Transcript Let`s move to the Adrenal Glands

Let’s move to the Adrenal
Glands
In this space, please draw an adrenal gland….
Where does it live, what is its shape?
Does it communicate with the kidney?
Did you include the inner and outer part of
the adrenal gland?
What are the 2 parts of the Adrenal
Gland???

Inner part is the _________ ________

What does the inner part secrete or
release?
 _____________________
 ______________________
What are the 2 parts of the Adrenal
Gland???

Outer part is the _________ ________
What does the outer part secrete or
release?
 _____________________
 _____________________
 ______________________

Sugar….Salt….and Sex
Let’s go with the Adrenal
Cortex first…..

3 Hormone types:
Glucocorticoids (Cortisol)
 Mineralocorticoids (Aldosterone)
 Androgens (Testosterone)

Or………..Sugar, Salt and Sex
Disorder #1 Cushing’s Disease
We are nurses taking care of a
patient with Cushing’s
Syndrome
What is Cushing’s syndrome?
 Too much _______________
 What is a synthetic form of cortisol that
you have probably administered in clinical
to your patients?
 Syndrome vs Disease………..

Too much Cortisol….

What do you remember about
cortisol or side effects of
glucocorticoids?
Write down here what you
remember…..
Cushing’s Syndrome vs
Cushing’s Disease
Syndrome is iatrogenically induced,
how?
 ________________________
 Cushing’s disease could be caused by
a tumor causing too much cortisol
release.
 Where could the tumor be located?
1. ________________ 2._____________
3. ___________________

Textbook Pic of Cushing’s
Syndrome/Disease
Can we live without
glucocorticoids or cortisol?

What does cortisol do in our body?
CHO (carbohydrate) metabolism
 Fatty acid mobilization
 Protein catabolism


Ding ding
Function of Cortisol or
Glucocorticoids:
***CHO Metabolism



What happens when we break down
carbohydrates?
Increase in amount of glucose formed
Increase in amount of glucose released
Therefore a major complication is
_______________________

Function of Cortisol:
*****Fat metabolism

What happens when we mobilize
fatty acids somewhere unusual?
Therefore we see some classic body
image changes in our patient-name
these here:
 ________________
 ________________
 ________________

Re Group for a POC Activity
Develop a plan of care for a patient
with Cushing’s Disease
 What are the priorities?


What can the nurse expect to see in
this patient?
Function of Cortisol:
****Protein breakdown or
catabolism
What happens in Cushing’s
syndrome with protein breakdown,
how does this look in our patients?
 ____________________________
 ____________________________

Re Group for a POC Activity

Develop a plan of care for a patient
with Cushing’s Disease

What kind of things can the nurse
call the physician about in
preventing complications in this
patient? SBAR ideas?
Clinical reasoning….

If glucocorticoids have a
mineralocorticoid like effect, what
would we see in our patients?
Too much Aldosterone or
Hyperaldosteronism
Excessive retention of Na and H2O
 Excessive excreting of K+

So what would we see in clinical in
our patients?
 _______________________
 _______________________

Still in the Adrenal
Cortex…now 2nd major group
of hormones

Mineralocorticoids or Aldosterone

You know this…what does
aldosterone do?

What stimulates its’ release?
Still in the Adrenal
Cortex…now 3rd major
group of hormones

Androgens or Testosterone
What happens if females have too
much testosterone?
 _____________
 _____________
 _____________

What diagnostic tests could
help diagnose Cushing’s
Disease?
Serum cortisol levels
 Serum ACTH levels
 CT scan of abdomen or adrenals
 MRI of brain to detect if pituitary
adenoma
 24 hour urine for cortisol

Normal Cortisol Levels
What would we expect to see in
Cushing’s, what would the graph
look like?

Try to draw here

So in summary, what effects the release of
cortisol?
________________________



What would the serum levels of cortisol be
at 8am vs 8pm?
________________________
Collaborative Management of
Cushing’s Disease


Need to know what first?????
_____________________________
Open adrenalectomy or laparoscopic
adrenalectomy if tumor or cancer of
adrenal gland
 What if it is an ectopic tumor releasing too
much ACTH? How would this be managed
or treated? __________________________
 What other surgery could be necessary?
 ______________________________________

Medications-Cushing’s Disease

Mitotane (Lysodren) which suppresses
cortisol production if surgery not an
option
Ketoconazole (Nizoral) inhibits cortisol
synthesis
 Activity: Look up doses and routes of
these medications and list as would be on
the MAR

Medications-Cushing’s Disease

Mitotane (Lysodren)

Ketoconazole (Nizoral)

Why would these be called a “medical
adrenalectomy”
Write a detail nurse’s note on
the appearance of the client’s
skin or “Prednisone skin”
Prednisone skin documentation

Skin is fragile, thin and has decreased
elasticity. Multiple areas on all 4
extremities of dark purple bruises.
What assessment findings would
you document?
Cushing’s Disease-During
Cushing’s Disease-After
Treatment
Now the innermost part of
Adrenal Gland
What is it called?
 _________________________
 What does it release?
 1.___________________
 2.___________________
 What “response” does it trigger?
 ____________________________

Ok let’s summarize, how to
collaboratively intervene in
patient with Cushing’s
disease/syndrome?
Disorder #2
Hyperaldosteronism
Too much aldosterone secretion
 What does aldosterone do?
 _________________
 _________________
 _________________
 Usually caused by a tumor on Adrenal
cortex

Clinical Manifestations:
Hyperaldosteronism
Headache due to Na and H2O retention
 HTN due to Na and H2O retention
 K+ excretion which leads to ________
 muscle weakness, fatigue
 cardiac dysrhythmias
 usually no edema

Diagnostic Tests:
Hyperaldosteronism

urinary K+

plasma aldosterone levels with low
plasma renin levels---WHY?

CT scan will reveal adenoma of adrenal
gland
EKG changes

Collaborative Management of
Hyperaldosteronism
Low sodium diet
 K+ sparing diuretic such as aldactone…
 How will this help perfectly???
 ___________________________
 Calcium channel blockers to treat the
elevated blood pressure
 Adrenalectomy

Disorder #3 Addison’s Disease

Which famous President had Addison’s
Disease?
What is Addison’s Disease

Too little of Sugar, Salt, and Sex
glucocorticoids
mineralocorticoids
androgens
Not enough Cortisol? POC
priorities
________________________
 ________________________
 ________________________
 ________________________

Not enough Aldosterone…..POC
priorities
______________________
 ______________________
 ______________________
 Salt craving—why?
 Not enough Androgens…what could be a
priority?
 ______________________

Diagnostic Studies-Addison’s
Disease

Serum cortisol levels
or
Urine cortisol high or low
 Hypo or hyper kalemic?
 Serum glucose levels
or

Serum aldosterone levels high or low?
 EKG peaked T waves due to hyperkalemia

In summary…
Low bp
 F & E imbalances
 Hypoglycemic
 Hyponatremia
 Hyperkalemia
 Nausea and Vomiting
 Dehydration
 Anxiety, irritable

Addisonian Crisis or Acute
Adrenal Crisis
Severe hypotension
 Tachycardia
 Severe nausea and vomiting
 Hypovolemic shock
 Hypoglycemia
 Hyponatremia
 Hyperkalemia

Emergency TreatmentAddisonian Crisis or Adrenal
Crisis
Rapid infusion of IV fluids (D5NS)
 Frequent VS and I & O
 May need to administer vasopressors to
bring up blood pressure
 Solucortef IVP until enough
glucocorticoid on board

Collaborative Management
Addison’s Disease
Oral glucocorticoids
 2/3 dose in am
 1/3 dose in pm
 DOC is Cortate po
 Oral mineralocorticoid
 Florinef 0.1mg po
 Lifelong hormone replacement
 Stress management

Patient Teaching-Addison’s –ding
ding
Salt additives for excess heat or humidity
 Daily glucocorticoid replacement
 Daily mineralocorticoid replacement
 List of all meds
 Medical identification device in wallet, or
in the form of a bracelet or necklace
 Conditions requiring larger dose of
hormones (surgery, trauma, happy stress)
 IM glucocorticoid administration by
patient (100mg hydrocortisone kit)

Disorder #4
Pheochromocytoma-in the
Adrenal Medulla

Rare, benign tumor of the adrenal medulla
Oh no, what are we going to see a hyper
secretion of???
 ___________________
 ___________________

Clinical Manifestations








Hallmark is hypertension-200/150 or >
NE and Epinepherine released
sporadically
Deep breathing
Profound sweating due to peripheral
vasoconstriction
Pounding HR
Headache
Visual disturbances
“Spells” or paroxysmal attacks
◦ Triggers can be from bladder distension,
exposure to cold, emotional distress
PheochromocytomaDiagnostic Studies
Increase serum NE and Epinepherine
levels
 Increase in urine metabolites of NE and
Epinepherine
 CT scan of adrenal gland(s)
 MRI of adrenal gland(s)

Collaborative ManagementPheochromocytoma
Adrenergic Blocker
1. Minipress to decrease bp
 Beta blocker
1. Inderal to decrease HR and bp and force
of contraction also helps reduce anxiety
 Monitor vs
 Adrenalectomy-usually laporoscopic
If having episode, elevate HOB and
complete bedrest

During surgery….and post op
Potent vasodilator Regitine or Nipride
administered due to manipulation of
tumor in the medulla and surge of NE and
Epi
 BP may be elevated initially, but can
bottom out post operatively, why?
 If not a surgical candidate, then drug
Demser (drug which inhibits
catecholamine synthesis) is given

Actual Case at UMCB:









25 yo male from Bastrop
Hx of Insulin dependent DM and
hypothyroidism
Admitted via ED and transferred to IMC then
to tele unit
On admission:
Na=118
K+=8.4
TSH=46.1
Low testosterone levels
16 lb weight loss past 6 weeks
What should be included in
POC?
What other data do you need?
What are this patient’s priorities?