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DEMS > Diabetes Treatments - PHARM > Flashcards

Diabetes Treatments - PHARM Flashcards

1
Q

In which patients are insulin treatments ESSENTIAL?

A

Type I diabetes. These patients no longer have insulin and therefore you must treat them with insulin (making up for what they lack)
*they are indicated for late and progressive type ii diabetes that is not able to be controlled with non-insulin treatments and lifestyle changes

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2
Q

What are the bolus insulins used for prandial therapy?

A 
• Humalog
		○ Lispro
	• Novolog
		○ Aspart
	• Glulisine 
		○ Aprida
	• Inhaled insulin (Afrezza)
*these agents can be effectively used in insulin pumps
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3
Q

What is the time to onset of the bolus insulins? What is their clearance time?

A

These are rapid acting and should be used for prandial therapy

  • Lispro, Aspart, Glulisine (Girls and Lads from sketchy)
  • they lead to a 15minute or so onset of insulin action
  • their peak action is about 1 hour
  • their activity lasts 3-5 hours in total
  • these agents can be effectivly used in insulin pumps
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4
Q

What are the short acting human insulins?

A

• Straight up regular insulin
• Humulin R
• Novolin R
○ Recombinant human insulin

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5
Q

When do you use intravenous insulin infusions?

A
  • Think regular, recombinant insulin here
    • DKA
    • Hyperosmolar hyperglycemic state
    • Inpatient hyperglycemia in which glycemic control is desired, like peri-operatively and ICU patients
    • IV insulin has immediate effect and rapid off-set (15 min or so)
    • Thus no benefit to using a rapid acting IV agent
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6
Q

What is the usual dose of regular, recombinant insulin in hospital setting therapy?

A
  • Hospital setting b/c regular insulin not often used in outpatient setting because of the difference in physiological timing
    • 5-15 units is the usual dose
    • This leads to clearance after 6-8 hours
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7
Q

What are the pharmacokinetic profiles of the short acting human insulins?

A
  • Regular insulin (recombinant insulin)
    • Not often used in outpatient b/c kinetics do not match well with physiologic needs
    • 30 min before meals
    • 30-60 minute onset with 2 hr peek
    • Duration is 6-8 hours if used in normal doses
    • 5-15 units are the normal dose
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8
Q

What are the “basal” insulins?

A

• These are the long acting ones that mimic the basal action of insulin in the body
• These are not prandial, but provide the insulin necessary to handle normal glucose fluctuations throughout the day
○ Remember thought that WELL CONTROLLED diabetes HbA1C is still 7%
• Glargine (Lantus)
• Detemir (Levemir)
• Degludec (Tresiba)
• Glargine U-300 (toujeo)

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9
Q

What makes the long acting insulins “long acting”

A

• They are formulated in a way that allows for less rapid dissolving and incorporation into the plasma
• Glargine has extra arginines that makes it precipitate in the subcutaneous neutral pH
○ Onset is 1.5 hr and 24 hour duration, taken once a day
• Detemir has an additional fatty acid chain which allows it to be more liphophilic and bind serum protein better, increasing duration of action to 12-20 hrs. usually taken 2X a day
• Degludec is the newest and has 42 hours of duration and is injected once daily

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10
Q

As far as drug mixing goes (insulin) what about NPH insulin vs. glargine?

A
  • Glargine can’t be mixed with other insulins because it’s stored in an acidic manner
    • NPH insulin and regular insulin CAN be mixed up in the same delivery stystem
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11
Q

What are the pharmacokinetics of NPH and Humulin insulin?

A
  • NPH = neutral protamine Hagedorn
    • The brand names are Humulin N, Novolin N
    • Another word to look for is sophane
    • Cloudy solution
    • 1-3 hour onset with 6-8 hour peek
    • Lasts 12-16 hours and is mostly used for the lunch-time peak in glucose
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12
Q

What is meant by “pre-mixed insulins”?

A

• Human: %NPH/%regular
○ Usually 70/30 or 50/50
• Humalog/regular is an option for the analogs
○ Humalog 75/25
§ Or 50/50
○ Novolog 70/30
• Allows for short term benefit for meals with longer action basal coverage
• Analog mixed - Injected 5-15 minutes before meal and have pharmacokinetics that are more physiologic than NPH/regular b/c of basal and spike mix

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13
Q

What is meant by basal bolus therapy?

A
  • This includes the basal, prandial and correctional insulin needs
    • You are mimicking with injection the normal insulin release of the body
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14
Q

Glargine, Detemir and NPH are used for what purpose?

A
  • These are basal insulin medications
    • Used for a patient to cover normal daily cyclical glucose spikes or hormone swings
    • Suppresses hepatic glucose output and lowers overall glucose levels throughout the day
    • Type 1 patients will develop DKA if they do not inject their basal insulin doses while type 2 patients will develop severe hyperglycemia but usually have enough endogenous insulin secretion to prevent ketoacidosis
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15
Q

If you wanted to start a patient on insulin therapy what is the estimate you can use to figure out the starting dose?

A
  • 0.2 units/kg/day is the weight based method
    • Titrated according to individual needs and circumstances
    • Type 2, which has some insulin resistance in it, think more along the 0.5 units/kg/day for basal insulin
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16
Q

Describe the treatment paradigm of prandial insulin

A

• Used to metabolize nutrients in a meal or snack and cover the postprandrial rise in glucose
• The rapid-acting insulins are used for this
○ Humalog, novolog, apidra
○ Girls and Lads - Glulisine, Aspart and Lispro
• You can estimate the dose according to the carbohydrate to insulin ratio (C:I)
• Number of grams of carbohydrates that 1 unit of insulin is anticipated to cover for that individual
○ Insulin sensitive individuals may require a C:I ratio of 15:1 or 20:1
○ Resistant is more 10:1 or 8:1

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17
Q

How do you go about determining the dose of insulin for CORRECTION?

A

• Correctional doses of insulin are used to correct a high blood glucose level
• Humalog, novolg, apidra and inhaled insulin all used
• Usually added to a prandial insulin dose
• You determine the correction factor or sensitivity factor by dividing a constant, 1600, by their total daily dose of insulin
• The resulting number is the number of mg/dL that the blood glucose is expected to drop with each unit of insulin given as a correction dose
• Normal sensitivity might have a correction factor of 50
○ 1 unit of rapid acting insulin would be expected to drop the glucose by 50mg/dL
• Resistence might look like a correction factor of 20
○ 1 unit will drop glucose 20mg/dL
• USE TARGET GLUCOSE OF 100mg/dL

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18
Q

Describe the general, overall treatment paradigm of type 1 diabetes patients

A
  • standard care is intensive multiple-dose insulin or basal bolus therapy
    • This provides more physiologic replacement of insulin
    • Allows for flexibility in timing, size and composition of meals
    • Pre-meal doses can be fixed according to carbohydrate content of a given meal
    • Must take into account lifestyle, motivation and preferences as well as cost
    • Glargine injected once daily provides basal coverage for about 24 hours (detemir is 2X daily))
    • Bolus dose is added to this before meal and additional correctional doses can be added as well according to correction factor
    • Also think of the glucose pumps and the artificial pancreas
19
Q

Describe the overall and general treatment paradigm for type 2 diabetes

A
  • Essentially use insulin in patients who have not achieved good control before
    • With data from home glucose monitoring, doses of rapid-acting insulin are added successively until glycemic control is achieved
    • In this case though, consider the use of all non-insulins before starting insulin therapy
    • Usually add insulin after 2-3 non-insulins are tried and are not effective in controlling the glucose target/goal
    • In cases of severe insulin deficiency you should use insulin right away
    • Fasting over 250, random over 300 and A1c over 10%
    • Use insulin at first and see if you can titrate down or off
    • Also use insulins in hyperglycemic hyperosmolar state or DKA
    • Discharge with insulin and maybe taper with outpatient follow up
20
Q

What are the different targets for treatment of diabetes?

A

• ADA recommends:
○ Less than 7% A1c
○ Fasting glucose - 70-130mg/dL
○ 2 hr post-meal glucose is less than 180mg/dL

21
Q

What are the lifestyle recommendations made in the treatment of diabetes?

A
  • Less calorie-dense foods
    • More complex carbohydrates (as opposed to simple like high fructose corn syrup?)
    • Higher fiber, lean proteins, smaller portions
    • Increase physical activity
    • Weight loss to normal range
22
Q

What is metformin?

A

• Biguanide drug
• Potentiates the suppressive effect of insulin on hepatic glucose production
• Does not stimulate insulin secretion or increase circulating insulin levels
• Risk of lactic acidosis lower than a different drug in this class which is pulled off the market
○ But the risk still exists
• Use eGFR to guide use, since renal failure may precipitate lactic acidosis

23
Q

What are the pros and cons to metformin use?

A 
• Pros
		○ Mechanism of action is more or less safe
		○ No hypoglycemia
		○ Inexpensive
		○ No weight gain (slight weight loss)
		○ Combinations are possible
			§ Sulfonylureas
			§ Thiazolidinediones
			§ DPP-4 inhibitor
			§ SGLT-2 inhibitor
	• Cons
		○ GI side effects - nausea, bloating, diarrhea
		○ Risk of lactic acidosis - contrast media, CHF, renal insufficiency, liver disease
24
Q

If metformin is not enough in your type 2 diabetes patient, and they have CV comorbidities, now what do you recommend?

A

• Add SGLT-2 or GLP-1RA to the regimen

25
Q

You have a 51 year old woman with a 9yr histor of T2DM, A1c of 8.4% and is only on metformin right now. What additional therapies can be recommended at this point

A 
• Again, have the lifestyle change conversation (always)
	• Drugs (essentially just add another one)
		○ Sulfonylurea
		○ Thiazolidinedione
		○ Basal insulin
		○ GLP-1 receptor agonist
		○ DPP-4 inhibitor
		○ SGLT-2 inhibitor
26
Q

What are the drug-specific considerations for thinking through additive glucose-lowering therapies?

A
  • Mechanism of action
    • Glucose-lowering effectiveness
    • Side effects
    • Cost
    • Convenience
    • Pharmacokinetics
    • Non-glycemic beneficial effects
27
Q

What are the patient-specific considerations for thinking through additive glucose-lowering therapies?

A
  • Baseline control
    • Stage of diabetes
    • Co-existing medical conditions
    • Tolerability of side effects
    • Social situation
    • Financial situation
    • Preference of therapy
28
Q

If a DM patient has primarily a problem with insulin resistance, what are the drugs of choice?

A
  • Metformin
    • GLP-1RA
    • DPP-4i
    • TZD
    • Insulin
29
Q

How many times per year should A1c be measured in a diabetic patient?

A
  • 2-4 times per year in ALL diabetic patients

* At that point you re-hash goals and talk about risk/benefit

30
Q

How much of a reduction in A1c can the standard T2DM non-insulin drugs be expected to give you?

A
  • Metformin - 1-2% reduction
    • Every other drug but insulin will give you a 0.5% reduction
    • The other exception is sulfonylureas, which can be expected to give you about the same reduction as does metformin
31
Q

What are the Incretins?

A

• GLP-1 = glucagon-like peptide 1
○ Very effective for lowering glucose in diabetes
• GIP = gastric inhibitory peptide
○ Secreted by cells in GI tract in response to food intake
○ Augments insulin secretion only if blood glucose is elevated

32
Q

What are incretins supposed to treat?

A
  • The incretin effect
    • This is the fact that there is insufficient insulin secretion AND insufficient glucagon supression in response to a meal in type 2 diabetes
33
Q

What are all the ways that GLP-1 lowers glucose?

A
  • Food intake will stimulate GLP-1 secretion from L cells of ileum
    • This stimulates glucose-dependent insulin secretion and SUPRESSES postprandial glucagon secretion
    • This leads to decreased hepatic glucose output, slowed gastric emptying and inhibited food uptake
    • The end result is a normalized blood glucose
34
Q

What is DPP-4 and why must it be inhibited?

A
  • DPP-4 is what breaks down GLP-1
    • DPP-4 = dipeptidyl peptidase 4
    • Inhibit it to allow GLP-1 agonists to do their work of inhibiting glucagon secretion
35
Q

What are the GLP-1 agonists you should know about?

A 
• Exenatide
		○ byetta
	• Liraglutide
		○ victoza
	• Exenatide qwk
		○ bydureon
	• Albiglutide
		○ tanzeum
	• Dulaglutide
		○ Trulicity
36
Q

What are the pros and cons of GLP-1 agonists?

A 
• Pros
		○ Multiple mechanisms of action to lower postprandial glucose
		○ Effects are glucose-dependent
		○ Weight loss
		○ Recent trial suggests CV benefit
	• Cons
		○ SC injections
		○ Side effects
		○ expensive
37
Q

What are the DPP-4 inhibitors to know about?

A 
• Sitagliptin
	• Saxagliptin
	• Linagliptin
	• Alogliptin
		○ Just remember the clips on the old hag's nose in the sketchy picture
38
Q

What are the pros and cons to the use of DPP-4 inhibitors?

A 
• Pros
		○ Multiple mechanisms of action to lower postprandial glucose
		○ Oral admin
		○ Once daily admin
		○ Weight neutral drugs
		○ Combination pill with metformin
	• Cons
		○ Less potent glucose-lowering effect
		○ Expensive
		○ Side effects
39
Q

What are the SGLT-2 inhibitors to know about?

A 
• Sodium glucose co-transporter 2 is what is being inhibited - in proximal tubule
	• Canagliflozin
		○ invokana
	• Dapagliflozin
		○ farxiga
	• Empagliflozin
		○ Jardiance
40
Q

What level of glucose can the normal kidney handle?

A
  • Filtered glucose load of about 180 g/day
    • Urinary glucose less than 0.5g/day
    • Glucose reabsorption occurs in the proximal tubule though the action of SGLT1 and 2
41
Q

What are the pros and cons of SGLT2 inhibitors?

A

• Pros
○ Novel mechanism for controlling glucose
○ Weight loss
○ Pill
○ At least 1 available as a combo pill with metformin
○ Recent trial suggesting CV benefit
• Cons
○ Increased risk for urinary tract and GU infections
○ Increased risk for low potassium
○ Expensive
○ Questionable long-term safety because they are new and not all that well studied far out

42
Q

What is the mechanism of action for sulfonylureas?

A
  • Close the ATP-sensitive K+ channels in the beta cell
    • Closing of the potassium channels will depolarize the beta cell and lead to influx of calcium and secretion of insulin granules
43
Q

What are the sulfonylureas to know?

A
  • Glyburide
    • Glipizide
    • glimepiride
44
Q

What are the pros and cons of the sulfonylureas for diabetes treatment?

A 
• Pros
		○ Inexpensive
		○ Combos available
			§ Metformin
			§ Thiazolidinediones
	• Cons
		○ Weight gain
		○ Hypoglycemia
		○ Loses effectiveness with longer duration of diabetes
			§ Since the beta cells are getting more and more burned out

DEMS (30 decks)

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