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Pharm S2015 > SG8: Diabetes > Flashcards

SG8: Diabetes Flashcards

1
Q

What are the current criteria for diagnosis of diabetes mellitus?

A
  1. FPG ≥ 126 mg/dl (7.0 mM). Fasting is defined as no caloric intake for at least 8 h.*

OR

  1. Two-hour plasma glucose≥200mg/dl (11.1mM) during an OGTT.Thetest should be performed as described by the World Health Organization, using a glucose load containing the equivalent of 75 g anhydrous glucose dissolved in water.*

OR

  1. Inapatientwithclassicsymptomsofhyperglycemiaorhyperglycemiccrisis,a random plasma glucose ≥ 200 mg/dl (11.1 mM).
  2. HbA1C ≥ 6.5%. The test should be performed in a laboratory using a method that is NGSP certified and standardized to the DCCT assay.*

OR

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2
Q

List the target goals for blood glucose, blood pressure and lipids for T2D

A

Blood glucose targets

HbA1C < 7%.
FPG < 130 mg/dL
Postprandial glucose concentrations < 180 mg/dL

Blood pressure and lipids targets

Blood pressure < 130/80 mm Hg
LDL < 100 mg/dL
HDL > 40 mg/dL for men and > 50 for women Triglycerides < 150 mg/dL

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3
Q

Metformin pharm

A

MOA: Biguanide acting via AMPK to decr GNG & incr glucose utilization

Decrease in HbA1C (%): 1.0-2.0

Plasma Insulin Levels: ↓ or –

Advantages: Weight neutral/ Weight loss

Disadvantages:

  • GI side effects.
  • Rarely lactic acidosis.
  • Contraindicated with renal and hepatic disease, hypoxia, alcoholism
  • Vitamin B12
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4
Q

Insulin pharm

A

Decrease in HbA1C (%): 1.5-3.5

Plasma Insulin Levels: ↑

Advantages:

  • No dose limit.
  • Rapidly effective.
  • Improved lipid profile

Disadvantages

  • 1-4 injections daily. Monitoring. Hypoglycemia.
  • Weight gain
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5
Q

Sulfonylureas Pharm

A

MOA: binds SUR1 blocking ATP sensitive K+ to stimulate insulin secretion

  • Tolbutamide, chlorpropromide, glyburide, glipizide, glimepiride

Decrease in HbA1C (%): 1.0-2.0

Plasma Insulin Levels: ↑

Advantages: Rapidly effective

Disadvantages: Weight gain. Hypoglycemia

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6
Q

Meglitinides pharm

A

MOA: same as sulfonylureas

  • Ex. Repaglinide, Nateglinide

Decrease in HbA1C (%): 0.5-1.5

Plasma Insulin Levels: ↑

Advantages: Short duration

Disadvantages:

  • Weight gain.
  • Hypoglycemia
  • Frequent dosing
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7
Q

TZD pharm

A

MOA: stimulate PPAR-gamma (TF) to promote glucose uptake and utilization, incr insulin sensitivity

  • Ex. glitazones

Decrease in HbA1C (%): 0.5-1.4

Plasma Insulin Levels: ↓

Advantages:

  • Improved lipid profile (pioglitazone)
  • No hypoglycemia

Disadvantages:

  • Fluid retention. Weight gain.
  • CHF
  • Requires perioidic LFT
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8
Q

alpha-glucosidase inhibitors pharm

A

MOA:

  • competitive inhibitors of brush borderalpha-glucosidase
  • Slows intestinal carbohydrate digestion/absorption
  • Ex. Acarbose, Miglitol

Decrease in HbA1C (%): 0.5-0.8

Advantages: Weight neutral

Disadvantages:

  • GI side effects (flatulence, diarrhea).
  • Frequent dosing schedule.
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9
Q

Exenatide pharm

A

MOA: incretin analog -> incr insulin secretion; resistant to dipeptidyl peptidase IV (DPP-IV)

Decrease in HbA1C (%): 0.5-1.0

Plasma Insulin Levels: ↑

Advantages: Weight loss

Disadvantages:

  • GI side effects (nausea/vomiting).
  • Pancreatitis.
  • Injectable.
  • Should not be used in patients with gastroparesis.
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10
Q

Pramlinitide

A

MOA:

  • Amylin analog -> cosecreted w insulin
  • ↓ Glucagon secretion
  • Slows gastric emptying

Decrease in HbA1C (%): 0.5-1.0

Advantages: Weight loss

Disadvantages:

  • 3 injections daily.
  • Frequent GI effects.
  • Long-term safety not established
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11
Q

Sitagliptin

A

MOA:

  • Selective inhibitor of DPP-IV
  • increases GLP-1 and insulin secretion
  • decr Glucagon secretion

Decrease in HbA1C (%): 0.5-0.8

Plasma Insulin Levels: ↑

Advantages: Weight neutral

Disadvantages: Long-term safety not established

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12
Q

Management of T2D

A

Step 1

Metformin therapy should be initiated concurrent with lifestyle intervention at diagnosis.

Step 2

If lifestyle intervention and metformin fail to achieve HbA1C ≤ 7%, another medication should be added within 2-3 months of the initiation of therapy.

The consensus is to choose either insulin or a sulfonylurea other than glyburide or chlorpropamide (glyburide and chlorpropamide are associated with a greater risk of hypoglycemia than newer sulfonylureas such as glimepiride and glipizide.)

The HbA1C level determines in part which agent is selected. For patients with HbA1C ≥ 8.5% or with symptoms secondary to hyperglycemia, insulin should be considered.

Step 3

If lifestyle, metformin, and a second drug do not achieve glycemic goals, the next step should be to start, or intensify, insulin therapy.

When insulin is started, insulin secretagogues should be discontinued.

Although addition of a third oral agent can be considered, especially if the HbA1C level is close to target (HbA1C < 8.0%), this approach is usually not preferred, as it is no more effective in lowering glycemia and is more costly than initiating or intensifying insulin.

Insulin is the most effective medication in lowering glycemia. It can decrease any level of elevated HbA1C to, or close to, the therapeutic goal. Unlike the other blood glucose–lowering medications, there is no maximum dose of insulin beyond which a therapeutic effect will not occur.

Relatively large doses of insulin (≥1 unit/kg), compared with those required to treat type 1 diabetes, may be necessary to overcome the insulin resistance of type 2 diabetes and lower HbA1C to goal.

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13
Q

What are the criteria for instituting insulin therapy in type 2 diabetes?

A
  • Insulin therapy is usually tried after lifestyle modification and other antihyperglycemic agents have failed.
  • In the case of severe hyperglycemia or an HbA1c > 10%, insulin, along with lifestyle modification may be warranted as initial therapy.
  • Patients with type 2 diabetes who experience ketonuria or symptoms such as polyuria, polydipsia, and weight loss, may also require insulin as initial therapy. After the symptoms of hyperglycemia dissipate, oral agents can be tried, and insulin may be discontinued if oral agents are sufficient to control blood glucose.
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14
Q

How should metformin therapy be monitored

A
  • HBA1c
  • LFT for Pt w liver disease
  • Renal function test (GFR, BUN: Cr ratio) for Pt w renal disease
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15
Q

What are the different types of insulin available?

A

Rapid-acting: onset 15 min; peak 30 to 90 min; duration 1 to 5 h

  • Lispro
  • Aspart
  • Glulisine

Short-acting: onset 30 min; peak 90 to 240 min; duration 5 to 8 h

  • Regular soluble

Intermediate- acting: onset 60 to 120 min; peak 6 to 12 h; 18 to 24 h

  • NPH
  • Lente

Long-acting: onset 60 to 300 min; no peak; duration ~24 h

  • Ultralente
  • Protamine zinc
  • Glargine: no peak
  • Detemir: no peak
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16
Q

What methods of insulin administration are available to achieve optimal glucose control?

A

2 methods have been used to achieve a similar pattern of insulin release:

  1. Basal-Bolus Insulin Regimens consisting of once to twice daily doses of basal insulin coupled with pre-meal doses of rapid or short-acting insulin.
  2. Insulin Pump Therapy (previously referred to as “continuous subcutaneous infusion of insulin”)
17
Q

Select a Basal-Bolus Insulin regimen for T1D

A

In general, individuals with type 1 DM require 0.5 to 1.0 U/kg per day of insulin divided into multiple doses. Initial insulin-dosing regimens should be conservative. Approximately 40 - 50% of the insulin should be given as basal insulin.

The insulin doses in such regimens should be adjusted based on self-monitoring of blood glucose (SMBG) results with the following general assumptions:

  • pre-breakfast (fasting) glucose is primarily determined by the prior bedtime basal insulin.
  • pre-lunch glucose is a function of the morning rapid-acting insulin
  • pre-dinner glucose is a function of the morning basal insulin or of the pre-lunch rapid-acting insulin.
  • bedtime glucose is a function of the pre-dinner rapid-acting insulin.
18
Q

Why is it important to treat his hypertension?

A

A 5 mmHg reduction in mean diastolic BP can produce a 37% reduction in microvascular complications, and a 10 mmHg reduction in mean systolic BP reduces the risk of MI by 11% and death related to diabetes by 15%.

19
Q

What is the recommended treatment for hypertension in diabetes?

A

130–139 mmHg or a diastolic blood pressure 80–89 mmHg:

  • lifestyle incl. DASH

Severe hypertension (systolic blood pressure ≥ 140 mmHg or diastolic blood pressure ≥ 90 mmHg):

  • ACEi and ARB
  • If needed, thiazide should be added to those with an estimated glomerular filtration rate (GFR) (see below) ≥ 30 ml/min/1.73 m2 and a loop diuretic for those with an estimated GFR < 30 ml/min/1.73 m2.
20
Q

What laboratory monitoring is recommended during lisinopril therapy?

A
  • serum K+
  • serum creatinine

The ACEI can increase serum potassium as a result of aldosterone reduction. Potassium increases with ACEI monotherapy are very small and typically do not result in hyperkalemia. This risk is increased, however, when used in patients with significant chronic kidney disease (estimated GFR <60 mL/minute/1.73 m2), or when used in combination with other drugs that can also raise potassium (i.e., an ARB, potassium-sparing diuretics, aldosterone antagonists).

ACEI therapy can also cause a small increase in serum creatinine, due to decreased vasoconstriction of the efferent arteriole in the kidney. This results in a small decrease in GFR that leads to a small increase in serum creatinine.

  • One common mistake is to discontinue an ACEI when there is a modest rise in serum creatinine. Increases in serum creatinine of up to 35% from the baseline creatinine value are safe and anticipated.
21
Q

What is the mechanism of action of statins?

A

inhibit HMG-CoA reductase, a key regulatory enzyme for cholesterol biosynthesis. As a result, hepatic cholesterol synthesis declines, surface LDL particle receptors increase, and LDL cholesterol clearance increases.

22
Q

What are the main adverse effects of statins?

A
  • hepatotoxicity
  • myopathy
  • rhabdomyolysis
  • In most of these cases, patients usually suffered from renal insufficiency or were taking drugs such as cyclosporine, itraconazole, erythromycin, gemfibrozil, or niacin. Plasma creatine kinase levels should be determined regularly.
23
Q

What are the beneficial cardiovascular pleiotropic effects of statins?

A

Pleiotropic effects of statins include:

  • improvement of endothelial dysfunction
  • increased nitric oxide bioavailability
  • antioxidant properties
  • inhibition of inflammatory responses
  • stabilization of atherosclerotic plaques.
24
Q

What is the cause of diabetic gastroparesis? How should H.D. be treated?

A

Diabetic gastroparesis

  • Pathophysiology: diabetic neuropathy affecting the autonomics of GIT (enteropathy), especially the vagus nerve damage.
  • Pharm: metoclopramide or erythromycin
    • Metoclopramide Adverse: Parkinsonism
25
Q

Canagliflozin

A

MOA:

  • Inhibits SGLT2 in the proximal nephron
  • Blocks glucose reabsorption by the kidney, increasing glucosuria

Advantages:

  • No hypoglycemia
  • Weight reduction Decreases BP

Disadvantages:

  • UTI
  • Polyuria
  • Volume depletion/hypotension
  • ↑LDL
  • ↑Creatinine (transient)
26
Q

Which therapeutic agents can be used for the management of the painful symptoms of diabetic neuropathy?

A
  • TCA considered for 1st line
  • Amitriptyline, imipramine: tertiary amines
  • Gabapentin & pregabalin
  • SNRI

Pharm S2015 (47 decks)

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