Endocrine system 4: adrenal glands

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Endocrine system

Keywords Endocrine system/

Hormones/Adrenal glands

This article has been

double-blind peer reviewed

In this article...

¡ñ Endocrine functions of the adrenal glands

¡ñ Hormones of the adrenal glands

¡ñ The role of adrenal gland hormones in mediating essential physiological processes

Endocrine system 4: adrenal glands

Key points

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There are two

adrenal glands: one

located above each

kidney

Adrenal glands

consist of two parts,

the cortex and the

medulla, which each

produce different

hormones

The adrenal cortex

produces a diverse

range of steroid

hormones, using

cholesterol as a

substrate

The main hormones

produced by the

medulla are the

¡®flight or fight¡¯

hormones

adrenaline and

noradrenaline

Authors Maria Andrade is honorary associate professor in biomedical science;

Zubeyde-Bayram Weston is senior lecturer in biomedical science; John Knight is

associate professor in biomedical science; all at College of Human and Health

Sciences, Swansea University.

Abstract The endocrine system consists of glands and tissues that produce and

secrete hormones to regulate and coordinate vital bodily functions. This article, the

fourth in an eight-part series on the endocrine system, explores the anatomy and

physiology of the adrenal glands, and describes how they regulate and coordinate

vital physiological processes in the body through hormonal action.

Citation Andrade M et al (2021) Endocrine system 4: adrenal glands. Nursing Times

[online]; 117: 8, 54-58.

T

his eight-part series on the endocrine system opened with an

overview of endocrine glands and

the role of hormones as chemical

signals that help maintain the homeostatic

balance that is essential to good health.

This fourth article examines the anatomy

and physiology of the adrenal glands.

Anatomy

There are two adrenal (suprarenal) glands:

one located immediately above each

kidney (Fig 1). They are yellow to orange in

Fig 1. Position and structure of the adrenal gland

Adrenal Gland

Medulla

Cortex

Left Kidney

JENNIFER N.R. SMITH

Capsule

Nursing Times [online] August 2021 / Vol 117 Issue 8

54

colour and are positioned retroperitoneally (behind the peritoneal membrane

lining the abdominal cavity). The right

adrenal gland is at, approximately, the

level of the 12th rib, while the left is located

slightly higher between the 11th and 12th

ribs (Perrier and Boger, 2005).

Normal, healthy adult adrenal glands

are relatively small ¨C they each weigh 4-6g,

and are around 3cm wide, 5cm high and

1cm thick; changes in size are often indicative of underlying pathology (Lack and

Paal, 2019; Westphalen and Bonnie, 2006).

The right adrenal gland is usually distinctly triangular in appearance, resembling a witch¡¯s hat, while the left is more

flattened and typically crescent shaped.

The adrenals are highly vascularised,

and each gland is supplied with oxygenated blood through superior, middle and

inferior suprarenal arteries; deoxygenated

blood is carried away from each gland via

an adrenal vein (Perrier and Boger, 2005).

Internal structure

Each adrenal gland is protected by a thick

collagen-rich outer capsule, with glandular tissues located beneath. The largest

portion is the outer region, called the

adrenal cortex, accounting for around 90%

of total adrenal volume (Gorman, 2013).



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The adrenal cortex produces a diverse

range of steroid hormones, using cholesterol as a substrate. These include the longterm stress hormone cortisol, aldosterone

(regulating levels of sodium and potassium in the blood) and a group of testosterone-like hormones called androgens.

The adrenal medulla is the inner region

of the adrenal gland, accounting for

around 10% of adrenal volume (Gorman,

2013), and produces adrenaline (epinephrine) and noradrenaline (norepinephrine).

These have diverse physiological effects,

but function primarily to activate the sympathetic branch of the autonomic nervous

system (ANS) and prepare the body for

immediate action (VanPutte et al, 2017).

Adrenal medulla

The major cells of the adrenal medulla are

called chromaffin cells because they take

up stains containing chromium salts

(Mubarik and Aeddula, 2021). Chromaffin

cells produce amino acid-derived hormones called catecholamines.

Adrenaline and noradrenaline

The two major catecholamines are adrenaline (epinephrine) and noradrenaline (norepinephrine), which are enzymatically

derived from the amino acid tyrosine.

These are commonly referred to as the

¡®fight-or-flight' hormones, and will be

explored later in this article.

Tyrosine is a non-essential amino acid

that can be obtained through diet or

derived from the essential amino acid phenylalanine. Chromaffin cells continually

take up tyrosine and, through the sequential actions of several enzymes, convert it

into the active catecholamines L-dopa,

dopamine, noradrenaline and adrenaline.

Tyrosine is also taken up by the neurons in

the ANS to generate noradrenaline, which

functions as a key neurotransmitter in the

sympathetic branch of the ANS.

In the adrenal medulla, adrenaline is

the major product of catecholamine biosynthesis, accounting for around 95% of

the medullary hormones released into the

blood (Berends et al, 2019).

Fight-or-flight response

When we perceive a threat (for example, by

a predator) or are in a potentially dangerous or exciting situation (for example,

at the top of a bungee jump), adrenaline

and smaller amounts of noradrenaline are

usually released. The bulk of noradrenaline in the circulation is derived from the

sympathetic nerve endings because the

sympathetic branch of the ANS is

Table 1. Major physiological effects of adrenaline

Target organ/tissue

Physiological effects

Heart

Interacts with beta-adrenergic receptors to accelerate heart

rate and increase force of myocardial contraction

Blood vessels

Vasoconstriction in skin and gastrointestinal tract, vasodilation

in the musculature, coronary and hepatic circulation

Respiratory tract

Increased respiratory rate and bronchodilation

Gastrointestinal tract

and liver

Reduced gut motility, reduced blood flow to gastrointestinal

tract, reduced digestion, increased breakdown of glycogen to

glucose in liver

Central nervous

system

Activation of the sympathetic branch of the autonomic

nervous system

activated in acutely stressful situations.

The adrenal medulla itself is innervated

with sympathetic nerve endings that,

when activated, initiate the release of more

adrenaline, further amplifying the fightor-flight response (Verberne et al, 2016).

Adrenaline and noradrenaline have multiple and diverse physiological effects that

prepare the body for immediate action. The

most-obvious effects of the sudden release

of catecholamines (adrenaline rush) primarily centre on the cardiovascular system.

Adrenaline binds to beta-adrenergic receptors associated with the sinoatrial node

(SAN) of the heart (Macdonald et al, 2020).

The SAN functions as the heart¡¯s natural

pacemaker and adrenaline dramatically

accelerates the heart rate, often way beyond

the upper limit for normal resting heart rate

of 100 beats per minute (bpm). This is often

perceived as a notable thumping in the

chest and, as cardiac output and blood pressure increase, the pulse may be perceived

(without palpation) in other areas of the

body, such as the neck and temples.

Adrenaline also further increases blood

pressure by promoting vasoconstriction in

the skin and gastrointestinal tract, hence

the expression of skin turning ¡®ashen with

fear¡¯ and the common sensation of ¡®butterflies in the stomach¡¯. Simultaneously,

adrenaline promotes vasodilation of the

arteries in the skeletal muscles and coronary circulation, diverting oxygenated

blood to the major muscle groups and

myocardium of the heart. Adrenaline

improves oxygen uptake by dilating the

airways and increasing the breathing rate,

increasing blood glucose, and improving

sensory perception and response times

while decreasing the perception of pain

(VanPutte et al, 2017). Cumulatively, this

enhances musculoskeletal function, so an

individual can put up an effective fight or

escape any potential threat (Table 1).

Nursing Times [online] August 2021 / Vol 117 Issue 8

55

The effects of adrenaline and noradrenaline are rapid and usually observed within

a few seconds of release; the primary effect

of adrenaline in accelerating heart rate

ensures its rapid distribution throughout

the body. Adrenaline is a short-acting hormone with a half life of around 2-3 minutes; it is rapidly metabolised by the liver

and excreted in the urine (Electronic Medicines Compendium, 2020).

Adrenal cortex

The adrenal cortex lies immediately below

the protective collagenous adrenal capsule

and continually takes up cholesterol as the

substrate to generate a diverse range of

steroid hormones. Histologically, the

cortex consists of three distinct layers of

tissue, each producing its own class of

steroid hormones:

¡ñ Zona glomerulosa (outer layer) ¨C synthesises mineralocorticoids that help

regulate electrolyte concentrations;

¡ñ Zona fasciculata (middle layer)

¨C synthesises glucocorticoids that

primarily function as long-term stress

hormones;

¡ñ Zona reticularis (inner layer) ¨C marks

the boundary between the cortex and

the medulla, producing a class of

testosterone-like hormones called

androgens.

Aldosterone

As their name suggests, the mineralocorticoid hormones produced by the zona glomerulosa regulate plasma concentrations

of minerals/salts (electrolytes). The most

important mineralocorticoid in humans is

aldosterone, which regulates blood concentrations of ionic sodium (Na+) and

ionic potassium (K+) .

Na+ and K+ ions are essential for maintaining membrane potentials and generating nerve impulses (action potentials),



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Fig 2. Renin angiotensin aldosterone system

Drop in blood pressure

Drop in fluid volume

Renin-angiotensin system

Liver

angiotensinogen

Renin release from kidney

NaCl

H2O

Renin acts on

angiotensinogen to

form angiotensin I

Aldosterone acts

on the kidneys to

stimulate

reabsorption of

salt (NaCl) and

water (H2O)

ACE

(angiotensin-converting

enzyme) within lungs

ACE acts on

angiotensin I to

form angiotensin II

JENNIFER N.R. SMITH

Angiotensin II acts on

the adrenal gland to

stimulate release of

aldosterone

so need tight regulation in the extracellular and intracellular fluids. To help this

balance, many cells have an active transport mechanism called the sodium-potassium pump, which uses membrane transporter proteins to pump K+ ions into cells

while pumping out Na+ ions (VanPutte et

al, 2017). This ensures most Na+ ions are

found in the extracellular fluids, with large

amounts accumulating in the blood

plasma, while most K+ ions are concentrated in the intracellular fluid.

Although this mechanism ensures the

correct distribution of Na+ and K+ between

the intracellular and extracellular compartments of the body, it is aldosterone

that fine tunes the plasma concentration

of Na+ and K+. In health, the normal

plasma concentration of Na+ is maintained at 135-145mmol/l, while the activity

of the sodium potassium pump keeps

plasma concentration of K+ much lower at

3.5-5.0mmol/l (Justice et al, 2019).

Aldosterone is released in response to

hyponatraemia (low blood sodium), most

commonly due to a lack of Na+ in the diet or

Na+ loss through sweating. Aldosterone

increases and normalises plasma Na+ con-

Angiotensin II acts

directly on blood

vessels, stimulating

vasoconstriction

(narrowing)

centrations by several mechanisms:

¡ñ Enhancing the reabsorption of Na+ into

the blood from the renal filtrate at the

distal convoluted tubule and collecting

duct of kidney nephrons;

¡ñ Promoting salt cravings to encourage

the intake of sodium-rich foods;

¡ñ Enhancing Na+ reabsorption into the

colon;

¡ñ Reducing loss of Na+ in sweat, saliva

and pancreatic juice (Byrd et al, 2018;

VanPutte et al, 2017).

Conversely, aldosterone secretion

reduces in response to hypernatriemia

(high blood sodium), such as following a

salty meal, allowing elimination of excess

Na+ in the urine, sweat and faeces.

Blood pressure regulation

The primary stimulus for aldosterone

release is the activation of the renin angiotensin aldosterone system (RAAS) (Byrd et

al, 2018). The RAAS is the most important

physiological mechanism for medium to

long-term control of blood pressure and is

centred around a plasma protein called

angiotensinogen, produced by the liver

(Atlas, 2007).

Nursing Times [online] August 2021 / Vol 117 Issue 8

56

When the kidneys detect a drop in blood

pressure, they produce the enzyme renin,

which converts angiotensinogen into an

inactive protein called angiotensin I. This

circulates in the plasma until it reaches the

lung tissue, where angiotensin-converting

enzymes (ACE) convert it into biologically

active angiotensin II. This primarily functions as a vasoconstrictor, helping to

restore blood pressure while simultaneously stimulating the release of aldosterone from the adrenal cortex.

Aldosterone promotes the reabsorption

of Na+ in the kidney, thereby increasing

plasma Na+ concentration (Fig 2). This

encourages the movement of water from

the tissues into the blood vessels by

osmosis, thereby increasing blood volume

and blood pressure.

Hyperkalaemia and hypokalaemia

Aldosterone also regulates concentration

of plasma K+ ions and is released in

response to hyperkalaemia (high blood

potassium), most commonly following

consumption of potassium-rich foods or

food supplements, such as bananas or lowsodium salt replacements containing

potassium chloride. Hyperkalaemia can

also follow major physical injury causing

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+

pump (Ookuma et al, 2015).

Severe hyperkalaemia requires urgent

assessment, as it can interfere with the

electrical conductive tissues of the heart,

leading to dangerous ventricular arrhythmias and, potentially, cardiac arrest (Weiss

et al, 2017). Aldosterone reduces and normalises the blood¨Cpotassium concentration, primarily by promoting the excretion

of K+ ions into the kidney nephrons for

elimination in the urine.

Hypokalaemia (low blood potassium)

can result from a lack of potassium in the

diet or a side-effect of some diuretic medications. Diuretics such as furosemide are

used to reduce oedema and treat high blood

pressure by eliminating excess fluids and

blood volume through increasing urine

output; however, this can lead to significant flushing out of K+. Hypokalaemia

inhibits aldosterone secretion, reducing

the secretion of K+ in the renal filtrate and

causing the retention of K+ in the blood.

Newer forms of potassium-sparing

diuretics are available, such as amiloride

or triamterene, which increase urine

output with minimal loss of K+ (Bit.ly/

BNFDiuretics).



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Primary aldosteronism

Primary aldosteronism (PA, also known as

Conn¡¯s syndrome) is a condition that is

most often caused by benign enlargement

(hyperplasia) of the adrenal glands or by

tumours in the adrenal cortex. It leads to

excess secretion of aldosterone, causing

hypernatraemia, which increases blood

volume and blood pressure. Around 5-10%

of cases of hypertension are thought to be

caused by PA (Young, 2019).

Patients with PA also usually show

hypokalaemia as increased aldosterone

promotes the rapid secretion of potassium

in the urine. Other signs and symptoms

include water retention and neurological/

psychological symptoms, including anxiety, demoralisation, stress, depression

and nervousness. When PA is caused by

tumours, surgery is usually the treatment

of choice; excess aldosterone secretion

caused by adrenal hyperplasia is usually

treated using aldosterone-blocking drugs

(Young, 2019).

Androgens

The zona reticularis secretes small

amounts of hormones called androgens,

which are structurally similar to the male

sex hormone, testosterone. Like testosterone, these hormones function as anabolic steroids of varying potency and promote the development of male physical

characteristics such as increased muscle

mass, growth of body and facial hair,

and deepening of the voice. In females,

androgens play key roles in the functioning of the musculoskeletal system,

heighten libido and form intermediates

for the biosynthesis of oestrogens (Handelsman, 2020).

Androgens, including synthetically

produced testosterone, are of clinical use

in people physically transitioning from

female to trans male, as they help ensure a

match between gender identity and physical body (gender congruence). Such masculinising hormone therapy, also known

as gender-affirming hormone therapy,

helps to block the activity of female sex

hormones, such as oestrogens, and suppress the normal menstrual cycle (Bit.ly/

MayoHormone).

Adrenal androgens are secreted by both

males and females, but their physiological

effects in males tend to be diluted by the

presence of testosterone produced by the

testes. Hypersecretion of androgens is

termed hyperandrogenism and, in early

life, can lead to premature (precocious)

puberty in boys; in cisgender females, it

can lead to potentially unwanted masculine

Fig 3. Hypothalamic-pituitaryadrenal axis

STRESSOR

Hypothalamus

Corticotropin-releasing

hormone

Anterior pituitary

Adrenocorticotropic

hormone

Adrenal gland

Cortisol

Metabolic effects

Negative feedback

patterns of hair growth and a disrupted

menstrual cycle (Utriainen et al, 2015).

Glucocorticoids

The zona fasciculata secretes the glucocorticoid hormones. The most important glucocorticoid in humans is cortisol, which

functions as a long-term stress hormone.

Long-term stressors, such as physical

injury, starvation or emotional stress, activate the hypothalamic-pituitary-adrenal

(HPA) axis, leading to the release of cortisol. As implied by their name, glucocorticoid hormones influence the blood¨C

glucose concentration; they work with

many other hormones, including insulin

and glucagon, to maintain glucose homeostasis (Kuo et al, 2015).

Cortisol release promotes a rise in

blood¨Cglucose concentration. This occurs

because cortisol stimulates the breakdown

of fat and protein, converting amino acid

residues and the glycerol portion of fat

into glucose; this biochemical process is

called gluconeogenesis (literally: the creation of new glucose). Gluconeogenesis

allows for blood¨Cglucose concentrations

to be maintained when food supplies are

limited and increased blood glucose provides a valuable energy resource for tissue

repair after physical injury.

Cortisol also influences the sleep/wake

cycle, mood and behaviour, and has a

variety of immunosupressant properties

(Kandhalu, 2013). In terms of immune

modulation, it is a powerful natural antiinflammatory molecule that helps limit

and control the inflammatory response.

Powerful steroidal anti-inflammatory

medications, such as hydrocortisone

creams commonly used to treat inflammatory skin conditions, mimic the effects of

cortisol (Fleischer et al, 2017). Recently

dexamethasone (another cortisol-like

drug) has been shown to improve survival

Nursing Times [online] August 2021 / Vol 117 Issue 8

57

in patients with severe Covid-19 infection,

primarily by reducing inflammation and

preventing over-reaction of the immune

system (Johnson and Vinetz, 2020).

HPA axis

Cortisol release is tightly regulated by

homeostatic mechanisms that rely on negative feedback. As seen in part 2 of this

series, the hypothalamus is a vital region

of the brain that acts as a crossover point

between the nervous system and the endocrine system. During periods of chronic

stress (both physical and emotional), the

hypothalamus releases corticotropinreleasing hormone (CRH). CRH is delivered to the anteror pituitary in the hypothalamic-pituitary portal circulation,

where it initiates the release of adrenocorticotropic hormone (ACTH).

ACTH circulates systemically and stimulates the release of cortisol from the

adrenal cortex. As cortisol is important in

regulating metabolism and influences a

variety of immune and behavioural

responses, the hypothalamus continually

monitors the plasma¨Ccortisol concentration. When levels of cortisol rise, the hypothalamus responds by reducing CRH

secretion; this decreases the release of

ACTH and, ultimately, cortisol secretion

(Fig 3).

The HPA axis also influences the release

of aldosterone and androgens, although

the exact mechanisms are poorly understood (Gallo-Payet, 2016).

Cushing¡¯s syndrome

Cushing¡¯s syndrome (CS) or hypercortisolism is characterised by increased secretion of cortisol. It is more prevalent in

women than men and, although it can

occur at any age, is most commonly

detected at 30-40 years. It is relatively rare,

with a reported incidence of around 1 in

200,000, but appears to be becoming more

common (Bit.ly/PFCushings). Most cases of

CS are caused by benign pituitary tumours

leading to excess secretion of ACTH, which

increases secretion of cortisol from the zona

fasiculata. More rarely, hypersecretion of

cortisol may be caused by adrenal tumours,

this uncommon form is referred to as

adrenal Cushing¡¯s (Pappachan et al, 2017).

An excess of cortisol results in major

physiological changes that are characteristic of CS. As cortisol is a glucocorticoid

that promotes gluconeogenesis, glucose

concentration typically increases, leading

to hyperglycaemia; this is associated with

lipolysis (breakdown of fats) and increased

protein catabolism (breakdown), which



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can lead to muscle wastage and thin, sticklike arms and legs.

A major characteristic of CS is abnormal

fat distribution, with increased centraltrunk obesity leading to large accumulations of abdominal fat, increased fat around

the face (moon face) and possible prominent fat between the shoulder blades (buffalo hump). Excess cortisol is also associated with a thinning of the skin, causing it

to bruise easily, and prominent striae

(stretch marks), particularly in areas of

rapid fat deposition, such as the abdomen.

Other common symptoms are fatigue, poor

concentration and memory, decreased

libido and loss of bone density, potentially

leading to osteoporosis (Nieman et al,

2008). How to treat CS depends on the cause

but surgical excision of tumours at the pituitary or adrenal glands is usually the treatment of choice.

Addison¡¯s disease

Addison¡¯s disease (AD) affects around 1 in

10,000 people (Bit.ly/ADSHGAddisons)

and is characterised by the reduced secretion of hormones from the adrenal cortex.

It is usually associated with depletion in all

three categories of adrenal steroid hormones (mineralocorticoids, glucocorticoids and androgens). There are many

known causes of AD, with autoimmune

destruction of the tissues of the adrenal

cortex the most common in developed

countries (Michels and Michels, 2014). The

depletion of aldosterone and cortisol after

damage to the zona glomerulosa and zona

fasiculata precipitates many of the symptoms associated with AD.

AD onset is usually insidious and often

goes unrecognised for long periods. Symptoms are incredibly diverse, hindering

diagnosis, particularly in the disease¡¯s early

stages. As the reduced secretion of the hormones of the adrenal cortex will activate

the HPA axis, AD is usually associated with

increased levels of ACTH. Part 2 of this

series highlighted that ACTH is structurally similar to melanocyte-stimulating hormone, which can lead to hyperpigmentation in areas of skin ¨C a common feature of

AD. The most common symptoms can usually be traced back to a lack of aldosterone,

cortisol or both as highlighted below:

¡ñ Lethargy, drowsiness and overwhelming exhaustion ¨C lack of cortisol

and aldosterone;

¡ñ Loss of appetite, nausea and unintentional weight loss ¨C lack of cortisol and

aldosterone;

¡ñ Hypotension and postural hypotension

¨C lack of aldosterone;

Hyperpigmentation, leading to dark

patches of skin ¨C increased ACTH;

¡ñ Hypoglycaemia ¨C lack of cortisol;

¡ñ Hyponatraemia and hyperkalaemia

¨C lack of aldosterone;

¡ñ Muscle weakness and cramping ¨C lack

of aldosterone;

¡ñ Poluria and increased thirst ¨C lack of

aldosterone;

¡ñ Low mood or irritability ¨C lack of

cortisol and aldosterone;

¡ñ Increased thirst ¨C lack of aldosterone

(Bit.ly/NHSAddisons).

Treatment and management of AD is

usually achieved through life-long synthetic hormone replacement therapy with

glucocorticoids (cortisone or hydrocortisone) and mineralocorticoids (fludrocortisone) (Bornstein et al, 2016).

Severe deficiency of aldosterone and

cortisol can be life-threatening and lead to

a medical emergency termed an adrenal

crisis. This is characterised by some or all

of the following symptoms:

¡ñ Rapid shallow breathing;

¡ñ Severe dehydration;

¡ñ Sweating;

¡ñ Pale, cold, clammy skin;

¡ñ Dizziness;

¡ñ Hypotension;

¡ñ Severe vomiting and diarrhoea;

¡ñ Abdominal pain or pain in the side;

¡ñ Fatigue and severe muscle weakness;

¡ñ Headache;

¡ñ Severe drowsiness or loss of consciousness (Bit.ly/NHSAddisons).

Unless treated quickly, adrenal crisis

can lead to convulsions, coma and death; it

is usually treated with intravenous hydrocortisone (Bornstein et al, 2016).

¡ñ

Conclusion

This article has explored the anatomy,

physiology and function of the adrenal

glands. Part 5 will focus on the pineal and

thymus glands. NT

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CLINICAL

SERIES

Endocrine system

Part 1: Overview of the endocrine system

and hormones

Part 2: Hypothalamus and pituitary gland

Part 3: Thyroid and parathyroid glands

Part 4: Adrenal glands

Part 5: Pineal and thymus glands

Part 6: Pancreas, stomach, liver, small

intestine

Part 7: Ovaries and testes, placenta

(pregnancy)

Part 8: Kidneys, heart and skin

May

Jun

Jul

Aug

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