Diabetes Mellitus

A chronic multisystem disease related to

Abnormal insulin production
Impaired insulin utilization
Or both
Leading cause of
End-stage renal disease…chronic kidney disease
Adult blindness…progressive (diabetic retinopathy)
Nontraumatic lower limb amputations
 Major contributing factor
Heart disease
Stroke

Incidence
20.8 million people with diabetes in the U.S…people that has been diagnosis
41 million people with prediabetes…borderline, if they don’t do something to change their lifestyle
they will end up with diabetes

Pathophysiology
Normal insulin metabolism
Insulin is produced by the β cells in the pancreas
•Islets of Langerhans
Released continuously into bloodstream in small increments (basal insulin…always insulin is been
produced) with larger amounts released after food intake
Stabilizes glucose range to 70 to 120 mg/dl
- normal fasting bloodsugar….70 to below 100 mg/dl
Two most common types
Type 1…autoimmune breakdown of the beta cell and pancreas they no longer produce insulin
Type 2...insulin resistance where the target cell are resistance to insulin , so insulin cant bind to target
cells and then we don’t have the glucose being able to get into the cell to be used for energy
Other types
Gestational diabetes are at risk for developing type II diabetes
Secondary diabetes…

Etiology: Theories link cause to single/ combination of these factors

Genetic
Autoimmune…beta cell in type 1 are destroyed
Viral…virus can cause diabetes
Environmental

Pathophysiology: Insulin
Insulin
↑ Insulin after a meal…in response to the intake of foods especially carbohydrates
•Stimulates storage of glucose as glycogen in liver and muscle
•Inhibits gluconeogenesis
•Enhances fat deposition…increase the chance of fat deposits being formed
↑ Protein synthesis
Insulin promotes glucose transport from bloodstream across cell membrane to cytoplasm of cell…
this is how serum blood sugar level decrease… ex..(insulin is a bridge that allows glucose to come
from bloodstream across the bridge and into target cell to be used for energy)…if there is no bridge the
glucose cant swim across to target cell to get there to be used for energy
o Decreases glucose in the bloodstream…. if the bridge is connected the glucose can go
into the cell then you have a serum blood sugar level drop…glucose is in the cell and no
longer in the bloodstream
Counterregulatory hormones…they counter the effect of insulin, they oppose insulin
Oppose effects of insulin
Increase blood glucose levels
Provide a regulated release of glucose for energy
Help maintain normal blood glucose levels
 Examples
•Glucagon, epinephrine, growth hormone, cortisol

Type 1 Diabetes Mellitus

Formerly known as “juvenile onset” or “insulin dependent” diabetes
Most often occurs in people under
30 years of age
Peak onset between ages 11 and 13: Type 1 need insulin because there beta cells are worn out, not
longer produce, are destroyed, but with Type 2 they beta cells will become so tired form over working
they give up, they will soon need insulin injection

Pathophysiology
End result of long-standing process
Progressive destruction of pancreatic β cells by body’s own T cells…self destruction process
Autoantibodies cause a reduction of 80% to 90% of normal β cell function before
manifestations/diagnosis occur
Causes
Genetic predisposition: r/t human leukocyte antigens (HLAs)
Exposure to a virus
Long preclinical period
Antibodies present for months to years before symptoms occur
Manifestations develop when pancreas can no longer produce insulin or enough to keep them from
becoming hyperglycemia
Rapid onset of symptoms…the pancreas can not keep the blood sugar down any more
Present at ER with ketoacidosis (DKA)

Type 1 Diabetes Mellitus:

Onset of Disease
History of recent, sudden, weight loss
Classic symptoms
Polydipsia…increase thirst
Polyuria…increase urination
Polyphagia …excessive hunger
Will require exogenous insulin (insulin that their body doesn’t make) to sustain life…supplement
from the outside
Diabetic ketoacidosis (DKA)
Occurs in absence of exogenous insulin
Life-threatening condition
Results in metabolic acidosis

Prediabetes…on the edge of become type 2 diabetic

- have a evaluated blood sugar levels, not yet high enough to official diagnosis them with diabetes
Known as impaired glucose tolerance (IGT) or impaired fasting glucose (IFG)
IGT: Fasting glucose levels higher than normal (>100 mg/dl, but <126 mg/dl)
IFG: 2-hour plasma glucose higher than normal (between 140 and 199 mg/dl)

Prediabetes
Not high enough for diabetes diagnosis
Increase risk for developing type 2 diabetes…if no preventive measures where taken…no exercise, no
change of diet
If no preventive measure taken—usually develop diabetes within 10 years
- DR. will place on metformin…oral agent for type 2 and prediabetes
Long-term damage already occurring
Heart, blood vessels
Usually present with no symptoms
Must watch for diabetes symptoms
 Polyuria
Polyphagia
Polydipsia

Type 2 Diabetes Mellitus

Most prevalent type of diabetes
Over 90% of patients with diabetes
Usually occurs in people over 35 years of age
80% to 90% of patients are overweight
Prevalence increases with age
Genetic basis
Greater in some ethnic populations
Increased rate in African Americans, Asian Americans, Hispanic Americans, and Native
Americans
Native Americans and Alaskan Natives: Highest rate of diabetes in the world

Pathophysiology
Pancreas continues to produce some endogenous insulin
Insulin produced is either insufficient or poorly utilized by tissues
Obesity (abdominal): Most powerful risk factor
 Genetic Mutation
Lead to insulin resistance
Increased risk for obesity
Four major metabolic abnormalities…the first two is more important
1. Insulin resistance
•Body tissues do not respond to insulin
•Insulin receptors either unresponsive or insufficient in number for insulin to bond to and
decrease the blood sugar
•Results in hyperglycemia
2. Pancreas ↓ ability to produce insulin
•β cells fatigued from compensating cause they are producing all of the insulin but the body
is not utilizing the insulin and the blood sugar goes up the pancreas thinks it needs more
insulin….the problem is the body can’t utilize
3. Inappropriate glucose production from liver
•Liver’s response of regulating release of glucose is haphazard
•Not considered a primary factor in development of type 2
4. Alteration in production of hormones and adipokines
•Play a role in glucose and fat metabolism
•Contribute to pathophysiology of type 2 diabetes
•Two main adipokines
•Adiponectin and leptin
Individuals with metabolic syndrome at increased risk for type 2 diabetes
Cluster of abnormalities that increase risk for cardiovascular disease and diabetes
Characterized by insulin resistance

Metabolic syndrome (3 or more):

Abdominal obesity (waist circumference):
Men: > 40 inches
Women: > 35 inches
Triglycerides: > or = 150mg/dl
HDL Cholesterol:…good
Men < 40mg/dl
Women < 50mg/dl
Blood Pressure: > or = 130/85
Fasting glucose: > or = 110
Exercise is the best treatment…can decrease insulin resistance
Type 2 Diabetes Mellitus: Onset of Disease
Gradual onset
Person may go many years with undetected hyperglycemia
Osmotic fluid/electrolyte loss from hyperglycemia may become severe
Hyperosmolar coma (HHNK)

Secondary Diabetes
Results from
Another medical condition
•Cushing syndrome
•Hyperthyroidism
•Pancreatitis
•Parenteral nutrition…huge amounts of glucose being dumped into vascular system, may
require insulin
•Cystic fibrosis
•Hematochromatosis
Treatment of a medical condition that causes abnormal blood glucose level
•Corticosteroids (Prednisone)…steroid often has to have there blood sugar check…watch for
hyperglycemia
•Thiazides
•Phenytoin (Dilantin)
•Atypical antipsychotics (clozapine)
Usually resolves when underlying condition treated
Type 1 Diabetes Mellitus: Clinical Manifestations
Classic symptoms
Polyuria (frequent urination)
Polydipsia (excessive thirst)
Polyphagia (excessive hunger)
Weight loss
Weakness
Fatigue

Type 2 Diabetes Mellitus: Clinical Manifestations

Nonspecific symptoms
May have classic symptoms of type 1
Fatigue
Recurrent infections
Recurrent vaginal yeast infections
Prolonged wound healing
Visual changes…high level of glucose, there can be changes in the lens

Diabetes Mellitus: Diagnostic Studies

Three methods of diagnosis
Fasting plasma glucose level > (greater) 126 mg/dl
Random or casual plasma glucose measurement ≥ 200 mg/dl plus symptoms
Two-hour OGTT level (random) ≥ 200 mg/dl using a glucose load of 75 g

Hemoglobin A1C test…

Useful in determining glycemic levels over time
Not diagnostic but monitors success of treatment and patient compliance
Shows the amount of glucose attached to hemoglobin molecules over RBC life span…when pt.
has fluctuation in glucose causes the glucose to stay attach to hemoglobin molecules, once it
attach it never let go….Hemoglobin A1C normal value is 4%-6%, this percent stays attach to the
hemoglobin molecule…someone with diabetes this percent can be very high, as high as 10% -
15%
 •90 to 120 days
Hemoglobin A1C (cont’d)
Regular assessments required
Ideal goal
•ADA ≤7.0%
Normal A1C reduces risk of retinopathy, nephropathy, and neuropathy…the tighter the glycemic
control or the more frequently that the patient is able to keep their blood sugar level at near normal
level this will reduce the risk for developing these complications.

Diabetes Mellitus: Collaborative Care

Goals of diabetes management
Decrease symptoms
Promote well-being
Prevent acute complications
Delay onset and progression of
long-term complications

Patient teaching
Nutritional therapy
Drug therapy
Exercise

Diabetes Mellitus: Treat to Target

Goals:
A 1c below 7%
B /P below 130/80
C holesterol: Triglyceride below 150mg/dl

Diabetes Mellitus: Treatment

Balancing Act: 3 points of treatment:
• Drugs,
• Nutrition
• Exercise
Drug Therapy
Insulin
Exogenous insulin
Insulin from an outside source
Required for type 1 diabetes
Prescribed for patient with type 2 diabetes who cannot control blood glucose by other means

Types of insulin
Human insulin
•Only type used today
•Prepared through genetic engineering
•Derived from common bacteria (Escherichia coli)…. Or…..
•Yeast cells
•Recombinant DNA technology used
Insulins differ in regard to onset, peak action, and duration
•Characterized as rapid-acting, short-acting, intermediate-acting, long-acting…insulin has to
be coordinated with meal, activity level and the peak puts them at risk for hypoglycemia
Different types of insulin may be used for combination therapy

Rapid-acting: Lispro (SQ, IV)(Humalog), Aspart (Novolog), and glulisine (Apidra), Exubera
(inhaled insulin, rapid acting)
Short-acting: Regular (SQ, IV)
Intermediate-acting: NPH (SQ)
Long-acting: Glargine (Lantus), detemir (Levemir) (SQ)
Regimen that closely mimics endogenous insulin production is basal-bolus
Long-acting (basal) once a day
Rapid/short-acting (bolus) before meals

Insulin preparations
Rapid-acting (bolus) lispro, aspart, apidra Lispro, aspart, glulisine
•Injected 0 to 15 minutes before meal
•Onset of action 15 minutes
•Peak: 60-90 minutes
Short-acting (bolus)
•Regular
•Injected 30 to 45 minutes before meal
•Onset of action 30 to 60 minutes
•Peak: 2-3 hours
Intermediate-acting NPH
•Injected once or twice daily (morning and evening)
•Onset of action 2-4 hours
•Peak 4-10 hours
•Duration: 10-16 hours
Long-acting (basal)lantus,
lantus, levemir
•Injected once a day at bedtime or in the morning
•Released steadily and continuously…mimic endogenous insulin
•No peak action…decreases the risk of hypoglycemia
•Duration: 24 hours
•Cannot be mixed with any other insulin or solution

Combination insulin:
NPH + regular
70/30
75/25
50/50
Storage of insulin
Do not heat/freeze
In-use vials may be left at room temperature up to 4 weeks
•Lantus only for 28 days
Extra insulin should be refrigerated
Avoid exposure to direct sunlight
Administration of insulin
Cannot be taken orally
Subcutaneous injection for
self-administration
IV administration…lispro (rapid) and regular (short)
- Exubera is inhaled
Fastest absorption from abdomen, followed by arm, thigh, buttock
Abdomen
•Preferred site
Rotate injections within one particular site…they will have same rate of absorption and that helps to keep the
triangle balance
Do not inject in site to be exercised, because it absorb more quickly and throws triangle off
balance
 Insulin Pen…might be more cost effective - multiuse vial, but change needle

Drug Therapy: Insulin

Insulin pump
Continuous subcutaneous infusion
Battery operated device
Connected via plastic tubing to a catheter inserted into subcutaneous tissue in abdominal wall
Potential for tight glucose control
- Change needle every 2-3 days
Inhaled insulin
Exubera…like Lispro (rapid acting)
•Rapid-acting, dry powder inhaled through mouth into lungs
•Not recommended for patients with asthma, bronchitis, or emphysema; smokers or those who
have smoked within the last 6 months
•PFT (pulmonary function test) required prior to treatment, in 6 months, then yearly
Side effects: hypoglycemia, cough, SOB, sore throat, dry mouth
Available in 1 and 3 mg blisters
1 mg = 3 units
3 mg = 8 units
Problems with insulin therapy
Hypoglycemia…keep in mid when insulin peak that when pt. are at a greater risk for hypoglycemia
episode
Allergic reactions…don’t see that much, but due to the additives
Lipodystrophy…don’t want to use this area for absorption…don’t use for 6 months
Somogyi effect
Dawn phenomenon
Somogyi effect…related to hypoglycemia during the night
•Rebound effect in which an overdose of insulin causes hypoglycemia during the hours of
sleep…due to taking too much, wrong dose, cant read syringe
•Counterregulatory hormones released
•Rebound hyperglycemia and ketosis occur
•Hyperglycemia upon waking
•Check blood sugar for hypoglycemia between 2a-4a
•Tx: decrease insulin
Dawn phenomenon
•Characterized by hyperglycemia present on awakening in the morning
•Due to release of counterregulatory hormones in predawn hours
•Growth hormone/cortisol possible factors…causing blood sugar to be high
•More common in adolescence and young adults r/t hormones
•Tx: increase insulin or adjust timing, we want to adjust the timing of the insulin so it will
last longer into morning hours, because it’s a basal dose
Not insulin
Work to improve mechanisms by which insulin and glucose are produced and used by the body
Work on three defects of type 2 diabetes
Insulin resistance
Decreased insulin production
Increased hepatic glucose production
 - Double diabetes…pt. that is diagnosis with type 1can acquire type 2…so they have both
pathophysiology going on

Drug Therapy: Oral Agents

Sulfonylureas
Meglitinides
Biguanides
α-Glucosidase inhibitors
Thiazolidinediones

Sulfonylureas
↑ Insulin production from pancreas
10% experience decreased effectiveness after prolonged use
Side effect: hypoglycemia; allergy to sulfa
Examples
•Glipizide (Glucotrol)
•Glyburide (DiaBeta)
•Glimepiride (Amaryl)
Meglitinides
↑ Insulin production from pancreas
Taken 30 minutes before each meal up to time of meal; mimics normal insulin response to food
intake
Should not be taken if meal skipped
Side effect: hypoglycemia
Examples
•Repaglinide (Prandin)
•Nateglinide (Starlix)
Biguanides
Reduce glucose production by liver
Enhance insulin sensitivity
Improve glucose transport into cells
Do not promote weight gain; no hypoglycemia
Used to prevent Type 2 diabetes in patients with prediabetes
Example
•Metformin (Glucophage)
Combination drugs:
Glucovance = metformin+glyburide…they have different actions

α-Glucosidase inhibitors
Slow down absorption of carbohydrate in small intestine
Take with food
Effective in lowering post-prandial blood sugar
- prevent big rapid increase of blood sugar
Example
•Acarbose (Precose)

Thiazolidinediones (“Insulin sensitizers”)

Most effective in those with insulin resistance
 Improves insulin sensitivity, transport, and utilization at target tissues…make target cell more
sensitive to insulin
Do not cause hypoglycemia
Can cause edema; should not be used in patients with heart failure
Examples
•Pioglitazone (Actos)
•Rosiglitazone (Avandia)

Amylin analog
Hormone secreted by β cells of pancreas
Cosecreted with insulin in response to food
Indicated for type 1 and type 2 diabetics
Slows gastric emptying, reduces postprandial glucagon secretion, increases satiety…make pt. feel
like they are full
 reduced food intake
Taken with insulin
- severe hypoglycemia can occur three hours after drug is taken…take before meals or before a snack
that has at least 250 calories or 30 grams of carbohydrates
Subcutaneous injection
•Thigh or abdomen
•Cannot be mixed with insulin
Example
•Pramlintide (Symlin)

Incretin mimetic…hormone produce in the gut/gi tract

Indicated for type 2 diabetes
Synthetic peptide
•Stimulates release of insulin from β cells
•Suppresses glucagon secretion
•Increases satiety Reduced food intake
•Slows gastric emptying
Not to be used with insulin…usually given with oral agents
Subcutaneous injection
- given before breakfast and dinner to prevent hypoglycemia (side effect)
Example
•Byetta

Drug Therapy: Other Agents

β-Adrenergic blockers
Mask symptoms of hypoglycemia
Prolong hypoglycemic effects of insulin
Thiazide/loop diuretics
Can potentiate hyperglycemia
•By inducing potassium loss
Diabetes: Nutritional Therapy
Cornerstone of care for person with diabetes
Most challenging for many people
Recommended that diabetes nurse educator and registered dietitian with diabetes experience be members
of team
- nutritional energy intake should be balance with energy output
American Diabetes Association (ADA)
 Guidelines indicate that within context of an overall healthy eating plan, person with diabetes can eat
same foods as person who does not have diabetes
Overall goal
•Assist people in making changes in nutrition and exercise habits that will lead to improved
metabolic control
Food composition
Nutrient balance of diabetic diet is essential
Nutritional energy intake should be balanced with energy output

Carbohydrates
Carbohydrates and monounsaturated fats should provide 45% to 65% of total energy intake
↓ Carbohydrate diets are not recommended for diabetics

Glycemic index (GI)

Term used to describe rise in blood glucose levels after consuming carbohydrate-containing food
•Foods with high GI will cause sharp rise in blood glucose level…such as white bread, rice,
potatoes
•Foods with low GI cause steady rise in blood glucose over a longer period of time…apple
Should be considered when formulating a meal plan
Fats
No more than 25% to 30% of meal plan’s total calories
•<7% from saturated fats
Protein
Contribute <10% of total energy consumed
Exercise
Essential part of diabetes management
↑ Insulin sensitivity at receptor sites
Lowers blood glucose levels
Contributes to weight loss

Several small carbohydrate snacks can be taken every 30 minutes during exercise to prevent
hypoglycemia
Best done after meals
Exercise plans should be started
•After medical clearance
•Slowly with gradual progression
Should be individualized
Monitor blood glucose levels before, during, and after exercise

Diabetes: Pancreas Transplant

Used for patients with type 1 diabetes who also have
End-stage renal disease
Had, or plan to have, a kidney transplant
Pancreas transplants alone are rare
Usually kidney and pancreas transplants done together
Eliminates need for exogenous insulin…will be on immunosuppressant for the rest of their life.
Can also eliminate hypoglycemia and hyperglycemia
Nursing Management:
Planning
Overall goals
Active patient participation
Few or no episodes of acute hyperglycemic emergencies or hypoglycemia
Maintain normal blood glucose levels
Prevent or delay chronic complications
 Lifestyle adjustments with minimal stress

Nursing Implementation
Health promotion
Identify those at risk
Routine screening for overweight adults over age 45
•FPG is preferred method in clinical settings
Acute intervention
Hypoglycemia
Diabetic ketoacidosis
Hyperosmolar hyperglycemic nonketotic
Stress of illness and surgery
•↑ Blood glucose level
• Continue regular meal plan
•↑ Intake of noncaloric fluids…food w/ sugar or carbohydrates, so they can get their source of
carbs
•More frequent BG checks
•Continue taking oral agents and insulin
•Frequent monitoring of blood glucose
Stress of illness and surgery
•Patients undergoing surgery or radiologic procedures requiring contrast medium should hold
their metformin day of surgery and 48 hours
•Begun after serum creatinine has been checked and is normal

Ambulatory and home care

Overall goal is to enable patient or caregiver to reach an optimal level of independence
Insulin therapy and oral agent
•Education on proper administration, adjustment and side effects
•Assessment of patient’s response to therapy
Personal hygiene
•Regular bathing with emphasis on foot care
•Daily brushing/flossing
•Dentist should be informed about diabetes diagnosis
Medical identification and travel card
•Must carry identification indicating diagnosis of diabetes
Patient and family teaching
•Educate on disease process, physical activity, medications, monitoring blood glucose, diet,
resources
•Enable patient to become most active participant in his/her care

Diabetes: Acute Complications

1. Diabetic ketoacidosis (DKA)
2. Hyperosmolar hyperglycemic syndrome (HHNK)
3. Hypoglycemia

Diabetic KetoAcidosis (DKA)

Hyperglycemic state
Caused by profound deficiency of insulin
Characterized by
•Hyperglycemia
•Ketosis
•Acidosis
•Dehydration
Most likely occurs in type 1
Precipitating factors
•Illness
•Infection
•Inadequate insulin dosage
 •Undiagnosed type 1
•Poor self-management
•Neglect
When supply of insulin insufficient
•Glucose cannot be properly used for energy
•Body breaks down fats stores
•Ketones are by-products of fat metabolism
•Alters pH balance, causing metabolic acidosis
•Ketone bodies excreted in urine
•Electrolytes become depleted, patient become dehydrated

Signs and symptoms of DKA

•Lethargy/weakness
•Early symptoms
•Dehydration
•Poor skin turgor
•Dry mucous membranes
•Tachycardia
•Orthostatic hypotension
•Abdominal pain
•N/V
•Kussmaul respirations…body is in a state of acidosis, trying to compensate to get rid of the extra
acid
•Rapid deep breathing…trying to blow off the carbon dioxide which is an acid, body trying to
get rid of the acid
•Attempt to reverse metabolic acidosis
•Sweet fruity odor on breath
Serious condition
•Must be treated promptly
Depending on signs/symptoms
•May or may not need hospitalization
Laboratory findings
•Blood glucose > 300 mg/dl
•Arterial blood pH below 7.30…normal ph in blood is 7.35 – 7.45 (7.3 or below is a state of
acidosis)
•Serum bicarbonate level <15 mEq/L…normal is 22-26
•Ketones in blood and urine
Correct fluid/electrolyte imbalance
•IV infusion 0.45% or 0.9% NaCl…1 Liter every few hours
•Restore urine output to go down, so dehydration stops
•Raise blood pressure
• When blood glucose levels approach 250 mg/dl
•5% dextrose added to regimen
•Prevent hypoglycemia
•Potassium replacement….high or low causes cardiac dysrhythmias (hypokalemia)
•Sodium bicarbonate…give an amp of sodium IV
•If pH <7…severe acidosis
Airway management
•Oxygen administration
Insulin therapy
 •Withheld until fluid resuscitation has begun
•Bolus followed by insulin drip

Hyperosmolar Hyperglycemic NonKetosis (HHNK)

Hyperglycemic state
Life-threatening syndrome
Fewer early S/S so BG levels continue to rise
Less common than DKA
Often occurs in patients with type 2 over 60 years of age
Patient has enough circulating insulin so ketoacidosis does not occur but not enough insulin to
prevent hyperglycemia…so the body does not have to break down fat to provide energy
Neurologic manifestations occur due to ↑ serum osmolality and intracellular dehydration…cause
fluid to shift from intracellular to extracellular
- so we see intracellular dehydration cause neurological manifestation…due high blood sugar and
fluid shift
•Seizures
•Coma
•Hemiparesis
Usually history of
•Inadequate fluid intake
•Increasing mental depression
•Polyuria
Laboratory values
•Blood glucose >400 mg/dl
•Increase in serum osmolality, because of high glucose concentration
•Absent/minimal ketone bodies…not a state of acidosis
Medical emergency, higher priority than DKA
High mortality rate, these pt. lose greater amount of fluid…need greater amount of fluid
Therapy similar to DKA
•Except HHNK requires greater fluid replacement

Nursing management DKA/HHNK

Patient closely monitored
•Administration
• IV fluids
•Insulin therapy
•Electrolytes
•Assessment
•Renal status
•Cardiopulmonary status
•Level of consciousness
•Signs of hypokalemia (dizziness and muscle weakness)
•Cardiac monitoring
 •Vital signs

Diabetes: Acute Complications

Hypoglycemia
Low blood glucose
Brain requires constant supply of glucose
Occurs when
•Too much insulin in proportion to glucose in the blood
•Blood glucose level less than 70 mg/dl
Common manifestations
•Confusion
•Irritability
•Diaphoresis…skin cold and clammy
•Tremors
•Hunger
•Weakness
•Visual disturbances
•Can mimic alcohol intoxication
Hypoglycemia…goes to top of list for priority of care
Untreated can progress to loss of consciousness, seizures, coma, and death
Hypoglycemic unawareness
•Person does not experience warning signs/symptoms, increasing risk for decreased blood glucose
levels
•Related to autonomic neuropathy
Causes
•Exercise
•Mismatch in timing
•Food intake and peak action of insulin or oral hypoglycemic agents
At the first sign
•Check blood glucose
•If <70 mg/dl, begin treatment
•If >70 mg/dl, investigate further for cause of signs/symptoms
•If monitoring equipment not available, treatment should be initiated
Treatment
•If alert enough to swallow
•15 to 20 g of a simple carbohydrate
•4 to 6 oz fruit juice
•Regular soft drink
•Avoid foods with fat
•Decrease absorption of sugar
 •If alert enough to swallow
•Do not overtreat
•Recheck blood sugar 15 minutes after treatment
•Repeat until blood sugar >70 mg/dl
•Patient should eat regularly scheduled meal/snack to prevent rebound hypoglycemia
•Check blood sugar again 45 minutes after treatment
•If no improvement after 2 or 3 doses of simple carbohydrate OR patient not alert enough to
swallow
Treatment of Hypoglycemia
•Administer 1 mg of glucagon IM or subcutaneously
•Side effect: Rebound hypoglycemia, if we don’t give them a long action carbohydrate
•Have patient ingest a complex carbohydrate after recovery
•In acute care settings
•20 to 50 ml of 50% dextrose IV push …does into vascular system

Diabetes: Chronic Complications

Angiopathy
Macrovascular
Macro
•Diseases of large and medium-sized blood vessels
•Cardiovascular
•Cerebrovascular
•Peripheral vascular
•Can occur in general population but occurs with greater frequency and with an earlier onset in diabetics
•Development promoted by altered lipid metabolism common to diabetes
•Tight glucose control may delay atherosclerotic process
•Risk factors
•Obesity
•Smoking
•Hypertension
•High-fat intake
•Sedentary lifestyle
•Patients with diabetes should be screened for dyslipidemia at diagnosis
Microvascular
Micro
• Occur only in patients with diabetes
•Result from thickening of vessel membranes in capillaries and arterioles
•In response to chronic hyperglycemia
Areas most noticeably affected
1. Eyes (retinopathy)
2. Kidneys (nephropathy)
3. Skin (dermopathy)
Clinical manifestations usually appear after 10 to 20 years of diabetes

Diabetic retinopathy
Microvascular damage to retina
•Result of chronic hyperglycemia
Most common cause of new cases of blindness in people 20 to 74 years
Nonproliferative versus proliferative
Nonproliferative
•Most common form
•Partial occlusion of small blood vessels in retina
•Causes development of microaneurysms
•Capillary fluid leaks out
•Retinal edema and eventually hard exudates or intraretinal hemorrhages occur
Proliferative
•Most severe form
•Involves retina and vitreous
 •When retinal capillaries become occluded
•Body forms new blood vessels
•Vessels are extremely fragile and hemorrhage easily
•Retinal detachment can occur
Earliest and most treatable stages often produces no changes in vision
Must have annual dilated eye examinations
Treatment
•Photocoagulation
•Most common
•Laser destroys ischemic areas of retina
•Prevents further visual loss
•Cryotherapy
•Used to treat peripheral areas of retina
•Probe creates frozen area until reaches specific point on retina
•Vitrectomy
•Aspiration of blood, membrane, fibers from inside eye through small incision
•Used when
•Vitreal hemorrhage does not clear in 6 months
•Threatened or actual retinal detachment

Diabetic nephropathy
Associated with damage to small blood vessels that supply the glomeruli of the kidney
Leading cause of end-stage renal disease
Critical factors for prevention/delay
•Tight glucose control
•Blood pressure management
•Angiotensin-converting enzyme (ACE) inhibitors
•Used even when not hypertensive
•Angiotensin II receptor antagonists Yearly screening
•Yearly screening: serum creatinine
60% to 70% of patients with diabetes have some degree of neuropathy
Nerve damage due to metabolic derangements of diabetes
Sensory versus autonomic neuropathy

Sensory neuropathy
•Distal symmetric
•Most common form
•Affects hands and/or feet bilaterally
•Characteristics include
•Loss of sensation, abnormal sensations, pain, and paresthesias
•Usually worse at night
•Foot injury and ulcerations can occur without the patient having pain
•Can cause atrophy of small muscles of hands/feet
•Treatment
•Tight blood glucose control
•Drug therapy
•Topical creams
•Tricyclic antidepressants
•Selective serotonin and norepinephrine reuptake inhibitors
•Antiseizure medications
Autonomic
•Can affect nearly all body systems
•Complications
•Gastroparesis
•Delayed gastric emptying
•Cardiovascular abnormalities
Diabetic neuropathy
Autonomic
 •Complications
•Sexual dysfunction
•Neurogenic bladder
Complications of foot and lower extremity
Foot complications
•Most common cause of hospitalization in diabetes
•Result from combination of microvascular and macrovascular diseases
Risk factors
•Sensory neuropathy
•Peripheral arterial disease
Other contributors
•Smoking
•Clotting abnormalities
•Impaired immune function
•Autonomic neuropathy
Integumentary complications
Acanthosis nigricans
•Dark, coarse, thickened skin
Infection
Diabetics more susceptible to infections
Defect in mobilization of inflammatory cells
Impairment of phagocytosis by neutrophils and monocytes
Loss of sensation may delay detection
Treatment must be prompt and vigorous