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IC 1.0 > Treating Diabetes > Flashcards

Treating Diabetes Flashcards

1
Q

What pathogenic changes are associated with type 1, 2, 3, and 4 diabetes?

A
  • type I: autoimmune destruction of beta-islet cells
  • type II: desensitized beta-islet cells or insulin-resistant peripheral tissues
  • type III: non-pancreatic causes
  • type IV: gestational diabetes
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2
Q

What are the treatment goals of diabetes?

A

treat the hyperglycemia to avoid long-term complications

  • fasting glucose< 120
  • 2-hour postprandial glucose < 150
  • A1c < 7
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3
Q

Generally speaking, what group of drugs are used to treat type 1 diabetics?

A

insulin alone

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4
Q

Describe insulin levels in those with type 2 diabetes.

A
  • initially insulin levels rise as the pancreas attempts to compensate for the insensitivity of peripheral tissues
  • eventually, the pancreas “burns out” and patients become insulin deficienct
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5
Q

Describe endogenous insulin production.

A
  • preporinsulin is produced
  • the signal sequence is cleaved, leaving proinsulin
  • C peptide is cleaved form the protein, leaving an alpha and beta chain linked by disulfide bonds
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6
Q

Describe the mechanism by which beta-islet cells sense glucose levels and respond by release insulin.

A
  • glucose is taken up via GLUT2, a low affinity transporter
  • glycolysis generates ATP
  • ATP closes a potassium channel in the surface, depolarizing the cell
  • the resulting calcium influx tiggers exocytosis of insulin
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7
Q

What intracellular change in beta-islet cells drives insulin release?

A

a growing ATP/ADP ratio, which signals the availability of energy, which closes potassium channels and depolarizes beta cells

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8
Q

How does insulin act on peripheral tissues?

A
  • it stimulates a tyrosine kinase receptor

- the resulting cascade induces expression of GLUT4 on the cell surface

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9
Q

What is the net effect of insulin?

A

stimulate uptake of blood glucose by cells for use and storage

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10
Q

Insulin is used in the treatment of which kinds of diabetics?

A
  • it is the only therapy for type 1
  • it is used in type 2, especially in the later stages when they become insulin deficient
  • also used post-pancreatectomy and in gestational diabetes
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11
Q

How do we classify our insulin therapies?

A

based on their duration of action

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12
Q

How are insulins administered at home? Why?

A

subcutaneous injection avoids a quick rise or fall in response to digestive nutrients

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13
Q

Insulin regimens are tailored to what aspects of a patient?

A
  • activity
  • diet
  • endogenous insulin levels and responsiveness
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14
Q

What is the primary adverse effect of insulin? What are other common side effects?

A
  • hypoglycemia is the primary concern

- allergy, lipoatrophy, weight gain, and insulin edema are all possible

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15
Q

Create a drug list

A

week 2, friday at 11

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16
Q

Which sorts of insulins are typically prescribed to diabetics and what are typical dosing programs?

A
  • start with a basal, low level insulin

- add a short-acting insulin to be administered just before eating if basal insulin isn’t sufficient

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17
Q

List the rapid-acting insulins.

A
  • Lispro
  • Aspart
  • Glulisine
18
Q

List the short-acting insulins.

A
  • Regular Novolin

- Regular Humulin

19
Q

List the intermediate-acting insulins.

A
  • NPH Humulin

- NPH Novolin

20
Q

List the long-acting insulins.

A
  • Detemir

- Glargine

21
Q

What are NPH insulins?

A

intermediate-acting insulins: those attached to NPH, a slowly dissolving crystal component

22
Q

Regular insulins act for what period of time?

A

peak between 2-4 hours after administration with continued effects for roughly 8-12 hours

23
Q

How long are deter and glargine active for?

A

nearly 24 hours

24
Q

How is diabetic ketoacidosis treated?

A
  • IV infusion of regular insulin at a low rate
  • possible addition of glucose to prevent hypoglycemia
  • fluid and electrolyte replacement
25
Q

Why does diabetic ketoacidosis cause fluid and electrolyte imbalances?

A
  • hyperglycemia exceeds the capacity for reabsorption of the PCT
  • excess glucose in the tubules pulls water out, leading to a diuresis
  • additionally, glucose and acidosis shift potassium out of cells and into the extracellular space
  • total potassium decreases as it is lost through the kidneys, despite a hyperkalemia
26
Q

Sulfonylureas

A
  • a group of insulin secretagogues
  • they bind to and activate SUR1, a subunit of the K/ATP channel, which depolarizes the cell to promote insulin release
  • also function by decreasing hepatic clearance of insulin and inhibit glucagon release by stimulating somatostatin release
  • second generation drugs have higher affinity for SUR1 and greater activity but carry a greater risk for hypoglycemia as a result
  • used in type 2 diabetics
  • oral formulations, circulates bound to albumin, metabolized in the liver, and excreted in the urine
  • adverse effects include hypoglycemia, weight gain, and allergic reaction (sulfa drug)
  • contraindicated in type 1 diabetics, pregnancy, breast-feeding mothers, and those with hepatic or renal insufficiency as poor clearance increases risk for hypoglycemia
27
Q

Why might you use a first generation sulfonylurea rather than a second?

A

because the first generation have lower activity and therefore pose less risk for hypoglycemia

28
Q

Meglitinides

A
  • a group of insulin secretagogues
  • similar to sulfonylureas except they aren’t sulfa drugs (avoid allergy) and bind a different site to activate the K/ATP channel
  • nateglinide has a more rapid onset than repaglinide
  • major adverse effect is hypoglycemia
  • cleared by the liver and contraindicated in those with hepatic insufficiency
29
Q

How does nateglinide compare to repaglinide?

A

nateglinide has a more rapid onset than repaglinide

30
Q

Metformin

A
  • a biguanide and first line therapy for type 2 DM
  • primary mechanism of action is by reducing hepatic gluconeogenesis, but it also increases insulin sensitivity
  • this is a euglycemic effect meaning that it helps maintain normal blood glucose levels without producing hypoglycemia
  • has the added effect of reducing plasma triglycerides
  • lactic acidosis is a rare, but life-threatening dose-related complication most often seen in those with renal insufficiency
  • GI side effects are common and may result in reduced B12 absorption
  • does not produce weight gain or hypoglycemia and is not a sulfa drug
  • taken with or after food and has a half life of 1.5-3 hours, not metabolized, excreted by the kidney
31
Q

Describe Metformin Lactic Acidosis

A
  • a metformin toxicity
  • by blocking gluconeogenesis, it may impair hepatic metabolism of lactic acid
  • this is more common in those with renal insufficiency and is dose-related
32
Q

Thiazolidinediones (TZDs)

A
  • a group of insulin sensitizers
  • they are PPARy agonists with some PPARa agonist activity (rosiglitazone has more PPARy affinity than pioglitazone)
  • in adipose tissue, PPARy promotes the transport of serum lipids to adipose tissue; in other tissues it promotes insulin sensitivity
  • as a result, there is less hepatic gluconeogensis and an enhanced uptake of glucose by skeletal muscles
  • they effectively reduce glucose and triglyceride levels
  • declining use because of significant weight gain, frequent hepatotoxicity, and congestive heart failure
33
Q

alpha-Glucosidase Inhibitors

A
  • a group of drugs that inhibit intestinal glucose absorption
  • they inhibit pancreatic amylase and intestinal glucosidase enzymes, thereby increasing the time required to absorb complex carbs and reduce post-prandial glucose peaks
  • unpopular today because there effects have been exceeded by newer drugs, but occasionally used in combination with other drugs
  • pose no risk for hypoglycemia, but increased glucose is deliver to gut bacteria and so flatulence, bloating, and diarrhea are common
  • not recommended for those with IBD or individuals who spend lots of time in closed spaces
34
Q

Incretins

A
  • GLP1/GIP analogs and inhibitors of dipeptidyl peptidase-4 (enzyme that degrades them)
  • they increase insulin release, decrease glucagon section, delay gastric emptying, and central suppression of appetite
  • effective in the treatment of diabetes and have the added benefit of weight loss
  • pose very little risk for hypoglycemia and GI upset is rare
  • no benefit from using a GLP analog with a DDP-4 inhibitor
35
Q

What is dipeptidyl peptidase-4?

A

an enzyme that degrades the incretins (GLP-1 and GIP) and are thus a target for diabetes therapy

36
Q

What are the physiologic roles of incretins?

A
  • they increase insulin release and suppress glucagon release
  • they slow gastric emptying
  • they act on the hypothalamus to suppress appetite
37
Q

Where are the incretins produced? What mediates their release?

A
  • they are produce by enteroendocrine L cells in the ileum

- they are released in response to nutrients entering the gut

38
Q

SGLT2 Inhibitors

A
  • a group of drugs that inhibit reabsorption of glucose from the proximal renal tubules
  • effective at controlling type 2 DM and promotes weight loss
  • major side effects include genital/urinary tract infections due to glycosuria and osmotic diuresis leading to hypotension
  • not effective in those with chronic kidney disease
39
Q

What are considered first line mono therapies for the treatment of type 2 diabetes?

A
  • metformin
  • incretins
  • SGLT-2 inhibitors
40
Q

Pramlintide

A
  • an amylin analog
  • serves to blunt glucagon secretion, delay gastric emptying, and decrease appetite (much like the incretins)
  • preprandial use as an adjunct to inulin improves glucose control in type 1 and 2 DM
  • however, poses a risk for hypoglycemia and GI symptoms, so incretins are preferred
  • metabolized and excreted by the kidneys
41
Q

Covesevalam

A
  • a bile acid sequestrate and cholesterol-lowering drug used for glucose control in type 2 DM
  • mechanism not fully known
  • can exacerbate hypertriglyceridemia
  • efficacy is modest and use questionable
42
Q

Bromocriptine

A
  • a dopamine agonist that lowers glucose levels through an unknown mechanism
  • adverse effects include nausea, fatigue, dizziness, vomiting, and headache
  • efficacy is modest and use is questionable

IC 1.0 (24 decks)

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