Download Endocrine 251 Handout LS Fall 2014

NUR 251
Endocrine Handout
Glands & Conditions of Focus
o Pancreas- Diabetes (I & II) & Diabetic keto-acidosis (DKA)
o Adrenal- Cushing's, Addison's & Pheocryocytoma
o Pituitary- Syndrome of Inappropriate Antidiuretic Hormone Secretion (SIADH) &
Diabetes Insipidus (DI)
Pancreas- Review
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Type I DM is the failure of the beta cells to secrete any or enough insulin
Most type II DM is the result of abnormalities of the insulin receptors
Located posterior to the liver- LUQ
Contains the islets of Langerhans (glands)
The islets contain alpha and beta cells which produces insulin and glucagon
Influences fat, protein and carbohydrate metabolism
Pancreas- Diabetes Review
Type 1 Diabetes
Body’s immune system destroys pancreatic beta cells. This can happen early in life of up into
adulthood
o 5-10% of all documented cases of DM
o Depends on insulin to sustain life
o Risk factors include autoimmune, genetic, and environmental factors
Type II Diabetes
90-95% of all diagnosed cases of DM
o Usually begins as insulin resistance, cells do not use insulin properly
o Associated with older age, obesity, family history of diabetes, prior history of
gestational diabetes, impaired glucose tolerance, physical inactivity, and
race/ethnicity.
o Most important risk factor is family history and obesity
Often the presentation is nonspecific, the client may go to physician with “other” problems
such as fatigue, visual problems, recurrent infection, prolonged wound healing, etc.
Clinical manifestations can occur so gradually that before the person knows it, he or she may
have complications. Presentation ranges from asymptomatic to profound ketosis and coma.
Polyuria, Polydipsia, Polyphagia, As times, ketones are present (ketosis), Hyperglycemia,
weight loss, weakness and fatigue
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Endocrine Handout
Monitoring of Pancreas Review
Blood glucose
Normal 70-110mg/dL (fasting). This is the basic monitoring test for diabetics
Glucose Tolerance Test (GTT)
GTT can take up to 3-5 hours, requires IV or oral administration of glucose and multiple blood
draws
Glycosylated Hemoglobin (HbA1c)
Monitors a diabetic’s glucose management over the past 3 months
Test result >7 is considered poor management of DM and/or an indicator of newly
diagnosed DM
How long should your patient fast before having a HbA1c test?
Common medications such as corticosteroids, oral contraceptives and albuterol often
elevate glucose levels and may require the client to have regular glucose checks and at
times, receive SQ insulin
What is total parenteral nutrition (TPN) and how can it impact glucose levels?
Daily Routines for Diabetics Review
o Glucose monitoring and recording
o Insulin injections and oral agent administration
o Know the signs and symptoms of hypo and hyperglycemia
o Meal planning, exercise/ daily activities
o Skin care & foot care
o Carry fast acting glucose at all times
o What lifestyles or circumstances can impact or alter the way in which a client
incorporates the daily routines listed above? What are the nurse’s roles in assisting
the client as a result?
Sick Day Schedule Review
o If you live alone, have someone call and check on you two or three times a day.
o NEVER omit insulin or diabetic meds, even if you can't eat.
o Test your blood sugar every 2-4 hours.
o Rest. Do not exercise during an illness
o Drink plenty of fluids to prevent dehydration
o Eat carbs of BS <150
NUR 251
Endocrine Handout
Call Your Doctor or Diabetes Educator if:
o You have an obvious infection
o Your illness lasts longer than 2 days
o You have vomiting or diarrhea more than 8 hours
o Your blood sugar is over 400 mg in two consecutive tests
o All urine tests are positive for large amounts of sugar
o You have moderate to large urine ketones for more than 8 hours
o You have extreme fatigue, shortness of breath, or dizziness
o Flu shots are recommended every year for people with diabetes
o Also, pneumonia vaccines and tetanus shots should be kept up to date
o Try to stay away from people who are sick, especially young children
o If you are around people who are sick, wash your hands often
Critical Thinking- Pancreas
What situation concerns you more? The client with a 42mg/dL glucose or the client with a
420 mg/dL glucose; or are you equally concerned?
Think- is one client more likely to have a rapid decline in status? Would one need your
attention first if you were caring for both clients?
Once you’ve prioritized, what interventions are needed for these clients? Are you able to
delegate any of the interventions to the LPN or CNA?
List your interventions based on priority, figuring in your delegations…
NUR 251
Endocrine Handout
Endocrine Conditions of Focus- Pancreas
o Hyperglycemia
o Hypoglycemia
o Ketoacidosis (DKA)
o Hyperglycemic Hyperosmolar Nonketotic Syndrome (HHNS)
Hypoglycemia is very dangerous as low sugar in the blood leads to low sugar in
the brain- confusion, stupor, coma and death
o Rapid, shallow respirations
o Nauseated
o Diaphoresis (cold sweats)
o Weakness and trembling
o Palpitations, tachycardia, jitters
o Technically a BGL below 70 mg/dl
hyperglycemia
Although dangerous,
still supplies the brain with sugar and is
more of a chronic concern in comparison to the immediate concerns of hypoglycemia
Treatments for Hypoglycemia Review
o Carbs, Peanut butter, cheese and crackers
o Recheck glucose 15 min after initial treatment, and treatment should be repeated
until achieving a glucose of 70.
o Once over 70, regular diet or snack to prevent hypoglycemia should be given
o Recheck glucose in 30-45 minutes
o Emergency treatment: D50 IV or glucagon (IV, SC, IM)
o At what rate is an amp of Dextrose 50% given?
SCENARIO- A client arrives in the ER via family member. The client is week and febrile
(101.2). Labs reveal the following: Serum glucose of 511 mg/dL, WBC 18.3 thousand, sodium
129 mEq, potassium 6.8 mEq, anion gap 17, positive serum ketones & arterial blood pH 7.29.
Analyze the labs and client presentation and make the connections to a “hyperglycemia”
diagnosis. Once completed, continue the scenario.
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Endocrine Handout
What is likely happening to this client as a result of hyperglycemia, as evidenced in
presentation and lab data?
SCENARIO ContWhy do you think the client is febrile?
Regardless if the client knew he was diabetic on his ER admission or not, what type of DM
do you think he has and why?
Based on the client's blood pH (7.29) and glucose of 511 mg/dL, what compensatory measure
is likely to be observed on this client and why?
What are your priority actions? Can you delegate any interventions to the ER Tech?
What was your correlation of the sodium and potassium levels to this state of
hyperglycemia?
Based on your interventions and the client’s condition, what specific assessments will you do
on this client and how frequently will you assess?
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Endocrine Handout
Hyperglycemia Review
 Polyuria
 Polydipsia
 Blurred vision
 Weight loss
 Polyphagia
 Increased and/or
unexplained sense of
fatigue
 Skin infections, wounds
don't heal easily
 Warm, dry skin
DKA- An acute life-threatening complication of uncontrolled IDDM (type I)
Urinary loss of water, potassium, ammonium and sodium results in hypovolemia, electrolyte
imbalance, extremely high glucose and breakdown of free fatty acids, causing acidosis,
often leading to coma
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Endocrine Handout
Basics of DKA
http://on.aol.com/video/what-is-hyperosmolar-nonketotic-hyperglycemic-coma-234756250
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Fruity breath (from acetone), dry mucous membranes from polyuria
Deep respirations possibly kussmaul respirations
Drowsiness, stupor or coma
Low BP from polyuria
Glucosuria and ketonuria
Polyuria and polydipsia
n/v, no hunger
Glucose: 300-800mg/dl
Kussmaul Breathing
http://www.youtube.com/watch?v=gy7VEVPnOn4&list=PLKBbwyYL5BYHR9uprSR3IZ9Z04iISRJo
Basics of HHSN- In comparison
http://on.aol.com/video/what-is-hyperosmolar-nonketotic-hyperglycemic-coma-234756250
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Elevated glucose
NO elevation of serum or urine ketones
NO fruity scent
NO acidosis
NO Kussmauls
Treat with fluids and decrease glucose levels
Awesome potassium movement VIDEO
http://www.dnatube.com/video/5282/Maintaining-potassium-level-in-cells
Since
DKA is an emergency, often we treat these clients in the ER or ICU settings
Due to impaired insulin action and hyper osmolality, use of potassium by skeletal muscle is
greatly diminished, leading to K+ shifting out of the cell (going extracellular) leading to
intracellular potassium depletion. Also, potassium is lost via osmotic diuresis causing
profound total body potassium deficiency.
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Endocrine Handout
Goal is to return to normal intracellular K+ levels, increase fluid volume and to lower glucose
Ketoacidosis Treatment
o Treatment involves IV Insulin, fluid administration & possibly IV potassium
o Why is IV K+ sometimes given when the potassium levels in the blood (extracellular)
are already so high in DKA?
o How quickly can IV K+ be given and how is it administered? (find this in your drug
reference)
o Are there ways in which potassium should not be given?
(DKA) Ketoacidosis Treatment
What type of insulin will be used to treat DKA and how can it be given as an IV infusion? (find
this in your text or drug reference)
If you were to mix & prepare this insulin for IV infusion, how would you make a 1:1 dilution
from this bottle?
Now that you have prepared your medication, prime your line and infuse the proper dose of
insulin based on this following order.
ORDER:
Infuse 0.1 U/kg of Regular insulin STAT
Client weight is 170 lbs
What rate will your pump be set at?
How to add a medication to an IV solution VIDEO
http://www.bing.com/videos/search?q=adding+medication+to+iv+solution&FORM=HDRSC3#
view=detail&mid=728DD66FCE3F15482859728DD66FCE3F15482859
NUR 251
Endocrine Handout
Importance of Insulin in Treatment of DKA
Critically ill patients with DKA should be given a loading dose of regular insulin at 0.1 units/kg
body weight to a maximum of 10 units followed by an infusion of regular insulin at 0.1
units/kg body weight/hour, to a maximum of 10 units/hour. Other doses and routes of insulin
administration have been studied, but these have not been evaluated outside of the
research setting or in critically ill patients.
Less seriously ill patients with DKA should be given an infusion of regular insulin at 0.1
units/kg body weight/hour without a loading dose to minimize the risk of hypoglycemia.
Insulin should not be started until hypovolemia has been addressed and serum potassium
has been confirmed to be > 3.5 mEq/L. Giving insulin to patients with a serum potassium
level < 3.5 mEq/L may precipitate life-threatening arrhythmias.
Expert opinion regarding the use of insulin for patients with HHNS is mixed because some
patients with HHNS achieve euglycemia (normal glucose levels) with fluid resuscitation
alone. However, if the patient’s serum glucose does not decrease by 50–70 mg/dl per hour
despite appropriate fluid management, a bolus of IV regular insulin at 0.1 units/kg body
weight to a maximum of 10 units may be given.
IV Insulin Protocol Example
Nursing Management of Insulin Infusion
If K+ < 3.3 at the time of insulin administration, promptly notify physician
Initiate insulin drip at 0.1 units/kg/hour (or other dose written by physician)
Monitor glucose q1 hour. Titrate insulin drip using the below table
TABLE: Insulin Drip Titration (for use after insulin drip initiation) Glucose (mg/dL) Insulin Drip
(units/hr)
Glucose >500
Increase drip by 4 units/hr (or 25 %, which ever increase is less)
Glucose 251-500
Do not adjust rate if blood glucose is decreasing by 50-75 mg/dL/hr
If blood glucose is NOT decreasing by 50-75 mg/dL/hr, then increase the drip rate by 2
units/hr
Glucose 151-250
When the plasma glucose reaches 250 mg/dl in DKA, decrease the insulin infusion rate
to 0.05 - 0.1 unit/kg/h IV fluids should contain D5W if glucose is <250mg/dL. Call
physician, if needed.
Glucose 101-150
Decrease insulin drip by 50%
Glucose 71-100
Hold insulin drip for 1 hour. (if still 71-100 at next hour, continue to hold and call MD
Glucose <70
Hold insulin drip (if not already held) , Give dextrose 50%, 12.5 grams IV, Contact
physician. Recheck blood, glucose in 15 minutes , Follow titration as above, Physician
may change IV fluids to D10W
NUR 251
Endocrine Handout
Would you consider the structured decrease in glucose for DKA to be a fast or slow?
Consider the likelihood of hypoglycemia and need for constant nursing assessment when
titrating insulin. This insulin protocol is an example of titration in action; the nurse should
stay at the bedside for close monitoring
Fluid Replacement
Critically ill patients with severe hyperglycemia resulting from DKA or HHNS should be
treated immediately with a bolus of normal saline. The average fluid deficit for patients with
DKA is 3–5 liters; fluid resuscitation in young, otherwise healthy patients should begin with a
rapid bolus of 1 liter of normal saline followed by an infusion of normal saline at 500 ml/hour
for several hours.
Patients with HHNS are often severely dehydrated, with cumulative fluid deficits of 10 liters
or more. However, because they tend to be older and sicker, they require careful
resuscitation. Expert opinion advocates for a rapid bolus of 250 ml of normal saline repeated
as needed until the patient is well perfused. Fluid therapy is then continued at a rate of 150–
250 ml/hour based on cardiopulmonary status and serum osmolality.
The choice and rate of IV fluid for patients with DKA who are not critically ill should be based
on their corrected serum sodium and overall fluid status. While awaiting laboratory study
results, most of these patients may be given a bolus of 500 ml of normal saline. Patients with
mild to moderate DKA should be given normal saline at 250 ml/hour; those with an elevated
corrected serum sodium should be given half-normal saline at 250 ml/hour.
As the nurse, also think about IV access, urine output, electrolyte imbalance, should the
client have a Foley? etc.
NUR 251
Endocrine Handout
Conditions of focus for the Adrenal glands are Cushing’s
Syndrome, Addison's Disease & Pheochromocytoma
Adrenal Glands
Adrenal Cortex is the outer shell that secretes corticoids (aldosterone, glucocorticoids and
hydrocortisone) and sex hormones
Adrenal Medulla is the Inner core produces epi/norepi via the sympathetic nervous system
Addison’s Disease
Addison’s is the result of the HYPO secretion of the adrenal cortex hormones
Condition is fatal if left untreated
Presentation
o Hypotension and weakness, bronze pigment of skin and mucous membranes
changes
o Emotional & electrolyte imbalances & Hypoglycemia
Interventions
o Monitor VS, I&O, fluid and electrolyte balance
o Inform the client on the need for life long steroid therapy, avoid stress and observe
for Addisonian crisis (acute adrenal insufficiency)
Clients with Addison’s are unable to tolerate physical or emotional stress without additional
supplemental cortisone. Keeping the patient stress and infection free is very important.
Why do you think infection prevention is such an important factor?
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Endocrine Handout
Cushing’s Syndrome
The HYPERsecretion of glucocorticosteriods from the adrenal cortex
Most commonly the result of prolonged administration of corticosteroids
Less likely from an adrenal gland tumor or benign tumor of the pituitary gland
Interventions:
o Monitor glucose, I&O, weight, administer insulin when ordered
o Teach about the risk for infection and skin tears
o Surgical removal of tumor on adrenal gland or taper off steroid therapy if possible
o Client’s body image concerns. Do the side effects of Cushing's remain after the cause
is removed?
Pheochromocytoma
Benign tumor on the adrenal gland leading to HYPERsecretion of epinephrine and
norepinephrine, causing persistent or intermittent hypertension
BP as high as 300/175
o Many times not very responsive to medications
o Extreme HTN leads to: CVA, kidney damage and retinopathy
Presentation
o Severe HTN
o Complaints of anxiety and heart palpitations
o Classic symptoms
 Severe pounding headache
 Tachycardia
 Profuse sweating
Interventions
o Surgical excision is usual treatment
o Non-surgical candidates can be treated with adrenergic blocking agents
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Endocrine Handout
Endocrine Conditions of Focus- Pituitary
What does the word diabetes mean? Knowing this can help explain what is happening in
Diabetes Insipidus and you will see that overall DM and DI have little in common
What does anti diuretic hormone (ADH) do in our bodies?
Diabetes Insipidus (DI)
The HYPOsecretion of ADH from the pituitary gland (and/or a deficiency of vasopressin)
resulting in the failure of reabsorption of water in the kidneys, thus, a largely increased
output. Can occur after trauma to the pituitary gland.
Presentation and Assessment
o Polyuria of 4-24 liters a day
o Polydipsia
o Dehydration
o Tachycardia & postural hypotension, why?
o Urine specific gravity (measurement of urine concentration) of < 1.006
o Why should we monitor VS, I & O, neuro, electrolyte and cardiac status?
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Endocrine Handout
Syndrome of Inappropriate Antidiuretic Hormone
Secretion (SIADH)
o Pituitary gland HYPER secretes ADH and leads to water intoxication
o May happen to those under great stress or trauma
o Severity depends on how rapid it progresses
o Most S/S appear when blood NA+ levels < 125mEq/L
Presentation- what are the reasons for each?
o Change in LOC and mental status
o Tachycardia and hypertension
o Weight gain
o Na+ less than 135mEq/L
Interventions- what are the reason for each?
o Monitor VS, I & O, daily weight, labs, fluid restrictions, fluid retention
o Monitor neurological and cardiac status
o Push foods high in Na+