What is Diabetes?

Describe a contributing factor to DM2.

A chronic multisystem disease to absence of or decrease in insulin production, or impaired insulin utilization, or both. 

Type 2 Insulin resistance. Obesity has a lot to do with it. It's hard for glucose to penetrate adipose tissue to move into cell.

5th leading cause of death nationally

Cost $174 billion/year

What system is responsible for DM?

Describe this system

Diabetes: a disorder of the endocrine system

Chemical messengers

Pancrease

What secreats insulin in pancreas?

What hormones are secreated and what do they do?

Islets of Langerhans sensitive insulin producing tissue
Secretes important hormones
Glucagon (alpha cells)
Insulin (beta cells)
Somatostatin (delta cells) regulates secretion of insulin and glucagon

What is the incidence of DM in the US?

Diagnosed and undiagnosed?

25.8 million, or 8.3 % of the U.S population.
Diagnosed 18.8 million
Undiagnosed 7.0 million

Blacks are 1.8 times more likely to develop diabetes than whites.
Blacks with diabetes are more likely than non – Hispanic whites to develop and to experience greater disability from diabetes related complications.
Death rates for Blacks with diabetes are 27% higher than whites.

Released into the bloodstream in small increments (increases Bld glu)
Released when food is ingested (bolus) (decreases Bld glu)

70-110 mg/dl

(Lewis 105-100 mg/dl)

Which tissues and muscles are considered insulin depenent?

Adipose tissue, cardiac, and skeletal muscle are considered  insulin dependent tissues

Type 1 DM

Prediabetes (At risk for)

Type 2 DM

Gestation (pregnancy)

Secondary (medically induced)

What is the etiology/pathophysiology of DM1?

Onset?

Treatment?

Long standing process in which the body’s own T cells attack and destroy pancreatic beta cells. A genetic and viral component are factors that may also be responsible.
Age of onset occurs in people under 30 years of age with peak onset between ages 11 and 13, but can occur at any age.
Manifestation develops when the pancreas can no longer produce insulin:
Onset of symptoms rapid
Typically lean body type
Sudden weight loss
Classic symptoms of polydipsia, polyuria,  polyphagia

Treatment requires a supply of insulin from an outside source

Onset of symptoms rapid
Typically lean body type
Sudden weight loss
Classic symptoms of polydipsia (exessive thirst) polyuria (large production of urine),  polyphagia (eating a lot)

What is the etilogy/pathophysiology of DM2?

Treatment?

Etiology/Pathophysiology:
The pancreas continues to produce insulin but it is insuffience or poorly utilized.
Type 2 accounts for 90% of clients who have diabetes, and it tends to run in families (genetic component)
Age of onset usually occurs in people over 35 years of age

Manifestation include a multitude of factors:
 Often without symptoms
Insulin resistance
Obesity
Inactivity
Treatment includes, diet, exercise, weight loss, oral medication, and/or may require insulin during periods of stress, illness, etc

Manifestation include a multitude of factors:
Often without symptoms
Insulin resistance
Obesity
Inactivity

Compare and contrast DM1 and DM2

Causes?

Peak onset?

Symptoms?

Treatment?

Insulin

DM1 little or 0

DM2 produced, but less efficient or poorly utilized

Causes

DM1 - Virus/autoimmure

DM2 -Associated with physical inactivity, obesity, insulin resistance

Peak onset

DM1 11-13 yrs

DM2 adult >35 (adolescents due to obesity)

Treatment

DM1 Requires insulin injections

DM2 Diet, exercise, weight loss, as well as medication are used to treat type 2 diabetes (oral agents)

Manifestations

DM1 Manifestation of symptoms is rapid with sudden weight loss and classic symptoms of:
Polydipsia, Polyuria, Polyphagia

DM2 Manifestation often without symptoms

Nutritional therapy

What are the nutrient balances of Carbs, Fats and Proteins in daily diets?

Carbohydrates - 45-65% of total energy intake.  Low carb diets are NOT recommended.  Whole grains, fruits, vegetables, low-fat milk

Fats - No more than 25-30% of total calories less than 7% from saturated fats

Protein - Less than 10% of total energy consumed

DM1 - Food intake is balanced w/insulin, and exercise pattern. The insulin schedule depends on theclient's eating habits and activity pattern

DM2 - Nutritionally adequate meal with a reduction of totl fat

Spacing meals to spread nutrient intake throughout the day

Weight loss of at least 5-7% of body weight

Regular exercise

1- Insulin resistance

2 - Decreased insulin production

3 - Increased hepatic glucose production

*Sulfonylureas - Glipizide (glucotrol, glucotrol XL) - drug class of choice. Increase insulin production in pancrease.
Meglitinides - Repaglinide (Prandin)
Biguanides - Metformin (Glucophage)
Glucosidase inhibitors - Acarbose (Precose)
Thiazolidinediones - Rosiglitazone (Avandia)

Rapid acting

Short acting

Intermediate acting

Long acting

Combination therapy

Rapid Acting

Onset?

Peak?

Duration?

Types?

Onset 15-30 min

Peak 30-90 min

Duration 3-5 hours

aspart/novolog

lispro/humalog

Short (Regular) acting insulin

Onset/Peak/Duration?

Types?

Onset 30-60 min

Peak - 2-3 hours

Duration 3-6 hours

regular/humulin R

novolin R, relionR

DBL check with Lewis

Intermediate acting insulin

Onset/peak/duration?

Types?

Onset 1-2 hr

Peak - 6-8 hr (Lewis 4-10)

Duration 12-16hr

NPH/humulin N

novolin N

Not getting used as much.  HMO's use because cheaper Too unpredictable for hypoglycemic reaction

Long acting insulin

Onset/peak/duration?

Type?

Onset 30min - 3 hr

Peak 10-20 hr (none)

Duration 20-36 hr

What is combination Therapy?

Types?

NPH/regular

NPH/rapid

For those who do not want more than one or two injections per day

What are the goals of DM mgmt?

Client teaching?

Promote well being
Reduce symptoms
Maitain bld glucose level
Prevent acute complications/delay onset and progression of long term complication

Client teaching

Self - bld glu monitoring

Nutritional therapy

Drug therapy

Exercise

Foot care

Check feet

Clean and dry

Cut toenails in a straight line

White clean socks (can see bleeding

Oil/moisturize but NOT inbetween toes

What are the names of some sulfonylureas?

What is the action?

Glipizide (glucofrol, glucotrol)

Glyburide (micronase, diabets, glynase)

Glimepiride (amaryl)

Primary action is to increase insuln production from the pancrease

What are some Meglitinides?

What is the action?

repaglinide (prandin)

nataglinide (starlix)

Increased insulin production from pancreas but they are more rapidly absorbed and eliminated than sulfonylureas so less likely to cause hypoglycemia.  When taken just before meals insulin production increases during and after meal mimicking normal bld glu

What are some glucosidase inhibitors "starch blockers"?

What is the action?

Acarbose (precose)

miglitol (glyset)

These drugs work by slowing down the absorption of carbohydrate in the small intestine.  Taken with the first bite of each meal they are most effective in lowering postprandial (after meal) blood glucose.  Effeciveness is measured by checking 2-hour postprandial  glucose levels

Name some Thiazolidinediones?

What is the action?

piolitazone (actos)

rosiglitazone (avandia)

Most effective in ppl who have insulin resistance.  They work by increasing the sensitivity of the insulin receptor sites in muscle, fat and liver cells  They do not increase insulin production so will not cause hypoglycemia when used in combo with sulfonylurea or insulin.

Name some Dipeptidyl peptidase - r?

What is it's action?

sitaliptin (janovia)

savaliptin (orglyza)

These medications inhibit DPP-r increase incretin hormones which inhibit glucagon release, which in turn increases insulin secretion, decreases gastric emptying, and decreases blood glucose levels. Since DPP-r inhibitors are glucose dependent they lower the potential for hypoglycemia.  The main benefit of these drugs over others for diabetes with simular effects is the absence of weight gain as a side fx

Name some Biquanides

What is the action?

metformin (glucophage)

lowering agent 1st action is to reduce glucose production in the liver.  It also enhances insulin sensitivity at the tissue level improving glucose transport into the cells.  It is the 1st choice drug for most ppl with DM2.  Does not promote weight gain like sulfonylureas.  Also used in prevention of diabetes in prediabetes.

IDDM - insulin dependet DM or Type 1/autoimmune destruction of beta cells 5-10% of all DM

NIDDM - Non-insulin dependent DM or Type 2/Insulin resistant 90% of DM

Infection releases hormones into the body which increase glucose levels in the blood.  WBC increase affects glucose too. Decreased glucose into the cells.  Increased liver glucose production.  REQUIRE MORE INSULIN

(See lewis)

Regular is short acting 30-60 min Peak 2-3 hr

NPH intermediate acting Onset 2-4 hrs, peak 4-10 hrs, last 16-20 hrs.  Very unpredictible.  Cloudy - need to roll. (See Lewis)

Stomach, most realiable neutral place for absorpting insulin and is very predictable.

Rotate at site to prevent lipodystrophy

Do NOT rotate anatomical areas different absorption rates

S/S Hypoglycemia?

Causes?

Blood glucose <70 mg/dL (3.9 mmol/L)
Cold, clammy skin
Numbness of fingers, toes, mouth
Rapid heartbeat
Emotional changes
S/S
Headache
Nervousness, tremors
Faintness, dizziness
Unsteady gait, slurred speech
Hunger

Thirst
Changes in vision
Seizures, coma

Causes

Alcohol intake without food
Too little food—delayed, omitted, inadequate intake
Too much diabetic medication
Too much exercise without compensation
Diabetes medication or food taken at wrong time
Loss of weight without change in medication
Use of β-adenergic blockers interfering with recognition of symptoms

S/S hyperglycemia?

Causes?

S/S

Dry skin

Dizziness

Decreased healing

Increase in urination
Increase in appetite followed by lack of appetite
Weakness, fatigue
Blurred vision
Headache
Glycosuria
Nausea and vomiting
Abdominal cramps
Progression to DKA or HHS

Causes

llness, infection
Corticosteroids
Too much food
Too little or no diabetes medication
Inactivity
Emotional, physical stress
Poor absorption of insulin

Livetime risk for people born in 2,000 for developing diabetes is:

1 in every 3 males

2 in every 5 females

Acute - immediately have to deal with Hypo/hyperglycemia

BG > 250 mg/dl

DKA (DM1 Ketones)

HHNS (DM2 - no ketones)

Microvascular - Eyes (retinopathy), kidneys (nephropathy), feet (neuropathy) >180 kidneys have problem flushing out glucose, periodontal disease

Macrovascular - lg vessels of heart and brain - Stroke, heart attack, peripheral vascular disease

Postprianal ?????

Fasting bld glucose

DM diagnosis

A1C

Normal FBG <90

FBG (venous draw no finger stick) with diabetes diagnosis (126 x2 or greater)

A1C <6.8

Lantus 24 hr 1 x day 2x if >50 units

Slow acting

Also referred to as diabetic acidosis and diabetic coma, is caused by a profound deficiency of insulin and is characterized by hyperglycemia, ketosis, acidosis, and dehydration. It is most likely to occur in people with type 1 diabetes but may be seen in type 2 in conditions of severe illness or stress when the pancreas cannot meet the extra demand for insulin.

Precipitating factors include illness and infection, inadequate insulin dosage, undiagnosed type 1 diabetes, poor self-management, and neglect.

Ketones are acidic by-products of fat metabolism that can cause serious problems when they become excessive in the blood. Ketosis alters the pH balance, causing metabolic acidosis to develop.

Signs and symptoms of DKA include manifestations of dehydration such as poor skin turgor, dry mucous membranes, tachycardia, and orthostatic hypotension. Early symptoms may include lethargy and weakness. As the patient becomes severely dehydrated, the skin becomes dry and loose, and the eyeballs become soft and sunken. Abdominal pain is another symptom of DKA that may be accompanied by anorexia and vomiting. Finally, Kussmaul respirations (rapid, deep breathing associated with dyspnea) are the body's attempt to reverse metabolic acidosis through the exhalation of excess carbon dioxide.

Renal failure, which may eventually occur from hypovolemic shock, causes the retention of ketones and glucose, and the acidosis progresses. Untreated, the patient becomes comatose as a result of dehydration, electrolyte imbalance, and acidosis.

Because fluid imbalance is potentially life threatening, the initial goal of therapy is to establish IV access and begin fluid and electrolyte replacement. Typically, an infusion of 0.45% or 0.9% NaCl at a rate to restore urine output to 30 to 60 mL/hr and to raise blood pressure constitutes the initial fluid therapy regimen. When blood glucose levels approach 250 mg/dL (13.9 mmol/L), 5% dextrose is added to the fluid regimen to prevent hypoglycemia.17

Eitiology DKA

Undiagnosed DM(1)

Inadequate treatment of existing DM

Insulin not taken as prescribed

Infection

Change in diet, insulin or exercise regimen

The management for both DKA and HHS is similar, except that HHS requires greater fluid replacement

Dry mouth

Thirst

Abdominal pain

Nausea and vomiting

Increasing restlessness, confusion and lethargy

Flushed dry skin

Eyes appear sunken

Breath order of ketones

Rapid weak pulse

Labored breathing (kussmaul resp)

Fever

Urinary frequency

Glucose >250 mg/dl

Glucosuria and ketonuria

 Initial Intervention

Ensure airway

Administer O2 via nasal canula or non-rebreather mask

Establish IV access with large bore catheter

Begin fluid resuscitation w/ 0.9% NaCl solution 1 l/hr until BP stabilizes and urine out put 30-60ml/hr

Begin continuous regular insulin drip 0.1 U/kg/hr

ID hx of DM,  time of last meal and time/amt last insulin inj

Ongoing monitoring

            VS, LOC, Cardiac rhythm O2 sat, and urine output

            Assess breath sounds for fluid overload

            Monitor glucose and K

            Administer K to correct Hypokalemia

            Administer HCO3 if severe acidosis (pH<7.0)

History and physical examination

Blood studies, including immediate blood glucose, complete blood count, pH, ketones, electrolytes, blood urea nitrogen, arterial or venous blood gases

Urinalysis, including specific gravity, glucose, acetone

Collaborative

Administration of intravenous fluids

Intravenous administration of short-acting insulin

Electrolyte replacement

Assessment of mental status

Recording of intake and output

Central venous pressure monitoring (if indicated)

Assessment of blood glucose levels

Assessment of blood and urine for ketones

ECG monitoring

Assessment of cardiovascular and respiratory status

Annual exam

Retinopathy – funduscopic (dilated eye exam) – fundus photography

Nephropathy – urine microalbuminuria, serum creatinine

Cardiovascular disease – risk factor assessment: HTN, Dyslipidemia, smoking family hx and presence of microalbuminuria and macroalbuminuira

Daily by patient

Neuropathy (foot and lower extremities)

Hyperosmolar hyperglycemic syndrome (HHS) is a life-threatening syndrome that can occur in the patient with diabetes who is able to produce enough insulin to prevent DKA but not enough to prevent severe hyperglycemia, osmotic diuresis, and extracellular fluid depletion  HHS is less common than DKA. It often occurs in patients over 60 years of age with type 2 diabete

The higher blood glucose levels increase serum osmolality and produce more severe neurologic manifestations, such as somnolence, coma, seizures, hemiparesis, and aphasia. Since these symptoms resemble a cerebrovascular accident (stroke),

HHS is often related to impaired thirst sensation and/or a functional inability to replace fluids. There is usually a history of inadequate fluid intake, increasing mental depression, and polyuri

Laboratory values in HHS include a blood glucose level greater than 600 mg/dL (33.33 mmol/L) and a marked increase in serum osmolality. Ketone bodies are absent or minimal in both blood and urine.

HHS constitutes a medical emergency and has a high mortality rate.

Electrolytes are monitored and replaced as needed. Hypokalemia is not as significant in HHS as it is in DKA, although fluid losses may result in milder potassium deficits that require replacement.

Assess vital signs, intake and output, tissue turgor, laboratory values, and cardiac monitoring to check the efficacy of fluid and electrolyte replacement. Patients with renal or cardiac compromise require special monitoring to avoid fluid overload during fluid replacement. This includes monitoring of serum osmolality and frequent assessment of cardiac, renal, and mental status.17

The management for both DKA and HHS is similar, except that HHS requires greater fluid replacement