Module 8: Diabetes

Question 1

Diabetes

Answer 1

-chronic multi system disease, results in hyperglycemia related to abnormal insulin production, impaired insulin use, or both

Question 2

Etiology of Diabetes

Answer 2

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

Question 3

Normal Glucose and Insulin Metabolism

Answer 3

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

Question 4

Insulin’s Role

Answer 4

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

Question 5

Type 1 DM

Answer 5

5-10% of all people with diabetes
Any age, generally people under 40

Question 6

Type 1 DM Etiology and Pathophysiology

Answer 6

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

Question 7

Type 1 Onset

Answer 7

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

Question 8

Type 2 DM

Answer 8

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

Question 9

Type 2 Onset

Answer 9

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

Question 10

Prediabetes

Answer 10

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

Question 11

Gestational DM

Answer 11

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

Question 12

Other Specific Types of Diabetes

Answer 12

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

Question 13

Clinical Manifestations
Type 1 DM

Answer 13

Classic symptoms
 Polyuria (frequent urination)
 Polydipsia (excessive thirst)
 Polyphagia (excessive hunger)

 Weight loss
 Weakness
 Fatigue
 Ketoacidosis (DKA)

Question 14

Clinical Manifestations
Type 2 DM

Answer 14

Nonspecific symptoms
 Classic symptoms of type 1 may manifest
 Fatigue
 Recurrent infection
 Recurrent vaginal yeast or candida infection
 Prolonged wound healing
 Visual problems

Question 15

Diabetes Diagnostic Studies

Answer 15

1. A1C level 6.5% or higher
2. Fasting plasma glucose (FPG) level > 126 mg/dL
3. 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
4. Classic symptoms of hyperglycemia or hyperglycemic crisis or a random plasma glucose level greater than 200 mg/dL

Question 16

A1C

Answer 16

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)

Question 17

Other Testing

Answer 17

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

Question 18

Diabetes Management Goals

Answer 18

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

Question 19

Drug Therapy - Insulin

Answer 19

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

Question 20

Insulin Plans

Answer 20

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

Question 21

Mealtime Insulin (Bolus)

Answer 21

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

Question 22

Long- or Intermediate-Acting
(Basal) Background Insulin

Answer 22

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

Question 23

Combination Insulin Therapy

Answer 23

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

Question 24

Insulin Storage

Answer 24

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

Question 25

Insulin Administration

Answer 25

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

Question 26

Insulin Pump

Answer 26

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

Question 27

Problems With Insulin Therapy

Answer 27

 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

Question 28

Inhaled Insulin

Answer 28

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

Question 29

Drug Therapy: Oral and Noninsulin
Injectable Agents

Answer 29

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

Question 30

Meds: Biguanides

Answer 30

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

Question 31

Meds: Sulfonylureas

Answer 31

Action: Increases insulin production from pancreas
 Major side effect: hypoglycemia

Examples:
 Glipizide (Glucotrol)
 Glyburide (Glynase)
 Glimepiride (Amaryl)

Question 32

Meglitinides

Answer 32

Action: Increases insulin production from pancreas
 Rapid onset: Decreases risk of hypoglycemia

Examples:
 Repaglinide (Prandin)
 Nateglinide (Starlix)

Question 33

Alpha- Glucosidase Inhibitors

Answer 33

“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)

Question 34

Thiazolidinediones

Answer 34

“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

Question 35

Dipeptidyl Peptidase–4 (DDP-4)
Inhibitors

Answer 35

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)

Question 36

Sodium-Glucose Co-Transporter 2
(SGLT2) Inhibitors

Answer 36

Action: block reabsorption of glucose by kidney
 Increase urinary glucose excretion

Examples:
 Canagliflozin (Invokana)
 Dapagliflozin (Farxiga)
 Empagliflozin (Jardiance)

Question 37

Dopamine Receptor Agonist

Answer 37

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

Question 38

Combination Oral Therapy

Answer 38

Combine 2 different classes of DM medications in one pill
 Advantage- fewer pills for patient to take

Question 39

Glucagon-Like Peptide-1
Receptor Agonists

Answer 39

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)

Question 40

What are Incretin Hormones?

Answer 40

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.

Question 41

Amylin Analogs

Answer 41

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

Question 42

Other drugs affecting glucose levels

Answer 42

Drug interactions can potentiate hypoglycemia and
hyperglycemia effects
 Examples:
* beta-adrenergic
* Thiazide and loop diuretics

Question 43

Nutrition Therapy

Answer 43

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

Question 44

Patient Teaching for Nutrition

Answer 44

-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

Question 45

Exercise Plan

Answer 45

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

Question 46

When to test glucose levels

Answer 46

Before meals
2 hours after first bite
suspected hypoglycemia
q 4 hours during illness
before and after exercise

Question 47

Hyperosmolar hyperglycemic syndrome (HHS)

Answer 47

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

Question 48

Diabetic Ketoacidosis (DKA) Etiology + Pathophysiology

Answer 48

-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

Question 49

DKA Clinical Manifestations

Answer 49

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

Question 50

DKA Treatment

Answer 50

-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

Question 51

Hypoglycemia

Answer 51

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

Question 52

Hypoglycemia Management

Answer 52

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

Question 53

Diabetes Complications: Angiopathy

Answer 53

-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

Question 54

Microvascular Complications

Answer 54

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

Question 55

Macrovascular Complications

Answer 55

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

Question 56

Retinopathy - a Microvascular Complication

Answer 56

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

Question 57

Nephropathy - A Microvascular Complication

Answer 57

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

Question 58

Neuropathy - Microvascular Complication

Answer 58

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

Question 59

Sensory Neuropathy

Answer 59

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

Question 60

Autonomic Neuropathy

Answer 60

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

Question 61

Foot and Lower Extremity
Complications of DM

Answer 61

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

Question 62

Skin Complications of DM

Answer 62

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

Question 63

Infection Complications of DM

Answer 63

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