Transcript Endocrine System

Endocrine System
JUSTINE WILLMAN MED, MSN, RN
2015-2016
Glands & Conditions of Focus
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PANCREAS- DIABETES (I & II) & DKA
ADRENAL- CUSHING'S, ADDISON'S & PHEOCRYOCYTOMA
PITUITARY- SYNDROME OF INAPPROPRIATE ANTIDIURETIC HORMONE
SECRETION (SIADH) & DIABETES INSIPIDUS (DI)
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 Type I DM is the failure of the beta cells to
Pancreas
Review
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
secrete any or enough insulin
 Most type II DM is the result of abnormalities of
the insulin receptors
Pancreas- Diabetes Review
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Type 1 Diabetes
Type II Diabetes
 Body’s immune system destroys
 90-95% of all diagnosed cases of
pancreatic beta cells. This can
happen early in life of up into
adulthood
 5-10% of all documented cases of
DM
 Depends on insulin to sustain life
 Risk factors include autoimmune,
genetic, and environmental
factors
DM
 Usually begins as insulin
resistance, cells do not use
insulin properly
 Associated with older age,
obesity, family history of
diabetes, prior history of
gestational diabetes, impaired
glucose tolerance, physical
inactivity, and race/ethnicity.
 Most important risk factor is
family history and obesity
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 Often the presentation is nonspecific, the client
Diabetes
Clinical
Manifestations
Review
Polyuria
Polydipsia
Polyphagia
As times, ketones are
present (ketosis)
Hyperglycemia, weight
loss, weakness and
fatigue
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.
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 Blood glucose
Monitoring of
Pancreas Review
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?
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?
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Daily Routines for
Diabetics Review
 Glucose monitoring and recording
 Insulin injections and oral agent administration
 Know the signs and symptoms of hypo and
hyperglycemia
 Meal planning, exercise/ daily activities
 Skin care & foot care
 Carry fast acting glucose at all times
 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?
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 If you live alone, have someone call and check on you
Sick Day Schedule
Review
Flu shots are
recommended every
year for people with
diabetes
Also, pneumonia
vaccines and tetanus
shots should be kept up
to date
Try to stay away from
people who are sick,
especially young children
If you are around people
who are sick, wash your
hands often
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two or three times a day.
NEVER omit insulin or diabetic meds, even if you can't
eat.
Test your blood sugar every 2-4 hours.
Rest. Do not exercise during an illness
Drink plenty of fluids to prevent dehydration
Eat carbs of BS <150
Call Your Doctor or Diabetes Educator if:
 You have an obvious infection
 Your illness lasts longer than 2 days
 You have vomiting or diarrhea more than 8 hours
 Your blood sugar is over 400 mg in two consecutive
tests
 All urine tests are positive for large amounts of sugar
 You have moderate to large urine ketones for more
than 8 hours
 You have extreme fatigue, shortness of breath, or
dizziness
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 What situation concerns you more? The client
Endocrine
Conditions of
Focus- Pancreas

Hyperglycemia
Hypoglycemia

Ketoacidosis (DKA)

Hyperglycemic
Hyperosmolar
Nonketotic Syndrome
(HHNS)
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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…
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Hypoglycemia is very
dangerous as low sugar in
the blood leads to low
sugar in the brainconfusion, stupor, coma
and death
Although dangerous,
hyperglycemia still
supplies the brain
with sugar and is more
of a chronic concern in
comparison to the
immediate concerns of
hypoglycemia
Rapid, shallow respirations
Nauseated
Diaphoresis (cold sweats)
Weakness and trembling
Palpitations, tachycardia, jitters
Technically a BGL below 70 mg/dl
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Treatments for
Hypoglycemia
Review
 Carbs, Peanut butter, cheese and crackers
 Recheck glucose 15 min after initial treatment,
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and treatment should be repeated until
achieving a glucose of 70.
Once over 70, regular diet or snack to prevent
hypoglycemia should be given
Recheck glucose in 30-45 minutes
Emergency treatment: D50 IV or glucagon (IV,
SC, IM)
At what rate is an amp of Dextrose 50% given?
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Hyperglycemia
Review
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Polyuria
Polydipsia
Blurred vision
Weight loss
Polyphagia
Increased and/or
unexplained sense of
fatigue
Skin infections,
wounds don't heal
easily
Warm, dry skin
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 on next slide.
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 What is likely happening to this client as a result of
Hyperglycemia
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View the next slide for a
visual on how low insulin
(leading to high blood
glucose) impacts the
body
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hyperglycemia, as evidenced in presentation and lab
data?
Why 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 measures are 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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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
Most commonly brought
on by infection
DKA vs. HHNS
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HHNS- Type II DM
DKA- Type I DM
Basics of DKA
http://www.bing.com/videos/search?q=what+is+dka&FORM=
HDRSC3#view=detail&mid=FD2E83EF5AD293D93915FD2E83EF
5AD293D93915
Kussmaul Breathing
 http://www.youtube.com/watch?v=gy7VEVPnOn4
&list=PLKBbwyYL5BYHR9u-prSR3IZ9Z04iISRJo
 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
Basics of HHSN
 http://on.aol.com/video/what-is-hyperosmolarnonketotic-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
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 Treatment involves IV Insulin, fluid administration &
Ketoacidosis
Treatment
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
(extracellular) leading to
intracellular potassium
depletion. Also, potassium is
lost via osmotic diuresis
causing profound total body
potassium deficiency.
Goal is to return to normal
intracellular K+ levels, increase
fluid volume and lower
glucose
possibly IV potassium
 Why is IV K+ sometimes given when the potassium
levels in the blood (extracellular) are already so high
in DKA?
 How quickly can IV K+ be given and how is it
administered? (find this in your drug reference)
 Are there ways in which potassium should not be
given?
Awesome potassium movement VIDEO
http://www.dnatube.com/video/5282/Maintaining-potassium-level-in-cells
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 What type of insulin will be used to treat DKA and
Ketoacidosis
Treatment
how can it be given as an IV infusion? (find this in your
drug reference)
 If you were to mix & prepare this insulin for IV
infusion, how would you make a 1:1 dilution from this
bottle?
ORDER:
Infuse 0.1 U/kg of
Regular insulin STAT
Client weight is 170 lbs
 Now that you have prepared your med, prime your
line and infuse the proper dose of insulin based on
the order to the left.
 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=H
DRSC3#view=detail&mid=728DD66FCE3F15482859728DD66FCE3F15482859
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
Importance of
Insulin for DKA
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Look at the next slide for
an example of IV insulin
protocol
Would you consider the
structured decrease in
glucose for DKA to be a
fast or slow?
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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.
doi: 10.2337/diaclin.29.2.51 Clinical Diabetes April 2011 vol. 29 no. 2 51-59
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IV Insulin
Protocol Example
Consider the likelihood of
hypoglycemia and need for
constant nursing assessment
This is an example of
titration in action, the nurse
should stay at the bedside
for close monitoring
Nursing Management of Insulin Infusion
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If K+ < 3.3 at the time of insulin administration, promptly notify physician
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Initiate insulin drip at 0.1 units/kg/hour (or other dose written by physician)
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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)
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Glucose >500
Increase drip by 4 units/hr (or 25 %, which ever increase is less)
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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
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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.
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Glucose 101-150
Decrease insulin drip by 50%
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Glucose 71-100
Hold insulin drip for 1 hour. (if still 71-100 at next hour, continue to hold and call MD
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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
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Fluid Replacement
Ketoacidosis
Treatment
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Fluid Replacement
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As the nurse, also think
about IV access, urine
output, electrolyte
imbalance, should the
client have a Foley? etc.
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.
doi: 10.2337/diaclin.29.2.51 Clinical Diabetes April 2011 vol. 29 no. 2 51-59
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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
Conditions of focus for the adrenal glands are
Cushing’s Syndrome, Addison's Disease &
Pheochromocytoma
Addison’s Disease
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 Addison’s is the result of the HYPO
secretion of the adrenal cortex
hormones
 Condition is fatal if left untreated
Presentation
 Hypotension and weakness
 Bronze pigment of skin and mucous
membranes changes
 Emotional disturbances
 Electrolyte imbalances
 Hypoglycemia
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Interventions
Addison’s
It is believed that
President Kennedy had
Addison’s
Consider the effects on
his body as a result of
the stress associated
with holding the
Presidency

Monitor VS, I&O, fluid and electrolyte balance
 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?
Cushing’s Syndrome
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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:
 Monitor glucose, I&O, weight
 Administer insulin when ordered
 Teach about the risk for infection and
skin tears
 Surgical removal of tumor on adrenal
gland or taper off steroid therapy if
possible
 Client’s body image concerns
 Do the side effects of Cushing's remain
after the cause is removed?

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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
Many times not very
responsive to medications
Extreme HTN leads to:
CVA, kidney damage and
retinopathy
Presentation
 Severe HTN
 Complaints of anxiety and heart palpitations
 Classic symptoms
 Severe pounding headache
 Tachycardia
 Profuse sweating
Interventions
 Surgical excision is usual treatment
 Non-surgical candidates can be treated with
adrenergic blocking agents
http://www.bing.com/videos/search?q=pheochromocytoma&qs=PA&sk=
&FORM=QBVR&pq=pheocry&sc=87&sp=1&qs=PA&sk=#view=detail&mid=919EA9B021DC73F5F5BE919EA9B
021DC73F5F5BE
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Endocrine
Conditions of
Focus- Pituitary
Diabetes Insipidus (DI)
Syndrome of Inappropriate
Antidiuretic Hormone
Secretion (SIADH)
 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?
http://www.bing.com/videos/search?q=diabetes+insipidus&qs=n&form=QBVR&pq=di
abetes+insipidus&sc=8-18&sp=1&sk=#view=detail&mid=942A92486701F91E0CDA942A92486701F91E0CDA
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Diabetes Insipidus
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
 Polyuria of 4-24 liters a day
 Polydipsia
 Dehydration
 Tachycardia & postural hypotension, why?
 Urine specific gravity (measurement of urine concentration)
of < 1.006
 Why should we monitor VS, I & O, neuro, electrolyte and
cardiac status?
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Syndrome of
Inappropriate
Antidiuretic Hormone
Secretion (SIADH)
Pituitary gland HYPER
secretes ADH and
leads to water
intoxication
May happen to those
under great stress or
trauma
Severity depends on how
rapid it progresses
Most S/S appear when
blood NA+ levels <
125mEq/L
Presentation- what are the reasons for each?
 Change in LOC and mental status
 Tachycardia and hypertension
 Weight gain
 Na+ less than 135mEq/L
Interventions- what are the reason for each?
 Monitor VS, I & O, daily weight, labs, fluid restrictions,
fluid retention
 Monitor neurological and cardiac status
 Push foods high in Na+
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