diabetes mellitus dedy

8/9/2019 Diabetes Mellitus Dedy

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Diabetes Mellitus

Barbara S. Hays

Winter, 2006


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Blood Glucose

(normal serum level 65 105 mg)

Inside CNS

Brain uses glucose as primary fuel Brain cannot store/produce glucose

Outside CNS

Fatty acids: stored as Glycogen (liver/muscles)

Triglycerides (fat cells)


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Blood glucose, cont.

Outside CNS, continued

Endocrine portion of pancreas: Islets of

Langerhans

Alpha cells make glucagon

counterregulatory, acts opposite of insulin

Beta cells make insulin

Allows body cells to store and use carbohydrate, fats,and protein


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Hyperglycemia

When blood glucose becomes high

INSULIN allows glucose to enter cells

Liver Production /storage of glycogen

Inhibits glycogen breakdown

Increased protein & fat synthesis (VLDL formation)

Muscles

Promotes protein and glycogen synthesis

Fat cells

Promotes storage of triglycerides


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Hyperglycemia

Drowsy

Flushed Thirsty


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Hypoglycemia

Glucagon: causes release of glucose from

liver

glycogenolysis (breakdown of glycogen toglucose)

glyconeogenesis of glucose not available

Lipolysis (breakdown of fat)

Proteolysis (breakdown of amino acids)


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Hypoglycemia

Weak, sweaty

Confused/irritable/disoriented


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Diabetes Mellitus

(problem with glucose metabolism) Major health problem US/worldwide

Complications [lousy blood vessels]

Blindness Renal failure

Amputations

[heart attacks and strokes]

[OB/neonatal complications]


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Diabetes Mellitus

The good news:

Blood glucose control reduces complicationsof Diabetes!


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Diabetes Mellitus

Absence (or ineffectiveness of ) insulin

Cellular resistance

Cells cant use glucose for energy Starvation mode

Compensatory breakdown of body fat/protein

Ketone bodies from faulty fat breakdown

Metabolic acidosis, compensatory breathing(Kussmals breathing)


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Diabetes Mellitus

HYPERGLYCEMIA: fluid/electrolyte

imbalance.

Polyuria Sodium, chloride, potassium excreted

Polydipsia from dehydration

Polyphagia: cells are starving, so person

feels hungry despite eating huge amounts offood. Starvation state remains until insulin is

available.


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Diabetes Mellitus

Complications of chronic hyperglycemia

Macrovascular complications

Cardiovascular disease (heart attack)

Cerebrovascular disease (strokes)

Microvascular

Blindness (retinal proliferation, macular degeneration)

Amputations

Diabetic neuropathy (diffuse, generalized, or focal)

Erectile dysfunction


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Classifying Diabetes Mellitus

Type I Diabetes: autoimmune

Beta cell destruction in genetically susceptibleperson

Some viral infections


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Classifying Diabetes Mellitus

Type II Diabetes

Reduction in ability of most cells to respond toinsulin

Poor control of liver glucose output

Decreased beta-cell function (eventual failure)


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Diabetes Mellitus

Major risk factors

Family history

Obesity

Origin (Afro-American, Hispanic, NativeAmerican, Asian-American)

Age (older than 45)

History of gestational diabetes

High cholesterol

Hypertension


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Diabetes Mellitus

Prevention of effects: combinationapproach

Increased exercise Decreases need for insulin

Reduce calorie intake Improves insulin sensitivity

Weight reduction Improves insulin action


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Triad of Treatment

Diet

Medication

Oral hypoglycemics

Insulins

Exercise


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Diabetes treatment

Exercise

Under physician supervision Check glucose prior


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Diabetes treatment

Diet

Lower calorie Fewer foods of high glycemic index

Spread meals evenly


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Diabetes treatment

Anti-Diabetic medications

Oral hypoglycemic agents (Easy p 297) Sulfonylureas

Thiazolidinediones Biguanides

Alpha-glucosidase inhibitors

D-phenylalinine derivatives

Combinations

Insulins (Easy Prototype Pro p 393)


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Sulfonylureas

Stimulate pancreas to secrete insulin

Glyburide (Diabeta) [Prototype Pro p 393] Glucotrol (Glipizide)

Diabenese (chlorpropamide)

Adverse reactions

Hypoglycemia

Water retention/edema

Photosensitivity

May need to add insulin in times of stress


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Biguanides

Decreases liver production of glucose

Decreases intestinal absorption of glucose

Improves cell sensitivity to insulin

Example: Metformin

GI upset, flatulence Cardiac (CHF, MI)


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Thiazolidinediones

Increase cellular sensitivity to insulin

Pioglitazone (Actos)

Rosiglitazone (Avandia)

Client should have liver enzymes

checked periodically


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D-Phenylalanine derivatives

Nateglinide (Starlix)

Rapid onset, short half-life

Good for those with rapid post prandial rise in

blood glucose


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Combinations

Glucovance

Glyburide and Metformin

Avandamet

Avandia and Metformin

[come tell me when you run into this

question]


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Insulin

Made in beta cells of the pancreas

Moves glucose into cells (thus acts likegrowth hormone in a way)

Moves potassium into cells (can buy time

in emergencies)


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Insulin preparations (Easy p 390)

given ONLY with syringes marked in units

Rapid acting (lispro,

asparte)

Short acting (regular)

Intermediate acting

(NPH)

Long acting Ultralente

[Glargine/Lantus]


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Your learning

Onset of action

Peak (blood glucose will be lowest then)

Duration


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Rapid acting insulin

Lispro (Humolog, Novolog Aspart)

Onset of action

15-30 minutes [may come on in 5 minutes]

Peak of action

1 - 2 hours

Duration

3 4 hours


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Short acting insulins

Regular (clear so can be given IV)

Onset of action

0.5 to 1 hour

Peak of action

2 4 hours

Duration of action

6 8 hours


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Intermediate acting insulins

NPH, Lente (chemicals added. Cloudy)

Onset of action

1 4 hours

Peak of action

4 12 hours

Duration of action

18 24 hours


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Long acting insulins

Ultralente

Onset of action

4 8 hours

Peak of action

18 hours

Duration of action

24 36 hours


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Once a day insulin

Glargine/Lantus

Cannot be diluted or mixed in syringe with any

other insulin

Slow, steady release

Daily dosing [usually at bedtime]

Refrigerated or tosses every 14 days


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Combination insulins

70/30 (70% NPH and 30% regular)

Humolog 70/30 (Humolog and regular)

Fewer injections

Rotate sites to decrease lipodystrophy


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Miscellaneous

Byetta for type II Diabetics taking

sulfonylureas or combination

Mimics physiologic glucose control

Inhances insulin secretion only in presence of

hyperglycemia

Insulin secretion decreases as blood glucose

approaches normal

Neutontin for Diabetic nerve pain


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Some things to know

Insulin moves potassium into cells

Good for emergency situations Dangerous if potassium level already low


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Some things to know

HHNK (Hyperglycemic HyperosmolarNon-

Ketotic Coma). Also called

HHNK

HNKS [syndrome]

Like dibetic ketoacidosis, without the ketones

Type II diabetic, makes enough insulin to avoid

ketones, but sugar guilds up to dangerous levels -

> cellular dehydration


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Some things to know

Dawn Phenomenon vs Somogis effect

Dawn phenomenon Blood sugar rises in early morning

Somogis (rebound) effect

Blood sugar rise in morning as reaction tohypoglycemic time during the night


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Some things to know

Diabetic foot care

Dry, cracked skin + poor circulation could =loss of a limb

For the most part nurses dont trim nails of

diabetic clients. Refer to Podiatrist.


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Typical diabetic foot ulcer


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diabetes mellitus dedy

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