Drugs for both Thyroid disorders and Diabetes

Excessive thyroid hormone; faster metabolic processes (tachycardia, heat intolerance, nervousness, tremors, body wasting, etc). Defined by low TSH.

What characterizes hyperthyroidism?

Inadequate thyroid hormone; slower metabolic processes (bradycardia, cold intolerance, weight gain, fatigue, mental impairment). Defined by high TSH.

What characterizes hypothyroidism?

Hypothalamus releases thyroid releasing hormone (TRH) which tells the anterior pituitary to release Thyroid Stimulating Hormone (TSH) mediated by cAMP.

What is the process of thyroid activation?

Giving patients thyroid hormone in the form of T3 (liothyronine), T4 (levothyroxine), a mix (liotrix) or iodine to make thyroid hormone with (iodide or potassium iodide). T4 is better tolerated, and has a better half life.

How is hypothyroidism (bascially) treated?

Mimic hyperthyroidism at toxic levels. Drugs that increase P-450 activity reduce drug effectiveness.

Adverse reactions to hypothyroidism medication—

Autoimmune disorders; Graves disease causes hyperthyroidism.

What typically causes hyper/hypothyroidism?

Inhibiting oxidation of iodine, and the coupling of iodotyrosines into T3/T4.

How do thioamides function to shut down T3/T4 synthesis? (Methimazole and Propylthiouracil (PTU) )

Methimazole has a longer half life and lower adverse effects, but it IS tetragenic. Both are hepatotoxic.

Why do we prefer methimazole over PTU?

Remove/destroy the thyroid gland (radioactive iodine)

Inhibiting hormone synthesis

Blocking hormone release

What are the options for treating hyperthyroidism?

With iodide, but it’s short term, orally or parentally. Used prior to surgery.

How do we block thyroid hormone release?

Beta cells in the pancreas are destroyed, leading to no insulin production and increased blood glucose levels.

What is diabetes type 1?

Insulin resistance or defective beta cells in the pancreas leads to higher blood glucose levels.

What is diabetes type 2?

Increased thirst (polydipsia), increased hunger (polyphagia), increases urination (polyuria), and weight loss.

Common type 1/2 diabetes symptoms?

Metformin administration and lifestyle changes

What’s the first 2 actions for type 2 diabetes treatment?

Beta cells monitor glucose blood levels. As those levels increase, glucose transporters take in glucose and phosphorylate, triggering insulin secretion.

How is insulin secreted from beta cells?

Hypoglycemia, weight gain, lipodystrophy

Adverse reactions to insulin therapy?

Rapid, short, intermediate and long acting preparations.

What are the 4 preparations for insulin therapy?

Regular (always intravenous)

Lispro

Aspart

Glulisine

What are the 5 rapid acting insulin preparations?

Neutral protamine Hagedorn; releases insulin slowly for a basal level of insulin.

What is the intermediate acting insulin preparation?

Glargine (releases slowly from a depot at inject site)

Detemir (binds to albumin for reservoir, long release)

Degludec (like glargine, but the depot is a multihexamer)

What are the long acting insulin preparations?

Intermediate and long release preparations

What preparations are NEVER administered via IV?

Standard is 1-2 injections a day.

Intensive is 3-5 injections a day. Hypoglycemia risk, but lower complications.

Standard vs intensive insulin treatment?

Delays gastric emptying time, decreases glucagon secretion, and improves satiety (fullness). Injected right before meals and with less insulin than usual.

How does pramlintide (Amylin analog, usually released with insulin) help with diabetes?

Oral glucose increases insulin more than IV glucose (the incretin effect). Incretin Mimetics mimic that effect, increasing glucose dependent insulin secretion in type 2 diabetics, and behave like amylin.

How do Incretin Mimetics (GLP-1 agonists, injected) help with diabetes?

They all end in “-tide”

What’s an easy way to tell whether a drug is a incretin mimetic?

Adverse incretin mimetic effects?

How do oral antidiabetic agents help with diabetes?

Reduces hepatic gluconeogenesis, reduces glucose absorption, and improves peripheral glucose uptake/sensitvity.

How does metformin (biguanide) help with diabetes?

Diarrhea, nausea and vomiting. Weight loss from lack of appetite. Contraindicated with severe renal disfunction

Metformin adverse reactions?

Blocking potassium channels in beta cells to promote insulin release. Work for 12-24 hours. May cause hypoglycemia, hyperinsulinemia and weight gain. Contraindicated with hepatic/renal insufficiency, and drug interactions.

How do sulfonylureas help with diabetes?

Mimic sulfonylureas (and so CANNOT be used together); they work faster and for a shorter period of time. Best for mealtimes.

How do meglitinides help with diabetes?

They all end in “-linide”

How can you tell a drug is a meglitinide?

Target PPAR receptors to make tissues in the body more sensitive to insulin. Cause fluid retention, osteopenia, MI’s, and angina.

How do thiazolidinediones (TZD’s) help with diabetes?

There are 2 of them, and both end in “-litazone”

How can you tell a drug is a TZD?

Preserve the incretin hormones that are normally released with insulin, promoting insulin secretion. Specifically might cause pancreatitis. CANNOT be combined with GLP-1 agonists.

How do dipeptidyl peptidase-4 (DPP-4) inhibitors help with diabetes?

There are 4 of them, and they all end in “-glyptin”

How can you tell a DPP-4 inhibitor?

Decrease glucose reabsorption in the kidney’s, meaning more glucose is excreted in the urine. Causes hypotension and UTI’s.

How do sodium-glucose cotransporter 2 inhibitors help with diabetes?

There are 4 of them, and they all end in “-gliflozin”

How can you tell a drug is a SGLT2 inhibitor?

Delay the digestion of carbohydrates, lowering postprandial glucose levels. May cause flatulence, diarrhea and abdominal cramping.

How do alpha-glucosidase inhibitors help with diabetes?