Week 3: Endocrine/Metabolism Flashcards
The pancreas functions as both ?
exocrine and an endocrine gland
Exocrine function of pancreas
associated with the digestive system because it produces and secretes digestive enzymes
endocrine function of pancreas
produces two important hormones in Islets of Langerhans, insulin and glucagon
Insulin
- (beta cells)
- stimulates the uptake of glucose by body cells thereby decreasing blood levels of glucose
Glucagon
- (alpha cells)
- stimulates the breakdown of glycogen and the release of glucose, thereby increasing blood levels of glucose
Polysaccharide consisting of numerous monosaccharide glucoses linked together. Stored as an energy source in liver & muscles
Glycogen
Functions of insulin
- 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
- 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)
Type I diabetes
- 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?
Type I Clinical Manifestations
- 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).
- fats
- Ketones
- Ketoacidosis
- high
- 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
Type 2 diabetes
What is beta-cell dysfunction?
- Major defect in individuals with type 2 diabetes
- Reduced ability of beta-cells to secrete insulin in response to hyperglycemia
Why does the Beta Cell fail?
- 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
Type 2 Clinical Manifestations
- Polydipsia – increased thirst
- Polyuria – increased urine
- Polyphagia – increased hunger
- Fatigue
- Blurred vision
- Slow healing infections
- Impotence in men
- 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?
Type 1
- 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?
Type 2
Hyperglycemia and the ICU is associated with?
Increased mortality, especially when 300 or above
Hyperglycemia following CABG >200 increased?
- 2x LOS
- 3x Vent duration
- 7X mortality
benefits of tight glycemic control
- infection rates down
- mortality rates down
- afib down 60% post up
Intensive treatment vs. traditional treatment
keeping it down below 110 vs down below 200 decreases LOS, earlier discharge from ICU, discharged home quicker, off the vent quicker
Severe hypoglycemia is defined as a blood glucose level?
less than 40, less than 50 = decrease in cerebral glucose availability
hypoglycemic episodes in the icu causes increased?
mortality, recurrent MI’s, and they do worse
Events Triggering Hospital Hypoglycemia
- 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
- 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?
Features Increasing the Risk of Hypoglycemia in an Inpatient Setting
What happens if the pt becomes hypoglycemic
- 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
AACE/ADA Recommended Target Glucose Levels in ICU Patients
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
AACE/ADA Target Glucose Levels in Non–ICU Patients
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
Monitor BG ? with IV insulin
monitor BG hourly with IV insulin
Continuous Variable Rate IV Insulin DripAtlanta Multiplier Method
- *(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)
All patients with hyperglycemia should have an ? drawn to aid in transition and discharge therapy
HbA1C
Methods of Screening for Hyperglycemia
- 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.
Converting to SC insulin from IV protocol? What’s the exception?
- 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
Initiating SC Basal Bolus. Starting total dose, basal dose, bolus doses, correction bolus
- 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
Correction Bolus Formula
- 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
Protocol for Treatment of Hypoglycemia
- 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
Determining IV insulin needs with TPN or enteral feeding
- 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.
If known diabetes or A1c >6%, what should the nurse do?
transition patient to basal bolus therapy once BG at goal and stable.
Diabetes service is contacted for?
all patients new to SC insulin.
- 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.
Diabetic Ketoacidosis (DKA)
- 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.
Hyperosmolar Hyperglycemic State (HHS)
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
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
Causes of DKA/HHS
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
- 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 ?
DKA/HHS
To correct pseudohyponatremia?
add 1.6 mEq of sodium to every 100mg/dL of glucose above normal
Anion gap is calculated by?
(Na+) – (Cl- + HCO3-)
Treatment of DKA
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
Treatment of HHS
- 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.
Hypophosphatemia, Cerebral edema, Myocardial infarction, DVT/PE, cardiac dysrhythmias
Possible complications of? Why do these happen?
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
