Ch. 59 Concepts of Care for Patients w/ DM Flashcards
Diabetes Mellitus (DM)
Common, chronic, complex disorder of impaired nutrient metabolism
Describes diseases of abnormal carbohydrate metabolism with a characteristic of hyperglycemia
Classification of Diabetes
Underlying problem causing a lack of insulin
Action and the severity of insulin deficiency
Type 1 DM
Insulin production is absent d/t autoimmune pancreatic beta-cell destruction
Abrupt onset, thirst, hunger, increased urine output, wt loss
Usually <30 yr old
All dependent on insulin
Type 1 DM Causes
Susceptible genes
Autoantigens
Environmental factors
Viruses - coxsackievirus, rubella, cytomegalovirus, EPV
Diet - early exposure to cow’s milk, high nitrates in water, low vitamin D
Type 1 DM Clinical Manifestations
Polyuria
Polyphagia
Polydipsia
Wt loss
Fatigue
Increased frequency of infections
Type 2 DM
Insulin resistance and decreased insulin secretion
Inability to suppress hepatic glucose production
Impaired glucose uptake
Type 2 DM Causes
Some beta cell dysfunction
Genetics
Ethnic groups - American Indians, Hispanics, Asians
What causes insulin resistance?
Develops from obesity and physical inactivity in a genetically susceptible adult
Type 2 DM is characterized by what?
Hyperglycemia d/t progressive loss of insulin secretion in beta cells > causes insulin resistance and insulin deficiency
Type 2 DM Clinical Manifestations
Polyuria
Nocturia
Polydipsia
Polyphagia
Recurrent infections
Prolonged wound healing
Visual changes
Fatigue
Decreased energy
Metabolic Syndrome
Simultaneous presence of metabolic factors that increase risk for developing type 2 DM and CVD
Metabolic Syndrome Characteristics
Abdominal obesity - waist circumference greater then or equal to 40in (men); greater then or equal to 35in (female)
Hyperglycemia
Hypertension
Hyperlipidemia
HDL < 40 (male); <50 (female)
Absence of Insulin
Lack of production or a problem with insulin use at cell receptors
Causes glucose to build up on the blood, causing hyperglycemia
What is required for glucose regulation?
Insulin to move glucose into many tissues
Basal Insulin Secretion
Low-level secretion during fasting
Prandial
Two-phase release after eating
An early burst of insulin secretion occurs within 10 minutes of eating, followed by an increasing release that lasts until BG levels return to normal
Classic Symptoms of DM
Polyuria
Polydipsia
Polyphagia (cells are starving)
Blurred vision
Weight loss
Acute Complications of Diabetes
Diabetic ketoacidosis (DKA)
Hyperglycemic-hyperosmolar state
Hypoglycemia
All 3 require emergent treatment and can be fatal if treatment is delayed or incorrect
Chronic Complications of Diabetes
Macrovascular - large blood vessels
Microvascular - small blood vessels
Develop from chronic hyperglycemia
Macrovascular Complication - Cardiovascular Disease (CVD)
CVD risk factors
Treatment is aggressive management of: HTN, hyperglycemia, hyperlipidemia
Priority - reduce modifiable risk factors by lifestyle modifications
CVD Risk Factors
Macrovascular Complication - Cerebrovascular Disease
Risk for stroke 2-4x higher in adults w/ DM
Increases likelihood of severe carotid atherosclerosis
Macrovascular Complication - Cerebrovascular Disease Additional Risk Factors
HTN
Hyperlipidemia
Nephropathy
Peripheral vascular disease
Alcohol
Tobacco
Macrovascular Complication - Reduced Immunity
Combination of vascular changes and hyperglycemia by reducing WBC activity, inhibiting gas exchange in tissues, and promoting growth of microbes
WBCs do not like to swim around in a sugary environment
Microvascular Complication - Eye & Vision
Blindness is 25x more common
Diabetic retinopathy r/t duration of diabetes
R/t blocked retinal blood vessels and cause them to leak, leading to retinal hypoxia
Proliferative Diabetic Retinopathy
Growth of new retinal blood vessels which are thin, fragile, and bleed easily leading to vision loss
Microvascular Complication - Diabetic Peripheral Neuropathy
Progressive deterioration of nerve function = muscle weakness, damage to nerve fibers
Damage causes pain at first, which is followed by loss of sensation
Onset slow
Microvascular Complication - Diabetic Autonomic Neuropathy
Due to failure of heart and arteries to respond to position changes by increasing HR and vascular tone
CAN, orthostatic hypotension, syncope
Can affect entire GI system (gastroparesis, neurogenic bladder, defective balancing hormones)
Microvascular Complication - Diabetic Nephropathy
Causes progressive albumin excretion and declining GFR
Changes in kidney = reduced function = kidney failure
Leading cause of ESRD = diabetic-kidney disease
Diabetic Nephropathy Risk Factors
10-15 yr history of DM
Poor blood glucose control
Uncontrolled HTN
Genetic predisposition
Microvascular Complication - Sexual Dysfunction
Due to damage to both nerve tissue and vascular tissue
Affects M & F
Made worse by poorly controlled BG levels
Other risk factors: obesity, HTM, tobacco use, some prescribed drugs
Microvascular Complication - Cognitive Dysfunction
Due to neuron damage, brain atrophy, cognitive impairment
DM increases risk for developing all types of dementia
Increases complications of neuropathy and retinopathy
Indications for Testing People for Type 2 Diabetes
BMI > 25
First-degree relative w/ DM
Physically inactive
High-risk ethnic population
Gave birth to baby weighing > 9 or had gestational diabetes
Hypertensive
A1C > 5.7%
Criteria for Diagnosis of Diabetes
A1C >6.5%
Fasting BG > or = to 126
Normal Blood Glucose Values
Fasting BG < 100 mg/dL
Glycosylated hemoglobin (A1C) 4%-6%
A1C Levels
Q6Months or quarterly
5.7%-6.4% prediabetes
> 6.5% diabetes
> 8% poorly controlled diabetes
Preventing Injury From Hyperglycemia
Maintaining BG levels in optimal target range
A1C maintained < or = to 7.0%
Majority of premeal BG levels 70-130
Peak after meal BG <180
Drug Therapy for Diabetes
Indicated for type 2
Type 1 requires insulin therapy
Insulin therapy indicated for type 2 when BG levels cannot be met
What is the most important thing to teach the patient on drug therapy with DM?
Antidiabetic drugs are not a substitute for dietary modification and exercise
Sulfonylureas (SU)
Insulin Stimulator
Glyburide; Glipizide
Used for patients who are still able to produce insulin
Sulfonylureas (SU) MOA
Stimulate insulin release from pancreatic beta cells
Sulfonylureas (SU) Pt Teaching
S/S of hypoglycemia
Take w/ or just before meals to prevent hypoglycemia
Report to provider any OTC or supplement use