2. Content
ā¢ Review of Anatomy
ā¢ Introduction
ā¢ Epidemiology
ā¢ Classification: (Type-I, Type-II, GDM and other)
ā¢ Diagnostic criteria
ā¢ Complications
ā¢ Treatment
ā¢ Nursing Management
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3. Anatomy and physiology of Pancrease
ā¢ Pancreas is a narrow, 6 inch long gland that
lies posterior and inferior to stomach on left
side of abdominal cavity.
ā¢ Pancreas extends laterally and superiorly
across abdomen from the curve of
duodenum to spleen.
ā¢ The head of pancreas, which connects to the
duodenum, is the widest region.
ā¢ The glandular tissue surrounds many small
ducts that drain into the central pancreatic
duct.
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4. Functions
Pancreas is a dual-function gland, having features of
both endocrine and exocrine glands.
Endocrine
ā¢ Pancreas with endocrine function is made of million
cell called islets of Langerhans.
ā¢ Four main cell types in the islets: Ī± alpha cells-
glucagon(increase glucose in blood), Ī² beta cells-
insulin (decrease glucose in blood), Ī delta cells-
somatostatin (regulates/stops Ī± and Ī² cells) and PP
cells , or Ī³ (gamma) cells, secrete pancreatic
polypeptide.
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6. Exocrine
ā¢ Secretes pancreatic fluid that contains digestive
enzymes that pass to small intestine.
ā¢ These enzymes help to further break down
carbohydrates, proteins and lipids (fats) in the chyme.
ā¢ Digestive enzymes include trypsin, chymotrypsin,
pancreatic lipase, and pancreatic amylase, and are
produced and secreted by acinar cells of the exocrine
pancreas.
ā¢ Specific cells lining pancreatic ducts, called
centroacinar cells, secrete bicarbonate- and salt-rich
solution into the small intestine.
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9. Introduction
ā¢ Diabetes Mellitus (DM) refers to a group of common
metabolic disorders that share the phenotype of
hyperglycemia.
ā¢ Caused by complex interaction of genetics and
environmental factor.
ā¢ Factors ā reduced insulin secretion, decreased glucose
utilization, and increased glucose production.
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10. Epidemiology
According to International Diabetes Federation,
South East Asia:
ļ 382 million people have diabetes in the world
and more than 72.1 million people in the South East
Asia Region; by 2035 this will rise to 123 million.
ļ There were 674,120 cases of diabetes in Nepal in
2013.
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11. Classification
ā¢ Type 1 diabetes (due to Ī²-cell destruction, usually
leading to absolute insulin deficiency).
ā¢ Type 2 diabetes (due to a progressive insulin
secretory defect on the background of insulin
resistance).
ā¢ Gestational diabetes mellitus (diabetes diagnosed
during pregnancy that is not clearly overt diabetes).
ā¢ Diabetes mellitus associated with other conditions
or causes.
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12. Prediabetes
Categories of increased risk for Diabetes (prediabetes)*
FBG 100 mg/dL (5.6 mmol/L) to 125 mg/dL (6.9 mmol/L) (IFG)
OR
2-h PG in the 75-g OGTT 140 mg/dL (7.8 mmol/L) to 199 mg/dL (11.0
mmol/L) (IGT)
OR
A1C 5.7ā6.4%
*For all three tests, risk is continuous, extending below the lower limit of the
range and becoming disproportionately greater at higher ends of the range.
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13. Diagnosis
Criteria for the diagnosis of Diabetes Mellitus
A1C ā„ 6.5%. The test should be performed in a laboratory using a method that is NGSP
certified and standardized to the DCCT assay.*
OR
FPG ā„ 126 mg/dL (7.0 mmol/L). Fasting is defined as no caloric intake for at least 8 h.*
OR
Two-hour PG ā„ 200 mg/dL (11.1 mmol/L) during an OGTT. The test should be
performed as described by the WHO, using a glucose load containing the equivalent of 75 g
anhydrous glucose dissolved in water.*
OR
In a patient with classic symptoms of hyperglycemia or hyperglycemic crisis, a
random plasma glucose ā„ 200 mg/dL (11.1 mmol/L).
*In the absence of unequivocal hyperglycemia, result should be confirmed by repeat
testing.
National Glycohemoglobin Standardization Program (NGSP)
Diabetes Control and Complications Trial (DCCT)
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14. Type 1 Diabetes
ā¢ Type 1diabetes was previously called insulin-dependent
diabetes or also called juvenile-onset diabetes, as it
often begins in childhood.
ā¢ Type 1 diabetes is characterized by destruction of the
pancreatic beta cells, leading to absolute insulin
deficiency.
ā¢ It is thought that combined genetic, immunologic and
possibly environmental (eg, viral) factors contribute to
beta cell destruction.
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15. DM Type 1 Pathology
Genetic Factor
ā¢ It is generally accepted that genetic susceptibility is a
underlying factor in the development of type 1
diabetes.
ā¢ People do not inherit type 1 diabetes itself; rather,
they inherit a genetic predisposition or tendency,
toward developing type 1 diabetes.
ā¢ This genetic tendency has been found in people with
certain HLA (human leukocyte antigen) types.
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16. contdā¦.
ā¢ One proposal is that reduced exposure to
microorganisms in early childhood limits maturation
of the immune system and increases susceptibility to
autoimmune disease (the 'hygiene hypothesis').
ā¢ Stress may precipitate type 1 diabetes by stimulating
the secretion of counter-regulatory hormones and
possibly by modulating immune activity.
ā¢ Dietary factors may also be important.
ā¢ Various nitrosamines (found in smoked and cured
meats) and coffee have been proposed as potentially
diabetogenic toxins.
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17. Clinical Features
ā¢ Polyuria: Caused by osmotic diuresis secondary to
hyperglycemia
ā¢ Thirst: response to the hyperosmolar state and dehydration
ā¢ Fatigue and weakness: may be caused by muscle wasting
from the catabolic state of insulin deficiency, hypovolemia,
and hypokalemia
ā¢ Extreme hunger with unintended weight loss
ā¢ Muscle cramps: caused by electrolyte imbalance
ā¢ Blurred vision: Glucose and its metabolites cause osmotic
swelling of the lens, altering its normal focal length
ā¢ Feeling numbness or tingling in feet
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18. Diagnosis
Age: before the age of 30. The incidence is 12 to 14
cases per 1,00,000 people younger than 20 years and
1 case per 500 people younger than 16 years.
Blood Tests:
ā¢ Fasting blood test (126 mg/dL (7 mmol/L) or higher
on two separate tests, is considered diabetes).
ā¢ (HbA1c) test: 6.5% or higher
ā¢ RBS level: 200 mg/dL (11.1 mmol/L) or higher
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19. Contdā¦
Immunologic Markers:
ā¢ Islet cell autoantibodies (ICAs) are a composite of
several different antibodies directed at pancreatic islet
molecules such as glutamic acid
decarboxylase(GAD), insulin and IA-2/ICA-512 and
serve as a marker of the autoimmune process of type
1 DM.
ā¢ Testing for ICAs can be useful in classifying the type
of DM as type 1 and in identifying nondiabetic
individuals at risk for developing type 1 DM.
Urine test: Ketone bodies
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20. Treatment
Insulin Therapy
1.Rapid acting insulin
ā¢ The rapid acting insulin is used as a bolus dosage.
ā¢ The action onsets in 15 minutes with peak actions in 30 to 90
minutes.
Drugs: Humalog or lispro, Novolog or aspart, Apidra or glulisine
2. Short acting insulin
ā¢ Short acting insulin action onsets within 30 minutes with the peak
action around 2 to 4 hours.
Drugs: Regular (R) humulin or novolin, Velosulin (for use in the
insulin pump)
3. Intermediate acting insulin I
ā¢ Action onsets within 1 to 2 hours with peak action of 4 to 10 hours.
ā¢ Drugs: NPH (N)
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21. 4. Long acting insulin
ā¢ It is usually given around bedtime.
ā¢ Action onset is roughly 1 to 2 hours with a sustained action
of 24 hours.
Drugs: Lantus (insulin glargine), Levemir (insulin detemir)
5. Premixed insulin
ā¢ Combination of specific proportions of intermediate-acting
and short-acting insulin in one bottle or insulin pen.
ā¢ These products are generally taken two or three times a day
before mealtime.
ā¢ Action onset is 30minutes to 4hours with sustained action
up to 24hours.
Drugs: Humulin 70/30, Novolin 70/30, Novolog 70/30,
Humulin 50/50, Humalog mix 75/25
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22. Treatment
ā¢ Dietary plan
ā¢ Regular check up of blood sugar levels: Blood
glucose to the near normal range, approximately 80ā
140 mg/dl
ā¢ Physically active or exercise
ā¢ Controlling blood pressure
ā¢ Monitoring cholesterol levels
ā¢ Transplantation of Pancreas
ā¢ Transplantation of Islet cells
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23. Prevention
Immunosuppressive drugs
ā¢ Cyclosporine A
ā¢ Anti-CD3 antibodies, including teplizumab and
otelixizumab, had suggested evidence of preserving
insulin production (as evidenced by sustained C-peptide
production) in newly diagnosed type 1 diabetes patients.
Diet
ā¢ Some research has suggested breastfeeding decreases the
risk in later life.
ā¢ Giving children 2000 IU of Vitamin D during their first
year of life is associated with reduced risk of type 1
diabetes, though the causal relationship is obscure.
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24. Type 2 Diabetes
ā¢ was previously referred to as non-insulin dependent diabetes
mellitus or adult onset diabetes.
ā¢ is a more complex condition than type 1 diabetes as there is a
combination of resistance to the actions of insulin in liver and
muscle together with impaired pancreatic Ī²-cell function
leading to 'relative' insulin deficiency.
ā¢ Insulin resistance appears to come first, and leads to elevated
insulin secretion in order to maintain normal blood glucose
levels.
ā¢ However, in susceptible individuals the pancreatic Ī² cells are
unable to sustain the increased demand for insulin and a
slowly progressive insulin deficiency develops.
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25. contdā¦
Insulin resistance
ā¢ refers to decreased tissue sensitivity to insulin.
ā¢ Normally, insulin binds to special receptors on cell surfaces
and initiates a series of reactions involved in glucose
metabolism.
ā¢ In type 2 diabetes, these intracellular reactions are diminished,
thus rendering insulin less effective at stimulating glucose
uptake by the tissues and at regulating glucose release by the
liver.
ā¢ The exact mechanisms that lead to insulin resistance and
impaired insulin secretion in type 2 diabetes are unknown,
although genetic factors are thought to play a role.
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26. contdā¦
Impaired pancreatic Ī²-cell function
ā¢ Insulin secretion and sensitivity are interrelated.
ā¢ In type 2 DM, insulin secretion initially increases in response
to insulin resistance to maintain normal glucose tolerance.
ā¢ Initially, the insulin secretory defect is mild and selectively
involves glucose-stimulated insulin secretion.
ā¢ The response to other nonglucose secretagogues, such as
arginine, is preserved.
ā¢ Eventually, the insulin secretory defect progresses to a state of
grossly inadequate insulin secretion.
ā¢ The reason for the decline in insulin secretory capacity in type
2 DM is unclear.
ā¢ The assumption is that a second genetic defectāsuperimposed
on insulin resistanceāleads to beta cell failure.
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27. Pathophysiology
ā¢ Type 2 DM is characterized by impaired insulin secretion, insulin
resistance, excessive hepatic glucose production, and abnormal
fat metabolism.
ā¢ Obesity (particularly visceral or central) is very common in type
2 DM.
ā¢ In the early stages of the disorder, glucose tolerance remains
near-normal, despite insulin resistance, because the pancreatic
beta cells compensate by increasing insulin output.
ā¢ As insulin resistance and compensatory hyperinsulinemia
progress, the pancreatic islets in certain individuals are unable to
sustain the hyperinsulinemic state.
ā¢ A further decline in insulin secretion and an increase in hepatic
glucose production lead to overt diabetes with fasting
hyperglycemia.
ā¢ Ultimately, beta cell failure may ensue.
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28. Risk factors for DM type 2
ā¢ Family history of diabetes (i.e., parent or sibling with type 2
diabetes): Both parents have type 2 DM, the risk approaches
40%.
ā¢ Obesity (BMI ā„25 kg/m2)
ā¢ Habitual physical inactivity
ā¢ Race/ethnicity (e.g., African American, Latino, Native
American, Asian American, Pacific Islander)
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29. contdā¦
ā¢ History of GDM or delivery of baby >4 kg (>9 lb)
ā¢ Hypertension (blood pressure ā„140/90 mmHg)
ā¢ HDL cholesterol level <35 mg/dL (0.90 mmol/L) and/or a
triglyceride level >250 mg/dL (2.82 mmol/L)
ā¢ Polycystic ovary syndrome
ā¢ History of vascular disease
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30. Treatment of DM type 2
ā¢ Type 2 diabetes management should begin with
Medical nutrition therapy (MNT).
ā¢ An exercise regimen to increase insulin sensitivity
and promote weight loss should also be instituted.
ā¢ Pharmacologic approaches to the management of
type 2 DM include oral glucose-lowering agents,
insulin, and other agents that improve glucose
control.
ā¢ Type 2 DM is a progressive disorder, requires
multiple therapeutic agents and often insulin
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31. Glucose-Lowering Agents
Sulfonylureas
ā¢ Primary action is directly stimulating the pancreas to
secrete insulin.
ā¢ Therefore, a functioning pancreas is necessary for
these agents to be effective, and they cannot be used
in patients with type 1 diabetes.
ā¢ These agents improve insulin action at the cellular
level and may also directly decrease glucose
production by the liver.
ā¢ The sulfonylureas can be divided into first- and
second-generation categories.
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33. Biguanides
ā¢ It produces antidiabetic effects by facilitating
insulinās action on peripheral receptor sites.
ā¢ Therefore, it can be used only in the presence of
insulin.
ā¢ There is some evidence that it also impairs glucose
absorption by the gut and inhibits hepatic
gluconeogenesis.
ā¢ Increases susceptibility to lactic acidosis.
ā¢ Contraindicate in patients with impaired renal or
hepatic function and in those who drink alcohol in
excess.
Drug: Metformin
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34. contdā¦
Alpha Glucosidase Inhibitors
ā¢ work by delaying the absorption of glucose in the
intestinal system, resulting in a lower postprandial
blood glucose level.
ā¢ must be taken immediately before a meal, making
therapeutic adherence.
ā¢ Side effects are diarrhea and flatulence.
ā¢ Drug: Acarbose (Precose)
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35. Thiazolidinediones
ā¢ enhance insulin action at the receptor site without
increasing insulin secretion from the beta cells of the
pancreas.
ā¢ may affect liver function; therefore, liver function studies
must be performed (monthly for the first 12 months of
treatment, and quarterly thereafter).
Drug: Pioglitazone (Actos), rosiglitazone (Avandia)
Meglitinides
ā¢ lower the blood glucose level by stimulating insulin
release from the pancreatic beta cells.
ā¢ Its effectiveness depends on the presence of functioning
beta cells.
Drug: Repaglinide (Prandin), nateglinide (Starix)
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36. ā¢ DDP 4 Inhibitors Drugs: sitagliptin, Saxagliptin,
Vildagliptin, Linagliptin
ā¢ GLP-1 analogues: GLP-1 analogues have been
found to be particularly effective in helping to
improve blood glucose levels by stimulating insulin
secretion and helping with weight loss.
Drugs:
ā¢ Dulaglutide (Trulicity)
ā¢ Exenatide (Byetta)
ā¢ Liraglutide (Victoza)
ā¢ Lixisenatide (Lyxumia)
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37. Prevention of DM type 2
ā¢ Lifestyle modifications and pharmacologic agents prevent
or delay the onset of DM.
ā¢ Weight loss of 7% of body weight and increasing physical
activity to at least 150 min/week of moderate activity
such as walking.
ā¢ The Diabetes Prevention Program (DPP) demonstrated
that intensive changes in lifestyle (diet and exercise for 30
min/d five times per week) in individuals with delayed
the development of type 2 DM by 58% and
ā¢ Metformin prevented or delayed diabetes by 31%.
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38. Gestational Diabetes
ā¢ Refers to hyperglycaemia occurring for the first time during
pregnancy.
ā¢ During normal pregnancy, insulin sensitivity is reduced
through the action of placental hormones (human placental
lactogen, estrogen, and cortisol) and this affects glucose
tolerance.
ā¢ GDM occurs in Ķ 4% of pregnancies in the United States
ā¢ Most women revert to normal glucose tolerance post-partum
but have a substantial risk (30ā60%) of developing DM later
in life.
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39. DETECTION & DIAGNOSIS OF GESTATIONAL
DIABETES MELLITUS (GDM)
Recommendations for diabetes in Pregnancy
Screen for undiagnosed type 2 diabetes at the first prenatal visit in those with risk
factors, using standard diagnostic criteria.
Screen for GDM at 24ā28 weeks of gestation in pregnant women not previously
known to have diabetes.
Screen women with GDM for persistent diabetes at 6ā12 weeks postpartum,
using the OGTT and nonpregnancy diagnostic criteria.
Women with a history of GDM should have lifelong screening for the
development of diabetes or prediabetes at least every 3 years.
Further research is needed to establish a uniform approach to diagnosing GDM.
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41. Other conditions or causes
ā¢ Genetic defects of Ī²-cell function
ā¢ Genetic defects of insulin action (e.g. leprechaunism,
lipodystrophies)
ā¢ Pancreatic disease (e.g. pancreatitis, pancreatectomy,
neoplastic disease, cystic fibrosis, fibrocalculous
pancreatopathy)
ā¢ Excess endogenous production of hormonal
antagonists to insulin (e.g. growth hormone-
acromegaly; glucocorticoids- Cushing's syndrome;
catecholamines- phaeochromocytoma; thyroid
hormones-thyrotoxicosis)
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42. Contdā¦..
ā¢ Drug-induced (e.g. corticosteroids, thiazide
diuretics, phenytoin)
ā¢ Viral infections (e.g. congenital rubella, mumps)
ā¢ Uncommon forms of immune-mediated diabetes
ā¢ Associated with genetic syndromes (e.g. Down's
syndrome; Klinefelter's syndrome; Turner's
syndrome
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43. Complications
Hypoglycemia (insulin reaction):
ā¢ occurs when the blood glucose falls to less
than 50 to 60 mg/dL (2.7 to 3.3 mmol/L).
ā¢ caused by too much insulin or oral
hypoglycemic agents, too little food, or
excessive physical activity.
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44. Clinical Manifestations
ā¢ grouped into two categories: adrenergic symptoms and central nervous system
(CNS) symptoms.
In mild hypoglycemia, as the blood glucose level falls, the sympathetic nervous
system is stimulated, resulting in a surge of epinephrine and norepinephrine.
This causes symptoms such as sweating, tremor, tachycardia, palpitation,
nervousness, and hunger.
In moderate hypoglycemia
ā¢ Fall in blood glucose level deprives the brain cells of needed fuel for
functioning.
ā¢ Signs of impaired function of the CNS may include inability to concentrate,
headache, lightheadedness, confusion, memory lapses, numbness of the lips and
tongue, slurred speech, impaired coordination, emotional changes, double
vision, and drowsiness.
ā¢ Any combination of these symptoms (in addition to adrenergic symptoms) may
occur with moderate hypoglycemia.
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45. Contdā¦
In severe hypoglycemia
ā¢ CNS function is so impaired that the patient needs the
assistance.
ā¢ Symptoms may include disoriented behavior,
seizures, difficulty arousing from sleep, or loss of
consciousness.
ā¢ Also can cause a coma and even death.
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46. Management of Hypoglycemia
ā¢ Immediate treatment must be given when hypoglycemia
occurs. The usual recommendation is 15 g of a fast-
acting concentrated source of carbohydrate .
ā¢ The equivalency of 15 grams of glucose (approximate
servings) are:
ļThree or four commercially prepared glucose tablets
ļ4 to 6 glass of fruit juice or regular soda
ļ6 to 10 Life Savers or other hard candies
ļ2 to 3 teaspoons of sugar or honey
ā¢ Injection of glucagon or intravenous glucose.
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47. Diabetic Ketoacidosis
ā¢ It is sometimes the first indication that a person has
type 1 diabetes, and can be a serious complication of
lack of insulin.
ā¢ It occurs when the body cannot use sugar (glucose) as
a fuel source because there is no insulin or not
enough insulin.
ā¢ Fat is used for fuel instead. When fat breaks down,
waste products called ketones build up in the body.
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48. Signs and symptoms of DKA
ā¢ Frequent urination
ā¢ Extreme thirstiness
ā¢ Abdominal pain
ā¢ Weight loss
ā¢ Deep, rapid breathing
ā¢ Fruity smell on breath (Smell of ketones being
released from body)
ā¢ Confusion
ā¢ Weakness- Muscle stiffness or aches
ā¢ Nausea and vomiting
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49. Chronic or Long-term Diabetes
Complications
Microvascular Complications
ā¢ Eye disease
ā¢ Retinopathy (nonproliferative/proliferative)
ā¢ Macular edema
ā¢ Neuropathy
ā¢ Sensory and motor (mono- and polyneuropathy)
ā¢ Autonomic
ā¢ Nephropathy
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51. Criteria for testing for diabetes in asymptomatic adult individuals
Testing should be considered in all adults who are overweight (BMI ā„25 kg/m2) and have
additional risk factors:
ā¢ physical inactivity
ā¢ first-degree relative with diabetes
ā¢ high-risk race/ethnicity (e.g., African American, Latino, Native American, Asian
American)
ā¢ women who delivered a baby weighing >9 lb or were diagnosed with GDM
ā¢ hypertension (ā„140/90 mmHg or on therapy for hypertension)
ā¢ HDL cholesterol level <35 mg/dL and/or a triglyceride level >250 mg/dL
ā¢ women with polycystic ovarian syndrome
ā¢ other clinical conditions associated with insulin resistance (e.g., severe obesity,
acanthosis nigricans)
ā¢ history of CVD
In the absence of the above criteria, testing for diabetes should begin at age 45 years.
FPG ā„126 mg/dL (7.0 mmol/L). Fasting is defined as no caloric intake for at least 8 h.
If results are normal, testing should be repeated at least at 3-year intervals, with
consideration of more frequent testing depending on initial results (e.g., those with
prediabetes should be tested yearly) and risk status.
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52. Testing for type 2 diabetes in asymptomatic children*
Criteria
ā¢ Overweight (BMI >85th percentile for age and sex, weight for height >85th
percentile, or weight >120% of ideal for height)
Plus any two of the following risk factors:
ā¢ Family history of type 2 diabetes in first- or second-degree relative
ā¢ Race/ethnicity (Native American, African American, Latino, Asian American,
Pacific Islander)
ā¢ Signs of insulin resistance or conditions associated with insulin resistance (
hypertension, dyslipidemia, polycystic ovarian syndrome, or small-for-
gestational-age birth weight)
ā¢ Maternal history of diabetes or GDM during the childās gestation
Age of initiation: age 10 years or at onset of puberty, if puberty occurs at a younger age
Frequency: every 3 years
*Persons aged 18 years and younger.
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53. Patient Education
1. Diabetes Education
ā¢ Self-monitoring of blood glucose
ā¢ Urine ketone monitoring (type 1 DM)
ā¢ Insulin administration: Insulin Therapy and insulin
preparations, types, time course of action, selecting and
rotating the injection site, complications of insulin therapy
(insulin lipodystrophy, local and systemic allergic reaction)
ā¢ Guidelines for diabetes management during illnesses
ā¢ Management of hypoglycemia
ā¢ Foot and skin care
ā¢ Diabetes management before, during, and after exercise and
ā¢ Risk factor modifying activities.
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54. contdā¦
2. Nutrition
ā¢ Medical nutrition therapy (MNT) is a term used by the ADA to describe
the optimal coordination of caloric intake with other aspects of diabetes
therapy (insulin, exercise, weight loss). The ADA has issued
recommendations for three types of MNT.
ā¢ Primary prevention measures of MNT are directed at preventing or
delaying the onset of type 2 DM in high-risk individuals (obese or with pre-
diabetes) by promoting weight reduction.
ā¢ Secondary prevention measures of MNT are directed at preventing or
delaying diabetes related complications in diabetic individuals by
improving glycemic control.
ā¢ Tertiary prevention measures of MNT are directed at managing diabetes-
related complications (cardiovascular disease, nephropathy) in diabetic
individuals. For example, in individuals with diabetes and chronic kidney
disease, protein intake should be limited to 0.8 g/kg of body weight per day.
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55. Nutritional Recommendation for Adults with
Diabetes
Fat
ā¢ 20ā35% of total caloric intake
ā¢ Saturated fat <7% of total calories
ā¢ <200 mg/d of dietary cholesterol
ā¢ Two or more servings of fish per week provide
omega-3 polyunsaturated fatty acids
ā¢ Minimal trans fat consumption
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56. Contdā¦
Carbohydrate
ā¢ 45ā65% of total caloric intake (low-carbohydrate
diets are not recommended)
ā¢ Amount and type of carbohydrate important (amount
of carbohydrate determined by estimating grams of
carbohydrate in diet; glycemic index reflects how
consumption of a particular food affects the blood
glucose).
ā¢ Sucrose-containing foods may be consumed with
adjustments in insulin dose
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57. Contdā¦
Protein
ā¢ 10ā35% of total caloric intake (high-protein diets are
not recommended)
Other components
ā¢ Fiber-containing foods may reduce postprandial
glucose
ā¢ Non nutrient sweeteners
Alcohol
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58. Contdā¦
3. Exercise
ā¢ For individuals with type 1 or type 2 DM, exercise is
also useful for lowering plasma glucose (during and
following exercise) and increasing insulin sensitivity.
ā¢ In patients with diabetes, the ADA recommends 150
min/ week (distributed over at least 3 days) of aerobic
physical activity.
ā¢ In patients with type 2 DM, the exercise regimen
should also include resistance training (weight lifting)
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59. Guidelines for ongoing medical care for
patients with diabetes
ā¢ Self-monitoring of blood glucose (individualized frequency)
ā¢ A1C testing (two to four times per year)
ā¢ Patient education in diabetes management (annual)
ā¢ Medical nutrition therapy and education (annual)
ā¢ Eye examination (annual)
ā¢ Foot examination (one to two times per year by physician;
daily by patient)
ā¢ Screening for diabetic nephropathy (annual)
ā¢ Blood pressure measurement (quarterly)
ā¢ Lipid profile and serum creatinine (estimate GFR) (annual)
ā¢ Influenza/pneumococcal immunizations
ā¢ Consider antiplatelet therapy
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60. Nursing Management
Assessment
1. Obtain a history of current problems, family history,
and general health history.
ā¢ Has the patient experienced polyuria, polydipsia,
polyphagia, and any other symptoms?
ā Number of years since diagnosis of diabetes
ā Family members diagnosed with diabetes, their
subsequent treatment, and complications
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61. Contdā¦
2. Perform a review of systems and physical examination to assess for
signs and symptoms of diabetes, general health of patient, and
presence of complications.
ā General: recent weight loss or gain, increased fatigue, tiredness,
anxiety
ā Skin: skin lesions, infections, dehydration, evidence of poor wound
healing
ā Eyes: changes in vision- floaters, halos, blurred vision, dry or
burning eyes, cataracts, glaucoma
ā Mouth: gingivitis, periodontal disease
ā Cardiovascular: orthostatic hypotension, cold extremities, weak
pedal pulses, leg claudication
ā GI: diarrhea, constipation, early satiety, bloating, increased
flatulence, hunger or thirst
ā Genitourinary (GU): increased urination, nocturia, impotence,
vaginal discharge
ā Neurologic: numbness and tingling of the extremities, decreased
pain and temperature perception, changes in gait and balance
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62. Nursing Diagnosis
ā¢ Imbalanced Nutrition: More than Body Requirements related
to intake in excess of activity expenditures
ā¢ Fear related to insulin injection
ā¢ Risk for Injury (hypoglycemia) related to effects of insulin,
inability to eat
ā¢ Activity Intolerance related to poor glucose control
ā¢ Deficient Knowledge related to use of oral hypoglycemic
agents
ā¢ Risk for Impaired Skin Integrity related to decreased sensation
and circulation to lower extremities
ā¢ Ineffective Coping related to chronic disease and complex
self-care regimen
621/1/2020 Prof. Dr. RS Mehta
63. Nursing Interventions
Improving Nutrition
ā¢ Assess current timing and content of meals.
ā¢ Advise patient on the importance of an individualized
meal plan in meeting weight-loss goals.
ā¢ Discuss the goals of dietary therapy for the patient.
ā¢ Setting a goal of a 10% (of patient's actual body
weight) weight loss over several months, reducing
blood sugar and other metabolic parameters.
ā¢ Explain the importance of exercise in
maintaining/reducing body weight.
631/1/2020 Prof. Dr. RS Mehta
64. Teaching about insulin
ā¢ Assist patient to reduce fear of injection by encouraging
verbalization of fears regarding insulin injection, and
identifying supportive coping techniques.
ā¢ Demonstrate and explain thoroughly the procedure for insulin
self-injection.
ā¢ Help patient to master technique by taking a step-by-step
approach.
ā Allow patient time to handle insulin and syringe to become
familiar with the equipment.
ā Teach self-injection first to alleviate fear of pain from
injection
ā¢ Review dosage and time of injections in relation to meals,
activity, and bedtime based on patient's individualized insulin
regimen
641/1/2020 Prof. Dr. RS Mehta
65. Improving activity tolerance
ā¢ Advise patient to assess blood glucose level before and
after strenuous exercise.
ā¢ Instruct patient to plan exercises on a regular basis each
day.
ā¢ Encourage patient to eat a carbohydrate snack before
exercising to avoid hypoglycemia.
ā¢ Advise patient that prolonged strenuous exercise may
require increased food at bedtime to avoid nocturnal
hypoglycemia.
ā¢ Instruct patient to avoid exercise whenever blood glucose
levels exceed 250 mg/day and urine ketones are present.
Patient should contact health care provider if levels
remain elevated.
651/1/2020 Prof. Dr. RS Mehta