Transcript Diabetes Mellitus - wcunurs120and121

Zoya Minasyan RN-MSN-Edu
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A chronic multisystem disease related to
◦ Abnormal insulin production
◦ Impaired insulin utilization
◦ Or both
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7th leading cause of death in the USA
Leading cause of adult blindness, end-stage
renal disease, and non traumatic lower limb
amputation.
Major contributing factor
◦ Heart disease
◦ Stroke
◦ Genetic
◦ Autoimmune
◦ Viral
◦ Environmental
Regardless of it’s cause, Diabetes is primarily a
disorder of glucose metabolism r/t absent or
insufficient insulin supply and/or poor utilization of
the insulin that is available.
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Two most common types
◦ Type 1
◦ Type 2
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Other types
◦ Gestational
◦ Prediabetes
◦ Secondary diabetes
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Normal insulin metabolism
◦ Produced by the  cells
 Islets of Langerhans of the pancreas.
◦ Released continuously into bloodstream in small
amounts; with larger amounts released after food.
◦ Stabilizes glucose range to 70 to 120 mg/dL
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Counter regulatory hormones-glucagon,
epinephrine, growth hormone and cortisol work
to oppose the effect of insulin; work to increase
blood glucose level by stimulating glucose
production and output by liver, and decreasing
the movement of glucose into the cells.
◦ Promotes glucose transport from bloodstream
across cell membrane to cytoplasm of cell
 Decreases glucose in the bloodstream
◦ ↑ insulin after a meal
 Stimulates storage of glucose as glycogen in liver and
muscle
 Inhibits gluconeogenesis
 Enhances fat deposition
 ↑ protein synthesis
Pancreas
Exocrine
pancreas
Endocrine
pancreas
releases digestive
juices through a
duct
releases hormones
into the blood
to the
duodenum
Endocrine
pancreas:
Islets of
Langerhans
Alpha
cells
Beta cells
Delta cells
PP cells
Somatostatin
Pancreatic
polypeptide
Insulin
Glucagon
and amylin
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Glucagon: causes cells to release stored food into
the blood
Insulin: allows cells to take up glucose from the
blood
Amylin: slows glucose absorption in small
intestine; suppresses glucagon secretion
Somatostatin: decreases GI activity; suppresses
glucagon and insulin secretion
Which pancreatic hormone decreases blood
glucose levels?
a. Glucagon
b. Insulin
c. Amylin
d. Somatostatin
Insulin
Insulin allows cells to take glucose from the
blood and use it for energy/to make ATP.
Because it stimulates movement of glucose
out of the blood and into the cells, blood
levels decrease when insulin is released.
b.
Tell whether the following statement is true or
false:
Type 2 DM is more common than Type 1 DM.
True
Type 1 DM is autoimmune (juvenile diabetes is
Type 1), and affects only 5% to 10% of the
diabetic population. Type 2 DM is associated
with risk factors like obesity, poor diet, and
sedentary lifestyle; 90% to 95% of diabetics
suffer from this type.
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Skeletal muscle and adipose tissues are
Insulin-dependent tissues; have receptors for
insulin
Other tissues (brain, liver, blood cells) do not
directly depend on insulin for glucose
transport; but require adequate glucose for
normal fx. Liver has receptor sites for hepatic
uptake of glucose and its conversion to
glycogen.
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“juvenile-onset” or “insulin-dependent”
diabetes, occurs in people younger than 40
years of age, and in younger children.
• Progressive destruction of pancreatic  cells by body’s
own T cells
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Caused by
◦ Genetic predisposition
 Related to human leukocyte antigens (HLAs)
◦ Exposure to a virus
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Manifestations develop when pancreas can no
longer produce insulin.
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Will require insulin
Diabetic ketoacidosis (DKA)
◦ Occurs in absence of insulin
◦ Life-threatening condition
◦ Results in metabolic acidosis
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Individuals already at risk for diabetes
Blood glucose is high but not high enough to be
diagnosed as having diabetes
Characterized by
◦ Impaired fasting glucose (IFG)
◦ Impaired glucose tolerance (IGT)
IFG: Fasting glucose levels are 100 to 125 mg/dL
IGT: 2-Hour plasma glucose levels are between 140
and 199 mg/dL
AIC is in range of 5.7% to 6.4%.
Must watch for diabetes symptoms
◦ Polyuria
◦ Polyphagia
◦ Polydipsia
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Usually occurs in
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people over 35 years of age,
overweight,
increases with age,
genetic basis.
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Four major metabolic abnormalities
◦ 1. Insulin resistance
 Body tissues do not respond to insulin which results in
hyperglycemia.
◦ 2. Pancreas ↓ ability to produce insulin
 β cells fatigued from compensating
 β-cell mass lost
◦ 3. Inappropriate glucose production from liver
◦ 4. Alteration in production of hormones
Individuals with metabolic syndrome also known as
syndrome X or insulin resistance syndrome are at
increased risk for type 2 diabetes
◦ risk for cardiovascular disease and diabetes
characterized by insulin resistance
Individuals with metabolic syndrome
◦ Elevated insulin levels, ↑ triglycerides, LDLs, ↓ HDLs,
hypertension
◦ Risk factors
 Central obesity, sedentary lifestyle, urbanization, certain
ethnicities(African Americans, Native Americans, Hispanics,
Asians)
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Gradual onset
Person may go many years with undetected
hyperglycemia.
Osmotic fluid/electrolyte loss from
hyperglycemia may become severe.
◦ Hyperosmolar coma(will discuss later)
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Develops during pregnancy
Detected at 24 to 28 weeks of gestation
Usually normal glucose levels at 6 weeks post
partum
Increased risk for cesarean delivery, and
neonatal complications
Increased risk for developing type 2 in 5 to
10 years
Therapy: First- nutritional, second -insulin
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Results from
◦ Another medical condition
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Cushing syndrome
Hyperthyroidism
Pancreatitis
Parenteral nutrition
Cystic fibrosis
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Corticosteroids (Prednisone)
Thiazides
Phenytoin (Dilantin)
Atypical antipsychotics (clozapine)
◦ Treatment of a medical condition that causes abnormal blood
glucose level
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Usually resolves when underlying condition treated
Drugs that can alter blood glucose levels are listed in
Table 49-8.
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Classic symptoms
◦ Polyuria (frequent urination)
◦ Polydipsia (excessive thirst)
◦ Polyphagia (excessive hunger)
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Weight loss
Weakness
Fatigue
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Nonspecific symptoms
◦ May have classic symptoms of type 1
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Fatigue
Recurrent infection
Recurrent vaginal yeast infection
Prolonged wound healing
Visual changes
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Four methods of diagnosis
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Hemoglobin A1C test
1.
2.
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AIC ≥ 6.5%
Fasting plasma glucose level >126 mg/dL
Random plasma glucose measurement ≥200 mg/dL
Two-hour OGTT(oral glucose tolerance test) level ≥200 mg/dL
when a glucose load of 75 g is used
◦ In 2010, recommended to be used as a diagnostic test
◦ Useful in determining glycemic levels over time
◦ Shows the amount of glucose attached to hemoglobin molecules
over RBC life span, approximately 120 days
◦ Ideal goal
 ADA ≤7.0%
 American College of Endocrinology <6.5%
◦ Normal A1C reduces risks of retinopathy, nephropathy, and
neuropathy.
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Goals of diabetes management
Decrease symptoms
Promote well being
Prevent acute complications
Delay onset and progression of long term
complications
◦ Patient teaching
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 Self-monitoring of blood glucose
◦ Nutritional therapy
◦ Drug therapy
◦ Exercise
◦ Insulin differ with regard to onset, peak action, and
duration.
 Characterized as rapid-acting, short-acting,
intermediate-acting, and long-acting
◦ Rapid-acting: Lispro (Humalog), Aspart (Novolog),
and glulisine (Apidra)
◦ Short-acting: Regular
◦ Intermediate-acting: NPH
◦ Long-acting: Glargine (Lantus), detemir (Levemir)
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Insulin preparations
◦ Rapid-acting (bolus)
 Lispro, aspart, glulisine
 Injected 0 to 15 minutes before meal
 Onset of action 15 minutes
◦ Short-acting (bolus)
 Regular
 Injected 30 to 45 minutes before meal
 Onset of action 30 to 60 minutes
◦ Long-acting (basal)
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Injected once a day at bedtime or in the morning
Released steadily and continuously
No peak action
Cannot be mixed with any other insulin or solution
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Storage of insulin
◦ Do not heat/freeze.
◦ In-use vials may be left at room temperature up to 4
weeks.
◦ Extra insulin should be refrigerated.
◦ Avoid exposure to direct sunlight.
◦ Administration of insulin
 Cannot be taken orally
 Subcutaneous injection for
self-administration
 IV administration
 Fastest absorption from abdomen, followed by arm, thigh,
and buttock
 Abdomen is the preferred site.
 Rotate injections within one particular site.
 Do not inject in site to be exercised.
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Administration of insulin
◦ Hand washing
◦ Do not recap needle
◦ 45- to 90-degree angle, depending on fat
thickness of the patient
◦ Insulin pens preloaded with insulin are now
available.
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Insulin pump
◦ Continuous subcutaneous infusion;
Battery-operated device
◦ Connected via plastic tubing to a
catheter inserted into subcutaneous
tissue in abdominal wall
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Problems with insulin therapy
◦ Hypoglycemia
◦ Allergic reaction
◦ Lipodystrophy(atrophy of SQ tissue)
◦ Somogyi effect( during the sleep hrs-decline in
blood glucose in respond to insulin;
counterregulatory hormones causes
gluconeogenesis which causes rebound
hyperglycemia and ketosis at night and in the
morning; sweats or nightmares, and high blood
glucose in am(recheck BG at 2 and 4 pm again)
◦ Dawn phenomenon( growth hormone and
cortisol: hyperglycemia in the morning)
◦ Sulfonylureas
 ↑ insulin production from pancreas
 ↓ chance of prolonged hypoglycemia
 Ex: glipizide (Glucotrol, Glucotrol XL), glyburide (Micronase, DiaBeta,
Glynase), and glimepiride (Amaryl).
◦ Meglitinides
 Increase insulin production from pancreas
 Taken 30 minutes before each meal up to time of meal
 Should not be taken if meal skipped
 Ex: repaglinide (Prandin) and nateglinide (Starlix).
◦ Biguanide
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Reduce glucose production by liver
Enhance insulin sensitivity at tissues
Improve glucose transport into cells
Do not promote weight gain
 Ex: Metformin (Glucophage)
◦ α-glucosidase inhibitors
 “Starch blockers”
 Slow down absorption of carbohydrate in small intestine
 Ex:Acarbose (Precose) and miglitol (Glyset)
◦ Thiazaolidinediones
 ↑ glucose uptake in muscle and ↓glucose production
 Ex: pioglitazone (Actos) and rosiglitazone (Avandia).
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Dipeptidyl peptidase-4 (DDP-4) inhibitor
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Slows the inactivation of incretin hormones(Gastric hormones-Ex:gastrin,secretin…)
Potential for hypoglycemia
Ex: Sitagliptin (Januvia)
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Hormone secreted by  cells of pancreas
Administered subcutaneously: thigh or abdomen
Slows gastric emptying
Ex: Pramlintide (Symlin)
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Synthetic peptide
Stimulates release of insulin from  cells
Subcutaneous injection
Suppresses glucagon secretion
Reduces food intake
Slows gastric emptying
Not to be used with insulin
Ex: Byetta
Saxagliptin (Onglyza) Amylin analog
Incretin mimetic
-adrenergic blockers
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Mask symptoms of hypoglycemia
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Can potentiate hyperglycemia
Thiazide/loop diuretics
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By inducing potassium loss
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American Diabetes Association (ADA)
◦ Overall goal
 Assist people in making changes in nutrition and
exercise habits that will lead to improved metabolic
control.
◦ Meal plan is based on individual’s usual food intake
and is balanced with insulin and exercise patterns.
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Carbohydrates
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Fats
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◦ Sugars, starches, and fiber
◦ minimum of 130 g/day; whole grains, along with fruits, vegetables, and low-fat
milk, should be included.
◦ Less than 200 mg/day of cholesterol and trans fats
Protein
Alcohol
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High in calories
No nutritive value
Detrimental effects on liver
Can cause severe hypoglycemia
• Alcohol inhibits gluconeogenesis (breakdown of glycogen to
glucose) by the liver. This can cause severe hypoglycemia in
patients on insulin or oral hypoglycemic medications that
increase insulin secretion.
• Moderate alcohol consumption can sometimes be safely
incorporated into the meal plan if blood glucose levels are well
controlled, and if the patient is not taking medications that will
cause adverse effects.
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Exercise
◦ Essential part of diabetes management
◦ ↑ insulin receptor sites
◦ Lowers blood glucose levels
◦ Contributes to weight loss
• The ADA recommends that individuals with diabetes should
perform at least 150 minutes per week of a moderate-intensity
aerobic physical activity.
• The ADA also encourages those with type 2 diabetes to perform
resistance training 3 times a week in the absence of
contraindications.
◦ 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.
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Past health history
◦ Viral infections
◦ Medications
◦ Recent surgery
Obesity
 Weight loss
 Thirst
 Hunger
 Poor healing
• Kussmaul respirations (Rapid, deep breathing)
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Ineffective self-health management
Risk for injury
Risk for infection
Powerlessness
Imbalanced nutrition: More than body
requirements
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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
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Health promotion
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Acute intervention for
◦ Identify those at risk, routine screening
◦ Hypoglycemia; Diabetic ketoacidosis; Hyperosmolar
hyperglycemic nonketotic syndrome.
◦ Stress of illness and surgery
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↑ blood glucose level
Continue taking oral agents and insulin.
Frequent monitoring of blood glucose
Patients undergoing surgery or radiologic procedures requiring
contrast medium should hold their metformin on day of surgery
and to 48 hour
Ambulatory and home care
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Overall goal is to reach an optimal level of independence
Insulin therapy and oral agents
Personal hygiene
Medical identification and travel card
Patient and family teaching
 Educate on disease process, physical activity, medications,
monitoring blood glucose, diet, resources.
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Knowledge
Balance of nutrition
Immune status
Health benefits
No injuries
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Diabetic ketoacidosis (DKA)
Hyperosmolar hyperglycemic syndrome (HHS)
Hypoglycemia
Table 49-17 compares the manifestations,
causes, management, and prevention of
hyperglycemia and hypoglycemia(page 1242)
◦ 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, and
Neglect
◦ When supply of insulin insufficient
 Glucose cannot be properly used for energy.
 Body breaks down fat stores.
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Ketones are by-products of fat metabolism.
Alter pH balance, causing metabolic acidosis
Ketone bodies excreted in urine
Electrolytes become depleted.
◦ Signs and symptoms
 Lethargy/weakness: early symptoms
 Dehydration
 Poor skin turgor
 Dry mucous membranes
 Tachycardia
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Orthostatic hypotension
Abdominal pain
Anorexia, vomiting
Kussmaul respirations
 Rapid deep breathing
 Attempt to reverse metabolic acidosis
 Sweet fruity odor
◦ Serious condition
 Must be treated promptly
Acute Complications
◦ Airway management
 Oxygen administration
◦ Correct fluid/electrolyte imbalance
 IV infusion 0.45% or 0.9% NaCl
 Restore urine output.
 Raise blood pressure.
 When blood glucose levels approach 250 mg/dL
 5% dextrose added to regimen
 Prevent hypoglycemia.
 Potassium replacement
 Sodium bicarbonate
◦ Insulin therapy
 Withheld until fluid resuscitation has begun.
 Bolus followed by insulin drip
Life-threatening syndrome
Less common than DKA
Often occurs in patients older than 60 years with type 2 DM
Patient has enough circulating insulin that ketoacidosis does not
occur.
◦ Neurologic manifestations occur because of ↑ serum osmolality.
◦ Usually history of
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 Inadequate fluid intake
 Increasing mental depression
 Polyuria
◦ Laboratory values
 Blood glucose >400 mg/dL
 Increase in serum osmolality
 Absent/minimal ketone bodies
◦ Medical emergency; high mortality rate
◦ Therapy similar to DKA, except HHS requires greater fluid
replacement
 Administration
 IV fluids
 Insulin therapy
 Electrolytes
 Assessment
 Renal status
 Cardiopulmonary status
 Level of consciousness
 Signs of potassium imbalance
 Cardiac monitoring
 Vital signs
◦ Low blood glucose
 Blood glucose level less than 70 mg/dL
◦ Common manifestations
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Confusion
Irritability
Diaphoresis
Tremors
Hunger
Weakness
Visual disturbances
◦ Untreated can progress to loss of consciousness,
seizures, coma, and death
• The
balance between blood glucose and insulin
can be disrupted by the administration of too
much insulin or medication, the ingestion of too
little food, delaying the time of eating, and
performing unusual amounts of exercise.
 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
 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
 Gels or tablets containing specific amounts of glucose
are convenient for carrying.
• Avoid large quantities of quick-acting carbohydrates, so that
rapid fluctuation to hyperglycemia does not occur.
◦ Treatment
 If alert enough to swallow
 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.
Patient not alert enough to swallow
 Administer 1 mg of glucagon IM or subcutaneously.
 Side effect: Rebound hypoglycemia
 Have patient ingest a complex carbohydrate after
recovery.
 In acute care settings
 20 to 50 mL of 50% dextrose IV push
◦ Macrovascular
 Diseases of large and medium-sized blood vessels
 one of the leading causes of diabetes-related deaths
 Tight glucose control may delay atherosclerotic
process.
 Risk factors
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Obesity
Smoking
Hypertension
High fat intake
Sedentary lifestyle
◦ Microvascular
 Result from thickening of vessel membranes in
capillaries and arterioles
 In response to chronic hyperglycemia
 Is specific to diabetes, unlike macrovascular
◦ Areas most noticeably affected
 Eyes (retinopathy)
 Kidneys (nephropathy)
 Skin (dermopathy)
◦ Clinical manifestations usually appear after 10 to
20 years of diabetes.
◦ Microvascular damage to retina
 Result of chronic hyperglycemia
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Diabetic retinopathy (cont’d)
◦ 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 intr-aretinal
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
 Produce vitreous contraction
 Retinal detachment can occur
◦ Treatment
 Laser photocoagulation
 Most common
 Laser destroys ischemic areas of retina
 Prevents further visual loss
 Vitrectomy
 Aspiration of blood, membrane, and fibers inside the eye
◦ damage to small blood vessels that supply the
glomeruli of the kidney
◦ Leading cause of end-stage renal disease
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Risk factors for the development of diabetic
nephropathy include hypertension, genetic
predisposition, smoking, and chronic
hyperglycemia.
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More than 60% of nontraumatic amputations in
the United States occur in people with 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. The pain is
often described as burning, cramping, crushing, or tearing.
 Usually worse at night
 Foot injury and ulcerations can occur without the patient
having pain.
 Can cause atrophy of small muscles of hands/feet
◦ Autonomic
 Can affect nearly all body systems
 Complications
 Gastroparesis
 Delayed gastric emptying
 Cardiovascular abnormalities
◦ 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
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Smoking
Clotting abnormalities.
Impaired immune function
Autonomic neuropathy
◦ Diabetic individuals more susceptible to infection
◦ Defect in mobilization of inflammatory cells
◦ Impairment of phagocytosis by neutrophils and
monocytes
◦ Loss of sensation may delay detection.
• process
of aging is associated with a reduction
in β-cell function, decreased insulin sensitivity,
and altered carbohydrate metabolism.
• diabetes has been found to contribute to a
greater rate of decline in cognitive function.
 Recognize limitations in physical activity and
visual acuity
 Education based on individual’s needs, using
slower pace .