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Type I Diabetes
- Due to autoimmune beta cell destruction, which results in zero insulin
- Untreated, can lead to ketoacidosis
- Onset is not common after 30 years
- 5-10% of diabetes
Type 2 Diabetes
- Manifested as insulin resistance, along with some degree of insulin
- 90% of diabetic cases
- Prevalence is increasing
Gestational Diabetes
- Onset of glucose intolerance in pregnancy
1. Drugs
o APs
o Beta-adrenergic antagonists
o Glucocorticoids
o Niacin
o Protease inhibitors
o Thiazide or loop diuretics
2. Overweight
3. Poor nutrition
4. Sedentary lifestyle
5. Age >40
6. Hypertension
7. High risk population

Regular insulin should be administered 20-30 min before eating meals . pen.BG levels will ↓ after mod exercise. or continuous s/c insulin infusion . nocturnal hypoglycemia) .Minimum of 3 blood glucose measurements daily for those on insulin regimens . along with resistance training 3 times per week . insulin lispro) . due to ↓ frequency of adverse reactions . and may be associated with fewer episodes of hypoglycemia (esp.Encourage aerobic exercise > or equal to 150 min per week.Schizophrenia Non-Pharm .Can be administered by syringe.Rapid-acting insulin analogues (insulin aspartame.The long acting insulin analogues (insulin detemir and insulin glargine) appear to produce more predictable effects than intermediate-acting human insulin (NPH). insulin glulisine.Animal insulin has been replaced by human preparations. but ↑ after intense activity (stress response) Monitoring - BP measures Foot examinations annually A1C measurements q 3 mo Serum creatinine annually Fasting lipid profile PHARMACOLOGIC CHOICES Type 1 Diabetes Insulin . enhances insulin sensitivity and lowers blood pressure and lipid levels . PCOS 10.8. Family history 9.Physical activity improves CVS function.SMBG is not necessary for patient on oral metformin .

hunger.In patients with A1C > or equal to 9% o Medication must be initiated immediately + diet and exercise o Combination therapy with 2 medications from different classes is recommended.Rapid acting insulin analogues can be given before or within 20 min of starting a meal Adverse Effects of Insulin Therapy . 2nd line: Insulin secretagogues (sulfonylureas and meglitinides) .Localized fat hypertrophy o Often result of frequent use of same injection site o Causes low or unpredictable absorption of insulin from the site TYPE 2 DM . o A1C should be reached within 6-12 months ANTIHYPERGLYCEMIC AGENTS 1.  DO NOT GIVE glucagon to malnourished patients or in alcoholinduced hypoglycemia. disorientation o Conscious patient: give oral glucose preparation of 20 g carbohydrate o Unconscious patient: 1 mg of glucagon IM or SC temporarily ↑ blood glucose. tachycardia.  Give IV 50 mL of 50% dextrose in these situations . altered behavior. nausea o Severe hypoglycemia: confusion. tremors.Hypoglycemia o Most commonly the result of either a missed meal or an unusual amount of exercise o Mild hypoglycemia is manifested by: sweating.Patients with A1C < 9% o Can initiate with just diet and exercise o But medication must be started if glycemic targets are not met within 23 months o 1st line: Monotherapy with metformin is usually recommended . difficulty speaking..

↓ hepatic glucose production.Sulfonylureas: a. but associated w/ ↑ risk of hypoglycemia ii. No increase in the rate of lactic acidosis compared to other antihyperglycemic agents g. 2nd gen SU: Gliclazide. is a biguanide c. to avoid possibilities of acute renal failure (which can ↑ chances of lactic acidosis) Thiazolidinediones (TZDs) o Pioglitazone and rosiglitazone are agonists at PPAR gamma receptors located in the cell nucleus o They ↑ insulin sensitivity and ↓ glood glucose and circulating insulin levels . Glyburide is inexpensive. SUs are 2nd line in T2DM therapy. Hold metformin pre-operatively and when imaging contrast agents are being given. glyburide i. 1st line for T2DM b. CI in patients with HF. Drugs that ↓ hepatic glucose production and/or ↑ tissue sensitivity to insulin (thiazolidinediones and metformin) Metformin (1st line) : a. renal or hepatic disease or hypoxemic states f. Typically not used due to PK profile and ↑ risk of DI b. they are either add-on or monotx in patients with CI to metformin Meglitinides o o o o o Nateglinide and repaglinide ↑ insulin release Meglitinides have a shorter duration of action than SUs They need to be taken just before meals to ↓ post-prandial glucose Should be omitted if meal is missed Repaglinide ↓ A1C = to SU. glimepiride. 1st gen SU: Chlorpropamide and Tobutamide i. Can ↑ hypoglycemic effects of insulin and sulfonylureas e. but has ↓ risk of hypoglycemia 2. may lower glucose absorption and ↑ insulin-mediated glucose uptake d.

o They ↑ peripheral glucose uptake. which ↓ postprandial glucose levels c. enhance fat cell sensitivity to insulin and ↓ hepatic glucose output o Low risk of hypoglycemia. given po  Lack of long term safety. ↑ GLP-1 action by 5 times o Appear to lower A1C to a greater extent than DPP-4 inhibitors o Can cause more initial nausea than DPP-4 inhibitors initially o Only available via S/C injections o Exenatide is approved for use in Canada. can be compounded w/ insulin and SU o Associated w/ weight gain. This delays digestion of starches and disaccharides. They do not significantly inhibit intestinal lactase d. and ↑ satiety o DPP-4 breaks down GLP-1 o DPP-4 inhibitors Saxagliptin and Sitagliptin are currently approved for use in Canada. o GLP-1 is secreted in response to food ingestion by endocrine cells found in the GI tract o GLP-1 ↑ insulin secretion. 2 line: Drugs that mimic or enhance incretin hormones (dipeptidyl peptidase-4 inhibitors and glucagon-like peptide-1 receptor agonists DPP-4 inhibitors: o Augment actions of GLP-1. slows gastric emptying. Acarbose inhibits intestinal alpha-glucosidases b. fluid retention and edema (which ↑ risk of HF) o ↑ risk of fractures of wrist and hip o Health Canada requires that new Rx for rosiglitazone includes patient informed consent to ensure risks and benefits are understood by patient nd 3. Can ↑ risk of HG when combined with insulin or insulin secretagogues . high cost make them 2nd line GLP-1 Analogues o GLP-1 agonists mimic actions of GLP-1. but not marketed 4. suppresses glucagon secretion during postprandial period. an endogenous “incretin” hormone. 3rd line: Drugs that delay or prevent the digestion or complex carbohydrates (alpha-glucosidase inhibitor acarbose) a. Does not cause hypoglycemia e.

as acarbose prevents digestion of sucrose INSULIN FOR T2DM . Hypoglycemia in these patients should be treated by glucose.Appropriate to use insulin when: o Max dose or maximally tolerated dose of oral agents is reached.2 units/kg of insulin NPH or long-acting analogue  Or. high upon initial presentation. oral antihyperglycemic agents gradually lose effectiveness over time . Dose is then adjusted (approx.f. Causes GI effects g. then intensive insulin has to be started immediately . risk of hypoglycemia o Requires self-monitoring . when A1C > 9% o Metabolic decompensation o Preconception and pregnancy . 2 units q 3 days) until < 7 mmol/L is reached  Oral antihyperglycemic agents other than metformin may need to be discontinued o If glycemic targets are not met with bedtime insulin + daytime oral AHG agent.1-0. yet A1C is > 7% o End organ damage (such as kidney failure). which renders oral agents inappropriate o Initial diagnosis.Insulin is best at ↓ A1C . except metformin o If glycemic values are v. then mealtime insulin injections may have to be given  Generally oral AHG agents are d/c when meal time insulin is started. rather than sucrose.Insulin is often delayed because: o Self-injection is seen as complex o Associated with weight gain.Due to progressive nature of T2DM.Commonly used insulin regimes: o Insulin is added to existed oral therapy  Daily HS injection of basal insulin at 0. empiric dose of 5-10 U of NPH or LA insulin (glargine or detemir).

Insulin goes into breast milk. but no risk as hormone is degraded in GI tract before reaching systemic circulation . continued into pregnancy.Should avoid hypoglycemia and avoid oral AHG agents . as retinopathy can be accelerated due to poor glycemic control . perinatal mortality. congenital malformations . continued throughout pregnancy.4-1 mg daily. neonatal hypoglycemia .Can use glyburide in pregnant women BREASTFEEDING .Gestational DM develops during pregnancy.Folic acid supplementation should begin at least 3 months prior to conception. Initial dose is 5mg daily. . allows for correction of abnormal results PREGNANCY AND BREASTFEEDING PREGNANCY . primarily due to insulin resistance that results from high levels of gestational hormones . Start with 40% of total daily dose (0. dose is reduced to 0.5 units/kg divided over 24 hours) given as basal insulin (NPH or long acting analogue)  20% of daily dose given before meals 3 times daily  Dose is then adjusted to reach glucose <7 mmol/L and 2 hour post prandial glucose < 10 mmol  Insulin may be given BID injections of premixed insulin with 2/3rd of daily dose (0.Pre-existing diabetes (T1DM or T2DM) ↑ risk of miscarriage. higher birth weight.5 units/kg) given before breakfast and remaining 1/3rd of dose given before evening meal  Flexible regimen. After 3 months gestation.Target A1C of <7% should be achieved before conception. and for a minimum of 6 months postpartum or until breastfeeding is done .Eye exam is important.GDM ↑ risk of fetal hyperinsuliemia. fetal macrosomia.Switch to an insulin regimen from oral hypoglycemic agents .

Glyburide and metformin can be used in women who were diabetic before/after pregnancy. in patients with TSH > 10 mU/L (normally 0. consider treatment.Clinical syndrome that results from a deficiency of thyroid hormone . THYROID DISORDERS HYPOTHYROIDISM . abnormal lipid profile. LEVOTHYROXINE (L-T4) o Goal of L-T4 therapy is to normalize the TSH level o Dosage adjustment is made every 4-6 weeks as needed o Generally it takes 6 weeks to attain a new steady state after dosage adjustments .GDM usually leaves 24 hours postpartum . hair Hypertension. but can be low or normal in pituitary or hypothalamic disease .3-6 mU/L). as insulin regimens can change as more calories are burned during BF .Rarely. o If confirmed.↑ Thyroid-stimulating hormone (TSH) measurement is sensitive indicator of hypothyroidism. in patients who are antithyroid peroxidase (anti-TPO) + or those planning a pregnancy Symptoms: - Fatigue Weight gain Impaired memory Constipation Cold intolerance Appearance: coarse features. bradycardia PHARMACOLOGIC CHOICES 1. symptoms of hypothyroidism. esp.BG should be monitored. dry skin.Subclinical hypothyroidism is defined as an ↑ TSH with normal thyroid hormone levels. can be due to resistance to thyroid hormone ..

1st trimester  TSH levels are low due to ↑ beta HCG levels .Thyroid hormone therapy is safe in pregnancy and BF TT . thyroid hormone requirements stabilize .Can cause lower IQ scores in children of women who had elevated TSH at the time of conception . this means under-treatment with thyroxine or new diagnosis of hypothyroidism .Women already taking thyroid hormone replacement prior to pregnancy should ↑ their thyroid hormone dose by 2 extra tabs per week.Women on thyroid hormone replacement or at risk of hypothyroidism should have preconception TSH measurement . so requirements for L-T4 (levothyroxine) may ↑ up to 50% during pregnancy to maintain TSH at around 1-3 mU/L .Postpartum.Manage just as in non-breastfeeding women .Throughout pregnancy.Thyroid binding globulins ↑ during pregnancy. immediately following a positive pregnancy test . don’t fix this if free T4 and free T3 levels are ok! .2. separate by 6 hours BREASTFEEDING .If TSH is not low in 1st trimester.TSH level is low in 1st trimester  normal.Follow with repeat TSH or adjust dose of thyroxine MANAGEMENT . LIOTHYRONINE (Triiodothyronine.Hypothyroidism can cause infertility and miscarriage .Iron ↓ absorption of thyroxine.Further dose adjustment should be based on TSH levels . T3) o T3 is used for short-term management of patients with thyroid cancer undergoing withdrawal of L-T4 o Little to no benefit for coming T3 and L-T4 PREGNANCY . women should check TSH level every 8-6 weeks following dose adjustment .

↓ production of thyroid hormones .Syndrome of excessive thyroid hormone production .Radioactive iodine uptake (RAIU) NonPharm . Methimazole (MMI) a.Treatment is indicated if patient is frail and/or elderly. such as hydrocortisone 100 mg q8h IV. fT3. rash. Radioactive iodine (131I) to destroy thyroid tissue in patients with Grave’s disease. S/E: allergy. or treatment with radioactive iodine c. Also treat with corticosteroids. Main risk is inducing hypothyroidism b. HYPERTHYROIDSIM . Should stop 5 days prior to thyroid scan. CI in pregnancy c.Subclinical hyperthyroidism is common. TSH is suppressed while thyroid hormone levels are normal .Thyroid scan . Rare: hepatoxicity.Large goitre Pharmacologic Choices 1.. followed by 100 ug IV daily.Thyroid surgery in patients with thyroid nodules . RAIU.In subclinical hyperthyroidism. has RF for atrial fibrillation. nephrotoxicity 3. Blocks conversion of T4 to T3 b. can be RF for atrial fibrillation . fT4 . Propylthiouracil (PTU) a. or has Sx of hyperthyroidism Lab Tests . Caution in patients with significant ophthalmopathy. or in patients on corticosteroids 2.TSH. agranulocytosis. toxic autonomous nodules and toxic multinodular goitres a.Myxedema coma is treated with levothyroxine 300-500 ug IV initially. ↓ production of thyroid hormones b.

c. Caution in patients with asthma and obstructive respiratory disorders 5. RAIU. nephrotoxicity e. IV sodium iodide c. Can be used to acutely manage severe hyperthyroidism . If possible avoid PTU in children in favor of methimazole due to concerns about heptatoxicity 4. Beta-adrenergic blockers a. Oral Lugol’s solution b. Blocks thyroid hormone production d. Iodine a. d. S/E: allergy. Used adjunctively in management of Grave’s disease or toxic nodules c. or treatment with radioactive iodine d. PTU may make thyroid resistant to radioactive iodine f. Block symptoms of adrenergic excess b. agranulocytosis. Rare: hepatoxicity. Should stop 5 days prior to thyroid scan. rash. Nonselective agents can ↓ conversion of T4 to T3.