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Older Adults Pt 2 > 11.1 Endocrine > Flashcards

11.1 Endocrine Flashcards

1
Q

Diabetes Mellitus

A
  • Disorder that results in hyperglycemia or elevated serum glucose
  • Number 1 cause of renal failure, lower-limb amputations and adult blindness
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2
Q

Glucose Control

A
  • 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
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3
Q

Islets of Langerhans

A
  • 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
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4
Q

Function of Insulin

A
  • 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
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5
Q

DIABETES LABS

A
  • 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+)
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6
Q

Type 1 Diabetes

A
  • 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)
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7
Q

Type 2 Diabetes

A
  • Insulin resistance and impaired insulin secretion
  • Onset usually around age 30 but incidence increasing due to childhood obesity
  • Slow, progressive glucose intolerance
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8
Q

Latent Autoimmune Diabetes of Adults (LADA)

A
  • 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
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9
Q

Gestational Diabetes

A
  • Glucose intolerance during pregnancy
  • Placental hormones cause insulin resistance and hyperglycemia
  • Increases risk of hypertensive disorders during pregnancy
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10
Q

Diabetes Associations

A
  • 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)
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11
Q

Risk Factors DM1

A
  • Early Onset
  • Genetic/Familial
  • Viral triggers or toxins
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12
Q

Risk Factors DM2

A
  • 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
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13
Q

DM1 Clinical Manifestations

A

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
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14
Q

DM2 Clinical Manifestations

A
  • Asymptomatic for years
  • Weakness
  • Vision Changes
  • Tingling/Numbness in Hands and Feet
  • Dry Skin
  • Skin lesions and wounds that heal slowly
  • Recurrent infection
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15
Q

Medical Management of Diabetes

A
  • Normalize insulin/glucose levels

- A1C Less than 7%

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16
Q

Nutritional Therapy

A
  • 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)
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17
Q

Exercise

A
  • 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
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18
Q

Sick Days Rule

A
  • 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
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19
Q

Pharmacologic Therapy

A

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

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20
Q

Insulin

A
  • 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

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21
Q

Insulin Storage

A
  • 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
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22
Q

Insulin Education

A
  • 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
23
Q

Rapid Insulin

A
  • 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

24
Q

Short Acting Insulin

A
  • Humulin R, Actrapid, Novolin

Onset - 30-60 minutes
Peak - 2-5 hours
Duration 6-8 hours

INJECT 20-30 MINUTES BEFORE MEALS

25
Q

Intermediate Insulin

A

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
26
Q

Long Insulin

A
  • 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

27
Q

Premixed Insulin

A

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

28
Q

Exenatide (Byetta)

A
  • Non-insulin injection used to improve glycemic control in DM2

Adverse Effects

  • Hypoglycemia
  • GI Issues
29
Q

Oral Antidiabetic Agents

A
  • Used for DM2 patients in conjunction with diet and exercise
  • Major adverse effect is hypoglycemia
  • Nurses should monitor blood glucose
30
Q

Non-Sulfonylureas

A
  • Glinides (Meglitinides)
  • Biguanides
  • Thiazolidinediones
  • Alpha-Glucosides Inhibitors
  • Gliptins
31
Q

Sulfonylureas

A

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
32
Q

Biguanides

A
  • 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)

33
Q

Glinides (Meglitinides)

A
  • 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
34
Q

Alpha Glucosidase Inhibitor

A

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.
35
Q

Thiazolidinediones (Glitazones)

A
  • Rosiglitazone (Avandia)
  • Improves cellular response to insulin (reduces insulin resistance)
  • Monitor liver enzymes before and during 1st year of therapy
36
Q

Gliptins

A
  • Improves beta cell health and suppresses glucagon

Sitagliptin (Januvia) - It is safe but may not be that efficient. Can be used with metformin

37
Q

Macrovascular Complications of DM

A
  • Accelerated Atherosclerosis
  • Coronary Artery Disease
  • Cerebrovascular Disease
  • Peripheral Vascular Disease
38
Q

Microvascular Complications of DM

A
  • Retinopathy

- Nephropathy

39
Q

Neuropathic Complications of DM

A
  • Peripheral neuropathy
  • Autonomic neuropathy
  • Hypoglycemic unawareness
  • Neuropathy
  • Sexual Dysfunction
40
Q

Morning Hyperglycemia

A
  • 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
41
Q

Hypoglycemia (Insulin Shock)

A
  • 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
42
Q

Glucagon

A
  • 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
43
Q

DKA

A
  • 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
44
Q

DKA Assessment

A
  • 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)
45
Q

DKA Treatment

A
  • 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)
46
Q

HHS (Hyperglycemic Hyperosmolarity Syndrome)

A
  • 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
47
Q

HHS Manifestations

A
  • Hypotension
  • Extreme Dehydration
  • Tachycardia
  • Neurological signs from cerebral dehydration
48
Q

Treatment of HHS

A
  • 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
49
Q

HHS MONITORING

A
  • Glucose
  • Renal Function (I&O)
  • ECG
  • Electrolytes
  • VS
  • Lung sounds (fluid overload)
50
Q

DKA

A
  • Hyperglycemia
  • Metabolic Acidosis
  • Ketonemia
  • Typically with DM1
51
Q

HHS

A
  • Severe Hyperglycemia
  • Elevated Serum Osmolarity
  • Fluid Volume Depletion
  • DM2
52
Q

DKA LAB VALUES

A 
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
53
Q

HHS LAB VALUES

A 
Glucose 600-1200
Sodium Normal
Potassium Normal
Osmolarity 330-380 (normal 275-295) 
Ketones normal
Bicarbonate normal
pH normal 
CO2 normal
Anion Gap normal

Older Adults Pt 2 (17 decks)

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