Practice Paper 3: Answers
Anthony B. Starr, Hiruni Jayasena, David Capewell, Saran Shantikumar in Get ahead! Medicine, 2016
Adrenocorticotropic hormone (ACTH; also known as corticotropin) is secreted from the anterior pituitary gland in response to corticotropin-releasing hormone (CRH) from the hypothalamus. ACTH acts on the adrenal cortex to stimulate the release of glucocorticoids and androgens into the circulation. In Cushing’s disease, a pituitary adenoma secretes large amounts of ACTH into the circulation, causing uninhibited glucocorticoid secretion. Patients with glucocorticoid and androgen excess suffer from Cushing’s syndrome, which consists of a vast array of clinical features, including hypertension, central weight gain, a moon face, poor quality skin, bruising, poor wound healing, hirsutism, acne, abdominal striae, oligomenorrhoea, osteoporosis, hyperglycaemia, polyuria, polydipsia, myopathy, depression and psychosis.
Complications of Hypovolemic and Septic Shock
Stephen M. Cohn, Matthew O. Dolich in Complications in Surgery and Trauma, 2014
Sheehan syndrome was described in 1937 as a disruption of the hypothalamic–pituitary axis secondary to peripartum hemorrhagic shock. Findings include hypothyroidism, adrenocortical insufficiency, failure of lactation, and cessation of menses, resulting from ischemic necrosis of the pituitary gland. In some cases, computed tomography or magnetic resonance imaging actually demonstrate an empty sella turcica. The lesser-known Simmonds syndrome is pituitary dysfunction in either gender following traumatic hemorrhage. A great deal of interest has centered on adrenocortical insufficiency from either hypovolemic or septic shock. The most obvious clinical manifestation of adrenocortical insufficiency is refractory hypotension, perpetrating a vicious cycle. Adrenocortical insufficiency has been variously defined as a baseline serum cortisol concentration <10–25 μm/dL or an increase of <9 μm/dL within 1 h following administration of 250 μm of cosyntropin. In some cohorts, more than half of the patients with sepsis or hemorrhagic shock have at least occult adrenocortical insufficiency on the basis of laboratory values.21 Severe hyperacute adrenal insufficiency is present at the time of admission in 16% of trauma patients with evidence of ongoing hemorrhage.22 Most recently, studies suggest the existence of relative adrenal insufficiency, defined by shock that improves following administration of steroid replacement therapy, regardless of serum laboratory values.
Stratified Risk Assessment for Urological Surgery
Anthony R. Mundy, John M. Fitzpatrick, David E. Neal, Nicholas J. R. George in The Scientific Basis of Urology, 2010
The daily basal dose of corticosteroid is equivalent to 7.5 mg of prednisolone or 30 mg of hydrocortisone (44). In patients with a normal endocrine response, cortisol secretion usually rises immediately after the start of surgery and can be modified by anesthetic intervention. In primary or secondary adrenal failure, the body’s physiological response to stress is impaired, and increases in cortisol levels will not occur. Patients who have been on long-term high dose steroids will also lack such a response because of suppression of the hypothalamic corticotropinreleasing hormone and pituitary adrenocorticotropic hormone secretion. Such individuals may have mild symptoms of adrenal insufficiency such as fatigue, malaise, arthralgia, depression, nausea, and low-grade fever. These patients usually respond poorly to stress. Failure of cortisol secretion may result in the circulatory collapse and hypotension characteristic of an “Addisonian” crisis.
Pituitary apoplexy mimicking meningoencephalitis: case report and scoping study
Published in Hospital Practice, 2020
Chun Chu, Gretchen A. Perilli, Casey Judge, Sen Sheng, Hussam A. Yacoub
An urgent CT of the head revealed a solid and cystic sellar and suprasellar lesion concerning for a pituitary adenoma or a craniopharyngioma. Repeated CSF analysis revealed pleocytosis of 16/mm3 and elevated protein of 96 mg/100 ml. A complete analysis of anterior pituitary hormones revealed panhypopituitarism (Table 1). Adrenocorticotropic hormone (ACTH) stimulation test with cosyntropin of 250 mcg was performed. Early morning cortisol baseline level was 4.8 ug/dl. After cosyntropin administration, cortisol levels were 15.2 ug/dl at 30 minutes and 17.8 ug/dl at 60 minutes, respectively. Hormone replacement therapy (HRT) with steroids, dexamethasone initially followed by hydrocortisone, and levothyroxine were initiated. A brain MRI showed a rim-enhancing sellar and suprasellar lesion with peripheral hyperintensity in T1-weighted sequence and hypointensity in gradient echo (GRE) sequence, consistent with a subacute pituitary hemorrhage (Figure 2).
Secondary adrenal insufficiency induced by long-term use of opioid analgesics
Published in Baylor University Medical Center Proceedings, 2019
Patients with secondary AI usually present with symptoms such as nausea, dizziness, and fatigue. Hypotension and adrenal crisis may occur.2 It is well established that cortisol can increase after cosyntropin stimulation in secondary hypoadrenalism. Some have used 20 ng/mL as the cutoff for serum cortisol. However, even a cortisol value above this should not preclude treatment with glucocorticoids if the clinical presentation is consistent with cortisol deficiency.3 Moreover, even low-dose cosyntropin testing may not predict response to glucocorticoids4 and thus initial cosyntropin testing may miss secondary cortisol deficiency.5 We agree with Burgos et al6 that the patient’s clinical presentation should be considered when interpreting cosyntropin tests. We believe that glucocorticoid treatment should not be withheld on the basis of a cortisol level if the clinical presentation is consistent with hypoadrenalism.
Adrenal function following acute discontinuation of glucocorticoids in children with acute lymphocytic leukemia: A prospective study
Published in Pediatric Hematology and Oncology, 2019
Noman Ahmad, Ibraheem Faisal Abosoudah, Mrouge Mohamed Sobaihi, Ali Hassan Algiraigri, Farh Roujouleh, Fatima Ghurab, Jean-Pierre Chanoine
The second HPA assessment was planned one week after the completion of the induction phase. Due to changes in the follow up schedule, some participants had this assessment during the second week. The HPA axis was assessed by the low dose (1 mcg) ACTH stimulation test. Serum cortisol and adrenocorticotropin (ACTH) levels were measured before intravenous administration of 1 mcg cosyntropin. Samples for serum cortisol were collected 20 and 30 minutes after cosyntropin injection. A 250 mcg vial of cosyntropin (Cortrosyn, Amphastar Pharmaceuticals Inc, USA) was serially diluted in 0.9% saline to achieve a 1 µg/mL solution.12 Serum cortisol level >500 nmol/L (18 mcg/dL) at 20 or 30 min was considered as reflecting normal HPA axis function and a serum cortisol level 300–500 nmol/L (10.8–18 mcg/dL) was considered as a partial response. Serum cortisol was measured by commercial competitive chemiluminescent immunoassay (Elecsys Cortisol II) in an analyzer Cobas e 411. The mean intra-assay coefficient of variation was 3.9%. ACTH was measured by electrochemiluminescence immunoassay (Elecsys ACTH) in an analyzer Cobas e 801, the mean intra-assay coefficient of variation was 3.4%.
Related Knowledge Centers
- Acth Stimulation Test
- Adrenal Insufficiency
- Anterior Pituitary
- Cortisol
- Peptide
- Tropic Hormone
- Corticosteroid
- Amino Acid
- Pituitary Gland
- Adrenal Gland