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1

insulin

is secreted by beta cells, which are one of four types of cells in the islets of Langerhans in the pancreas. Insulin is an anabolic or storage, hormone. When we eat, insulin secretion increases and moves glucose from the blood into the muscle, liver, and fat cells

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insulin does

1. Transports and metabolizes glucose for energy
2. Stimulates storage of glucose in the liver and muscle (in the form of glycogen)
3. Accelerates transport of amino acids ( derived dietary protein) into cells
4. Insulin inhibits the breakdown of stored glucose, protein, and fat.

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during fasting, the pancreas

continuously releases a small amount of insulin (basal insulin). Yet another pancreatic hormone glucagon by the alpha cells of the islets of Langerhans is released when glucose levels are decreased and stimulate the liver to release stored glucose. The insulin and the glucagon together maintain a constant level of glucose in the blood by stimulating the release of glucose from the liver.

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Glycogenolysis is

The liver produces glucose through the breakdown of glycogen

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Gluconeogensis

after 8-12 hours without food*, the liver forms glucose from the breakdown of noncarbohydrate substances, including amino acids

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Type I

characterized by destruction of the pancreatic beta-cell destruction. Thought to be an autoimmune disease causing the destruction of Beta Cells resulting in decreased insulin production, unchecked glucose production by the liver, and fasting hyperglycemia. Also, glucose from food cannot be stored in the liver but instead remains in the blood stream. WHY>>> contributes to postprandial (after meals) hyperglycemia
(body does not produce insulin)

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When glucose level exceed renal threshold (usually 180 to 200 mg/dL) osmotic diuresis occurs and can result in

glycosuria (glucose in the urine because the kidneys may not reabsorb all of the filtered glucose)

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What is osmotic diuresis –

when excess glucose is excreted in the urine, it is accompanied by excessive loss of fluids and electrolytes

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Because insulin normally inhibits glycogenolysis

(breakdown of stored glucose) and gluconeogenesis (production of new glucose from amino acids and other substrates), these processes occur in an unrestricted fashion resulting is further hyperglycemia.

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ketones

the byproducts of fat breakdown

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ketone bodies are acids that disturb the acid-base balance of the body when they accumulate in excessive amounts.

The resulting diabetic ketoacidosis (DKA) may cause signs and symptoms such as abdominal pain, nausea, vomiting, hyperventilation (kusmaus resp), a fruity breathe odor, and if, left untreated, altered level of consciousness, coma, and death, Initiation of insulin treatment, along with fluid and electrolytes as needed is essential to treat hyperglycemia and DKA and rapidly improves the metabolic abnormalities. **

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Type II

1. Insulin resistance – refers to a decreased tissue sensitivity to insulin. Normally, insulin binds to special receptors on cell surfaces and initiates a series of reactions involved in glucose metabolism.
2. Impaired Insulin secretion- Book does not provide a lot of detail but answer the following…. (so body does not respond to insulin or not enough insulin)

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Metabolic syndrome is what?

To overcome insulin resistance and to prevent the buildup of glucose in the blood, increased amounts of insulin must be secreted to maintain the glucose level. Includes hypertension, hypercholesterolemia, and abdominal obesity. However, if the beta cells cannot keep up with the increased demand for insulin, the glucose level rises and type 2 diabetes develops

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Why no ketones in type II*

still enough insulin produced to break down fats

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main difference between type I and II*

ketones

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“three Ps”

polyuria (increased urination), polydispia (increased thirst), and polyphagia (increased appetite)
polyuria and polydispia occur as a result of the excess loss of fluid associated with osmotic diuresis. Patients also experience plyphagia that results from the carabolic state induced by insulin deficiency and the breakdown of proteins and fats. Poor wound healing, vaginal infections, yeast infections, blurred vision

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symptoms type II

Fatigue, Irritability, polyuria, polydipsia, polyphagia, poor healing, vaginal infections, blurred vision
other symptoms: fatigue and weakness, sudden vision changes, tingling or numbness in hands or feet, dry skin, skin lesions or wounds that are slow to heal, and recurrent infections

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What is important with type II

Pt education is very important with type II

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Assessment tests

FPG- Fasting plasma glucose- blood glucose determination obtained in the lab after fasting for more than 8 hours
Random Glucose-
2 hours Postload- glucose level 2 hours after receiving glucose
hemoglobin A1c – less than 7
UA – if ketones in urine, albumin, infection
EKG
Cholesterol -

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risk factors:

Family history, age, elevated tri, high cholesterol, and obesity

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important assessment things

Look for skin breakdown (esp feet) (peripheral neurophy)
eye assessment – specs/floaters – caused by hemmoraging, damange to retina/ blood supply to retina (retnophy)
renal failure – nephropy – deteration of renal tubules, albumin leaking into the urine

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Rapid acting agents

lispro (humalog), aspart (novalog), glulisine (apidra)

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rapid acting indications

used for rapid reduction of glucose level, to treat postprandial hyperglycemia, and/or to prevent noctural hypoglycemia

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Lispro (humalog)

onset (10-15 min) peak (1 hour) duration (2-4 hours)

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Aspart (Novalog)

onset (5-15 min) peak (40-50 min) duration (2-4 hr)

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Glulisine (Apidra)

onset (5-15 min) peak (30-60 min) duration (2hr)

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short acting agents

Regular (humalog R, novolin R, iletin II regular

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short acting onset peak duration

onset (1/2-1 hr) peak (2-3 hr) duration (4-6 hr)

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short acting indications

usually admin 20-30 min before a meal, may be taken alone or in combo with larger acting insulin

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intermediate acting agents

NPH, (Humulin N, iletin II lente, Iletin II NPH, Novolin L, Novolin N)

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NPH

onset (2-4 hr) peak (4-12hr) duration(16-20hr)

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Humalin N

onset (3-4 hr) peak (4-12 hr) duration (16-20hr)

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intermediate acting indications

usually taken after food

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very long acting agents

glarine (lantus), detemir (levemir)

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long acting onset peak duration

onset (1h) peak (continuous no peak) duration (24 hr)

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long acting indications

used for basal dose

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insulin pumps

usually given to type I
know home regiment
Insulin Pumps- Continuous SubQ insulin infusion involves an external device
What is basal rate – 0.5-2.0 units/h
Bolus dose- carb exchange? 1 unit of every 15 carbohydrates would require 3 units for a meal with 45 g of carbohydrates
Make sure change site so no scar tissue

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insulin pump disadvantages

unexpected disruptions in the flow of insulin from the pump that may occur if the tubing or needle becomes occluded, if supply of insulin runs out, or if the battery is depleted, increasing the risk of DKA; potentional for infection at needle insertion sites, hypocemia, occlusion
Most Common Risk factors: ketoacidosis
Do not abruptly stop infusion pump

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Sulfonlyureas Nursing Implications-

• Monitor pt for hypoglycemia
• Monitor blood glucose and urine ketone levels to assess effectiveness of therapy
• Pts at high risk for hypoglycemia: advanced age, renal insufficiency
• When taken with beta-adrenergic blocking agents may mask usual warning sings and symptoms of hypoglycemia
• Check renal function*

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Glucophage Nursing Implications-

• Monitor for lactic acidosis and hypoglycemia
• Monitor renal function
• Pts taking metformin are at increased risk of acute renal failure and lactic acidosis with use of iodinated contrast material for diagnostic studies; metformin should be stopped 48h prior to and for 48h after use of contrast agent or until renal function is evaluated and normal – risk for lactic acidosis**

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in general oral medications

monitor glucose levels, liver and renal function. Maintain diet and exercise program. Teach S&S of hypoglycemia.
Acute issues- covered in advanced nursing (DKA with type 1, HHNS with type 2)

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long term complications

Macrovascular Complications- results in the changes in the medium to the large blood vessels. Blood vessel walls thicken, sclerose, and become occuled by plque that adheres to the vessel walls-blocking flow. Resulting in CAD, PVD, CVD (3 main types)

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diabetic retinopathy

is caused by changes in the small blood vessels in the retina, the area of the eye that receives images and sends information about the images to the brain
Clinical Manifestations: painless process, blurry vision secondary to macular edema occurs in some pts, pts with significant degree of proliferative retinopathy and some hemorrhaging may not experience major visual changes (symptoms of hemorrhaging: floaters or cobwebs in the visual field, sudden visual changes including spotty or hazy vision, or complete loss of vision)

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diabetic retinopathy assessment

Diagnosis is by direct visualization of the retina through dilated pupils with an opthalmoscope or with a technique known as fluorescein angiophraghy that can document the type and activity of the retinopathy.

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diabetic retinopathy nursing management

implementing the individual plan of care and providing pt education. Education focuses on prevention through regular ophthalmologic examinations and blood glucose control and self-management of eye care regimens. If vision loss occurs, nursing care must also address the pts adjustment to impaired vision and use of adaptive advices for diabetes self-care as well as ADLs

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Nephropathy

secondary to diabetic microvascular changes in the kidney.
Clinical Manifestations: renal failure progresses, the catabolism of both exogenous and endogenous insulin decreases, and frequent hypoglycemic episodes may result

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Nephropathy assessment

Urine checked annually for presence of micoalbumin. Test for serume creatinine and BUN levels. Diagnostic testing for cardiac or other systemic disorders

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Nephropathy

• Control of hypertension
• Prevention or vigorous treatment of urinary tract infections
• Avoidance of nephrotoxic substances
• Adjustment of medications as renal function changes
• Low sodium diet
• Low protein diet

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peripheral neuropathy

most commonly affects the distal portions of the nerves, especially the nerves of the lower extremities; it affects both sides of the body symmetrically and may spread in a proximal direction.
Management: Varies approaches to pain management
med for pain – neurontin, nonopoid, antidepressants, seizure medication*
Teach foot care to treat problems early*

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Ace inhibitors –

to lower bp and decreases microalbumin

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Microvascular problems – *

how glucose interferes with lumen; coronary artery disease
Will have atypical symptoms of chest pain
GI delay – food just sit because not be digested because not a lot of muscle so lack of emptying – give regulin to increase GI motility
Bladder – nerve damage to bladder so urinary retention, treated with app. Antibiotics

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Special Issues with Diabetic patient’s hospital and undergoing surgery

1. During times of stress glucose levels tend to increase d/t stress hormones increase. If not controlled osmotic diuresis could happen leading to excessive fluid and electrolyte loss.
2. Hypoglycemia
3. Wound health and preventing infection- reason for tight glucose control.

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Hyperglycemia during hospitalization –A number of factors may contribute to hyperglycemia; examples include:

• Changes in the usual treatment regimen - at increased risk because now experiencing something different than home regimen, Less activity in hospital
• Medications
• IV dextrose – increase glucose levels
• Overly vigorous treatment of hypoglycemia
• Inappropriate withholding of insulin or inappropriate use of “sliding scales”
• Mismatched timing of meals and insulin

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hyperglycemia nursing actings

to correct some of the factors, assessment of home routine is important, monitoring blood glucose

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Hypoglycemia During Hospitalization- usually results from too much insulin or delays in eating. Examples include:

• Overuse of “sliding scale” regular insulin
• Lack of change insulin dosage when dietary intake is changed – due to NPO status
• Overly vigorous treatment of hyperglycemia
• Delayed meal after administration of lispro, aspart, or glulisine

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hypoglycemia treatment

assess the pattern of glucose values and avoid giving doses of insulin, arrange for snacks to be given