Module 8: Diabetes Flashcards
Diabetes
-chronic multi system disease, results in hyperglycemia related to abnormal insulin production, impaired insulin use, or both
Etiology of Diabetes
Theory of causes single or combination of factor(s):
Genetic
Autoimmune
Environmental
Primarily a disorder of glucose metabolism related to
absent/insufficient insulin and/or ineffective use of available insulin
American Diabetes Association (ADA) recognizes 4
different classes of diabetes:
Type I
Type 2
Gestational
Other
Normal Glucose and Insulin Metabolism
Insulin—hormone produced by beta-cells in islets of Langerhans
Released continuously into bloodstream in small increments with larger amounts released after food
* Daily amount of insulin secreted by adult = 40 to 50 U
Stabilizes glucose level in range of 74 to 106 mg/dL
Insulin’s Role
Promotes glucose transport from the bloodstream across the cell membrane to the cytoplasm of the cell
Cells break down glucose to make energy
* Liver and muscle cells store excess glucose as glycogen
* insulin—inhibits gluconeogenesis, enhances fat deposition, and increases protein synthesis
* insulin—release of stored glucose from liver, protein from muscle, and fat from adipose tissue
Skeletal muscle and adipose tissue—have receptors for
insulin; insulin-dependent
Insulin “unlocks” receptors so glucose can move into the cell to be used for energy
Other tissues don’t require insulin for glucose transport but still require glucose to function
Liver cells—not insulin-dependent but have receptor sites to facilitate uptake of glucose and convert it to glycogen
Counterregulatory hormones
Glucagon, epinephrine, growth hormone, cortisol
Oppose effects of insulin
Stimulate glucose production and release by the liver
Decrease movement of glucose into cell
Help maintain normal glucose levels
Insulin is synthesized from proinsulin (precursor)
Enzymes split proinsulin into insulin and C-peptide in equal amounts
Serum and urine C-peptide measurement is a useful indicator of beta-cell function and insulin levels
Type 1 DM
5-10% of all people with diabetes
Any age, generally people under 40
Type 1 DM Etiology and Pathophysiology
Autoimmune disorder
Body develops antibodies against insulin and/or pancreatic β cells that produce insulin resulting in not enough insulin to survive
Genetic link
Genetic predisposition (HLAs, human leukocyte antigens, involved in immune response) and exposure to virus contribute to immune-related type 1 DM
Idiopathic diabetes—inherited
Latent autoimmune diabetes in adults (LADA)—slow, progressive type 1 DM
Type 1 Onset
Islet cell autoantibodies present for months to years before onset of symptoms
Manifestations develop when pancreas can no longer make enough insulin—then rapid onset with ketoacidosis
Recent history of sudden weight loss and polydipsia, polyuria, and polyphagia
Requires exogenous insulin
Patient may have temporary (3 to 12 months) remission after starting treatment
Type 2 DM
90-95% of all diabetes
Many risk factors - family history, obesity/overweight, and advanced age
Increased prevalence in children and in ethnic groups
Pancreas usually makes some endogenous insulin but
Not enough insulin is produced and/or body does not use insulin effectively
Major distinction
Presence of endogenous insulin
In type 1 diabetes, there is an absence of endogenous insulin
Genetic link—likely multiple genes and metabolic
abnormalities
1. Insulin resistance
2. Decreased insulin production by pancreas
3. Inappropriate hepatic glucose production
4. Production of hormones and cytokines by adipose tissue (adipokines)
5. The brain, kidneys, and gut have roles in developing type 2 DM
Metabolic syndrome increases risk for
type 2 DM
Increased glucose levels
Abdominal obesity
high BP
High triglyceride levels
Decreased HDLs levels
* 3 of 5 components = metabolic syndrome
Type 2 Onset
Gradual onset
Person may go many years with undetected Hyperglycemia
Often discovered with routine laboratory testing
High glucose or hemoglobin A1C
At time of diagnosis
* About 50% to 80% of β cells are no longer secreting insulin
* Average person has had diabetes for 6.5 years
Prediabetes
Increased risk for developing type 2 diabetes
Impaired glucose tolerance (IGT)
* OGTT—140 to 199 mg/dL
Impaired fasting glucose (IFG)
* Fasting glucose of 100 to 125 mg/dL
May have both IGT and IFG
Intermediate stage between normal glucose homeostasis and DM
Asymptomatic but long-term damage may already be
occurring, especially heart and blood vessels
Patient teaching important
Undergo screening; glucose and A1C
Learn and manage risk factors
Monitor for symptoms of diabetes
Maintain healthy weight, exercise, make healthy food choices
Gestational DM
Develops during pregnancy; 2% to 10% in United States
risk for cesarean delivery and perinatal/neonatal
complications
Screen high-risk patients first visit
Obese, advanced maternal age, family history
Average-risk—24 to 28 weeks of gestation
Usually glucose levels normal 6 weeks post partum
Up to 63% chance of type 2 within 16 years
Other Specific Types of Diabetes
Results from injury to, interference with, or destruction
of β-cell function in the pancreas
From medical conditions and/or drugs
Resolves when underlying condition is treated or drug is discontinued
Clinical Manifestations
Type 1 DM
Classic symptoms
Polyuria (frequent urination)
Polydipsia (excessive thirst)
Polyphagia (excessive hunger)
Weight loss
Weakness
Fatigue
Ketoacidosis (DKA)
Clinical Manifestations
Type 2 DM
Nonspecific symptoms
Classic symptoms of type 1 may manifest
Fatigue
Recurrent infection
Recurrent vaginal yeast or candida infection
Prolonged wound healing
Visual problems
Diabetes Diagnostic Studies
- A1C level 6.5% or higher
- Fasting plasma glucose (FPG) level > 126 mg/dL
- 2-hour plasma glucose level during OGTT greater than 200 mg/dL (with glucose load of 75 g)
* Repeat criteria 1 to 3 on another visit to confirm
* Be attentive to influencing factors - Classic symptoms of hyperglycemia or hyperglycemic crisis or a random plasma glucose level greater than 200 mg/dL
A1C
Glycosylated hemoglobin reflects glucose levels over past 2 to 3 months
* Glucose attaches to hemoglobin molecule; higher the glucose levels = higher the A1C
Used to diagnose, monitor response to therapy, and screen patients with prediabetes
Goal: Less than 6.5% to 7% (reduces complications)
Other Testing
Fructosamine
Reflects glycemia in previous 1 to 3 weeks
* May show change before A1C
Used for hemoglobinopathies or short-term measurement of glucose levels
Islet cell autoantibody testing
Other:
Lipids, BUN, creatinine, electrolytes
Albuminuria and urine acetone
BP, ECG, eye exam, dental exam, foot exam, neurologic exam, ABI, weight
Diabetes Management Goals
Goals of diabetes management
Reduce symptoms
Promote well-being
Prevent acute complications
Prevent or delay onset and progression of
long-term complications
Meeting goals of ABCs of Diabetes lowers risk of heart attack
-A1C, BP, Cholesterol
Patient and caregiver teaching
Nutrition therapy
Drug therapy—glucose-lowering agents
* Insulin, oral agents, noninsulin injectable agents
Exercise
Self-monitoring of glucose
Type 2—healthy eating, regular exercise, and healthy
weight may be sufficient
May need medication as disease progresses
Drug Therapy - Insulin
Exogenous injected insulin
Insulin from an outside source
* Multiple daily injections or insulin pump
Required for type 1 diabetes
Prescribed for patients with type 2 diabetes during times of stress or as disease progresses and unable to manage glucose levels with previous therapies
Human insulin
Genetically engineered in laboratories from E. coli or yeast cells
Insulins differ by onset, peak action, and duration. They are categorized as
Rapid-acting
Short-acting
Intermediate-acting
Long-acting
Insulin Plans
Basal-bolus regimen
Intensive or physiologic insulin therapy—most closely mimics endogenous insulin production
Administer multiple daily injections (or insulin pump) with frequent self-monitoring of glucose (or continuous glucose monitoring system)
Bolus—rapid- or short-acting insulin before meals
Basal—intermediate- or long-acting (background) insulin once or twice a day
Goal: glucose level as close to normal as possible as much of the time as possible
Patient and HCP work together to choose a plan based on:
Desired and feasible glucose levels
Lifestyle
Food choices
Activity pattern
Less intense plans work for some people
Mealtime Insulin (Bolus)
Manage postprandial glucose levels
Insulin preparations
Rapid-acting synthetic (bolus)—mimic natural insulin in response to meals
* Aspart, glulisine, and lispro
* Onset of action 15 minutes
* Injected within 15 minutes of mealtime
Short-acting regular (bolus)
* Onset of action 30 to 60 minutes
* Injected 30 to 45 minutes before meal
More likely to cause hypoglycemia
Long- or Intermediate-Acting
(Basal) Background Insulin
Used with mealtime insulin to manage glucose levels in
between meals and overnight
Long-acting (basal)
* Degludec (Tresiba), detemir (Levemir), and glargine (Lantus, Toujeo, Basaglar)
* Released steadily and continuously with no peak action for many people; onset varies
* Administered once or twice a day
* Do not mix or dilute with any other insulin or solution
Intermediate-acting insulin (NPH)
Duration 12 to 18 hours
Peak 4 to 12 hours
Can mix with short- and rapid-acting insulins
Never given IV
Combination Insulin Therapy
Can mix short- or rapid-acting insulin with intermediate-acting insulin in same syringe
Provides mealtime and basal coverage in one injection
Commercially premixed formula or pen; flexible dosing limited
May self-mix from two vials
Consider visual, manual, or cognitive skills
Insulin Storage
Extreme temperatures can make insulin less effective [less than
32° F (0° C) or greater than 86° F (30° C)]
Vials and pens may be left at room temperature up to 4 weeks
Refrigerate extra unopened insulin
Avoid exposing to direct sunlight
Hot climates—use thermos or cooler
Store prefilled syringes upright
1 week if 2 insulin types
30 days for one type
Insulin Administration
Given by subcutaneous injection
* Avoid IM—risk of hypoglycemia
Regular insulin may be given IV
Cannot be taken orally—inactivated by gastric fluids
Steps for insulin injection
Absorption is fastest from abdomen, followed by arm, thigh, and buttock
Abdomen is often preferred site
Do not inject in site that will be exercised
Rotate injections within and between sites
U100 insulin—1 mL contains 100 U of insulin; must be
used with U100-marked syringe
Syringes marked for units
0.3 and 0.5 mL syringes have 1 U increments
1 mL syringe has 2 U increments
Needle sizes vary in length and gauge
6 mm (½ in), 8 mm (5⁄16 in), and 12.7 mm (½ in)
Administer at 90 degrees
Extremely thin or muscular at 45 degrees
Self-injection
* Only user recaps syringe
* No alcohol swab; wash with soap and water
* In hospital, follow policy to cleanse site
Insulin pen
* Portable, convenient, compact, discrete
* Various lengths and gauges
* Good option for patients with decreased vision
* Patient education and printed instructions
Insulin Pump
Continuous subcutaneous infusion of rapid-acting insulin
Small device connected to a catheter inserted into
subcutaneous tissue in abdominal wall
Some pumps are tubing-free
Change set and site every 2 to 3 days
Program basal and bolus doses that increase or decrease throughout the day based on carbohydrate intake, activity, or illness
Check glucose 4 to 8x/day or continuous monitoring
Major advantage—keeps glucose in a tighter range; avoid highs and lows
Careful programming and constant monitoring makes it possible as delivery is similar to normal physiologic pattern
More flexibility with meals and activities
Potential concerns of insulin pump
Infection at insertion site
Risk for DKA
Cost of pump and supplies
Attached to a device
Problems With Insulin Therapy
Hypoglycemia
Allergic reactions
-Local or systemic (rare)
-Other: preservative or latex or rubber stopper
Lipodystrophy—Changes in subcutaneous tissue
-Atrophy—wasting of subcutaneous tissue; indentations
-Hypertrophy—thickening of subcutaneous tissue
-Overuse of site; alters absorption of insulin
Somogyi effect
High dose of insulin causes decreased glucose during the night
Release of counterregulatory hormones causes rebound hyperglycemia
* Danger of this effect: when glucose checked in the morning and increased insulin is given
* Determine if Somogyi effect by checking glucose between 2 to 4 A.M.
Assess patient for headache, night sweats, or nightmares
Treatment is a bedtime snack, reducing the dose of insulin, or both
Dawn phenomenon
Morning hyperglycemia present on awakening
May be due to release of counterregulatory hormones in predawn hours
* Growth hormone and cortisol
* More severe in adolescence and young adulthood—peak time for growth hormone
Treatment is increase in insulin or adjustment of
administration time
Inhaled Insulin
Afrezza
Rapid-acting inhaled insulin
Administered at beginning of each meal or within 20 minutes after starting a meal
Used in combination with long-acting insulin for type 1 DM
Common adverse reactions: hypoglycemia, cough, throat pain or irritation
Not recommended for treatment of DKA, smokers; patients with asthma or COPD due to risk of bronchospasm
Drug Therapy: Oral and Noninsulin
Injectable Agents
Work to improve the mechanisms by which the body makes and uses insulin and glucose
Work on 3 defects of type 2 DM
-Insulin resistance
-Decreased insulin production
-Increased hepatic glucose production
Can be used in combination
Meds: Biguanides
Metformin (Glucophage)
Most effective 1st line treatment for type 2
* Available as immediate release, extended release, liquid forms
Action: reduces glucose production by liver
Enhances insulin sensitivity
Improves glucose transport
May cause weight loss
Used in prevention of type 2 diabetes
Withhold if patient is undergoing surgery or radiologic
procedure with contrast medium
24-48 hrs before and at least 48 hrs after when serum creatinine WNL
Contraindications
Renal, liver, cardiac disease; lactic acidosis
Iodine based contrast medium can cause AKI
Excessive alcohol intake
Meds: Sulfonylureas
Action: Increases insulin production from pancreas
Major side effect: hypoglycemia
Examples:
Glipizide (Glucotrol)
Glyburide (Glynase)
Glimepiride (Amaryl)
Meglitinides
Action: Increases insulin production from pancreas
Rapid onset: Decreases risk of hypoglycemia
Examples:
Repaglinide (Prandin)
Nateglinide (Starlix)
Alpha- Glucosidase Inhibitors
“Starch blockers”
Slow down absorption of carbohydrate in small intestine
Take with first bite of each meal
Check 2-hour postprandial glucose to determine
effectiveness
Examples:
Acarbose (Precose)
Miglitol (Glyset)
Thiazolidinediones
“Insulin sensitizers”
Most effective in those with insulin resistance
Improve insulin sensitivity, transport, and utilization at target tissues
Examples:
Pioglitazone (Actos)
Rosiglitazone (Avandia)
Rarely used because of adverse effects
Dipeptidyl Peptidase–4 (DDP-4)
Inhibitors
Incretin hormones
Increases insulin synthesis and release from
pancreas and decreases hepatic glucose production
Levels increase after a meal
Action: DDP-4 inhibitors block action of DDP-4- inactivates incretin hormones
Examples (“gliptins”)
* Alogliptin (Nesina)
* Sitagliptin (Januvia)
* Saxagliptin (Onglyza)
* Sitagliptin (Januvia)
Sodium-Glucose Co-Transporter 2
(SGLT2) Inhibitors
Action: block reabsorption of glucose by kidney
Increase urinary glucose excretion
Examples:
Canagliflozin (Invokana)
Dapagliflozin (Farxiga)
Empagliflozin (Jardiance)
Dopamine Receptor Agonist
Bromocriptine (Cycloset)—improves glucose levels
Mechanism of action unknown; the thought is that patients with type 2 diabetes have low levels of dopamine that may interfere with the body’s ability to control glucose
Action: increases dopamine receptor activity
Alone or in combination with other type 2 DM treatments
Combination Oral Therapy
Combine 2 different classes of DM medications in one pill
Advantage- fewer pills for patient to take
Glucagon-Like Peptide-1
Receptor Agonists
Action: simulate glucagon-like peptide–1 (GLP-1); one of the incretin hormones
Increase insulin synthesis and release
Inhibit glucagon secretion
Slow gastric emptying
Increases satiety, reduces food intake
Monotherapy or adjunct therapy for type 2 who don’t
achieve optimal glucose levels on OAs (oral agents)
Administered by subcutaneous injection in prefilled pen; frequency varies by medication
Examples:
Albiglutide (Tanzeum)
Dulaglutide (Trulicity)
Exenatide (Byetta)
Exenatide ER (Bydureon)
Liraglutide (Victoza)
Lixisenatide (Adlyxin)
Semaglutide (Ozempic)
What are Incretin Hormones?
Incretin hormones are a group of metabolic hormones that significantly decrease blood glucose levels by augmenting the secretion of insulin from the pancreas after eating, even before blood glucose levels become elevated. They also slow the rate of absorption of nutrients into the blood stream by reducing gastric emptying and may directly reduce food intake. The two most well-known incretins are Glucagon-like peptide-1 (GLP-1) and Gastric inhibitory polypeptide (GIP), also known as glucose-dependent insulinotropic polypeptide.
Functions of Incretin Hormones
Stimulate Insulin Secretion: Incretins enhance the secretion of insulin by the pancreas in a glucose-dependent manner, meaning the stimulation of insulin release is more pronounced when glucose levels in the blood are high. This helps to prevent the overproduction of insulin and reduces the risk of hypoglycemia (low blood sugar levels).
Inhibit Glucagon Secretion: In addition to promoting insulin release, incretins help regulate blood glucose levels by inhibiting the secretion of glucagon, a hormone that increases blood glucose levels by stimulating glucose production in the liver.
Slow Gastric Emptying: Incretins slow down the rate at which the stomach empties its contents into the small intestine, leading to a slower absorption of glucose into the bloodstream. This helps prevent spikes in blood glucose levels following meals.
Reduce Appetite: Some incretins, particularly GLP-1, can decrease appetite and promote satiety, contributing to weight management in individuals with obesity or type 2 diabetes.
GLP-1 Receptor Agonists: These are synthetic versions of GLP-1 or compounds that mimic the action of GLP-1, enhancing insulin secretion, suppressing glucagon release, and often leading to weight loss. They are administered via injection.
Dipeptidyl Peptidase-4 (DPP-4) Inhibitors: These oral medications work by inhibiting the enzyme DPP-4, which breaks down incretin hormones. By preventing the breakdown of GLP-1 and GIP, DPP-4 inhibitors extend the action of these endogenous incretins.
Amylin Analogs
Amylin—hormone secreted by beta-cells in response to food intake
slows gastric emptying, reduces postprandial glucagon
secretion, and increases satiety
Example
Pramlintide (Symlin)
* Used concurrently with mealtime insulin but can’t mix together in same syringe; decreased bolus insulin dose
Administer before meals with at least 250 cal
Watch for severe hypoglycemia ~ 3 hours after injection; have fast-acting glucose available
Other drugs affecting glucose levels
Drug interactions can potentiate hypoglycemia and
hyperglycemia effects
Examples:
* beta-adrenergic
* Thiazide and loop diuretics
Nutrition Therapy
Registered dietitian with expertise in diabetes management
Others: nurses, CDEs, CNS, social worker, HCPs
ADA guidelines
Person with DM can eat the same foods as without DM
Overall goal: Achieve and maintain safe and healthy glucose levels
Prevent or reduce the risk of complications
Achieve lipid profiles and BP that reduce risk for CVD
Prevent or slow development of chronic complications
Individual needs; personal, cultural preferences
Maintain pleasure of eating with healthy choices
To have flexibility - rapid-acting insulin, multiple daily injections, insulin pump (for Type 1)
-Moderate weight loss improves insulin sensitivity; appropriate serving sizes, reduced trans/saturated fats, regular exercise; monitor A1C, lipids, BP (type 2)
-Fiber helps control glucose levels
-20-35% total calories from fat
*Healthy fats come from plants (nuts, seeds, avocado)
Alcohol
-inhibits gluconeogenesis from liver, can cause severe hypoglycemia
-eat carbs when drinking
Patient Teaching for Nutrition
-Carb counting, track # of carbs per meal
-Serving size, typically 15g CHO, 45-60g per meal
-Insulin dose based on number of g; example: 1 unit per 15 g CHO
*teach patient to read labels and serving sizes
-My Plate guidelines; 1/2 non starchy veggies, 1/4 starch, 1/4 protein
Exercise Plan
At least 150 min/week moderate intensity
Strength 3x week
Decreases insulin resistance and glucose levels
Weight loss
Reduce need for DM drugs (type 2)
Reduce triglycerides and LDL , ↑ HDL
Decrease BP and improve circulation
Be careful that physical activity can cause hypoglycemia
**exercise 1 hour after a meal or have a 10-15g CHO snack first
**carby snack every 30 min to prevent hypoglycemia
**Effects of glucose lowering can last up to 48 hours after exercise
**Carry fast acting source of carbs
-If you’re frequently hypoglycemic after exercise, talk to provider about decreasing meds
**Strenuous exercise is perceived as stress by the body, temporarily increases glucose levels
**For type 1 - delay activity if glucose is over 250mg/dl and ketones are present in urine, will make it worse
When to test glucose levels
Before meals
2 hours after first bite
suspected hypoglycemia
q 4 hours during illness
before and after exercise
Hyperosmolar hyperglycemic syndrome (HHS)
a serious complication of diabetes mellitus, most commonly type 2 diabetes. It is characterized by extremely high blood glucose levels, significant dehydration, and an increased serum osmolality, without the significant ketoacidosis typically seen in diabetic ketoacidosis (DKA), which is more common in type 1 diabetes.
Key Features of HHS
Severe Hyperglycemia: Blood glucose levels in HHS can exceed 600 mg/dL (33.3 mmol/L), and in extreme cases, can reach 1000 mg/dL (55.5 mmol/L) or even higher.
Dehydration: Patients with HHS experience profound dehydration due to osmotic diuresis caused by high blood glucose levels, leading to increased urination and loss of fluids and electrolytes.
Increased Serum Osmolality: Osmolality, a measure of the solute concentration in the blood, is significantly increased in HHS, often exceeding 320 mOsm/kg. This hyperosmolarity leads to the movement of water out of cells, exacerbating dehydration.
Absence of Significant Ketoacidosis: Unlike DKA, HHS patients have minimal or no ketonemia and acidosis. This is because even the small amount of insulin present in most type 2 diabetes patients is enough to prevent ketone body production but not enough to control blood glucose levels.
Symptoms and Signs
Symptoms of HHS develop over days to weeks and may include:
Extreme thirst and dry mouth
Increased urination
Weakness
Confusion or altered consciousness, possibly progressing to coma
Seizures (in severe cases due to extreme hyperosmolarity)
Risk Factors
HHS is often precipitated by a stressor in individuals with compromised fluid intake or increased fluid loss. Common precipitating factors include:
Infections (e.g., pneumonia, urinary tract infections)
Acute illness
Medications that impair glucose tolerance (e.g., corticosteroids)
Inadequate fluid intake
Poorly managed or undiagnosed diabetes
Treatment
The management of HHS involves:
Rapid Rehydration: Administration of intravenous fluids to correct dehydration and reduce blood glucose levels.
Insulin Therapy: Low-dose insulin to gradually reduce blood glucose levels, avoiding rapid shifts in osmolality that can lead to cerebral edema.
Electrolyte Replacement: Particularly potassium, as levels may drop rapidly once insulin therapy is initiated and osmotic diuresis decreases.
Treatment of Precipitating Causes: Such as antibiotics for infections.
Monitoring: Close monitoring of vital signs, fluid balance, blood glucose levels, electrolytes, and mental status.
Management similar to DKA
IV insulin and NaCl infusions
* Add dextrose when glucose levels ~ 250 mg/dL
More fluid replacement needed
* Hemodynamic monitoring to avoid overload
Monitor: fluid and electrolytes (*K+), serum osmolality, VS, I &O, skin turgor, neuro, renal, and cardiac status
Correct underlying precipitating cause
Diabetic Ketoacidosis (DKA) Etiology + Pathophysiology
-Caused by huge insulin deficiency
Characterized by
Hyperglycemia
Ketosis
Acidosis
Dehydration
Most likely to occur in type 1 DM
May occur in people with type 2 DM with severe illness or stress
Precipitating factors:
Illness
Infection
Inadequate insulin dosage
Undiagnosed type 1 DM
Lack of education, understanding, or resources
Neglect
Insulin deficiency
Body burns fat as fuel source
By-product of fat metabolism—acidic ketones alter pH (metabolic acidosis)
Ketones excreted in urine along with electrolytes (cations)
Impairs protein synthesis, causes protein degradation resulting in nitrogen loss from tissues
Insulin deficiency
Stimulates glucose production from amino acids in liver leading to further hyperglycemia
Hyperglycemia may cause osmotic diuresis
Without treatment:
Severe depletion of sodium, potassium, chloride, magnesium, and phosphate
Acidosis
vomiting and further fluid and electrolyte losses
Hypovolemia followed by shock may cause renal
failure, causing retention of ketones and glucose and
further acidosis
Dehydration, electrolyte imbalance, and acidosis
causes coma and if not treated, death
DKA Clinical Manifestations
Dehydration
Dry mucous membranes
Tachycardia
Orthostatic hypotension
Early: Lethargy and weakness
As progresses:
Skin dry and loose; eyes soft and sunken
Abdominal pain, anorexia, nausea/vomiting
Kussmaul respirations
Sweet, fruity breath odor (acetone)
Glucose level of greater than or equal to 250 mg/dL
Blood pH lower than 7.30
Serum bicarbonate level less than 16 mEq/L
Moderate to high ketone levels in urine or serum
DKA Treatment
-Less severe - outpatient
-Hospitalization:
Severe fluid and electrolyte imbalance, fever,
nausea/vomiting, diarrhea, altered mental state, cause of DKA
Ability to communicate with health care provider every few hours
Emergency management
Ensure patent airway; administer O2
Establish IV access; begin fluid resuscitation to replace extracellular and intercellular fluid and correct electrolyte balance
* NaCl 0.45% or 0.9%; add 5% to 10% dextrose when glucose level approaches 250 mg/dL
* Restore urine output to 30 to 60 mL/hr
Protect from cerebral edema; monitor for fluid overload, renal or cardiac compromise
Monitor and replace potassium before starting insulin
therapy; drives K+ into cells leading to hypokalemia;
potentially life-threatening
IV regular insulin drip 0.1 U/kg/hr to correct
hyperglycemia and ketosis
* 36 to 54 mg/dL/hr drop in serum glucose will avoid
complications
Hypoglycemia
Too much insulin in proportion to glucose in the blood
Glucose level < 70 mg/dL
Neuroendocrine hormones released
Autonomic nervous system activated
Epinephrine released
Common manifestations
Shakiness
Palpitations
Nervousness
Diaphoresis
Anxiety
Hunger
Pallor
Altered mental function—“neuroglycopenia”
Difficulty speaking
Visual disturbances
Stupor
Confusion
Coma
Mimics alcohol intoxication
Untreated hypoglycemia can progress to loss of consciousness, seizures, coma, and death
Hypoglycemia unawareness
No warning signs/symptoms until glucose level critically low
* Incoherent, combative, loss of consciousness
Related to diabetes-related autonomic neuropathy and secretion of counterregulatory hormones
Patients at risk should keep glucose levels somewhat higher
Causes
Too much insulin or oral hypoglycemic agents
Too little food
Delaying time of eating
Too much exercise
Usually occurs at peak time for meds or with disruption in daily routine
Symptoms can also occur when high glucose level falls too rapidly
Hypoglycemia Management
Check glucose level
If less than 70 mg/dL, begin treatment
If greater than 70 mg/dL, investigate further for cause of signs/symptoms
If monitoring equipment not available, treatment should be initiated
Treatment: Rule of 15
Consume 15 g of a simple carbohydrate
* Fruit juice or regular soft drink, 4 to 6 oz
* Commercial products; gels or tablets
Recheck glucose level in 15 minutes
* Repeat if still < 70 g/dL; if remains low after 2 to 3x, contact HCP
* If glucose stable; give carb and protein
Avoid foods with fat; slows glucose absorption
Avoid overtreatment
Treatment in Acute Care Settings
Treatment in acute care settings
* 50% dextrose 20 to 50 mL IV push
Patient not alert enough to swallow or no IV access; also teach family/caregiver
* Glucagon 1 mg IM or subcutaneously
Watch for nausea; prevent aspiration
May not be effective with alcohol-related liver disease, starvation or adrenal insufficiency
Explore reason why occurred
Diabetes Complications: Angiopathy
-chronic disease of blood vessels, generic
-caused by chronic hyperglycemia
Leading cause of diabetes-related death
68% CVD and 16% stroke age 65 and older
2 categories
Macrovascular
Microvascular complications
Theories of how chronic hyperglycemia damages cells and tissues:
Accumulation of damaging by-products of glucose
metabolism (e.g. sorbitol) is associated with damage to nerve cells
Formation of abnormal glucose molecules in the basement membrane of small blood vessels that circulate to the eyes and kidneys
Derangement in RBC function results in decreased tissue oxygenation
Microvascular Complications
Diseases of large and medium-sized blood vessels
Cerebrovascular disease
Cardiovascular disease
Peripheral vascular disease
Greater frequency and earlier onset in patients with
diabetes
Women 4 to 6x risk for CVD
Men 2 to 3x risk for CVD those without DM
Thickening of vessel membranes in capillaries and
arterioles from chronic hyperglycemia
Areas most affected
Eyes—retinopathy
Kidneys—nephropathy
Nerves—neuropathy
Macrovascular Complications
Decrease and treat CVD risk factors
Obesity—nutrition and exercise
Smoking—blood vessel disease, stroke and lower extremity amputation; cessation
Hypertension—optimize BP; decrease CV and renal disease
High fat intake/dyslipidemia; statin and lifestyle interventions
Sedentary lifestyle—exercise
Retinopathy - a Microvascular Complication
Microvascular damage to retina due to chronic
hyperglycemia, nephropathy, and HTN
Most common cause of new cases of adult blindness
Two classifications
Nonproliferative- more common
Proliferative- more severe
Nonproliferative
Partial occlusion of small blood vessels in retina causes microaneurysms
Weakened walls cause fluid leaks resulting in edema and eventually hard exudates or hemorrhages
Mild to severe loss of vision
* Retina (macula) involvement—severe
Proliferative
Involves retina and vitreous
Retinal capillary occlusion results in compensation with new
blood vessels formed (neovascularization)very fragile and
bleed easily
* Patient see black or red spots or lines
Can cause retinal detachment
* Macula involvement causes vision loss
Glaucoma and cataracts can also occur
Initially no changes in vision
Annual eye exam with dilation to monitor
Maintain healthy glucose levels and manage
hypertension
Treatments
Laser photocoagulation
* Most common
* Laser destroys ischemic areas of retina
Vitrectomy
* Aspiration of blood, membrane, and fibers inside the eye
Iluvien
* injectable micro-insert that delivers corticosteroids flucinolone acetonide for 36 months
Vascular endothelial growth factor (VEGF) blocking drugs—reduce inflammation
Nephropathy - A Microvascular Complication
Damage to small blood vessels that supply the glomeruli of the kidney
Leading cause of end-stage renal disease in U.S.
20% to 40% of people with diabetes have it
Risk factors
Hypertension
Genetics
Smoking
Chronic hyperglycemia
Annual screening for albuminuria and albumin-to-creatinine ratio
If albuminuria present, drugs to delay progression
* ACE inhibitors or angiotensin II receptor blockers
Control of hypertension and glucose levels in a healthy range is imperative
Neuropathy - Microvascular Complication
Nerve damage due to metabolic imbalances of diabetes
60% to 70% of patients with diabetes have some degree of neuropathy
Sensory neuropathy—most common
* Loss of protective sensation in lower extremities, results in increased risk of amputation
* 60% of nontraumatic amputation is related to diabetes
Screen
* Type 2— time of diagnosis
* Type 1— 5 years after diagnosis
Theory: persistent hyperglycemia causes accumulation of sorbitol and fructose that damages nerves
Reduced nerve conduction and demyelination
Ischemic damage to peripheral nerves
May precede, accompany, or follow diagnosis
Classifications
Sensory or autonomic
Sensory Neuropathy
Distal symmetric polyneuropathy
Most common form
Affects hands and/or feet bilaterally; “stocking-glove
neuropathy”
Loss of sensation, abnormal sensations, pain, and
paresthesias
* Pain—burning, cramping, crushing, tearing; worse or only occurs at night
Paresthesias— tingling, burning, itching; “walking on
pillows or numb feet;”
Hyperesthesia
Complete or partial loss of sensitivity to touch or
temperature is common
Foot injury and ulcerations may occur without patient ever having pain
Small muscles of hands and feet may be affected causing deformity and limited fine movement
Treatment
Managing glucose levels
Drug therapy
* Topical creams
* Tricyclic antidepressants
* Selective serotonin and norepinephrine reuptake inhibitors
* Antiseizure medications
* Pregabalin
Autonomic Neuropathy
Can affect nearly all body systems and lead to
* Hypoglycemic unawareness, bowel incontinence and diarrhea, and urinary retention
Gastroparesis can cause:
* Delayed gastric emptying resulting in anorexia, nausea, vomiting, GERD, feeling full, hypoglycemia
Cardiovascular abnormalities
* Postural hypotension/falls, resting tachycardia, painless myocardial infarction
Sexual function
* Erectile dysfunction—often first manifestation
* Decreased libido
* Vaginal infections
Neurogenic bladder can cause urinary retention
* Empty frequently, use Credé’s maneuver
* Cholinergic agonist drugs
* Self-catheterization
Foot and Lower Extremity
Complications of DM
Microvascular and macrovascular diseases increases risk for injury and infection
Sensory neuropathy and PAD are major risk factors.
Other factors clotting abnormalities, impaired immune function, autonomic neuropathy
Smoking increases risk
Sensory neuropathy may cause loss of protective
sensation (LOPS) prevents awareness of injury; major risk factor for amputation
Peripheral artery disease (PAD)
Decreased blood flow = decreased O2, WBCs, and nutrients causes longer wound healing, increased risk for infection
Patient teaching: Foot care
Proper footwear
Avoidance of foot injury
Skin and nail care
Daily inspection of feet
Prompt treatment of small problems
Diligent wound care for foot ulcers
Neuropathic arthropathy (Charcot’s foot)
-Joint dysfunction and footdrop may cause ulcers
Skin Complications of DM
Diabetic dermopathy—most common
* Red-brown, round or oval patches
* Scaly then flat and indented; shins
Acanthosis nigricans—manifestation of insulin resistance
* Velvety light brown to black skin thickening; flexures, axillae, and neck
Necrobiosis lipoidica diabeticorum
* Red-yellow lesions; atrophic skin, shiny and transparent
Infection Complications of DM
Defect in mobilization of inflammatory cells and impaired phagocytosis
Recurring or persistent infections
* C. albicans, boils, and furuncles; cystitis
Antibiotics—prompt and vigorous
Patient teaching to prevent infection
Hand hygiene, avoid exposure
Flu and pneumococcal vaccine
