Presentation on theme: "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?"— Presentation transcript:
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?
Lots of Group Activities so let’s get into our groups Group 1: Group 2: Group 3: Group 4: Group 5: Group 6:
Now come up with a Name of your Group Group 1: Group 2: Group 3: Group 4: Group 5: Group 6:
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? _____________________ ______________________
Let’s go with the Adrenal Cortex first….. 3 Hormone types: Glucocorticoids (Cortisol) Mineralocorticoids (Aldosterone) Androgens (Testosterone) Or………..Sugar, Salt and Sex Activity: Giving you 10 minutes, get in your group and create a jingle, song or rap about these 3 types of hormones…..
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…..
Do you need to look up cortisol? Consult with your team and combine what you all know about cortisol? Record data here: _______________________
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. ___________________
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 2 nd major group of hormones Mineralocorticoids or Aldosterone You know this…what does aldosterone do? What stimulates its’ release?
Still in the Adrenal Cortex…now 3 rd 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
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.
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 Treatment- Addisonian 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
Pheochromocytoma- Diagnostic 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 Management- Pheochromocytoma 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