Adrenal Insufficiency Lec.5.pdf

ORAL SURGERY ENDOCRINE AND METABOLIC DISEASE ADRENAL INSUFFICIENCY 1 The Adrenal gland - small (6–8 g) endocrine glands, at the superior pole of a kidney. - Each gland contains an outer cortex and an inner medulla. - Medulla; functions as a sympathetic ganglion and secretes catecholamines...

ORAL SURGERY ENDOCRINE AND METABOLIC DISEASE ADRENAL INSUFFICIENCY 1 The Adrenal gland - small (6–8 g) endocrine glands, at the superior pole of a kidney. - Each gland contains an outer cortex and an inner medulla. - Medulla; functions as a sympathetic ganglion and secretes catecholamines, primarily epinephrine. - Cortex secretes steroid hormones (3 main classes) all derived from cholesterol - Cortex consists of three zones; i- Outer zone (zona glomerulosa)→mineralocorticoids→mainly aldosterone; regulates levels of sodium and potassium→ control of intravascular volume and blood pressure. ii- middle zone (zona fasciculata)→ glucocorticoids→mainly Cortisol; 1- acts as an insulin antagonist; increasing blood levels and peripheral use of glucose by activating gluconeogenesis and inhibiting glucose uptake in peripheral tissues 2- activates lipolysis in adipose tissue →release of free fatty acids into circulation. 3- increases blood pressure by potentiating the vasoconstrictor action of catecholamines and angiotensin II 4- antiinflammatory action 5- activates osteoclasts and inhibits osteoblasts iii- innermost zone (zona reticularis)→ androgens, or sex hormones. 1.1 CORTISOL Is regulated through activity of the hypothalamic–pituitary–adrenal (HPA) axis. Stress stimulates the hypothalamus to release corticotropin-releasing hormone (CRH), which stimulates the secretion of adrenocorticotropic hormone (ACTH) by the anterior pituitary. ACTH stimulates the adrenal cortex to secrete cortisol. Plasma cortisol levels are increased within a few minutes will eventually inhibit the production of CRH and ACTH (negative feedback loop). Cortisol secretion follows a circadian pattern; Peak levels around the time of waking (morning) and are lowest in the evening and night. The normal secretion rate ≈ 20mg/24 hr. Synthetic glucocorticoids (cortisol-like drugs) used in the treatment of autoimmune and inflammatory diseases (e.g., rheumatoid arthritis, systemic lupus erythematosus, asthma, hepatitis, inflammatory bowel disease, dermatoses, mucositis) can affect adrenal function. 1.2 ALDOSTERONE Aldosterone promotes sodium and water retention and potassium excretion. Aldosterone secretion is predominantly regulated by the renin–angiotensin system and extracellular potassium levels and less so by plasma sodium levels. Aldosterone secretion is stimulated by a fall in renal blood pressure, which results from decreased intravascular volume or a sodium imbalance → renin release from the kidney→activates angiotensinogen→angiotensin I→angiotensin II→stimulates secretion of aldosterone When blood pressure rises, renin–angiotensin release diminishes, serving as a negative feedback loop. 2 ADRENAL GLANDS DISORDERS These can be discussed in two categories; 2.1 HYPERADRENALISM - Excessive secretion of adrenal cortisol, mineralocorticoids, androgens, or estrogen in isolation or combination - most commonly glucocorticoid excess - If caused by pathophysiology→Cushing disease. - Cushing syndrome is a generalized state caused by excessive cortisol in the body, regardless of the cause. 2.2 ADRENAL INSUFFICIENCY Divided into three categories: 1- Primary adrenocortical insufficiency (Addison disease) occurs when the adrenal cortex is destroyed or the gland is removed. 2- Secondary adrenocortical insufficiency; due to pituitary disease, lack of responsiveness of the adrenal glands to ACTH, or critical illness. 3- Tertiary adrenal insufficiency; due to hypothalamus impaired function commonly caused by chronic use of corticosteroids. 2.2.1 ETIOLOGY A- Primary adrenocortical insufficiency 1- autoimmune disease 2- chronic infectious disease (tuberculosis, HIV, cytomegalovirus, and fungal infection) 3- malignancy. 4- Hemorrhage (e.g., heparin use) 5- Sepsis 6- adrenalectomy, 7- genetic mutations (e.g., adrenoleukodystrophy) 8- drugs (e.g., that increase cortisol metabolism) B- Secondary adrenocortical insufficiency; 1- Lesions of the pituitary gland (e.g., tumor), 2- Removal of the pituitary gland 3- Cranial irradiation of the pituitary gland 4- Head trauma 5- Lack of responsiveness of the adrenal glands to ACTH 6- Critical illness (e.g., sepsis, liver cirrhosis). C- Tertiary adrenal insufficiency results from 1- Defective hypothalamus function 2- chronic administration of corticosteroids. 3- administration of specific drugs (Antidepressant, Antifungal, Antipsychotic, Antisteroid, Antituberculosis... etc.) 4- critical illness (burns, trauma) 5- systemic infection NOTEs; - Corticosteroids can be administered by a variety of Routes. Corticosteroids that are topically applied or repeatedly locally injected or inhaled rarely induce adrenal suppression - prolonged topical corticosteroids on large areas may cause adrenal suppression - Inhaled corticosteroids in frequent and high doses may cause suppression - Doses above 400 to 500 μg/day (children) or 800 to 1000 μg/day (adults) of beclomethasone dipropionate equivalent (depending on body mass) considered the cutoff point (adrenal suppression is probable) - HPA may returns to respond to stress within 14 days even when supraphysiologic doses were given for 1 month or longer. 3 COMPLICATIONS A- Addison disease Lack of cortisol results in 1- impaired metabolism of glucose, fat, and protein 2- hypotension, 3- increased ACTH secretion 4- impaired fluid excretion 5- excessive pigmentation 6- inability to tolerate stress (maintenance of vascular reactivity, blood pressure and cardiac output). Aldosterone deficiency results in inability to conserve sodium and eliminate potassium and hydrogen ions, leading to hypovolemia, hyperkalemia, and acidosis. B- Secondary and tertiary adrenal insufficiency; Unlike primary adrenal insufficiency, aldosterone is not impaired because its secretion is ACTH independent. C- Adrenal Crisis; Potentially life-threatening complication of adrenal insufficiency triggered by stress (emotional and physical). The condition occurs among those with primary adrenal insufficiency. It evolves over a few hours S&S include; sunken eyes, profuse sweating, hypotension, weak pulse, cyanosis, abdominal pain, nausea, vomiting, weakness, headache, dehydration, fever, dyspnea, myalgias, arthralgia, hyponatremia, and eosinophilia. If not treated rapidly→hypothermia, severe hypotension, hypoglycemia, confusion, and circulatory collapse→death. 4 CLINICAL PRESENTATION 4.1 SIGNS AND SYMPTOMS 4.1.1 HYPOADRENALISM. S & S Nonspecific→delays in diagnosis (appears after 90% of the cortices destroyed) Addison disease - weakness, fatigue, abdominal pain, and hyperpigmentation of the skin (i.e., skin areas subjected to pressure: elbows, knuckles, palmar creases) and mucous membranes. Hypotension, anorexia, salt craving, myalgia, hypoglycemia, and weight loss - Inability to tolerate emotional or physical stress→adrenal crisis Secondary and tertiary adrenal insufficiency - limited to glucocorticoids. - NO hyperpigmentation or any symptoms unless the patient is significantly stressed→adrenal crisis (rare) 4.1.2HYPERADRENALISM. Produce four syndromes - Androgen-related disorders; rare, affect the reproductive organs - Mineralocorticoid excess (primary aldosteronism); hypertension, hypokalemia, and dependent edema - glucocorticoid excess (endogenous or exogenous); most common→ Cushing syndrome→weight gain, a broad and round face (“moon facies”), a “buffalo hump” on the upper back, abdominal striae, hypertension, hirsutism, acne, diabetes mellitus, heart failure, osteoporosis, psychiatric disorders, insomnia, peptic ulceration, cataract, glaucoma, growth suppression, and delayed wound healing. - estrogen-related disorders 5 LABORATORYFINDINGS - morning cortisol range 10–20 μg/dL. Late afternoon 3–10 μg/dL). - Levels of plasma corticotropin are high with primary adrenal insufficiency and low with secondary adrenal insufficiency. - A subnormal test response to standard-dose corticotropin (cortisol level1hour) procedure. 7.3 HYPERADRENALISM. - likelihood of having hypertension, diabetes, delayed wound healing, osteoporosis, and peptic ulcer - blood pressure should be taken at baseline and monitored during dental appointments. - Blood glucose levels should be determined - Follow-up appointments arranged to assess proper wound healing and periodic measures of periodontal bone loss (why?) - measures that promote one mineralization should be taken - extensive neck manipulation should be avoided (why?) - postoperative analgesics should not include NSAIDS 7.4ADRENAL INSUFFICIENCY 1 RISK OF INFECTION AND BLEEDING Generally, not an issue. 2 BLOOD PRESSURE - throughout invasive procedures evaluated at 5-minute intervals and before the patient leaves the office - A systolic blood pressure below 100 mm Hg or a diastolic pressure at or below 60 mm Hg represents hypotension→ corrective action 1- proper patient positioning (i.e., head lower than feet), 2- fluid replacement 3- administration of vasopressors 4- evaluation for signs of adrenal dysfunction (adrenal crisis) versus hypoglycemia; 3 CAPACITY TO TOLERATE CARE - Adrenal crisis risk is highest in those with 1- primary adrenal insufficiency 2- fever, trauma, stressful surgical procedures, or general anesthesia and have primary or severe secondary adrenal insufficiency→ delay treatment until medically stabilized. - patients with primary adrenal insufficiency are recommended to receive corticosteroid supplementation only when 1- surgery or general anesthesia is being performed or 2- management of a dental or systemic infection - patients with secondary or tertiary adrenal insufficiency may undergo routine dental treatment without the need for supplemental glucocorticoids. - Well-controlled secondary adrenal insufficiency patients are recommended to take their usual daily dose of steroid within 2 hours of the surgery with no supplementation dose - Patients undergoing surgery → monitored for blood and fluid loss (postoperatively)→if hypotension→IV fluids→if hypotension persists→ additional doses of corticosteroid - Patients are returned to their usual glucocorticoid dosage as soon as their vital signs are stabilized. - Additional measures minimize the risk of adrenal crisis due to surgery; 1- Surgery scheduled in the morning 2- Stress reduction (Nitrous oxide–oxygen inhalation and benzodiazepine sedation) 3- Barbiturates used cautiously (enhance the metabolism of cortisol) 4- Inhibitors of corticosteroid production discontinued at least 24 hours before surgery (consult a physician) 5- Surgeries > 1hr considered major surgery →steroid supplementation. 6- fasting state can contribute to hypoglycemia→ mimic features of adrenal crisis (no glucocorticoids needed) 4 DRUG CONSIDERATIONS AND INTERACTIONS. To minimizes stress → good postoperative pain control; long-acting local anesthetics (e.g., bupivacaine) and analgesics at the end of the procedure. cortisol levels generally increased 1–5 hours postoperatively, and the rise in cortisol levels is blunted by the use of analgesics and midazolam. 5 EMERGENCY ACTION. Immediate treatment during adrenal crisis; 1- proper patient positioning (i.e., head lower than feet), 2- fluid replacement 3- administration of vasopressors 4- administration of 100 mg of hydrocortisone or 4 mg of dexamethasone IV 5- immediate transportation to a medical facility. 6 ORAL MANIFESTATIONS 1- Diffuse or focal brown macular pigmentation of the oral mucous membranes in primary adrenal insufficiency 2- Pigmentation of sun-exposed skin in areas of friction occurs after the appearance of oral pigmentation and is accompanied by lethargy 3- Patients with secondary or tertiary adrenal insufficiency prone to delayed healing and may have increased susceptibility to infection but do not develop hyperpigmentation.