Addison’s Disease vs Cushing’s Syndrome Nursing

Posted on May 2, 2016 by MaryO

Cushing’s and Addison’s Disease. An endocrine NCLEX review on how to differentiate between Cushing’s Syndrome/Disease vs Addison’s and Addisonian Crisis. In this video, I will discuss the pathophysiology, signs & symptoms, and nursing interventions for these endocrine disorders of the adrenal cortex and pituitary glands.

 

Addison’s Disease and Cushing’s Syndrome/Disease review notes for nursing school and NCLEX exam. In nursing school and for the NCLEX exam, you will need to know how to provide care to a patient with either Addison’s Disease or Cushing’s.

However, many students get these two endocrine disorders confused, but these review notes will help you differentiate between them.

These NCLEX review notes will cover:

  • Signs and Symptoms of Addison’s Disease vs Cushing’s
  • Causes of Addison’s Disease and Cushing’s
  • Nursing Management of Addison’s Disease and Cushing’s

After reviewing these notes, don’t forget to take the Addison’s Disease vs Cushing’s Quiz.

Addison’s Disease vs Cushing’s

Major Players in these endocrine disorders:

  • Adrenal Cortex
  • Steroid Hormones
    • Corticosteroids (specifically Aldosterone (mineralocorticoid) & Cortisol (glucocorticoid)

Role of Adrenal Cortex: releases steroid hormones and sex hormones

Role of Aldosterone: regulates blood pressure through renin-angiotensin-aldosterone system, helps retain sodium and secretes potassium (balances sodium and potassium levels).

Role of Cortisol: “STRESS Hormone” helps the body deal with stress such as illness or injury, increases blood glucose though glucose metabolism, break downs fats, proteins, and carbs, regulates electrolytes.

Cushing’s (Syndrome & Disease)

Cushing’s: hyper-secretion of CORTISOL (watch video for clever ways to remember this)

Cushing’s Syndrome vs Cushing’s Disease

Cushing’s Syndrome: caused by an outside cause or medical treatment such as glucocorticoid therapy

Cushing’s Disease: caused from an inside source due to the pituitary gland producing too much ACTH (Adrenocorticotropic hormone) which causes the adrenal cortex to release too much cortisol.

Signs & Symptoms of Cushing’s

Remember the mnemonic: “STRESSED” (remember there is too much of the STRESS hormone CORTISOL)

Skin fragile

Truncal obesity with small arms

Rounded face (appears like moon), Reproductive issues amennorhea and ED in male(due to adrenal cortex’s role in secreting sex hormones)

Ecchymosis, Elevated blood pressure

Striae on the extremities and abdomen (Purplish)

Sugar extremely high (hyperglycemia)

Excessive body hair especially in women…and Hirsutism (women starting to have male characteristics), Electrolytes imbalance: hypokalemia

Dorsocervical fat pad (Buffalo hump), Depression

Causes of Cushing’s

  • Glucocorticoid drug therapy ex: Prednisone
  • Body causing it: due to tumors and cancer on the *pituitary glands or adrenal cortex, or genetic predisposition

Nursing Management for Cushing’s Syndrome

  • Prep patient for Hypophysectomy to remove the pituitary tumor
  • Prep patient for Adrenalectomy:
    • If this is done educate pt about cortisol replacement therapy after surgery
  • Risk for infection and skin breakdown
  • Monitor electrolytes blood sugar, potassium, sodium, and calcium levels

Addison’s Disease

Addison’s: Hyposecretion of Aldosterone & Cortisol (watch the video for a clever way on how to remember this and not get it confused with Cushing’s)

Signs & Symptoms of Addison’s Disease

Remember the phrase: “Low STEROID Hormones” (remember you have low production of aldosterone & cortisol which are STEROID hormones)

Sodium & Sugar low (due to low levels of cortisol which is responsible for retention sodium and increases blood glucose), Salt cravings

Tired and muscle weakness

Electrolyte imbalance of high Potassium and high Calcium

Reproductive changes…irregular menstrual cycle and ED in men

lOw blood pressure (at risk for vascular collapse)….aldosterone plays a role in regulating BP

Increased pigmentation of the skin (hyperpigmentation of the skin)

Diarrhea and nausea, Depression

Causes of Addison’s Disease

  • Autoimmune due to the adrenal cortex becoming damaged due to the body attacking itself:
    • Tuberculosis/infections
    • Cancer
    • Hemorrhaging of the adrenal cortex due to a trauma

Nursing Management of Addison’s Disease

  • Watching glucose and K+ level
  • Administer medications to replace the low hormone levels of cortisol and aldosterone
  • For replacing cortisol:
    • ex: Prednisone, Hydrocortisone
      • Education: Patient needs to report if they are having stress such as illness, surgery, or extra stress in life ( will need to increase dosage), take medication exactly as prescribed….don’t stop abruptly without consulting with MD.
  • For replacing aldosterone:
    • ex: Fludrocortisone aka Florinef
      • Education: consume enough salt..may need extra salt
  • Wearing a medical alert bracelet
  • Eat diet high in proteins and carbs, and make sure to consume enough sodium
  • Avoid illnesses, stress, strenuous exercise

Watch for Addisonian Crisis

This develops when Addison’s Disease isn’t treated.

In addisonian crisis, the patient has extremely LOW CORTISOL levels (life threatening).

Remember the 5 S’s

  1. Sudden pain in stomach, back, and legs
  2. Syncope (going unconscious)
  3. Shock
  4. Super low blood pressure
  5. Severe vomiting, diarrhea and headache
  • NEED IV Cortisol STAT:
    • Solu-Cortef and IV fluids (D5NS to keep blood sugar and sodium levels good and fluid status)
  • Watch for risk for infection, neuro status (confusion, agitation), electrolyte levels (sodium and potassium, glucose)

Addison’s vs Cushing’s Quiz

 

From http://www.registerednursern.com/addisons-disease-vs-cushings-review-notes-for-nclex/

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Genetics of adrenal diseases in 2014: Genetics improves understanding of adrenocortical tumours

Posted on December 17, 2014 by MaryO

2014 has seen advances in our understanding of benign and malignant tumours of the adrenal cortex, particularly in Cushing syndrome. Modern genetics has generated a flurry of data. The challenge is to give sense to them; however, the difficulties of collecting the clinical data must not be underestimated.

Download this information at http://www.nature.com/nrendo/journal/vaop/ncurrent/full/nrendo.2014.215.html

  • References
  1. Beuschlein, F. et al. Constitutive activation of PKA catalytic subunit in adrenal Cushing’s syndrome. N. Engl. J. Med. 370, 1019–1028 (2014).
  2. Goh, G. et al. Recurrent activating mutation in PRKACA in cortisol-producing adrenal tumors. Nat. Genet. 46, 613–617 (2014).
  3. Sato, Y. et al. Recurrent somatic mutations underlie corticotropin-independent Cushing’s syndrome. Science 344, 917–920 (2014).
  4. Cao, Y. et al. Activating hotspot L205R mutation in PRKACA and adrenal Cushing’s syndrome. Science 344, 913–917 (2014).
  5. Assié, G. et al. ARMC5 mutations in macronodular adrenal hyperplasia with Cushing’s syndrome. N. Engl. J. Med. 369, 2105–2114 (2013).
  6. Assié, G. et al. Integrated genomic characterization of adrenocortical carcinoma. Nat. Genet. 46, 607–612 (2014).
  7. Beuschlein, F. et al. Somatic mutations in ATP1A1 and ATP2B3 lead to aldosterone-producing adenomas and secondary hypertension. Nat. Genet. 45, 440–444 (2013).
  8. Scholl, U. I. et al. Somatic and germline CACNA1D calcium channel mutations in aldosterone-producing adenomas and primary aldosteronism. Nat. Genet. 45,1050–1054 (2013).
  9. Azizan, E. A. et al. Somatic mutations in ATP1A1 and CACNA1D underlie a common subtype of adrenal hypertension. Nat. Genet. 45, 1055–1060 (2013).
  10. Fernandes-Rosa, F. L. et al. Genetic spectrum and clinical correlates of somatic mutations in aldosterone-producing adenoma. Hypertension 64, 354–361 (2014).

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Mutations Drive Unrestrained Secretion

Posted on December 11, 2014 by MaryO
The USP8 mutations identified in adenomas of the pituitary gland lead to overproduction of ACTH. Panel A: ACTH-producing cells in a normal gland. The other panels show cells non-mutant (B) or mutant (C) for USP8. Credit: S. Sbiera, Universität Würzburg

The USP8 mutations identified in adenomas of the pituitary gland lead to overproduction of ACTH. Panel A: ACTH-producing cells in a normal gland. The other panels show cells non-mutant (B) or mutant (C) for USP8. Credit: S. Sbiera, Universität Würzburg

Benign tumors in the pituitary gland lead to uncontrolled secretion of the stress hormone cortisol by the cells of the adrenal cortex. An international research effort has now characterized a new mechanism that triggers the syndrome.

Many individuals who suffer from Cushing syndrome are easy to recognize: They tend to be overweight particularly around the waist, and have round faces and bull necks. In addition to these obvious features, most of them have high blood pressure, develop muscle weakness, become diabetic and are extremely susceptible to infection. Cushing syndrome can often be treated effectively by surgical intervention, but patients succumb to infections or cardiovascular disease if the condition is left untreated.

In their efforts to understand how benign tumors in the pituitary provoke the development of Cushing’s disease, researchers based in Munich, Würzburg and Tokyo led by Professor Martin Reincke (Director of LMU’s Medical Clinic IV at Munich University Medical Center) have now pinpointed a novel molecular mechanism responsible for the condition. The results of the study have just appeared in Nature Genetics.

The perils of incessant secretion

All of the symptoms that typify Cushing syndrome are attributable to the unregulated secretion of the hormone cortisol – generally referred to as cortisone. Cortisol is normally released into the bloodstream only in stress situations, and helps the organism to cope with the challenge. However, when secreted in an uncontrolled fashion, the result is physiological havoc. Cortisol is synthesized in, and secreted by specialized cells in the adrenal cortex in response to the binding of a different hormone, the adrenocorticotropic hormone (ACTH). ACTH in turn is produced in the pituitary gland. Excessive cell proliferation in the pituitary can result in the formation of benign tumors (adenomas), which may lead to overproduction of ACTH and a corresponding increase in the level of circulating cortisol. However, the connecting links between the two processes are incompletely understood.

“We have now shown that tumor cells in more than one-third of patients with Cushing’s disease carry a mutation in one specific gene, which codes for an enzyme called ubiquitin-specific protease 8,” says Martin Fassnacht (Würzburg University Hospital), one of the authors of the publication. The mutation was discovered in the course of a detailed genetic characterization of benign tumors of the pituitary gland that overproduced ACTH.

Protease defect sets off a chain reaction

Ubiquitin-specific protease 8 (USP8) is one of a family of enzymes which play a key role in the destruction of proteins that are required only transiently by cells. One such protein is the receptor for epidermal growth factor (EGF), which is degraded and disposed of only when the USP8 gene is inactive, and no USP8 protein is present. The collaboration found that the effect of the mutations identified in pituitary tumor tissues is to keep the USP8 permanently active. As a consequence, the EGF receptor escapes demolition, and is instead recycled to its site of action on the cell membrane. The upshot of this is a life-threatening chain reaction, in which unrestrained synthesis of ACTH leads to uninhibited secretion of cortisol. “The identification of mutations in USP8 is a significant finding, because it opens up entirely new diagnostic and therapeutic approaches to the management of Cushing’s disease,” Martin Reincke adds.

Long-term focus on Cushing’s disease

Indeed, this is not the first time that the collaboration between the teams in Munich and Würzburg has shed light on the pathogenesis of Cushing’s disease. The two groups have previously identified mutations in a gene that is expressed in the adrenal cortex as a frequent cause of the pathological secretion of cortisol in a different patient population. The results of that study appeared in February 2014 in the “New England Journal of Medicine“. And only last week, a paper providing a detailed characterization of the molecular effects of the latter set of mutations was published in “Nature Communications“.

Explore further: Cushing’s syndrome: A genetic basis for cortisol excess

More information: “Mutations in the deubiquitinase gene USP8 cause Cushing’s disease.” Nature Genetics (2014) DOI: 10.1038/ng.3166

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Etomidate drip quickly curbs severe hypercortisolism

Posted on August 1, 2014 by MaryO

By: BRUCE JANCIN, Clinical Endocrinology News Digital Network

JULY 31, 2014

AT ICE/ENDO 2014

VITALS  Key clinical point: The anesthetic induction agent etomidate is a potent suppressor of cortisol synthesis in the adrenal cortex at subhypnotic doses, making it a safe and effective agent for management of severe hypercortisolism in Cushing’s syndrome.

Major finding: Continuous infusion of etomidate using a standardized protocol resulted in a reduction in serum cortisol from a mean of 138 mcg/dL to a goal range of 10-20 mcg/dL in an average of 64 hours.

Data source: This was a retrospective case series involving six patients with severe hypercortisolism caused by adrenocorticotropic hormone–dependent Cushing’s syndrome.

Disclosures: The study was carried out with institutional funds. The presenter reported having no financial conflicts.

Continuous intravenous infusion of etomidate safely and swiftly gains control of severe hypercortisolism in patients with adrenocorticotropic hormone–dependent Cushing’s syndrome when conventional presurgical oral treatment is problematic.

“From our cumulative experience, we have now developed a standardized titrated etomidate infusion protocol, which should provide clinicians with a simple, safe, and effective means to lower serum cortisol in patients with severe clinical, metabolic, and neuropsychiatric consequences of prodigious hypercortisolism as a bridge to definitive medical or surgical therapy,” explained Dr. Katarzyna G. Zarnecki at the joint meeting of the International Congress of Endocrinology and the Endocrine Society.

Etomidate (Amidate) is a sedative hypnotic agent with an excellent cardiovascular safety profile. It is widely used in emergency settings, such as reduction of dislocated joints and cardioversion. It suppresses adrenal steroidogenesis by potently inhibiting 11-beta hydroxylase. Fortunately for endocrinologic purposes, etomidate suppresses cortisol synthesis even at subhypnotic doses. In using it off label for management of severe hypercortisolism, it’s essential to keep the drug at subhypnotic doses, meaning not more than 0.3 mg/kg per hour, emphasized Dr. Zarnecki of the University of Wisconsin, Milwaukee.

Dr. Zarnecki and her coworkers utilize as their standard etomidate infusion protocol an initial 5-mg bolus followed by an infusion at 0.02 mg/kg per hour, with dose titration in increments of 0.01-0.02 mg/kg per hour every 4-6 hours based on changes in serum cortisol level. The goal is to bring the cortisol down to a target range of 10-20 mcg/dL.

She presented an illustrative six-patient series in which she and her colleagues turned to continuous infusion of etomidate because conventional oral therapy would have taken too long to rein in the severe hypercortisolism or because medication side effects were intolerable.

Mean baseline pretreatment serum cortisol was 138 mcg/dL, with an adrenocorticotropic hormone level of 419 pg/mL. Five of the six patients reached the goal of 10-20 mcg/dL in an average time of 64 hours. The mean rate of serum cortisol reduction was 1.93 mcg/dL per hour. The average etomidate infusion rate at the time the target level was reached was 0.07 mg/kg per hour, with a maximum rate of 0.1 mg/kg per hour. Monitoring via the Richmond Agitation Sedation Scale confirmed that none of the patients experienced sedative effects.

In the sole patient who didn’t reach goal, etomidate therapy was suspended because the patient entered palliative care because of extensive tumor progression.

Dr. Zarnecki reported having no financial conflicts of interest.

From Clinical Endocrinology News

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Adrenal Glands

Posted on June 23, 2013 by MaryO

adrenal-glandsAnatomy of the adrenal glands:

Adrenal glands, which are also called suprarenal glands, are small, triangular glands located on top of both kidneys. An adrenal gland is made of two parts: the outer region is called the adrenal cortex and the inner region is called the adrenal medulla.

Function of the adrenal glands:

The adrenal glands work interactively with the hypothalamus and pituitary gland in the following process:

  • the hypothalamus produces corticotropin-releasing hormones, which stimulate the pituitary gland.
  • the pituitary gland, in turn, produces corticotropin hormones, which stimulate the adrenal glands to produce corticosteroid hormones.

Both parts of the adrenal glands — the adrenal cortex and the adrenal medulla — perform very separate functions.

What is the adrenal cortex?

The adrenal cortex, the outer portion of the adrenal gland, secretes hormones that have an effect on the body’s metabolism, on chemicals in the blood, and on certain body characteristics. The adrenal cortex secretes corticosteroids and other hormones directly into the bloodstream. The hormones produced by the adrenal cortex include:

  • corticosteroid hormones
    • hydrocortisone hormone – this hormone, also known as cortisol, controls the body’s use of fats, proteins, and carbohydrates.
    • corticosterone – this hormone, together with hydrocortisone hormones, suppresses inflammatory reactions in the body and also affects the immune system.
  • aldosterone hormone – this hormone inhibits the level of sodium excreted into the urine, maintaining blood volume and blood pressure.
  • androgenic steroids (androgen hormones) – these hormones have minimal effect on the development of male characteristics.

What is the adrenal medulla?

The adrenal medulla, the inner part of the adrenal gland, is not essential to life, but helps a person in coping with physical and emotional stress. The adrenal medulla secretes the following hormones:

  • epinephrine (also called adrenaline) – this hormone increases the heart rate and force of heart contractions, facilitates blood flow to the muscles and brain, causes relaxation of smooth muscles, helps with conversion of glycogen to glucose in the liver, and other activities.
  • norepinephrine (also called noradrenaline) – this hormone has little effect on smooth muscle, metabolic processes, and cardiac output, but has strong vasoconstrictive effects, thus increasing blood pressure.

From: University of Maryland Center for Diabetes and Endocrinology

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