Autoimmune polyendocrine syndrome type 1 treatment is based on the symptoms that are presented by the affected individual, additionally there is:

- Hormone replacement

- Systemic antifungal treatment

- Immunosuppressive treatment

Immunosuppressive therapy may be used in "type I" of this condition, ketoconazole can be used for "autoimmune polyendocrine syndrome type I" under certain conditions The component diseases are managed as usual, the challenge is to detect the possibility of any of the syndromes, and to anticipate other manifestations. For example, in a person with known Type 2 autoimmune polyendocrine syndrome but no features of Addison's disease, regular screening for antibodies against 21-hydroxylase may prompt early intervention and hydrocortisone replacement to prevent characteristic crises

Often, this disease is treated by giving aspirin to inhibit platelet activation, and/or warfarin as an anticoagulant. The goal of the prophylactic treatment with warfarin is to maintain the patient's INR between 2.0 and 3.0. It is not usually done in patients who have had no thrombotic symptoms.

Anticoagulation appears to prevent miscarriage in pregnant women. In pregnancy, low molecular weight heparin and low-dose aspirin are used instead of warfarin because of warfarin's teratogenicity. Women with recurrent miscarriage are often advised to take aspirin and to start low molecular weight heparin treatment after missing a menstrual cycle. In refractory cases plasmapheresis may be used.

Autoimmune polyendocrine syndromes (APS) occur when more than one autoimmune disease occurs in endocrine glands. These syndromes are also called Polyendocrine Autoimmune Disorders. In Type 3, autoimmune thyroiditis and another endocrine autoimmune disease are present, but the adrenal cortex is not involved.

The long-term prognosis for APS is determined mainly by recurrent thrombosis, which may occur in up to 29% of patients, sometimes despite antithrombotic therapy.

Autoimmune polyendocrine syndrome type 1 (APS-1), also known as autoimmune polyendocrinopathy-candidiasis–ectodermal dystrophy/dysplasia (APECED), autoimmune polyglandular syndrome type 1, Whitaker syndrome, or candidiasis-hypoparathyroidism–Addison's disease syndrome, is a subtype of autoimmune polyendocrine syndrome (autoimmune polyglandular syndrome) in which multiple endocrine glands dysfunction as a result of autoimmunity. It is a genetic disorder inherited in autosomal recessive fashion due to a defect in the "AIRE" gene (autoimmune regulator), which is located on chromosome 21 and normally confers immune tolerance.

Management of autoimmune polyendocrine syndrome type 2 consists of the following:

Standard therapy involves intravenous injections of glucocorticoids and large volumes of intravenous saline solution with dextrose (glucose). This treatment usually brings rapid improvement. If intravenous access is not immediately available, intramuscular injection of glucocorticoids can be used. When the patient can take fluids and medications by mouth, the amount of glucocorticoids is decreased until a maintenance dose is reached. If aldosterone is deficient, maintenance therapy also includes oral doses of fludrocortisone acetate.

Treatment for Addison's disease involves replacing the missing cortisol, sometimes in the form of hydrocortisone tablets, or prednisone tablets in a dosing regimen that mimics the physiological concentrations of cortisol. Alternatively, one-quarter as much prednisolone may be used for equal glucocorticoid effect as hydrocortisone. Treatment is usually lifelong. In addition, many patients require fludrocortisone as replacement for the missing aldosterone.

People with Addison's are often advised to carry information on them (e.g., in the form of a MedicAlert bracelet or information card) for the attention of emergency medical services personnel who might need to attend to their needs. It is also recommended that a needle, syringe, and injectable form of cortisol be carried for emergencies. People with Addison's disease are advised to increase their medication during periods of illness or when undergoing surgery or dental treatment. Immediate medical attention is needed when severe infections, vomiting, or diarrhea occur, as these conditions can precipitate an Addisonian crisis. A patient who is vomiting may require injections of hydrocortisone instead.

Autoimmune polyendocrine syndromes (APSs), also called autoimmune polyglandular syndromes (APSs), polyglandular autoimmune syndromes (PGASs), or polyendocrine autoimmune syndromes, are a heterogeneous group of rare diseases characterized by autoimmune activity against more than one endocrine organ, although non-endocrine organs can be affected.There are three types of APS or (in terms that mean the same thing) three APSs, and there are a number of other diseases which have endocrine autoimmunity.

Autoimmune polyendocrine syndrome type 2, a form of autoimmune polyendocrine syndrome also known as Schmidt's syndrome, or APS-II, is the most common form of the polyglandular failure syndromes. It is heterogeneous and has not been linked to one gene. Rather, individuals are at a higher risk when they carry a particular human leukocyte antigen (HLA-DQ2, HLA-DQ8 and HLA-DR4). APS-II affects women to a greater degree than men.

Catastrophic antiphospholipid syndrome (CAPS), also known as Asherson's syndrome, is an acute and complex biological process that leads to occlusion of small vessels of various organs. It was first described by Ronald Asherson in 1992. The syndrome exhibits thrombotic microangiopathy, multiple organ thrombosis, and in some cases tissue necrosis and is considered an extreme or catastrophic variant of the antiphospholipid syndrome.

CAPS has a mortality rate of about 50%. With the establishment of a CAPS-Registry more has been learned about this syndrome, but its cause remains unknown. Infection, trauma, medication, and/or surgery can be identified in about half the cases as a "trigger". It is thought that cytokines are activated leading to a cytokine storm with the potentially fatal consequences of organ failure. A low platelet count is a common finding. Individuals with CAPS often exhibit a positive test to antilipid antibodies, typically IgG, and may or may not have a history of lupus or another connective tissue disease. Association with another disease such as lupus is called a secondary APS unless it includes the defining criteria for CAPS.

Clinically, the syndrome affects at least three organs and may affect many organs systems. Peripheral thrombosis may be encountered affecting veins and arteries. Intraabdominal thrombosis may lead to pain. Cardiovascular, nervous, kidney, and lung system complications are common. The affected individual may exhibit skin purpura and necrosis. Cerebral manifestations may lead to encephalopathy and seizures. Myocardial infarctions may occur. Strokes may occur due to the arterial clotting involvement. Death may result from multiple organ failure.

Treatments may involve the following steps:

- Prevention includes the use of antibiotics for infection and parenteral anticoagulation for susceptible patients.

- Specific therapy includes the use of intravenous heparin and corticosteroids, and possibly plasma exchanges, intravenous immunoglobulin.

- Additional steps may have to be taken to manage circulatory problems, kidney failure, and respiratory distress.

- When maintaining survival of the disease treatments also include high doses of Rituxan (Rituximab) to maintain stability.

Causes of acute adrenal insufficiency are mainly sudden withdrawal of long-term corticosteroid therapy, Waterhouse-Friderichsen syndrome, and stress in people with underlying chronic adrenal insufficiency. The latter is termed critical illness–related corticosteroid insufficiency.

For chronic adrenal insufficiency, the major contributors are autoimmune adrenalitis (Addison's Disease), tuberculosis, AIDS, and metastatic disease. Minor causes of chronic adrenal insufficiency are systemic amyloidosis, fungal infections, hemochromatosis, and sarcoidosis.

Autoimmune adrenalitis may be part of Type 2 autoimmune polyglandular syndrome, which can include type 1 diabetes, hyperthyroidism, and autoimmune thyroid disease (also known as autoimmune thyroiditis, Hashimoto's thyroiditis, and Hashimoto's disease). Hypogonadism may also present with this syndrome. Other diseases that are more common in people with autoimmune adrenalitis include premature ovarian failure, celiac disease, and autoimmune gastritis with pernicious anemia.

Adrenoleukodystrophy can also cause adrenal insufficiency.

Adrenal insufficiency can also result when a patient has a craniopharyngioma, which is a histologically benign tumor that can damage the pituitary gland and so cause the adrenal glands not to function. This would be an example of secondary adrenal insufficiency syndrome.

Causes of adrenal insufficiency can be categorized by the mechanism through which they cause the adrenal glands to produce insufficient cortisol. These are adrenal dysgenesis (the gland has not formed adequately during development), impaired steroidogenesis (the gland is present but is biochemically unable to produce cortisol) or adrenal destruction (disease processes leading to glandular damage).

The best diagnostic tool to confirm adrenal insufficiency is the ACTH stimulation test; however, if a patient is suspected to be suffering from an acute adrenal crisis, immediate treatment with IV corticosteroids is imperative and should not be delayed for any testing, as the patient's health can deteriorate rapidly and result in death without replacing the corticosteroids.

Dexamethasone should be used as the corticosteroid if the plan is to do the ACTH stimulation test at a later time as it is the only corticosteroid that will not affect the test results.

If not performed during crisis, then labs to be run should include: random cortisol, serum ACTH, aldosterone, renin, potassium and sodium. A CT of the adrenal glands can be used to check for structural abnormalities of the adrenal glands. An MRI of the pituitary can be used to check for structural abnormalities of the pituitary. However, in order to check the functionality of the Hypothalamic Pituitary Adrenal (HPA) Axis the entire axis must be tested by way of ACTH stimulation test, CRH stimulation test and perhaps an Insulin Tolerance Test (ITT). In order to check for Addison’s Disease, the auto-immune type of primary adrenal insufficiency, labs should be drawn to check 21-hydroxylase autoantibodies.

Treatment for perfectionism can be approached from many therapeutic directions. Some examples of psychotherapy include: cognitive-behavioral therapy (the challenging of irrational thoughts and formation of alternative ways of coping and thinking), psychoanalytic therapy (an analysis of underlying motives and issues), group therapy (where two or more clients work with one or more therapists about a specific issue, this is beneficial for those who feel as if they are the only one experiencing a certain problem), humanistic therapy (person-centered therapy where the positive aspects are highlighted), and self-therapy (personal time for the person where journaling, self-discipline, self-monitoring, and honesty with self are essential). Cognitive-behavioral therapy has been shown to successfully help perfectionists in reducing social anxiety, public self-consciousness, and perfectionism. By using this approach, a person can begin to recognize his or her irrational thinking and find an alternative way to approach situations. Cognitive-behavioral therapy is intended to help the person understand that it is okay to make mistakes sometimes and that those mistakes can become lessons learned.

Re-entry ventricular arrhythmia is a type of paroxysmal tachycardia occurring in the ventricle where the cause of the arrhythmia is due to the electric signal not completing the normal circuit, but rather an alternative circuit looping back upon itself. There develops a self-perpetuating rapid and abnormal activation. ("Circus Movement" is another term for this.) Conditions necessary for re-entry include a combination of unidirectional block and slowed conduction. Circus movement may also occur on a smaller scale within the AV node (dual AV nodal physiology), a large bypass tract is not necessary.

Re-entry is divided into two major types: [Anatomically Defined] re-entry and [Functionally Defined] re-entry. The circus movement can occur around an anatomical or functional core. Either type may occur alone, or together.

"Anatomically" defined re-entry has a fixed anatomic pathway. Anomalous conduction via accessory pathways (APs) create the re-entry circuit (which are also called bypass tracts), that exist between the atria and ventricles. Wolff–Parkinson–White syndrome (WPW) is an example of anatomically defined re-entry. WPW syndrome is an atrioventricular re-entrant tachycardia (AVRT), secondary to an accessory pathway that connects the epicardial surfaces of the atrium and ventricle along the AV groove. The majority of time symptomatic WPW fits the definition of AVRT (Supraventricular tachycardia) however AVNRT (dual AV nodal physiology) exist in ~10% of patients with WPW syndrome creating the possibility of spontaneous atrial fibrillation degenerating into ventricular fibrillation (VF). The fact that WPW patients are young and do not have structural heart disease, lead to using catheter ablation of the APs with the elimination of the atrial fibrillation as well as the episodes of re-entrant ventricular tachycardia. This elimination of the atrial fibrillation with ablation implies APs have some pathophysiologic role in the development of a-fib in the WPW patient.

"Functionally" defined re-entry does not require the alternative anatomically defined circuit accessory pathways and it may not reside in just one location. Ventricular fibrillation (VF) following ventricular tachycardia (VT) may be described as a functionally defined re-entry problem caused by multiple mini re-entrant circuits spontaneously created within the ventricular myocardium. The original re-entrant circuit breaks down into multiple mini reentrant circuits. (VF becoming the grand finale of a single prolonged VT larger circus movement, propagating change in the "functional core" of the ventricular myocardium, dissipating mini reentrant circuits, exhibited as ventricular fibrillation.) Ischemia, electrolyte, pH abnormalities, or bradycardia are potential causes of functionally defined re-entry due to changes in the properties of the cardiac tissue's functional core. (No accessory pathway required)

Perfectionism, in psychology, is a personality trait characterized by a person's striving for flawlessness and setting high performance standards, accompanied by critical self-evaluations and concerns regarding others' evaluations. It is best conceptualized as a multidimensional characteristic, as psychologists agree that there are many positive and negative aspects. In its maladaptive form, perfectionism drives people to attempt to achieve an unattainable ideal, while their adaptive perfectionism can sometimes motivate them to reach their goals. In the end, they derive pleasure from doing so. When perfectionists do not reach their goals, they often fall into depression.