Insulins

Main cause of diabetes

Dysfunction of the pancreas or burn out

Autoimmune disease that destroys pancreatic beta cells → little to no insulin produced; patient requires exogenous insulin; diagnosed in childhood (makes up 10% of cases)

T1DM

A combination of hyperglycemia and insulin resistance/lack of sensitivity. Pancreas “burns out” over time as insulin resistance develops

• Patient’s caloric intake raises so much that body makes more insulin, and body become less responsive to insulin

• Is also a supply & demand issue where body’s demand for insulin is high and supply can’t keep up; patient has chronic state of pumping out insulin which burns out pancreas

• Makes up 90% of cases

T2DM

Pancreatic cells that produce and secrete insulin (lower BG)

Beta cells

Pancreatic cells that produce and secrete glucagon (raise BG)

Alpha cells

Pancreatic cells that produce and secrete somatostatin

S cells

Why does pancreas become dysfunctional in type 2 diabetes?

• Patient’s caloric intake raises so much that body makes more insulin, and body become less responsive to insulin

• Is also a supply & demand issue where body’s demand for insulin is high and supply can’t keep up; patient has chronic state of pumping out insulin which burns out pancreas/pancreas can’t keep up with high caloric intake

• Patient develops insulin resistance

Insulin that your body (pancreatic beta cells) produces

Endogenous insulin

Insulin that is given as a medication

Exogenous insulin

Background insulin; insulin that remains in bloodstream and controls glycemic index throughout the day. DOES NOT account for glycemic spikes

• prolonged duration; do not peak

Basal insulin

Type of insulin that is first line INSULIN for controlling hyperglycemia; has prolonged duration but does not peak; counteracts hormonal fluctuations (e.g. cortisol)

Basal insulin

A dose to control BG after consuming meals (post prandial); controls glycemic spikes; used in combination with basal insulin (that acts throughout the day)

• Is fast acting

• Can cause hypoglycemia more commonly

Bolus insulin (rapid/short-acting)

Bolus vs basal insulin

Bolus insulin → control BG after meals (glycemic spikes)

• Can cause hypoglycemia more commonly; is faster acting

Basal insulin → control BG throughout the day

Insulin that has

• O: 15 min or less

• P: peaks at 30-90 min OR (1-2 hrs)

• D: is 3-5 hrs

Rapid-acting insulin

Insulin that has

• O: 30 min – 1 hr

• P: peaks at 2-3 hrs OR 1.5 hrs

• D: is 5-7 hrs

Regular/short-acting insulin

Insulin that has

• O: 1-2 hrs

• P: peaks at 8-12 hrs

• D: is 18-24 (take half a day; take twice a day)

Intermediate-acting insulin (NPH)

Insulin that has

• O: 1-2 hrs

• P: does not peak

• D: duration stays in background for 18-24 (some formulations can last longer; lasts all day)

Long-acting insulin (AKA basal insulin)

Examples of bolus dose insulin

Rapid-acting or regular/short-acting insulin

Why give rapid-acting or short-acting (regular) bolus insulin before meals?

Patient will be hypoglycemic if they don’t eat (e.g. BG 180). Check BG an hour before and after administration (for regular insulin, check 2 hrs after)

When does cortisol peak?

When patient wakes up in the morning (6 AM) → High BG

Insulin indication 

• Diabetes → All of type 1; only some of type 2 (depends on genetic, caloric intake; when beta cells no longer produce endogenous insulin)

• ESRD (management of acute hyperkalemia) + given with dextrose

• As an antidote (CCBs + BBs)

All type 1 and type 2 diabetic patients need insulin. True or false?

False

Lab test used to diagnose someone with diabetes; is average glucose for the past 2-3 months

Hgb A1C

Hgb A1C is 5.7-6.4% =

Pre-diabetes stage; less than 5.7% = normal

Hgb A1C ≥ 6.5%

Formally diagnosed diabetes; beta cell function is diminished

First line treatment for diabetes

Lifestyle modifications (diet, exercise)

What does hyperglycemia do to the body?

High glucose in bloodstream cause blood to become sluggish/viscous → cause retinopathy, nephropathy, neuropathy, cardiovascular risk

Insulin ROA

Typically SubQ injection; Afrezza is inhaled; type 1 diabetics may have a pump

The only insulin that can be given IV

Regular (short-acting) insulin

SE of insulin

• Hypoglycemia (most common/dangerous SE)

• Assess for hypoglycemia depending on insulin type

S&S of hypoglycemia

• Sweating

• Pallor

• Hunger

• Irritability

• Lack of coordination

• Sleepiness

SPHILS (S&S of hyperglycemia

S – Sweating

P – Pallor

H – Hunger

I – Irritability/aggressive

L – Lack of coordination

S – Sleepiness

Interventions for hypoglycemia

• Awake AAOx4 (responsive) patient → 15-15 rule

• Unresponsive patient → if IV access present, give 25g D50 IV push; no IV → IM glucagon (patient may develop anxiousness, tachycardia, NV)

15-15 rule

• For hypoglycemic awake AAOx4 patients and can tolerate PO

• Give 15 g rapidly absorbed carb (e.g. juice, tsp of sugar, glucose products) → check BG in 15 mins

• Repeat until BG WNL

Interventions to treat a hypoglycemic patient that is unresponsive, AMS, airway not protected, can’t swallow

• If IV access → administer a 25-50% glucose solution such as 25g D50 IV push (could develop hyperglycemia)

• If no IV → IM 0.5 OR 1 mg glucagon (patient may develop anxiousness, tachycardia, NV)

• FREQUENT monitoring

Diabetes is a major, if not the major cause of

• Acquired vision loss

• Kidney failure

• Non-traumatic lower extremity amputation

S&S of hyperglycemia (diabetes)

• Common symptoms: polyuria, polydipsia, polyphagia, neurological symptoms 

• T1DM: DKA → diabetic ketoacidosis; acetone → fruity body odor

• T2DM: Hyperosmolar hyperglycemic non-ketotic syndrome (HHNK) → no acetone, no fruity body odor

Autoimmune diabetes; patient is young; moderate genetic disposition, no insulin = ketosis, usually not obese. Needs insulin to live

T1DM

T2DM has a

Strong genetic disposition, patient is usually obese

No oral drugs are currently approved to treat T1DM. True or false?

True

Diabetes insipidus is a type of DM. True or false?

False

Hormonally active, may increase insulin resistance

Fat cells

Carry nutrients, contain potassium

RBCs

Criteria for diabetes

• Hgb A1c ≥ 6.5%

• Fasting glucose (nothing eat/drink for 8 hrs) > 126

• OGTT (2hr after administering sugary drink) > 200 mg/dL

A1C values

• Normal < 5.7% 

• Prediabetes ≥ 5.7-6.4%

• Diabetes ≥ 6.5%

FBG values

Taken 8 hrs after no meals/drinks

• Normal < 100 mg/dL

• Prediabetes ≥ 100 mg/dL

• Diabetes ≥ 126 mg/dL

OGTT values

• Normal < 140 mg/dL

• Prediabetes ≥ 140 mg/dL

• Diabetes ≥ 200 mg/dL

Insulin therapy is always needed in T1DM (AKA IDDM). True or false?

True

Insulin therapy is sometimes, or eventually needed in NIDDM or T2DM 

Up to 1/3 of the time

Name the rapid-acting insulins

• AKA the “logs”

• Lispro (HumaLOG)

• Aspart (NovoLOG)

• Glulisine (Apridra) 

LAG (rapid-acting insulins)

L – Lispro (HumaLOG)

A – Aspart (NovoLOG)

G – Glulisine (Apridra)

Rapid-acting insulin indication

For post-prandial hyperglycemia (mimic bolus insulin dose)

The only insulin appropriate for acute management of

• DKA

• HHS (Hyperosmolar Hyperglycemic State; leads to dehydration)

• Acute hyperkalemia

IV regular insulin (short-acting insulin)

Short-acting insulin indication

• Only insulin for acute management of DKA, HHS, acute hyperkalemia (IV form)

• Only insulin that can be given IV

Name the intermediate acting insulins

NPH, (Humulin N, Novolin N)

Intermediate acting insulins is cloudy, this is abnormal. True or false?

False

Insulins that mimic bolus insulins

Rapid-acting & short-acting (regular) insulin; negate post-prandial BG spike

Insulins that provide basal dosing

Intermediate and long-acting insulins

Long-acting insulin has a peak. True or false?

False

Hypoglycemia is defined as BG < ______ mg/dL

70

• Can occur with rapid correction of BG by antidiabetics/insulin

• Patient may have AMS (confused, agitated)

• Can be life-threatening → prompt recognition and treatment

Hypoglycemia

Hallmarks of T2DM

• 3 Ps; Polyuria, polydipsia, polyphagia,

• Blurred vision (retinopathy), neurological symptoms 

How to mix intermediate insulin (NPH) and and regular insulin

(CLEAR BEFORE CLOUDY) or RN

1. Clean both vials

2. Inject air into cloudy (NPH)

3. Inject air into regular 

4. Withdraw regular

5. Withdraw NPH

Give patient insulin at night, patient experiences S&S of hypoglycemia (jittery, nauseous, irritable) during the night. Patient experiences rebound effect during the morning and experiences massive hyperglycemia. 2 am or 3am; nurse should check BG. If it’s very low, and then high in morning = Somogyi effect → treat by giving patient a snack such as crackers just before patient sleeps

Somogyi effect

Patient gets insulin at night, but patient gets rebound hyperglycemia during the morning. Patient does not have an episode of hypoglycemia during the night.

Dawn phenomenon

S&S of hypoglycemia

• Sweating

• Hungry

• Lethargic

• Irritable/AMS

• Pallor

• Sleepy

SHLIPS (S&S of hypoglycemia)

S – Sleepy

H – Hungry

L – Lethargic

I – Irritable/AMS

P – Pallor

S – Sweating

What insulins can be mixed?

• Rapid or regular can be mixed with intermediate

• Rapid/regular mix doesn’t make sense → both are bolus

• DO NOT mix long-acting → give alone

NPH (intermediate-acting insulin) considerations

Ideally taken BID. If patient needs 10 units, give ⅔ dose in the morning, and ⅓ in the evening

• Only insulin that’s normally cloudy

• Can be mixed with regular or rapid insulin

Cloudy regular insulin = 

Expired/spoiled → replace

RN =

Regular before Intermediated (clear before cloudy when mixing)

Brand name and drug class for metformin

Glucophage; biguanide

Diagnosing diabetes

1. FBG > 126 mg/dL

2. OGTT > 200 mg/dL (after 2 hrs)

3. Hgb A1C > 6.5%

4. Random glucose ≥ 200 mL/dL

T1DM vs T2DM presentation

• T1DM = Usually thinner, younger

• T2DM = Obese, acanthosis nigricans, ↑ triglycerides

A cluster of findings that increase r/o

• T2DM

• CVD

• Stroke

Metabolic Syndrome

Diagnostic criteria for metabolic syndrome

• Abdominal obesity

• Increased triglycerides

• Decreased HDL

• HTN

• Elevated FBG

Treatment of DKA

1. Replace fluids/fluid resuscitation FIRST

2. IV regular insulin 0.1 units/kg/hr

3. Replace K+ (insulin pulls glucose AND potassium with it)

Treatment of HHS

• 6+ liters of 0.9% NS (treat profound dehydration)

• IV regular insulin

Name the long-acting insulins

• Glargine (Lantus/SoloStar)

• Detemir (Levemir)

• Degludec (Tresiba)

• Semglee (Glargine)

• Basaglar (Glargine)

Long-acting insulin that lasts ultra-long

Degludec (Tresiba) 

When to take intermediate-acting insulin doses?

BID

• 2/3 dose in the morning

• 1/3 at night

• Complication of T1DM

• Breakdown of fats/muscles to use as fuel (bc absence of insulin)

  • Acetone

  • B-hydroxybutyrate

• Metabolic acidosis

• Hyperglycemia

• Abd pain (unique to DKA)

• Dehydration/diuresis

DKA

• Complication of T2DM

• Still have some insulin

  • Have just enough insulin to stay out of DKA

  • Blood sugar creeps up (slow onset)

• No ketones

• Glucose > 500, 600, 700

• More profound dehydration

• Neurological manifestations (unique to HHS)

HHS

Name the short-acting (regular) insulins

End in R: Humulin R & Novolin R

Nursing considerations for rapid-acting insulin

• Meal must be IN SIGHT

• Food must be at bedside

• Highest r/o hypoglycemia

Regular insulin ROA

SubQ, IM, IV