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NUR4630 > Week 3: Endocrine/Metabolism > Flashcards

Week 3: Endocrine/Metabolism Flashcards

1
Q

The pancreas functions as both ?

A

exocrine and an endocrine gland

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2
Q

Exocrine function of pancreas

A

associated with the digestive system because it produces and secretes digestive enzymes

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3
Q

endocrine function of pancreas

A

produces two important hormones in Islets of Langerhans, insulin and glucagon

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4
Q

Insulin

A
  • (beta cells)
  • stimulates the uptake of glucose by body cells thereby decreasing blood levels of glucose
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5
Q

Glucagon

A
  • (alpha cells)
  • stimulates the breakdown of glycogen and the release of glucose, thereby increasing blood levels of glucose
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6
Q

Polysaccharide consisting of numerous monosaccharide glucoses linked together. Stored as an energy source in liver & muscles

A

Glycogen

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7
Q

Functions of insulin

A
  • Enables glucose to be transported into cells for energy for the body
  • Converts glucose to glycogen to be stored in muscles and the liver
  • Facilitates conversion of excess glucose to fat
  • Prevents the breakdown of body protein for energy
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8
Q
  • Not fully understood
  • Current thoughts
  • Viral exposure triggers immune response that also attack the beta cells in the Islets of Langerhans.
  • Genetic propensity also believed to be involved.
  • Some drug therapies destroy the beta cells
  • Pyrinuron (no longer used in the US)
  • Zanosar (used in the treatment of pancreatic cancer)
A

Type I diabetes

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9
Q
  • Polyuria – increased urine
  • Polydipsia – increased thirst
  • Polyphagia – increased hunger
  • 3 ‘Ps”
  • Weight loss
  • Fatigue
  • Nausea, vomiting
  • Ketoacidosis may be a presenting sign

clinical manifestations for?

A

Type I Clinical Manifestations

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10
Q
  • As cells cannot get glucose, they burn (1) as an alternate energy source
  • (2) are produced by the breakdown of fat and muscle, and are toxic at high levels
  • Ketones in the blood cause a condition called “acidosis” or “(3)” (low blood pH)
  • Urine testing detects ketones in the urine
  • Blood glucose levels are also (4).
A
  1. fats
  2. Ketones
  3. Ketoacidosis
  4. high
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11
Q
  • Most common form of diabetes (90%+ of all cases)
  • _Risk factors: _Obesity, Family history, Sedentary lifestyle, Ethnicity (African American, Hispanic, and Native Americans), Hypertension, Hyperlipidemia, Over the age of 45 years
  • Combination of physiological factors contribute: Impaired insulin production,
  • Insulin resistance
  • These individuals may have both
  • Hyperinsulinemia
  • Hyperglycemia
A

Type 2 diabetes

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12
Q

What is beta-cell dysfunction?

A
  • Major defect in individuals with type 2 diabetes
  • Reduced ability of beta-cells to secrete insulin in response to hyperglycemia
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13
Q

Why does the Beta Cell fail?

A
  • at the physiological level both glucose and free fatty acids stimulate insulin secretions, so beta cell dysfunction occurs as a result of a combination of this increased glucose and free fatty acid being present
  • but also genetic predisposition
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14
Q

Type 2 Clinical Manifestations

A
  • Polydipsia – increased thirst
  • Polyuria – increased urine
  • Polyphagia – increased hunger
  • Fatigue
  • Blurred vision
  • Slow healing infections
  • Impotence in men
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15
Q
  • Usually under 30
  • Rapid onset
  • Normal or underweight
  • Little or no insulin
  • Ketosis common
  • Autoimmune plus environmental factors
  • Genetic Propensity possible
  • Treated with insulin, diet and exercise

Type 1 or type 2?

A

Type 1

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16
Q
  • Usually over 40
  • Gradual onset
  • Most have insulin resistance
  • Ketosis rare
  • Part of metabolic insulin resistance syndrome
  • Strongly hereditary
  • Obesity in 80% of Cases
  • Diet & exercise, progressing to tablets, then insulin

Type 1 or type 2?

A

Type 2

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17
Q

Hyperglycemia and the ICU is associated with?

A

Increased mortality, especially when 300 or above

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18
Q

Hyperglycemia following CABG >200 increased?

A
  • 2x LOS
  • 3x Vent duration
  • 7X mortality
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19
Q

benefits of tight glycemic control

A
  • infection rates down
  • mortality rates down
  • afib down 60% post up
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20
Q

Intensive treatment vs. traditional treatment

A

keeping it down below 110 vs down below 200 decreases LOS, earlier discharge from ICU, discharged home quicker, off the vent quicker

21
Q

Severe hypoglycemia is defined as a blood glucose level?

A

less than 40, less than 50 = decrease in cerebral glucose availability

22
Q

hypoglycemic episodes in the icu causes increased?

A

mortality, recurrent MI’s, and they do worse

23
Q

Events Triggering Hospital Hypoglycemia

A
  • Transportation off ward, causing meal delay
  • Failure to measure blood glucose before insulin doses
  • New NPO status
  • Interruption of: IV dextrose therapy, Total parenteral nutrition, Enteral feedings, Continuous venovenous hemodialysis
24
Q
  • Concurrent illness (cerebral vascular accident, congestive heart failure, shock, sepsis)
  • Concurrent medications (Beta-blockers, quinolones, epinephrine)
  • Advanced age
  • Renal failure
  • Liver disease
  • Ventilator use

These increase risk of?

A

Features Increasing the Risk of Hypoglycemia in an Inpatient Setting

25
Q

What happens if the pt becomes hypoglycemic

A
  • Tachycardia and high blood pressure
  • Myocardial ischemia: Silent ischemia, angina, infarction
  • Cardiac arrhythmias: Transiently prolonged corrected QT interval,Increased QT dispersion
  • Sudden death
  • CVA
  • Decreased brain function
26
Q

AACE/ADA Recommended Target Glucose Levels in ICU Patients

A

ICU setting:

  • Starting threshold of no higher than 180 mg/dL
  • Once IV insulin is started, the glucose level should be maintained between 140 and 180 mg/dL
  • Lower glucose targets (110-140 mg/dL) may be appropriate in selected patients
  • Targets <110 mg/dL or >180 mg/dL are not recommended

<110: not recommended

110-140: acceptable (surgical pts)

140-180: Recommended

>180: NOT RECOMMENDED

27
Q

AACE/ADA Target Glucose Levels in Non–ICU Patients

A

Non–ICU setting:

  • Premeal glucose targets <140 mg/dL
  • Random BG <180 mg/dL
  • To avoid hypoglycemia, reassess insulin regimen if BG levels fall below 100 mg/dL
  • Occasional patients may be maintained with a glucose range below and/or above these cut-points

Hypoglycemia: <70

Severed hypoglycemia: <40

28
Q

Monitor BG ? with IV insulin

A

monitor BG hourly with IV insulin

29
Q

Continuous Variable Rate IV Insulin DripAtlanta Multiplier Method

A
  • *(formula on test) Starting Rate Units / hour = (BG – 60) x 0.02, where BG is current Blood Glucose and 0.02 is the multiplier
  • Check glucose every hour and adjust drip
  • Adjust Multiplier to keep in desired glucose target range (90 to 120 in ICU; 100 to 140 on floor)
30
Q

All patients with hyperglycemia should have an ? drawn to aid in transition and discharge therapy

A

HbA1C

31
Q

Methods of Screening for Hyperglycemia

A
  • Finger stick blood glucose on admission or use of the glucose done on the biochemical profile
  • If glucose >110 mg/dL fasting or >140 mg/dL random, place in appropriate protocol and continue monitoring
  • Draw Hemoglobin A1C for help in deciding who needs transition from IV to SC insulin and what treatment is needed at home, including insulin.
32
Q

Converting to SC insulin from IV protocol? What’s the exception?

A
  • If More than 0.5 u/hr IV insulin required with normal BG, start long-acting insulin (glargine). Exception: if no prior DM and normal A1C, may not need SC insulin
  • Must start SC insulin at least 1 to 2 hours before stopping IV insulin
  • Some centers start long-acting insulin on initiation of IV insulin or the night before stopping the drip
33
Q

Initiating SC Basal Bolus. Starting total dose, basal dose, bolus doses, correction bolus

A
  • Starting total dose = 0.5 x wgt. in kg. Wt. is 100 kg; 0.5 x 100 = 50 units
  • Basal dose (glargine) = 50% of starting dose at HS. 0.5 x 50 = 25 units at HS
  • Bolus doses (rapid analog) = 50% of starting dose. 0.5 x 50 = 25 divided by 3 = ~8 units pc (tid)
  • Correction bolus = (BG - 100)/ CF, where CF = 1700/total daily dose; CF = 30
34
Q

Correction Bolus Formula

A
  • Current BG - Ideal BG/ Glucose Correction factor
  • Example:
    Current BG: 250 mg/dl
    Ideal BG: 100 mg/dl
    Glucose Correction Factor: 30 mg/dl
  • so 250-100/correction factor of 30= 5 units
  • * ON TEST*
  • Add that correction factor to current dose to calculate how much you’re giving
35
Q

Protocol for Treatment of Hypoglycemia

A
  • Any BG <60 mg/dl: D50 = (100-BG) x 0.4 ml IV
  • Recheck in 15 minutes and retreat if needed
  • If eating, may use 15 gm of rapid CHO
  • Do Not Hold Insulin When BG Normal
36
Q

Determining IV insulin needs with TPN or enteral feeding

A
  • For TPN, add insulin to TPN bag with correction SC every 4 to 6 hours
  • For enteral feedings, give Glargine or Detemir every 12 hours or NPH every 8 hours or Regular every 6 hours with correction SC every 4 to 6 hours.
37
Q

If known diabetes or A1c >6%, what should the nurse do?

A

transition patient to basal bolus therapy once BG at goal and stable.

38
Q

Diabetes service is contacted for?

A

all patients new to SC insulin.

39
Q
  • A state of absolute or relative insulin deficiency aggravated by ensuing hyperglycemia, dehydration, and acidosis-producing derangements in intermediary metabolism, including production of serum acetone.
  • Can occur in both Type I Diabetes and Type II Diabetes: In type II diabetics with insulin deficiency/dependence
  • The presenting symptom for ~ 25% of Type I Diabetics.
A

Diabetic Ketoacidosis (DKA)

40
Q
  • An acute metabolic complication of diabetes mellitus characterized by impaired mental status and elevated plasma osmolality in a patient with hyperglycemia.
  • Occurs predominately in Type II Diabetics
  • A few reports of cases in type I diabetics.
  • The presenting symptom for 30-40% of Type II diabetics.
A

Hyperosmolar Hyperglycemic State (HHS)

41
Q

Severe DKA vs HHS. Which is which?

? ?

Plasma glucose level: >250 >600

Arterial pH: <7.00 >7.30

Sodium Bicarb: <10 >15

Urine Ketones: positive small

Serum Ketones: positive small

Serum Osmolality variable >320

Anion Gap: >12 variable

Mental Status: Stupor/Coma

A

DKA HHS

Plasma glucose level: >250 >600

Arterial pH: <7.00 >7.30

Sodium Bicarb: <10 >15

Urine Ketones: positive small

Serum Ketones: positive small

Serum Osmolality variable >320

Anion Gap: >12 variable

Mental Status: Stupor/Coma

42
Q

Causes of DKA/HHS

A

Stressful precipitating event that results in increased catecholamines, cortisol, glucagon.

  • Infection (pneumonia, UTI)
  • Alcohol, drugs
  • Stroke
  • Myocardial Infarction
  • Pancreatitis
  • Trauma
  • Medications (steroids, thiazide diuretics)
  • Non-compliance with insulin
43
Q
  • Polyuria
  • Polydypsia
  • Blurred vision
  • Nausea/Vomiting
  • Abdominal Pain
  • Fatigue
  • Confusion
  • Obtundation
  • Hypotension, tachycardia
  • Kussmaul breathing (deep, labored breaths)
  • Fruity odor to breath (due to acetone)
  • Dry mucus membranes

Symptoms and findings of ?

A

DKA/HHS

44
Q

To correct pseudohyponatremia?

A

add 1.6 mEq of sodium to every 100mg/dL of glucose above normal

45
Q

Anion gap is calculated by?

A

(Na+) – (Cl- + HCO3-)

46
Q

Treatment of DKA

A

HYDRATION!!!

  • Normal Saline:500-1000 cc/hr for 4 hours, then 250 – 500 cc/hr for 4 hours, then 125-250 cc/hr
  • Once glucose is < 200, should change fluids to D5 ½ NS until insulin drip is stopped

Insulin

  • Insulin drip: Bolus: 0.15 units/kg, then infuse at 0.1 mg/kg/hr
  • Ideally should decrease glucose 50-100 mg/dL per hour
  • In DKA: Change to subcutaneous regimen once anion gap has closed and patient is ready to eat.
  • Need to give long-acting insulin dose several hours prior to stopping insulin drip.

Accuchecks

  • Every 1 hour initially, then every 2 hours, and so on.
  • Serial Electrolytes
  • Potassium repletion
  • Should add potassium to IV fluids once potassium < 5
47
Q

Treatment of HHS

A
  • Hydration!!!: Even more important than in DKA
  • Find underlying cause and treat!
  • Insulin drip: Should be started only once aggressive hydration has taken place. Switch to subcutaneous regimen once glucose < 200 and patient eating.
  • Serial Electrolytes: Potassium replacement.
48
Q

Hypophosphatemia, Cerebral edema, Myocardial infarction, DVT/PE, cardiac dysrhythmias

Possible complications of? Why do these happen?

A

Possible Complications of DKA

  • Hypophosphatemia: Occurs after aggressive hydration/treatment. Monitor phosphorus and replete as needed to keep > 1
  • Cerebral edema: Rare, but life threatening. Usually in pediatric, adolescent patients. Symptoms:Headache, altered mental status. Treat with mannitol, hyperventilation
  • Myocardial infarction, DVT/PE, cardiac dysrhythmias
49
Q
A

NUR4630 (34 decks)

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