight gain/edema
- ↑ risk of bladder cancer after 1 year of use - ) 8-12 weeks
Lispro U-100, Lispro U-200
- ) What class?
- )
1.)Rapid-Acting Insulin
Degludec U-100/U-200
- ) Drug class?
- ) MOA?
- ) Ultra-long acting
2. ) Forms multihexamers upon injection→ gradual removal of zinc to slow dissociation.
Metformin
- ) Drug class?
- ) MOA?
- ) ADR’s
- ) Caution with? why?
- ) Biguanide
- )Activates AMP-kinase in liver→ gluconeogenesis
- )Diarrhea
- ) Caution w/ pts w/ ↓ renal func due to risk of lactic acidosis
Glyburide
- ) Drug class?
- ) MOA?
- ) Caution with what pt’s?
- ) Hypoglycemia?
- ) 2nd gen sulfonylureas
- ) Binds to 140-kDA SU receptor → blocks K+ channel in beta cells → increased insulin release
- ) Caution with pts with ↓ renal function→ accumulation of active metabolite
- ) Highest risk of hypoglycemia with glyburide due to its really long half life
Basal vs. Bolus
-Basal: Constant low level release
→ To maintain glucose homeostasis in the fasting state
-Bolus: Meal stimulated
→ To cover meal stimulated Burts of glucose
Bromocriptine
- ) MOA?
- ) ADR?
1.) Unknown
→ we think it may ↑ insulin sensitivity
2.) Nausa
Afrezza
- ) What class?
- ) C/I?
- ) ADR’s
- ) Inhaled Insulin-Rapid Acting
- ) C/I in Pt’s w/
- COPD
- ASTHMA= ↑ bronchoconstriction
- SMOKER - ) Cough
- ) What is hypoglycemia?
2. ) How do you treat it?
- ) glucose < 70mg/dL
2. ) Oral/IV -glucose OR glucagon injection
Determir
- ) Drug class?
- ) MOA?
- ) C/I?
- ) Long acting
- ) injected as neural pH→ becomes 98% bound to albumin → slow distribution into the tissues
- ) pts with low albumin → hypoglycemia
Dapagliflozin
- ) Drug class?
- ) MOA?
- )ADR?→ can lead to?
- ) Sodium glucose transport -2 inhibitors (SGLT-2 inhibitors)
- ) Inhibits SGLT-2 → increased urinary glucose excretion
- ) Polyuria→ dehydration
Saxagliptin
- ) Drug Class
- ) MOA?
- ) C/I?
- ) DDP-4 inhibitors
- ) Inhibits DDP-4 enzyme → REDUCE breakdown of GLP-1
- ) HF & 34A inhibitors
Acarbose
- ) Drug class?
- ) MOA?
- ) ADR?
- ) Best taken ?
- ) Alpha-glucosidase inhibitors
- ) Inhibits small intestine enzymes that break down carbs→ delays absorption so there is reduced post prandial glucose
- ) GI issues: FARTING
- ) Best taken before meal
Chlorpropamide
- ) Drug class?
- ) MOA?
- ) Caution with what pt’s?
- )1st gen Sulfonylureas
- ) Binds to 140-kDA SU receptor→ blocks K+ channel in beta cells → increased insulin release
- ) Caution with pts with ↓ renal function→ accumulation of active metabolite
What is the role of Amylin
complements insulin by:
-suppressing post prandial glucagon release & slow gastric emptying
→ gastric emptying: slow process at which CARBS GET DIGESTED so there is LESS of a spike in our blood sugar AFTER we eat
→ Glucagon: responsible for sending signal to the liver to ↑ blood glucose
Miglitol
- ) Drug class?
- ) MOA?
- ) ADR?
- ) Best taken ?
- ) Alpha-glucosidase inhibitors
- ) Inhibits small intestine enzymes that break down carbs→ delays absorption so there is reduced post prandial glucose
- ) GI issues: FARTING
- ) Best taken before meal