11.1 Endocrine Flashcards
Diabetes Mellitus
- Disorder that results in hyperglycemia or elevated serum glucose
- Number 1 cause of renal failure, lower-limb amputations and adult blindness
Glucose Control
- Negative Feedback System
- Decrease in insulin, increase in glucagon and glucogenesis
- This leads to an increase in blood glucose
INCREASE IN BLOOD GLUCOSE CAN LEAD DOWN 2 PATHS
1st
- Decrease in glucagon
- Decrease of hepatic glucose production
- Decrease in blood glucose
2nd
- Increase in insulin released from beta cells
- Removal of glucose from the blood
- Decrease in blood glucose
Islets of Langerhans
- Area in the pancreas that contain alpha and beta cells.
- Beta cells produce insulin which lowers blood glucose
- Alpha cells create glucagon which raise blood glucose
- Catecholamines such as epinephrine inhibit insulin release by stimulating alpha receptors or stimulate insulin release by stimulating beta receptors
- Growth hormones rise in response to hypoglycemia and can cause insulin resistance
- Glucocorticoids (cortisol) exacerbate hyperglycemia
Function of Insulin
- Transports and metabolizes glucose for energy
- Stimulates storage of glucose in the liver and muscles as glycogen
- Signals liver to stop releasing glucose
- Enhances storage of dietary fat as adipose tissue
- Accelerates the transport of amino acids into cells
- Inhibits breakdown of stored glucose, protein, and fat
DIABETES LABS
- Random Plasma Glucose
(Diabetes - >200) - Fasting Plasma Glucose
(Normal <100)
(Prediabetes 100-125)
(Diabetes >126) - 75mg Oral GTT at 2 Hours
(Normal <140)
(Prediabetes 140-199)
(Diabetes >200) - A1C
(Normal 3.9-6.5)
(Prediabetes 5.7-6.4)
(Diabetes 6.5+)
Type 1 Diabetes
- Destruction of beta cells
DM1A
- Commonly referred to as type 1 which is immune mediated diabetes.
- Absolute lack of insulin, elevated blood glucose, breakdown of fat and protein
- Common in younger people but can occur at any age
- Insulin inhibits lipolysis (breakdown of fat)
- Ketosis happens in Type 1 Diabetes where fatty acids are converted to ketones in the liver
- All 1A diabetes need exogenous insulin
DM1B (Idiopathic)
- No evidence of immune mediated beta cell destruction
- Strongly inherited (mainly African and Asian descent)
Type 2 Diabetes
- Insulin resistance and impaired insulin secretion
- Onset usually around age 30 but incidence increasing due to childhood obesity
- Slow, progressive glucose intolerance
Latent Autoimmune Diabetes of Adults (LADA)
- Development of autoimmune beta-cell destruction in pancreas is slower than DM1 and DM2
- They are not insulin dependent in the first 6 months of disease onset
- Same clinical manifestations as DM1 and DM2
Gestational Diabetes
- Glucose intolerance during pregnancy
- Placental hormones cause insulin resistance and hyperglycemia
- Increases risk of hypertensive disorders during pregnancy
Diabetes Associations
- Associated with a number of genetic syndromes/disorders
- Down Syndrome
- Klinefelter’s Syndrome (Boys with extra X Chromosome)
- Turner’s Syndrome (Girls with missing X Chromosome)
Risk Factors DM1
- Early Onset
- Genetic/Familial
- Viral triggers or toxins
Risk Factors DM2
- Obesity
- Age
- Hypertension over 140/90
- HDL 35 mg/dL or less
- Triglycerides 250 mg/dL or more
- History of gestational diabetes
- History of baby over 9 pounds
DM1 Clinical Manifestations
Polyuria - Excessive urination. Hyperglycemia causes osmotic diuresis. More glucose is filtered by the kidneys than can be reabsorbed so there is also signs of glycosuria
Polydipsia - Increased blood sugar leads water to leave cells into extracellular fluid. This causes intracellular dehydration and stimulation of thirst
Polyphagia - Depletion of cellular stores of carbohydrates, fats, and protein lead to cellular starvation and sensation of hunger
OTHER MANIFESTATIONS
- Weight loss due to polyuria and loss of fat/protein used for energy
- Fatigue due to glucose from food not being utilized properly
DM2 Clinical Manifestations
- Asymptomatic for years
- Weakness
- Vision Changes
- Tingling/Numbness in Hands and Feet
- Dry Skin
- Skin lesions and wounds that heal slowly
- Recurrent infection
Medical Management of Diabetes
- Normalize insulin/glucose levels
- A1C Less than 7%
Nutritional Therapy
- Maintaining reasonable body weight
- Control total caloric intake
- Normalize lipid and blood pressure to avoid heart disease
MEAL PLANNING
- Consider food preferences, lifestyle, and usual eating times.
- Review history of diet and need for weight loss
- Work with nutritionist to determine caloric requirement
- 50-60% Carbs, 30% Fat (less than 10% saturated fat and 300mg cholesterol), 10-20% protein from non-animal sources
GLYCEMIC INDEX
- Avoid sharp rapid increases in blood glucose after food is eaten
- Glycemic index describes how much a certain food increases blood glucose after eating
- Combination of starchy foods, protein and fat slows absorption and lowers glycemic index
- Raw/Whole foods have slower response than cooked/chopped/pureed
- Whole fruits have fiber which decrease glycemic index opposed to juice
- Eat foods with sugar with other slowly absorbed foods to lower glycemic index
OTHER CONCERNS
- Alcohol is absorbed before other nutrients and does not require insulin for absorption. Large amounts turn to fat which increases risk of DKA
- Nutritive sweeteners have calories nonnutritive sweeteners do not.
- Food labels (honey, brown sugar, corn syrup, flour, saturated fats (coconut/palm oil), hydrogenated vegetable fat, animal fat is contraindicated in people with high lipid value)
Exercise
- Lowers blood sugar, helps weight loss, lowers CVD risk
- Insulin must be adjusted because exercise lowers blood sugar levels
- Eat 15g carbohydrate snack before moderate exercise (to prevent hypoglycemia)
GENERAL CONSIDERAIONS - Exercise 3 days a week (with no more than 2 days in between exercise sessions)
- Resistance training 2 times a week with DM2
- Exercise same time of day and same duration
- Protect the feet, inspect the feet, prevent trauma to the feet due to neuropathy
- Avoid extreme temperatures while exercising
- Do not exercise when you are in poor metabolic control
Sick Days Rule
- Take insulin or oral antidiabetics as usual even if sick
- Test glucose/ketones every 3-4 hours
- Report elevated glucose and ketones to provider
- Take supplemental regular insulin every 3-4 hours if needed
- Eat soft food if they cannot follow their normal meal plan
- Liquids such as orange juice every 30min - 1hour to provide calories if vomiting, diarrhea, or fever
- Report n/v and diarrhea due to dangers of extreme fluid loss
- Hospitalization may be required if patient cannot retain fluids to avoid DKA and Coma
Pharmacologic Therapy
DM1 - Insulin, diet, exercise
DM2 - Begins with lifestyle change
ORDER OF MEDICATION
- Starts with 1 type of oral hypoglycemic
- Advances to 2 types of oral hypoglycemics
- Advances to either 3 drugs or 1 drug and insulin
- Advances to insulin only
Insulin
- Promotes cellular uptake of glucose and metabolism
- 1-4 injections a day
- Used to manage DM, treat DKA, promote uptake of potassium into cells, aids growth hormone (GH) deficiency
- SUBQ injection is absorbed slow and steady (upper arm is the slowest and abdomen is the fastest)
- Regular insulin is the only one that can be given IV
ADVERSE EFFECTS
- Hypoglycemia, fatigue, headache, nausea, irritability, trembling
COMPLICATIONS
- Allergic reactions, lipodystrophy, resistance to injected insulin, morning hyperglycemia
Insulin Storage
- Refrigerator (DO NOT FREEZE)
- Can be used for 1 month after opening
- Vials are stable for 1 month in room temperature and 3 months in fridge
- Prefilled syringes are stable in fridge for 1 week with needle pointing up
- Keep out of sunlight and extreme heat
Insulin Education
- Use/Action of Insulin
- Symptoms of Hypo/Hyperglycemia
- Blood Glucose Monitoring
HOW TO SELF INJECT INSULIN
- Aseptic
- Action/Peak Times
- Sites of administration/safe disposal of equipment
- Site rotations
- Sick Days
- Diet modifications
- Stress and glucose control
Rapid Insulin
- Humalog, Lispro
Onset - Less than 15 minutes
Peak - 60-90 minutes
Duration - 3-5 Hours - Novolog, Aspart
Onset - Less than 15 minutes
Peak - 60-120 minutes
Duration - 3-5 hours
INJECT 10-15 MINUTES BEFORE MEALS
USED IN CONJUNCTION WITH LONGER ACTING INSULIN
Short Acting Insulin
- Humulin R, Actrapid, Novolin
Onset - 30-60 minutes
Peak - 2-5 hours
Duration 6-8 hours
INJECT 20-30 MINUTES BEFORE MEALS
Intermediate Insulin
NPH (N), LENTE (L)
Onset - 1-2 hours
Peak - 4-12 hours
Duration - 18-24 hours
- USED TWICE A DAY
- COMBINED WITH RAPID OR SHORT ACTING INSULIN
Long Insulin
- Ultralente (U), Lantus, Glargine, Levemir, Detemir
Onset - 30 min - 3 hours
Peak - 10-20 hours
Duration - 20-26 hours
COVERS INSULIN NEEDS FOR 24 HOURS
COMBINED WITH RAPID OR SHORT ACTING INSULIN IF NEEDED
Premixed Insulin
Humulin 70/30, Novolog 70/30, Novolin 70/30
Onset - 15-30 minutes
Peak - 2-4 hours
Duration - Up to 24 hours
COMBINATION OF INTERMEDIATE AND SHORT ACTING INSULIN
COMMONLY USE TWICE DAILY BEFORE MEALS
Exenatide (Byetta)
- Non-insulin injection used to improve glycemic control in DM2
Adverse Effects
- Hypoglycemia
- GI Issues
Oral Antidiabetic Agents
- Used for DM2 patients in conjunction with diet and exercise
- Major adverse effect is hypoglycemia
- Nurses should monitor blood glucose
Non-Sulfonylureas
- Glinides (Meglitinides)
- Biguanides
- Thiazolidinediones
- Alpha-Glucosides Inhibitors
- Gliptins
Sulfonylureas
Glyburide (DiaBeta, Micronase)
- Treats type 2 DM
- Onset 2 hours, absorbed in GI Tract
- Stimulates pancreatic beta cells to release insulin and increase insulin sensitivity
- Do not use for type 1 diabetics or hypersensitivity to sulfa drugs
ADVERSE EFFECTS - Allergies, hypoglycemia (more likely with renal or liver damage)
- GI issues, photosensitivity, hemolytic anemia, hyponatremia
- Syndrome of inappropriate antidiuretic hormone (SIADH)
- Administer drug before breakfast and keep stored tightly capped at room temperature
- Educate patient on hypoglycemia
Biguanides
- Metformin (Glucophage)
- Drug of choice for initial therapy in DM2
- Suppresses hepatic glucose production and enhances insulin sensitivity
- Do not use for patients with hepatic/renal impairment, HF, alcoholism, and metabolic acidosis
- ADVERSE EFFECTS include anorexia, n/v, weight loss, GI issues, bloody dyscrasias.
TOXICITY
- Lactic Acidosis (hyperventilation, myalgias (muscle aches), malaise, unusual somnolence (drowsy)
Glinides (Meglitinides)
- Repaglinide (Prandin) and Nateglidine (Starlix)
- Take 30 minutes before meals and duration is 1-2 hours
- Stimulates release of insulin and increases insulin sensitivity
- Side effects are hypoglycemia and weight gain
Alpha Glucosidase Inhibitor
Acarbose (Precose)
- Only oral hypoglycemic that does not rely on insulin
- Delays absorption of carbohydrates causing smaller rise in blood glucose
- Do not use in patients with bowel or chronic liver disease
- Use oral glucose tablets for hypoglycemia instead of sugar because sugar will not be absorbed. Cannot cause hypoglycemia on its own.
Thiazolidinediones (Glitazones)
- Rosiglitazone (Avandia)
- Improves cellular response to insulin (reduces insulin resistance)
- Monitor liver enzymes before and during 1st year of therapy
Gliptins
- Improves beta cell health and suppresses glucagon
Sitagliptin (Januvia) - It is safe but may not be that efficient. Can be used with metformin
Macrovascular Complications of DM
- Accelerated Atherosclerosis
- Coronary Artery Disease
- Cerebrovascular Disease
- Peripheral Vascular Disease
Microvascular Complications of DM
- Retinopathy
- Nephropathy
Neuropathic Complications of DM
- Peripheral neuropathy
- Autonomic neuropathy
- Hypoglycemic unawareness
- Neuropathy
- Sexual Dysfunction
Morning Hyperglycemia
- Progressive rise in blood sugar from bedtime to morning
- Managed by taking evening dose of intermediate/long insulin
SOMOGYI PHENOMENON
- Hypoglycemia at 3am followed by hyperglycemia which increases insulin levels, that again causes hypoglycemia at night which triggers stress and catecholamines which leads to 5am hyperglycemia.
- Treated by decreasing intermediate insulin dose at night, or eating a snack before bed
DAWN PHENOMENON
- Early morning hyperglycemia with no hypoglycemia at night.
- Caused by increase in GH at night
- Glucose is normal until 3am then turns into hyperglycemia
- Managed by changing time of evening intermediate insulin to bedtime
Hypoglycemia (Insulin Shock)
- Blood glucose lower than 50-60
- Caused by medication, insulin, excessive physical activity, or too little food
MANIFESTATIONS
- Sweating, tremors, tachycardia, palpitations, nervousness, hunger, headache, confusion, memory lapse, drowsiness, slurred speech, disorientation, seizures, loss of consciousness
MANAGEMENT
- Give 15g of fast-acting carbohydrates such as 3-4 glucose tablets or soda (not diet). Retest blood glucose in 15 minutes, if still less than 70 mg/dL or if symptoms persist re-give 15g of carbs.
- After, provide a snack with protein and carbohydrates
- If patient is not conscious or cannot swallow, give 25-50 mL of 50% dextrose IV or 1 mg glucagon if IV glucose not available
Glucagon
- Restores consciousness for extreme hypoglycemia due to insulin overdose
- ONLY USE IF IV GLUCOSE IS NOT AVAILABLE
- Stimulates glycogenolysis (breakdown of glycogen into glucose)
- DOES NOT WORK WHEN PATIENT IS IN STARVATION BECAUSE THEY MAY NOT HAVE GLYCOGEN STORES LEFT
- Takes 20 minutes to work (IM,IV,SC,INTRANASAL)
- Comes in powder form
DKA
- Caused by abnormal metabolism of carbohydrates, protein and fat when glucose is not available.
- Due to lack of insulin and increase in glucagon
- Liver makes glucose but usage of glucose decreases
- Ketones are made as a bi-product of protein and and fat breakdown
- Causes ACIDOSIS, OSMOTIC DIURESIS (URINATION), ELETROLYTE DISTURBANCES
- AVOID EXERCISE WHEN KETONES ARE IN URINE
DKA Assessment
- Hyperglycemia, Dehydration, Acidosis
- Elevated blood glucose
- Ketoacidosis (low serum bicarbonate, low pH, low PCO2 from respiratory compensation (KUSSMAULS RESPIRATIONS)
- Ketones are found in blood and urine
- Electrolyte imbalance due to dehydration (increased creatinine, hematocrit, and BUN)
DKA Treatment
- ABC’s (patent airways and oxygen administration)
- Rehydration with 0.45-0.9% saline (monitor I&O)
- IV insulin until glucose reaches 250, then add glucose into IV fluids (monitor glucose hourly)
- Monitor potassium especially when reversing acidosis
MONITOR
- Glucose
- Renal function (I&O)
- ECG
- Electrolytes
- VS
- Lung sounds (fluid overload)
HHS (Hyperglycemic Hyperosmolarity Syndrome)
- Caused by lack of insulin but does not show ketones
- Causes Diuresis, Loss of Water, Hypernatremia, Increase Osmolarity
- Glucose can reach 800, 1000+ is deadly
HHS Manifestations
- Hypotension
- Extreme Dehydration
- Tachycardia
- Neurological signs from cerebral dehydration
Treatment of HHS
- ABC’s (patent airways and oxygen administration)
- Rehydrate with NS (requires more fluid than DKA)
- Continuous IV infusion of Regular Insulin, when glucose hits 250, add glucose back into IV fluids.
- Monitor serum glucose and potassium
- Rehydration causes plasma volume of potassium to decrease so they may become hypokalemic and insulin also causes potassium to move back into cells
HHS MONITORING
- Glucose
- Renal Function (I&O)
- ECG
- Electrolytes
- VS
- Lung sounds (fluid overload)
DKA
- Hyperglycemia
- Metabolic Acidosis
- Ketonemia
- Typically with DM1
HHS
- Severe Hyperglycemia
- Elevated Serum Osmolarity
- Fluid Volume Depletion
- DM2
DKA LAB VALUES
Glucose - 250-600 Sodium - 125-135 Potassium - May be elevated Osmolarity - 300-320 (normal is 275-295) Plasma Ketones increased Bicarbonate <15 pH - 6.8-7.3 CO2 - 20-30 Anion Gap Elevated
HHS LAB VALUES
Glucose 600-1200 Sodium Normal Potassium Normal Osmolarity 330-380 (normal 275-295) Ketones normal Bicarbonate normal pH normal CO2 normal Anion Gap normal
