Diabetes

• unmodified, relatively rapid onset and short
• duration, clear solution. Only form that can be administered IV* Administered
• SC absorption is slightly delayed. Does not need to be refrigerated.

Adm. 30-60 minutes before meals

• rapid acting analog. Effects begin within
• 15-30 minutes of SC inj. Last 3-6 hours.
• Acts faster than Regular insulin.
• Adm. Immediately before eating.
• Use in combination with intermediate or long acting insulin preparations.

• analog of human insulin with a rapid onset (10-20 minutes) and short duration (3-5 hours).
• Inject immediately before meals.
• Can be mixed with other preparations (NPH)

• Prepared by conjugating regular insulin with Protamine (a large molecule).
• The presence of the large molecule retards absorption, resulting in delayed onset of action.

• Produced by complexing reg. insulin with Zinc, which changes the physical state , thereby reducing solubility.
• Less allergenic than NPH

• Modified human insulin with a prolonged duration of action (atleast 24 hours). Indicated for once daily injections SC. Administer at bedtime.
• Slowly absorbed, relatively steady levels over 24 hours.

• Cannot be mixed with other insulins even
• though it is clear !

Sulfonylureas

Meglitinides

Biguanides ( Metformin )

Thiazolidinediones (Glitazones)

Alpha Glucosidase Inhibitors

Promote insulin release

Derived from sulfonamide antibiotics

Maybe used alone or in combination

First & second generation ( 2nd. Generation more potent)

• Tolbutamide
• (Orinase)*

Amaryl(Glimeperide), Diabeta(Glyburide)

• Glucotrol XL(Glipizide)
• Use in patients with Type II DM

Stimulates release of insulin from pancreas

Readily absorbed after oral administration

Peak levels in 3-5 hours

• Hepatic metabolism & renal excretion
• monitor for renal impairment ( Cr.Cl)

Indicated for Type II DM

Stimulate release of insulin from pancreas

Similar mechanism of action like sulfonylureas

Blood levels peak within 1 hour

Side effect is hypoglycemia

• Repaglinide(Prandin), Nateglinide(
• Starlix)

• Metformin (Glucophage) lowers blood glucose 1° by decreasing production of glucose from
• the liver. Suppresses gluconeogenesis. Enhances glucose uptake.
• Does not cause hypoglycemia
• Excreted renally; monitor renal function
• Use alone or in combination
• Side Effects: Decreased appetite, nausea and
• diarrhea, decreased absorption of B12 and folic acid
• Lactic Acidosis
• Metformin and the Biguanides
• inhibit mitochondrial oxidation of lactic acid and can cause lactic acidosis.
• Avoid in patients with liver disease, ETOH XS., heart failure and shock

• Reduce glucose by decreasing insulin
• resistance.
• Glitazones cause volume increase which can lead to heart failure and edema
• Benefits take several weeks to develop
• Mixed effects on plasma lipid levels: raises
• LDL, and HDL, lowers triglycerides

• Act to delay the absorption of CHO
• Use in Type II DM
• Reduces the rise in glucose
• Maybe used in combination with other drugs
• Causes flatulence, cramps and abdominal
• distention, borborygmus
• and diarrhea

• Insulin Replacement ¨Initial IV bolus (.1U/kg BW) followed by continuous infusion at.1U/kg/hr.
• Bicarbonate for Acidosis¨Controversial (pH<6.9-7.1) treat empirically
• Water and Sodium replacement ¨NS or I/2NS 8-10 liters for adults
• Potassium replacement nNormalization of glucose levels

—FPG diagnostic at > 126mg/dl

—2 hour OGTT > 200 mg/dl

—Random glucose ( non-fasting) >200

—Hgb AIC < 7.0%

• —Lispro (Humalog) prior to meals
• —Also consider Glargine (Lantus)with 24hr. coverage

• —Rebound effect in which an overdose of insulin induces
• hypoglycemia, the counterregulatory system will cause an
• increase glucose causing hyperglycemia and in some cases ketosis

• —Treatment typically consists of small protein snacks
• before bedtime

• —Characterized by hyperglycemia on awakening due to Counterregulatory secretion of GH
• & cortisol. Most severe during
• adolescence and young adulthood

—Adjustment in insulin dosing and timing is needed

• —Worldwide, infection
• is the cause of DKA in about 30-50% of cases, with pneumonia, and UTI being the
• most common etiologies

• —Once DKA becomes
• apparent patient will exhibit Kussmaul’s respirations as a result of metabolic acidosis,
• abdominal pain and vomiting

—

• Less common than DKA but more serious is HHS which is a hyperosmolar state 2° to hyperglycemia
• but with little or no ketosis

• —***Insulin therapy to correct hyperglycemia is always
• secondary to aggressive fluid infusion in HHS

• 12-24 hours prior to the development of DKA the patientmay experience progressive weakness, blurred vision, polyuria and polydipsia—
• The patient becomes extremely volume depleted
• —His temperature may range from hypothermic to febrile ifinfection precipitated event.

• Profound deficiency of insulin characterized by
• hyperglycemia (>250 mg/dl), ketosis, acidosis, glucosuria and dehydration

—May have marked left shift if underlying infection

• —Most often seen in TYPE1, may occur in TYPE 2 to a
• lesser degree

—When circulating supply of insulin is not sufficient , glucose cannot be properly used for energy

—Body breaks down fat stores as a 2nd. Source of fuel

—Ketones are acid by-products that build up

—Ketosis alters ph= metabolic acidosis

—Ketonuria occurs along with depletion of electrolytes while attempting maintain electrical neutrality

Restoring perfusion

—Arrest ongoing ketoneogensis

—Correct electrolyte losses

—Avoid hypokalemia

—Avoid hypoglycemia

• Initial goal is to establish fluid & electrolyte
• replacement, improve volume status

• —IV NS (open) titrate for urine output 30-60ml/hr…this
• will correct Na, K, HCO3.

• —Replace 50% of the deficit in first 8 hours and
• remaining deficit within next 16 hours

• —Early K replacement is essential (insulin deficiency may
• cause K to move extracellularly, total body deficit
• of K)

• —Understand that initially K can be alarmingly high but
• will drop with treatment

—IV insulin therapy ( bolus of .1-.15U/kg)

• —Typically seen in
• Type 2 patients, they can make a certain amount of insulin so they ward off
• KETOSIS

• —Have severe
• hyperglycemia

—Osmotic diuresis resulting in osmolarity over 300 mosm/kg

• —Extracellular fluid
• depletion

• —Typically an have
• glucose in XS 900-1000mg/dl. Before manifestations

—Similar to DKA

—Fluid hydration .9% NS (greater than in DKA)

—Regular Insulin IV

—May require some Dextrose to prevent hypoglycemia

—Type II & metabolic syndrome

• —Presence of insulin* increases lipolysis and breakdown of TG
• in adipocytes this results in
• increase in Free Fatty Acids…increase VLDL

• —VLDL leads to increase in LDL and circulating
• cholesterol

—Treatment option for patients with type 1 DM

—K-P performed together in most instances

—Rare to perform only pancreas txpl.

—Only partially successful in reversing long term microangiopathies and neuropathies.

• —Pancreatic Islet transplant another potential treatment
• measure

Produced by the alpha cells

• ¨Increase plasma glucose
• levels and relaxes smooth muscle
• of the GI tract

• ¨Glucagon causes glucose levels to
• rise

• ¨For sever hypoglycemia IV glucose
• is preferred

¨May be administered parenterally IV, IM, SC (0.5-1mg)

¨insulin

¨sulfonamides

¨aminoglycosides

¨penicillin

• suppression of hepatic glucose
• production

lowering of triglyceride levels

enhanced insulin sensitivity

all of the above

¨Hypoglycemia

¨GI distress

¨lactic acidosis

¨diarrhea

¨sensitizing insulin receptors

• ¨decreasing carbohydrate
• absorption

¨increasing insulin secretion

• ¨decreasing hepatic glucose
• production

n

¨enhancing insulin production

¨sensitizing insulin receptors

• ¨decreasing hepatic glucose
• production

¨inhibiting CHO absorption