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MHD2/Pharm - Endocrine > Pharm - Diabetes Drugs > Flashcards

Pharm - Diabetes Drugs Flashcards

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1
Q

What is the difference between type 1 and type 2 diabetes mellitus?

A

Type 1 is caused by autoimmune destruction of insulin producing beta cells, leading to insulin deficiency.

Type 2 is caused by insulin resistance.

Both cause hyperglycemia

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2
Q

Role of insulin and glucagon in high glucose states

A

Insulin release is triggered and glucagon release is suppressed. This promotes an anabolic state in which liver, adipose, and muscle uptake glucose resulting in a decrease in serum glucose.

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3
Q

Role of insulin and glucagon in low glucose states

A

Unopposed action of glucagon causes an increase in gluconeogenesis and glycogenolysis in the liver, which increases serum glucose levels. Adipose and muscle also release products for gluconeogenesis.

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4
Q

Symptoms of type 1 DM

A 
Polyuria, polydipsia, glucosuria
Weight loss despite polyphagia
Fatigue
Blurred vision
Ketoacidosis
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5
Q

Symptoms of type 2 DM

A

Obesity, fatigue, polyuria, polydipsia

Many are asymptomatic

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6
Q

What are the fasting plasma glucose and postprandial plasma glucose levels that characterize pre-diabetes and diabetes

A

Prediabetes: fasting glucose 100-125 mg/dL, postprandial glucose 140-199 mg/dL

Diabetes: fasting glucose > 126 mg/dL, posprandial glucose > 200 mg/dL

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7
Q

What is the cutoff for HbA1c in terms of diagnosis of diabetes?

A

Diabetes HbA1c > 6.5%

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8
Q

What are chronic complications of sustained hyperglycemia?

A

Retinopathy, neuropathy, nephropathy, CVD, peripheral vascular disease

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9
Q

What is the major side effect of intensive therapy for glycemic control?

A

Increased risk of hypoglycemia

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10
Q

What is the main treatment for type 1 diabetes?

A

Insulin replacement therapy is the only teratment for glycemic control and survival for T1DM

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11
Q

What two kinds of insulin are given to type 1 diabetics?

A

Basal insulin and postprandial insulin

-This mimics normal physiologic production of insulin

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12
Q

What is the action of insulin on the liver?

A

Inhibits hepatic glucose production (decreased gluconeogenesis, decreased glycogenolysis)
Inhibits secretion of glucagon

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13
Q

What is the action of insulin on muscle?

A

GLUT4 transporter upregulated, increased glucose uptake

AA uptake and protein synthesis (decreased AA and precursors to the liver)

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14
Q

What is the action of insulin on adipose?

A

GLUT4 transporter upregulated, increased glucose uptake

Inhibits lipolysis and promotes TG storage, decreased precursors to liver

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15
Q

Which insulin preparations are used postprandially?

A 
Rapid acting (Insulin aspart, lispro, glulisine)
Regular insulin
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16
Q

Which insulin preparations are used for basal control/fasting protection?

A 
Intermediate acting (NPS insulin)
Long acting (insulin glargine, detmir)
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17
Q

How does the structure of rapid acting insulin preparations differ from regular insulin?

A

Rapid acting insulin have AA substitutions and are monomeric as opposed to the hexameric form of regular insulin. Monomeric forms are absorbed faster and therefore have faster onset, peak and duration.

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18
Q

What is the structure of NPH insulin?

A

Insulin conjugated with protamine peptide that needs to be cleaved before absorption. This allows for a slower onset, peak and duration to provide overnight coverage

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19
Q

How do glargine and detmir insulin differ?

A

Glargine has an AA substitution that preciptiates at body temperature. Detmir has a fatty acid side chain that increases albumin binding. Both slow the onset, peak and duration to provide overnight coverage.

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20
Q

What is the route of insulin administration?

A

Subcutaneously from injections (syringe, or pen) or continuous infusion

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21
Q

What is a complication associated with injection of insulin?

A

If sites are not rotated, lipodystrophy can occur at the injection site

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22
Q

What is conventional insulin therapy?

A

2x daily injections of pre-mixed NPH (50-75%) & regular insulin (25-50%)

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23
Q

What is intensive insulin therapy?

A

1-2x daily injections of basal insulin
Pre-meal bolus of rapid/fast acting insulin (dose determined by blood glucose levels, size/composition of meal, activity level)

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24
Q

Symptoms associated with mild hypoglycemia

A

Tremor
Palpitations
Sweating
Intense hunger

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25
Symptoms associated with moderate hypoglycemia
Headache Mood change & irritability Decreased attention, drowsiness My need assistance to help themselves
26
Symptoms associated with severe hypoglycemia
Unresponsiveness Unconsciousness Convulsions Death
27
What are the recommended treatments for moderate hypoglycemia? severe hypoglycemia?
Moderate: Oral simple carbohydrates Severe: IV glucose or glucagon
28
What is the best treatment for type 2 diabetes mellitus?
Diet and exercise improves insulin sensitivity, blood glucose, blood pressure, lipid profiles and longevity
29
What surgical option is available for obese type 2 diabetics?
Roux-en-Y gastric bypass restores normoglycemia, decreases visceral obesity and improves pancreatic function
30
What are the classes of drugs used to treat type 2 diabetes?
``` Insulin sensitizers Insulin secretagogues Incretin mimics/modulators Inhibitors of carbohydrate digestion Insulin Amylin Others ```
31
What are the insulin sensitizer drugs?
Biguanides like Metformin | Thiazolidinediones like pioglitazone and rosiglitazone
32
What is the initial drug of choice for all type 2 diabetes that cannot control glucose with lifestyle modifications alone?
Metformin
33
What are the effects of metformin?
Decreased fasting plasma glucose due to decreased hepatic gluconeogenesis and increased insulin sensitivity/glucose uptake by muscle, liver and adipose
34
What is required for metformin effectiveness?
Insulin is required for metformin to work. Metformin does not increase insulin production.
35
What are the major advantages of metformin treatment compared to other diabetes drugs?
There is no risk for hypoglycemia Not associated with weight gain Improves lipid profile Decreases frequency of MI, and mortality
36
What is the mechanism of action of metformin?
Inhibits complex I of mitochondria leading to an increase in AMP. This antagonizes glucagon by inhibiting adenylate cyclase and activates AMP-dependent protein kinase which causes decreased plasma glucose and decreased insulin resistance.
37
What adverse effects are associated with metformin treatment?
Well tolerated Can cause GI side effects (metallic/fishy taste), nausea, diarrhea Inhibits B12 absorption (can lead to megaloblastic anemia) Rare: Lactic acidosis
38
What patients are at increased risk for lactic acidosis associated with metformin treatment?
Patients with renal/liver insufficiency, CHF, MI, hypoxic states These patients are predisposed to a fatal buildup of lactic acid because metformin inhibits hepatic clearance and is eliminated renally
39
What are the contraindications for metformin treatment?
``` Pregnant/lactating women Impaired renal/liver function Elderly Iodinated contrast agents (cause renal failure) Predisposition to lactic acidosis ```
40
What is the mechanism of action of the thiazolidinediones?
Agonists of PPAR gamma in adipose, skeletal muscle, liver, heart and macrophages leads to increased insulin sensitivity and decreased plasma glucose by altering gene expression.
41
What proteins are upregulated by PPAR gamma agonists?
GLUT4: glucose uptake in adipose, muscle liver Adiponectin: increased insulin sensitivity Genes involved in FFA uptake and oxidation
42
What is the indication for thiazolidinediones?
Approved for T2DM monotherapy or combo therapy with metformin, sulfonylureas or insulin
43
How long do thiazolidinediones take to achieve maximum effect?
6-14 weeks
44
What adverse effects are associated with thiazolidinediones?
``` Weight gain Fluid retention (Na + H2O retention, risk for heart failure) Bone fracture risk in women Bladder cancer Hepatotoxicity ```
45
What are the contraindications for thiazolidinediones?
Liver disease Heart failure Pregnancy
46
What classes of drugs are the insulin secretagogues?
Sulfonylureas and Meglitinides
47
What are the primary differences between sulfonylureas and meglitinides?
Sulfonylureas are slower onset and have long half livers. They affect fasting glucose levels Meglitinides are rapid onset and have short half lives. They affect postprandial glucose
48
What drugs are sulfonylureas?
First gen: chlorpropamide, tolbutamide | Second gen: glimepiride, glyburide, glipizide
49
What is the mechanism of action of sulfonylurea drugs?
Stimulate beta cells to secrete insulin by binding to and closing the K+/ATP ion channel. This leads to membrane depolarization, influx of Ca2+ and secretion of insulin granules.
50
What are the effects of sulfonylureas?
Long duration glucose lowering (reduce fasting plasma glucose) - reduces FPG 50-70 mg/dL
51
What does sulfonylurea activity depend on?
Functional beta cells. As disease progresses, beta cell function declines and sulfonylurea drugs become less effective
52
What adverse effects are associated with sulfonylurea drugs?
Hypoglycemia | Weight gain
53
Which sulfonylurea drug is safer and why?
Glipizide is safer than glyburide and glimepiride because it is short acting and broken down into an inactive metabolite. Better option for patients with renal insufficiency.
54
What are contraindications for sulfonylurea treatment?
Elderly patients & renal/liver dysfunction Patients with T1DM Pregnant/lactating women Sulfa allergies
55
What drug-drug interactions are associated with sulfonylureas?
Highly protein bound, many interactions with drugs like (salicylates, beta blockers, warfarin, fibrates ... etc.)
56
Which drugs are meglitinides?
Repaglinide and nateglinide
57
What is the mechanism of action of meglitinides?
Similar to sulfonylureas | Close K+/ATP channel leading to membrane depolarization, secretion of insulin granules
58
What are the indications for meglitineds?
Used to reduce postprandial hyperglycemia (taken prior to/with meals)
59
What is the difference between nateglinide and repaglinide?
Nateglinide affects only postprandial glucose | Repaglinide affects postprandial and fasting glucose
60
What is a good alternative to sulfonylurea treatment in the presence of renal insufficiency?
Repaglinide, which is metabolized completely in the liver (CYP3A4)
61
What are containdications for meglitinide treatment?
Liver disease | Pregnancy
62
What are adverse effects of meglitinides?
Hypoglycemia (less frequency than sulfonylurea) | Weight gain
63
What are the two classes of incretin mimetics/modulators?
GLP-1 homologs | DPP4 inhibitors
64
What is the incretin effect?
Insulin levels rise higher in response to oral glucose than equivalent levels of IV glucose due to polypeptide hormone factors produced by the GI tract (ex: GLP1 from L cells)
65
What are the GLP-1 homologs?
Exenatide and Liraglutide
66
What is the mechanism of action of GLP-1 homologs?
-Binds GLP-1 receptor on pancreatic beta cells to potentiate glucose-induced insulin secretion when glucose levels are high (low risk for hypoglycemia) -suppresses hepatic glucose production by inhibiting glucagon production -Slows gastric emptying (reduce glucose absorption) Increases satiety (reduce food intake)
67
Indications for GLP-1 homologs
Alternative to starting insulin in T2Dm patients not responding to other anti-diabetic medications Reduces fasting and post-prandial glucose Moderate weight loss effects
68
What adverse effects are associated with GLP-1 homologs?
Nausea, vomiting, diarrhea
69
What are the DPP4 inhibitors?
Sitagliptin, Saxagliptin
70
What is the mechanism of action of DPP4 inhibitors?
DPP4 is the enzyme responsible for breaking down GLP1. By inhibiting this enzyme, the action of GLP1 is promoted
71
What drugs are alpha glucosidase inhibitors?
Acarbose | Miglitol
72
What is the mechanism of action of alpha glucosidase inhibitors
These drugs inhibit the brush border enzyme responsible for hydrolysis of dietary carbohydrates into absorbable glucose molecules, thus delaying glucose absorption
73
Indications for alpha glucosidase inhibitors
Control of postprandial hyperglycemia
74
What side effects are associated with alpha glucosidase inhibitors?
GI: unabsorbed carbs cause abdominal pain, flatulence
75
What are contraindications for alpha-glucosidase inhibitors?
Any GI disease: chronic, IBD, colonic ulceration or intestinal obstruction
76
What are the SGLT2 inhibitor drugs?
Canagliflozin | Dapagliflozin
77
What is the mechanism of action of SGLT2 inhibitors?
Reduce hyperglycemia by inhibiting SGLT2 transporters in proximal renal tubule. This leads to increased glucose excretion in the urine.
78
What are indications for SGLT2 inhibitors?
Improved glycemic control (monotherapy or combo) Reduced body weight Reduced BP
79
What are adverse effects of SGLT2 inhibitors?
``` UTI and mycotic infections Thirst/dehydration Hypotension Increased LDL Hyperkalemia ```
80
What are the contraindications for SGLT2 inhibitors?
Renal impairment
81
What is the mechanism of action of bromocriptine?
Dopamine agonist Normalizes decreased AM dopamine levels in T2DM patients which improves glucose tolerance, insulin sensitivity, serum FFAs and decreases vascular pathology
82
What is Colesevelam?
A bile acid binding resin used to lower LDL Also reduces blood glucose by indirectly increasing GLP-1 expression. Used as adjunct with metformin, sulfonylureas or insulin
83
What is the most effective medication at lowering hyperglycemia in T2DM patients?
Insulin is indicated for initial therapy in patients presenting with HbA1c > 10%
84
What is the dosing difference between insulin for T1DM and T2DM
T2 diabetics are resistant to insulin, so much larger doses are needed
85
What is pramlintide?
An amylin homolog used for postprandial glucose controle. It slows gastric emptying and increases satiety while inhibiting hepatic gluconeogenesis and postprandial glucagon
86
What is the indication for pramlintide?
Used to treat T1 and T2DM using insulin that are not adequately controlled. Additive effects with insulin, so insulin dose is lowered when administered together with amylin
87
What are the adverse effects of pramlintide?
Nausea, vomiting, anorexia, headache | Hypoglycemia risk with insulin
88
If metformin treatment alone does not work to control glucose, what combinations can be tried?
``` Metformin +: Sulfonylurea Thiazolidinedione Exenatide Insulin ```

MHD2/Pharm - Endocrine (7 decks)

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