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Home , Adrenal cortex, Adrenal gland, Endocrine system

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Clinical Practice Keywords / /Adrenal Systems of This article has been Endocrine system double-blind peer reviewed In this article... ● Endocrine functions of the adrenal glands ● Hormones of the adrenal glands ● The role of adrenal hormones in mediating essential physiological processes

Endocrine system 4: adrenal glands

Key points Authors Maria Andrade is honorary associate professor in biomedical science; There are two Zubeyde-Bayram Weston is senior lecturer in biomedical science; John Knight is adrenal glands: one associate professor in biomedical science; all at College of and Health located above each Sciences, Swansea University. NT SELF- Abstract The endocrine system consists of glands and tissues that produce and ASSESSMENT Adrenal glands secrete hormones to regulate and coordinate vital bodily functions. This article, the Test your consist of two parts, fourth in an eight-part series on the endocrine system, explores the and knowledge. the and the of the adrenal glands, and describes how they regulate and coordinate After reading this medulla, which each vital physiological processes in the body through hormonal action. article go to produce different nursingtimes.net/ NTSAAdrenal hormones Citation Andrade M et al (2021) Endocrine system 4: adrenal glands. Nursing Times If you score 80% [online]; 117: 8, 54-58. or more, you will The receive a certificate produces a diverse that you can use range of as revalidation his eight-part series on the endo- colour and are positioned retroperito- evidence. hormones, using crine system opened with an neally (behind the peritoneal membrane as a overview of endocrine glands and lining the ). The right substrate Tthe role of hormones as chemical is at, approximately, the signals that help maintain the homeostatic level of the 12th , while the left is located The main hormones balance that is essential to good health. slightly higher between the 11th and 12th produced by the This fourth article examines the anatomy (Perrier and Boger, 2005). medulla are the and physiology of the adrenal glands. Normal, healthy adult adrenal glands ‘flight or fight’ are relatively small – they each weigh 4-6g, hormones Anatomy and are around 3cm wide, 5cm high and and There are two adrenal (suprarenal) glands: 1cm thick; changes in size are often indica- noradrenaline one located immediately above each tive of underlying pathology (Lack and kidney (Fig 1). They are yellow to orange in Paal, 2019; Westphalen and Bonnie, 2006). The right adrenal gland is usually dis- Fig 1. Position and structure of the adrenal gland tinctly triangular in appearance, resem- bling a witch’s hat, while the left is more flattened and typically crescent shaped. The adrenals are highly vascularised, Adrenal Gland and each gland is supplied with oxygen- ated blood through superior, middle and Medulla inferior suprarenal ; deoxygenated blood is carried away from each gland via Cortex an adrenal (Perrier and Boger, 2005). Internal structure Left Kidney Capsule Each adrenal gland is protected by a thick collagen-rich outer capsule, with glan- dular tissues located beneath. The largest portion is the outer region, called the adrenal cortex, accounting for around 90%

JENNIFER N.R. SMITH JENNIFER of total adrenal volume (Gorman, 2013).

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The adrenal cortex produces a diverse range of steroid hormones, using choles- Table 1. Major physiological effects of adrenaline terol as a substrate. These include the long- Target / Physiological effects term , Interacts with beta-adrenergic receptors to accelerate heart (regulating levels of sodium and potas- rate and increase force of myocardial contraction sium in the blood) and a group of testos- terone-like hormones called . Blood vessels Vasoconstriction in skin and , The is the inner region in the musculature, coronary and hepatic circulation of the adrenal gland, accounting for Increased respiratory rate and bronchodilation around 10% of adrenal volume (Gorman, 2013), and produces adrenaline (epineph- Gastrointestinal tract Reduced gut motility, reduced blood flow to gastrointestinal rine) and noradrenaline (). and tract, reduced , increased breakdown of glycogen to These have diverse physiological effects, in liver but function primarily to activate the sym- Central nervous Activation of the sympathetic branch of the autonomic pathetic branch of the autonomic nervous system system (ANS) and prepare the body for immediate action (VanPutte et al, 2017). activated in acutely stressful situations. The effects of adrenaline and noradren- Adrenal medulla The adrenal medulla itself is innervated aline are rapid and usually observed within The major cells of the adrenal medulla are with sympathetic endings that, a few seconds of release; the primary effect called chromaffin cells because they take when activated, initiate the release of more of adrenaline in accelerating heart rate up stains containing salts adrenaline, further amplifying the fight- ensures its rapid distribution throughout (Mubarik and Aeddula, 2021). Chromaffin or-flight response (Verberne et al, 2016). the body. Adrenaline is a short-acting hor- cells produce -derived hor- Adrenaline and noradrenaline have mul- mone with a half life of around 2-3 min- mones called . tiple and diverse physiological effects that utes; it is rapidly metabolised by the liver prepare the body for immediate action. The and excreted in the urine (Electronic Medi- Adrenaline and noradrenaline most-obvious effects of the sudden release cines Compendium, 2020). The two major catecholamines are adrena- of catecholamines (adrenaline rush) pri- line () and noradrenaline (nor- marily centre on the cardiovascular system. Adrenal cortex epinephrine), which are enzymatically Adrenaline binds to beta-adrenergic recep- The adrenal cortex lies immediately below derived from the amino acid . tors associated with the sinoatrial node the protective collagenous adrenal capsule These are commonly referred to as the (SAN) of the heart (Macdonald et al, 2020). and continually takes up cholesterol as the ‘fight-or-flight' hormones, and will be The SAN functions as the heart’s natural substrate to generate a diverse range of explored later in this article. pacemaker and adrenaline dramatically steroid hormones. Histologically, the Tyrosine is a non-essential amino acid accelerates the heart rate, often way beyond cortex consists of three distinct layers of that can be obtained through diet or the upper limit for normal resting heart rate tissue, each producing its own class of derived from the essential amino acid phe- of 100 beats per minute (bpm). This is often steroid hormones: nylalanine. Chromaffin cells continually perceived as a notable thumping in the ● (outer layer) – synthe- take up tyrosine and, through the sequen- chest and, as and blood pres- sises that help tial actions of several , convert it sure increase, the pulse may be perceived regulate concentrations; into the active catecholamines L-dopa, (without palpation) in other areas of the ● (middle layer) , noradrenaline and adrenaline. body, such as the neck and temples. – synthesises that Tyrosine is also taken up by the in Adrenaline also further increases blood primarily function as long-term stress the ANS to generate noradrenaline, which pressure by promoting vasoconstriction in hormones; functions as a key in the the skin and gastrointestinal tract, hence ● (inner layer) – marks sympathetic branch of the ANS. the expression of skin turning ‘ashen with the boundary between the cortex and In the adrenal medulla, adrenaline is fear’ and the common sensation of ‘butter- the medulla, producing a class of the major product of bio- flies in the ’. Simultaneously, -like hormones called synthesis, accounting for around 95% of adrenaline promotes vasodilation of the androgens. the medullary hormones released into the arteries in the skeletal muscles and coro- blood (Berends et al, 2019). nary circulation, diverting oxygenated Aldosterone blood to the major muscle groups and As their name suggests, the mineralocorti- Fight-or-flight response myocardium of the heart. Adrenaline coid hormones produced by the zona glo- When we perceive a threat (for example, by improves oxygen uptake by dilating the merulosa regulate plasma concentrations a predator) or are in a potentially dan- airways and increasing the breathing rate, of minerals/salts (). The most gerous or exciting situation (for example, increasing blood glucose, and improving important in is at the top of a bungee jump), adrenaline sensory and response times aldosterone, which regulates blood con- and smaller amounts of noradrenaline are while decreasing the perception of pain centrations of ionic sodium (Na+) and usually released. The bulk of noradrena- (VanPutte et al, 2017). Cumulatively, this ionic (K+) . line in the circulation is derived from the enhances musculoskeletal function, so an Na+ and K+ ions are essential for main- sympathetic nerve endings because the individual can put up an effective fight or taining membrane potentials and gener- sympathetic branch of the ANS is escape any potential threat (Table 1). ating nerve impulses (action potentials),

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Fig 2. aldosterone system When the kidneys detect a drop in , they produce the renin, which converts angiotensinogen into an Drop in blood pressure Drop in fluid volume inactive called angiotensin I. This circulates in the plasma until it reaches the Renin-angiotensin system tissue, where angiotensin-converting Liver enzymes (ACE) convert it into biologically active angiotensin II. This primarily func- tions as a vasoconstrictor, helping to angiotensinogen restore blood pressure while simultane- Renin release from kidney ously stimulating the release of aldos- terone from the adrenal cortex. Aldosterone promotes the NaCl Renin acts on of Na+ in the kidney, thereby increasing HO angiotensinogen to plasma Na+ concentration (Fig 2). This form angiotensin I encourages the movement of water from Aldosterone acts ACE the tissues into the blood vessels by on the kidneys to (angiotensin-converting osmosis, thereby increasing stimulate enzyme) within and blood pressure. reabsorption of salt (NaCl) and water (H2O) Hyperkalaemia and hypokalaemia Aldosterone also regulates concentration ACE acts on of plasma K+ ions and is released in angiotensin I to response to hyperkalaemia (high blood form angiotensin II potassium), most commonly following consumption of potassium-rich foods or food supplements, such as bananas or low- Angiotensin II acts sodium salt replacements containing Angiotensin II acts on directly on blood the adrenal gland to vessels, stimulating potassium chloride. Hyperkalaemia can stimulate release of vasoconstriction also follow major physical injury causing aldosterone (narrowing) disruption of cell membranes (for example, a burn), leading to the release of large amounts of intracellular potassium that have accumulated via the Na+ K+ so need tight regulation in the extracel- centrations by several mechanisms: pump (Ookuma et al, 2015). lular and intracellular fluids. To help this ● Enhancing the reabsorption of Na+ into Severe hyperkalaemia requires urgent balance, many cells have an active trans- the blood from the renal filtrate at the assessment, as it can interfere with the port mechanism called the sodium-potas- and collecting electrical conductive tissues of the heart, sium pump, which uses membrane trans- of kidney ; leading to dangerous ventricular arrhyth- porter to pump K+ ions into cells ● Promoting salt cravings to encourage mias and, potentially, cardiac arrest (Weiss while pumping out Na+ ions (VanPutte et the intake of sodium-rich foods; et al, 2017). Aldosterone reduces and nor- al, 2017). This ensures most Na+ ions are ● Enhancing Na+ reabsorption into the malises the blood–potassium concentra- found in the extracellular fluids, with large colon; tion, primarily by promoting the amounts accumulating in the blood ● Reducing loss of Na+ in sweat, saliva of K+ ions into the kidney nephrons for plasma, while most K+ ions are concen- and (Byrd et al, 2018; elimination in the urine. trated in the intracellular fluid. VanPutte et al, 2017). Hypokalaemia (low blood potassium) Although this mechanism ensures the Conversely, aldosterone secretion can result from a lack of potassium in the correct distribution of Na+ and K+ between reduces in response to hypernatriemia diet or a side-effect of some diuretic medi- the intracellular and extracellular com- (high blood sodium), such as following a cations. Diuretics such as furosemide are partments of the body, it is aldosterone salty meal, allowing elimination of excess used to reduce oedema and treat high blood that fine tunes the plasma concentration Na+ in the urine, sweat and faeces. pressure by eliminating excess fluids and of Na+ and K+. In health, the normal blood volume through increasing urine plasma concentration of Na+ is main- Blood pressure regulation output; however, this can lead to signifi- tained at 135-145mmol/l, while the activity The primary for aldosterone cant flushing out of K+. Hypokalaemia of the sodium potassium pump keeps release is the activation of the renin angio- inhibits aldosterone secretion, reducing plasma concentration of K+ much lower at tensin aldosterone system (RAAS) (Byrd et the secretion of K+ in the renal filtrate and 3.5-5.0mmol/l (Justice et al, 2019). al, 2018). The RAAS is the most important causing the retention of K+ in the blood. Aldosterone is released in response to physiological mechanism for medium to Newer forms of potassium-sparing hyponatraemia (low blood sodium), most long-term control of blood pressure and is diuretics are available, such as amiloride commonly due to a lack of Na+ in the diet or centred around a plasma protein called or triamterene, which increase urine Na+ loss through sweating. Aldosterone angiotensinogen, produced by the liver output with minimal loss of K+ (Bit.ly/

JENNIFER N.R. SMITH JENNIFER increases and normalises plasma Na+ con- (Atlas, 2007). BNFDiuretics).

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Primary aldosteronism Fig 3. Hypothalamic-pituitary- in patients with severe Covid-19 infection, (PA, also known as adrenal axis primarily by reducing and Conn’s syndrome) is a condition that is preventing over-reaction of the immune most often caused by benign enlargement system (Johnson and Vinetz, 2020). () of the adrenal glands or by tumours in the adrenal cortex. It leads to HPA axis Corticotropin-releasing excess secretion of aldosterone, causing hormone Cortisol release is tightly regulated by hypernatraemia, which increases blood homeostatic mechanisms that rely on neg- volume and blood pressure. Around 5-10% ative . As seen in part 2 of this Adrenocorticotropic of cases of are thought to be hormone series, the hypothalamus is a vital region caused by PA (Young, 2019). of the brain that acts as a crossover point Patients with PA also usually show Adrenal gland between the nervous system and the endo- Cortisol hypokalaemia as increased aldosterone crine system. During periods of chronic promotes the rapid secretion of potassium Metabolic effects stress (both physical and emotional), the in the urine. Other signs and symptoms hypothalamus releases corticotropin- include water retention and neurological/ releasing hormone (CRH). CRH is deliv- psychological symptoms, including anx- ered to the anteror pituitary in the hypo- iety, demoralisation, stress, depression patterns of hair growth and a disrupted thalamic-pituitary portal circulation, and nervousness. When PA is caused by menstrual cycle (Utriainen et al, 2015). where it initiates the release of adrenocor- tumours, surgery is usually the treatment ticotropic hormone (ACTH). of choice; excess aldosterone secretion Glucocorticoids ACTH circulates systemically and stim- caused by adrenal hyperplasia is usually The zona fasciculata secretes the glucocor- ulates the release of cortisol from the treated using aldosterone-blocking drugs ticoid hormones. The most important glu- adrenal cortex. As cortisol is important in (Young, 2019). cocorticoid in humans is cortisol, which regulating and influences a functions as a long-term stress hormone. variety of immune and behavioural Androgens Long-term , such as physical responses, the hypothalamus continually The zona reticularis secretes small injury, starvation or emotional stress, acti- monitors the plasma–cortisol concentra- amounts of hormones called androgens, vate the hypothalamic-pituitary-adrenal tion. When levels of cortisol rise, the hypo- which are structurally similar to the male (HPA) axis, leading to the release of cor- responds by reducing CRH , testosterone. Like testos- tisol. As implied by their name, glucocor- secretion; this decreases the release of terone, these hormones function as ana- ticoid hormones influence the blood– ACTH and, ultimately, cortisol secretion bolic of varying potency and pro- glucose concentration; they work with (Fig 3). mote the development of male physical many other hormones, including The HPA axis also influences the release characteristics such as increased muscle and , to maintain glucose homeo- of aldosterone and androgens, although mass, growth of body and facial hair, stasis (Kuo et al, 2015). the exact mechanisms are poorly under- and deepening of the voice. In females, Cortisol release promotes a rise in stood (Gallo-Payet, 2016). androgens play key roles in the func- blood–glucose concentration. This occurs tioning of the musculoskeletal system, because cortisol stimulates the breakdown Cushing’s syndrome heighten and form intermediates of fat and protein, converting amino acid Cushing’s syndrome (CS) or hypercorti- for the biosynthesis of oestrogens (Han- residues and the glycerol portion of fat solism is characterised by increased secre- delsman, 2020). into glucose; this biochemical process is tion of cortisol. It is more prevalent in Androgens, including synthetically called (literally: the crea- women than men and, although it can produced testosterone, are of clinical use tion of new glucose). Gluconeogenesis occur at any age, is most commonly in people physically transitioning from allows for blood–glucose concentrations detected at 30-40 years. It is relatively rare, female to trans male, as they help ensure a to be maintained when food supplies are with a reported incidence of around 1 in match between gender identity and phys- limited and increased blood glucose pro- 200,000, but appears to be becoming more ical body (gender congruence). Such mas- vides a valuable energy resource for tissue common (Bit.ly/PFCushings). Most cases of culinising hormone therapy, also known repair after physical injury. CS are caused by benign pituitary tumours as gender-affirming hormone therapy, Cortisol also influences the /wake leading to excess secretion of ACTH, which helps to block the activity of female sex cycle, mood and behaviour, and has a increases secretion of cortisol from the zona hormones, such as oestrogens, and sup- variety of immunosupressant properties fasiculata. More rarely, hypersecretion of press the normal menstrual cycle (Bit.ly/ (Kandhalu, 2013). In terms of immune cortisol may be caused by adrenal tumours, MayoHormone). modulation, it is a powerful natural anti- this uncommon form is referred to as Adrenal androgens are secreted by both inflammatory molecule that helps limit adrenal Cushing’s (Pappachan et al, 2017). males and females, but their physiological and control the inflammatory response. An excess of cortisol results in major effects in males tend to be diluted by the Powerful steroidal anti-inflammatory physiological changes that are character- presence of testosterone produced by the medications, such as istic of CS. As cortisol is a testes. Hypersecretion of androgens is creams commonly used to treat inflamma- that promotes gluconeogenesis, glucose termed and, in early tory skin conditions, mimic the effects of concentration typically increases, leading life, can lead to premature (precocious) cortisol (Fleischer et al, 2017). Recently to hyperglycaemia; this is associated with in boys; in cisgender females, it (another cortisol-like lipolysis (breakdown of fats) and increased can lead to potentially unwanted masculine drug) has been shown to improve survival protein catabolism (breakdown), which

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can lead to muscle wastage and thin, stick- ● , leading to dark Fleischer DM et al (2017) Atopic dermatitis: skin care and topical therapies. Seminars in Cutaneous like arms and legs. patches of skin – increased ACTH; Medicine and Surgery; 36: 3, 104-110. A major characteristic of CS is abnormal ● Hypoglycaemia – lack of cortisol; Gallo-Payet N (2016) 60 YEARS OF POMC: Adrenal fat distribution, with increased central- ● Hyponatraemia and hyperkalaemia and extra-adrenal functions of ACTH. Journal of Molecular ; 56: 4, T135-T156. trunk leading to large accumula- – lack of aldosterone; Gorman LS (2013) The adrenal gland: common tions of abdominal fat, increased fat around ● Muscle weakness and cramping – lack disease states and suspected new applications. Clinical Laboratory Science; 26: 2, 118-125. the face (moon face) and possible promi- of aldosterone; Handelsman DJ (2020) physiology, nent fat between the shoulder blades (buf- ● Poluria and increased – lack of , use and misuse. In: Feingold KR et falo hump). Excess cortisol is also associ- aldosterone; al (eds) Endotext. MDText.com Inc. Johnson RM, Vinetz JM (2020) Dexamethasone in ● ated with a thinning of the skin, causing it Low mood or irritability – lack of the management of covid -19. BMJ; 370: m2648. to bruise easily, and prominent striae cortisol and aldosterone; Justice S et al (2019) Biochemistry Reference (), particularly in areas of ● Increased thirst – lack of aldosterone Ranges Document. Oxford University Hospitals NHS Foundation Trust. rapid fat deposition, such as the . (Bit.ly/NHSAddisons). Kandhalu P (2013) Effects of cortisol on physical Other common symptoms are fatigue, poor Treatment and management of AD is and psychological aspects of the body and usually achieved through life-long syn- effective ways by which one can reduce stress. concentration and memory, decreased Berkeley Scientific Journal; 18: 1, 14-16. libido and loss of density, potentially thetic hormone replacement therapy with Kuo T et al (2015) Regulation of glucose leading to (Nieman et al, glucocorticoids ( or hydrocorti- by glucocorticoids. Advances in Experimental Medicine and Biology; 872: 99–126. 2008). How to treat CS depends on the cause sone) and mineralocorticoids (fludrocorti- Lack EE, Paal E (2019) Adrenal glands. In: Cheng L but surgical excision of tumours at the pitu- sone) (Bornstein et al, 2016). et al (eds) Urologic Surgical Pathology. Saunders. itary or adrenal glands is usually the treat- Severe deficiency of aldosterone and MacDonald EA et al (2020) Neurohumoral control of sinoatrial node activity and heart rate: insight ment of choice. cortisol can be life-threatening and lead to from experimental models and findings from a medical emergency termed an adrenal humans. Frontiers in Physiology; 11: 170. Addison’s disease crisis. This is characterised by some or all Michels A, Michels N (2014) Addison disease: early detection and treatment principles. American Addison’s disease (AD) affects around 1 in of the following symptoms: Family Physician; 89: 7, 563-568. 10,000 people (Bit.ly/ADSHGAddisons) ● Rapid shallow breathing; Mubarik A, Aeddula NR (2021) ● . StatPearls Publishing. and is characterised by the reduced secre- Severe dehydration; Nieman LK et al (2008) The diagnosis of Cushing’s tion of hormones from the adrenal cortex. ● Sweating; syndrome: an Endocrine Society clinical practice It is usually associated with depletion in all ● Pale, cold, clammy skin; guideline. The Journal of Clinical Endocrinology & Metabolism; 93: 5, 1526–1540. ● three categories of hor- Dizziness; Ookuma T et al (2015) The clinical relevance of mones (mineralocorticoids, glucocorti- ● ; plasma potassium abnormalities on admission in coids and androgens). There are many ● Severe vomiting and diarrhoea; trauma patients: a retrospective observational study. Journal of Intensive Care; 3: 1: 37. known causes of AD, with autoimmune ● Abdominal pain or pain in the side; Pappachan JM et al (2017) Cushing’s syndrome: a destruction of the tissues of the adrenal ● Fatigue and severe muscle weakness; practical approach to diagnosis and differential cortex the most common in developed ● Headache; diagnoses. Journal of Clinical Pathology; 70: 4, 350-359. countries (Michels and Michels, 2014). The ● Severe drowsiness or loss of conscious- Perrier ND, Boger MS (2005) Surgical Anatomy. In: depletion of aldosterone and cortisol after ness (Bit.ly/NHSAddisons). Linos D, van Heerden JA (eds) Adrenal Glands: Diagnostic Aspects and Surgical Therapy. Springer. damage to the zona glomerulosa and zona Unless treated quickly, Utriainen P et al (2015) Premature : a fasiculata precipitates many of the symp- can lead to convulsions, and death; it common condition with variable presentation. toms associated with AD. is usually treated with intravenous hydro- Hormone Research in Paediatrics; 83: 4, 221-231. VanPutte CL et al (2017) Seeley’s Anatomy and AD onset is usually insidious and often cortisone (Bornstein et al, 2016). Physiology. McGraw-Hill. goes unrecognised for long periods. Symp- Verberne AJM et al (2016) Adrenaline: insights into toms are incredibly diverse, hindering Conclusion its metabolic roles in hypoglycaemia and . British Journal of Pharmacology; 173: 9, 1425–1437. diagnosis, particularly in the disease’s early This article has explored the anatomy, Weiss JN et al (2017) Electrophysiology of stages. As the reduced secretion of the hor- physiology and function of the adrenal and hyperkalemia. Circulation: mones of the adrenal cortex will activate glands. Part 5 will focus on the pineal and Arrhythmia and Electrophysiology; 10: e004667. Westphalen CA, Bonnie N (2006) CT and MRI of the HPA axis, AD is usually associated with glands. NT adrenal masses. Applied Radiology; 35: 8, 10-26. increased levels of ACTH. Part 2 of this Young WF (2019) Diagnosis and treatment of primary aldosteronism: practical clinical perspectives. series highlighted that ACTH is structur- References Journal of ; 285: 2, 126–148. ally similar to melanocyte-stimulating hor- Atlas SA (2007) The renin-angiotensin aldosterone system: pathophysiological role and mone, which can lead to hyperpigmenta- pharmacologic inhibition. Journal of Managed Care CLINICAL Endocrine system tion in areas of skin – a common feature of and Specialty Pharmacy; 13: 8 Suppl B, 9-20. SERIES AD. The most common symptoms can usu- Berends AMA et al (2019) Intricacies of the molecular machinery of catecholamine biosynthesis Part 1: Overview of the endocrine system ally be traced back to a lack of aldosterone, and secretion by chromaffin cells of the normal and hormones May adrenal medulla and in and cortisol or both as highlighted below: Part 2: Hypothalamus and Jun . ; 11: 8, 1121. ● Lethargy, drowsiness and over- Bornstein SR et al (2016) Diagnosis and treatment of Part 3: and parathyroid glands Jul whelming exhaustion – lack of cortisol primary : an Endocrine Society Part 4: Adrenal glands Aug and aldosterone; clinical practice guideline. The Journal of Clinical Part 5: Pineal and thymus glands Sep Endocrinology and Metabolism; 101: 2, 364–389. ● Part 6: , stomach, liver, small Loss of appetite, nausea and uninten- Byrd JB et al (2018) Primary aldosteronism: tional weight loss – lack of cortisol and practical approach to diagnosis and management. intestine Oct aldosterone; Circulation; 138: 8, 823-835. Part 7: and testes, Electronic Medicines Compendium (2020) (pregnancy) Nov ● Hypotension and postural hypotension Adrenaline (epinephrine) injection BP 1 in 1000. Part 8: Kidneys, heart and skin Dec – lack of aldosterone; medicines.org.uk, 1 April.

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