ADRENAL HORMONES

(INTRODUCTION)

Dr. Manal Kh. Abdulrazak

Assistant prof. of Medicine
Department of Medicine
Baghdad College of Medicine
 Objectives
At the end of this presentation, the student should be
able to:
Describe the functions of the adrenal hormones.
Describe the pharmacological actions and therapeutic
principles of corticosteroids.
Describe the side effects of steroid abuse.
 Review of Anatomy and Function
• Capsule
• Cortex (outer) has 3 zones:
1- Zona glomerulosa : mineralocorticoids, mainly
aldosterone, responsible for the regulation of BP.
It affects the distal convoluted tubule and
collecting duct of the kidney (increased
reabsorption of Na + and excretion of both K + and
H + ions.
2- Zona fasciculata: glucocorticoids, such as
11-deoxycorticosterone, corticosterone, and
cortisol in humans.
3- Zona reticularis: produces androgens, mainly
dehydroepiandrosterone (DHEA), DHEA sulfate
(DHEA-S), and androstenedione (the precursor to
testosterone) in humans.

• Medulla (core of the gland)

• It secretes norepinephrine and epinephrine.
Catecholamines (aa tyrosine ), water-soluble, the
major hormones underlying the fight-or-flight
response.
• Receives input from the sympathetic nervous
system through preganglionic fibers originating in
the thoracic spinal cord from T5–T11.
• Cortisol also promotes epinephrine synthesis.
 Basal secretions
Group Hormone Daily
secretions
Glucocorticoids • Cortisol 5 – 30 mg
• Corticosterone 2 – 5 mg
Mineralocorticoids • Aldosterone 5 – 150 mcg
• 11- deoxycorticosterone Trace
Sex Hormones
•Androgen • DHEA 15 – 30 mg
•Progestogen • Progesterone 0.4 – 0.8 mg
•Oestrogen • Oestradiol Trace

From Essential of Pharmacotherapeutics, ed. FSK Barar. P.351

 Cholesterol ACTH

Oestriol
Pregnenolone 17-α- Hydroxy Dehydro-epi
pregnenolone androsterone

Progesterone 17- Hydroxy Andro-

Oestrone
progesterone stenedione

11-Desoxy- 21,β hydroxylase

corticosterone
11- Desoxy-
cortisol
Corticosterone
11,β hydroxylase
18-Hydroxy-
corticosterone

ALDOSTERONE CORTISOL TESTOSTERONE OESTRADIOL

 Pharmacological Actions

1. Carbohydrate 8. Stomach
2. Protein 9. Blood
3. Lipid 10. Anti-inflammatory
4. Electrolyte & water 11. Immunosuppressant
5. CVS 12. Respiratory system
6. Sk. Muscle 13. Growth & Cell Division
7. CNS 14. Calcium metabolism
Actions: Carbohydrate and protein metabolism
Negative nitrogen balance & hyperglycaemia

• Gluconeogenesis
– Peripheral actions (mobilize AA & glucose and
glycogen)
– Hepatic actions

• Peripheral utilization of glucose

• Glycogen deposition in liver

(activation of hepatic glycogen synthase)
Actions: Lipid metabolism

• Redistribution of Fat
• Buffalo hump
• Supraclavicular fat
• Moon face

• Promote adipokinetic agents activity

(glucagon, growth hormone, adrenaline, and
thyroxine)
Actions: Electrolyte and water balance

• Aldosterone is more important

• Act on D.T. & C.D. of kidney
– Na+ reabsorption
– Urinary excretion of K+ and H+
Actions: Cardiovascular system

• Restrict capillary permeability

• Maintain tone of arterioles
• Myocardial contractility

Mineralocorticoid induced hypertension ??

Na+ sensitize blood vessels to the action of

catecholamines & angiotensin
Actions: Skeletal Muscles

Needed for maintaining the normal function of

Sk. muscle
Addison's disease: weakness & fatique is due to
inadequacy of circulatory system
Prolonged use:
Steroid myopathy
 Actions: CNS

• Direct:
– Mood
– Behaviour
– Brain excitability
• Indirect:
– maintain glucose, circulation and electrolyte
balance

ICP (pseudotumor cerebri) - Rare

Actions: Stomach

Aggravate peptic ulcer. May be due to

– Acid & pepsin secretion

– immune response to H.Pylori

Actions: Blood

RBC: Hb & RBC content

(erythrophagocytosis )

WBC: Lymphocytes, eosinophils, monocytes,

basophils
Actions: Anti-inflammatory

• Recruitment of WBC & monocyte- macrophage

into affected area & elaboration of chemotactic
substances
• Lipocortin
• TNF from phagocytic cells
• IL1 from monocyte-macrophage
• Formation of Plasminogen Activator
• Fibroblastic activity
• Expression of cyclooxygenase II
 Corticosteroids

Lipocortin
Phospholipids

Phospholipase A2

Arachidonic acids

lipoxygenase Cycylooxygenase

Prostaglandins,
Leukotriene Thromboxane
PAF by lipocortin Prostacyclins
Anti-inflammatory actions of corticosteroids

Corticosteroid inhibitory effect

 Immunosuppressive & anti-allergic actions

• Suppresses all types of hypersensitivity &

allergic phenomenon.
• At High dose: Interfere with all steps of
immunological response.
• Causes greater suppression of CMI (graft
rejection & delayed hypersensitivity).
• Transplant rejection: antigen expression from
grafted tissues, delay revascularization,
sensitisation of T lymphocytes.
 Actions: Growth & Cell division

• Inhibit cell division or synthesis of DNA.

• Delay the process of healing.
• Retard the growth of children.
 Actions: Calcium metabolism

• Intestinal absorption

• Renal excretion

• Excessive loss of calcium from

spongy bones (e.g., vertebrae, ribs )
 Actions: Respiratory system

• Not bronchodilators
• Most potent and most effective anti-
inflammatory.
• Effects not seen immediately (delay 6 or
more hrs).
• Inhaled corticosteroids are used for long
term control.
 Endocrinology lecture 4
ADRENAL GLAND HYPERFUNCTION
Manal Kh. Aladhadh
Professor of Internal Medicine
Department of Medicine
College of Medicine - University of
Baghdad
 Objectives
At the end of this lecture, the student should be able to:
❑Define Cushing’s syndrome.
❑Recognize the etiology of Cushing’s syndrome.
❑Describe the clinical features and complication
of Cushing’s disease
❑Outline the diagnosis and treatment options
Cushing’s syndrome.
❑Describe the clinical features, diagnostic
investigations and management plan of
Pheochromocytoma.
 CASE SCENARIO
❖A 28 y old unmarried female presented with
5m history of weight gain, bruising easily,
menstrual irregularity and abdominal stretching
marks.
❖On examination she is obese and hypertensive
❖Her blood tests reveal hypokalemia
What is your clinical approach to reach to the
diagnosis?
 Cushing’s Syndrome
• A multisystem disorder resulting from
chronic exposure to inappropriately elevated
concentrations of free circulating
glucocorticoids produced within the body
(endogenous) or introduced from outside
the body (exogenous).
 Causes of Cushing's Syndrome
❑ ACTH- Dependent Cushing‘s (90%)
1- Cushing's disease (75%)
2- Ectopic ACTH syndrome(15%): Bronchial or
pancreatic carcinoid tumors, small cell lung cancer,
medullary thyroid carcinoma, pheochromocytoma
❑ ACTH- Independent Cushing‘s F/M (4:1) (10%)
▪ Adrenocortical adenoma
▪ Adrenocortical CA
▪ Bilateral adrenal hyperplasia
▪ Iatrogenic (exogenous) Cushing’s syndrome
(ACTH treatment, Glucocorticoid treatment)
❑Pseudo-Cushing's syndrome
Chronic activation of (HPA), usually mild and
temporary.
• Major depressive disorder
• Alcoholism
• Obesity, PCOS
• Obstructive sleep apnea
 Cushing’s Disease
• (ACTH- producing pituitary adenoma)
• Most common cause of Cushing’s syndrome
• F/M (4:1), more in male in prepuberty cases
• 3rd or 4th decade of life
• Microadenoma in 90% of cases
• Usually sporadic
 Clinical features
• Truncal obesity • Purplish wide striae
• Moon face • Proximal muscle weakness
• Fat deposits (supraclavicular • Osteoporosis
fossa and buffalo hump) • DM
• HTN • Avascular necrosis
• Hirsutism • Wound healing impaired
• Amenorrhea and impotence • Pysch. symptoms
• Depression • Hyperpigmentation
• Thin skin • Hypokalemic alkalosis
• Easy bruising
• Hypercoagulation
 Ectopic ACTH
All the previous symptoms but…..
• Ectopic dominated by :
– Hypokalemic alkalosis (dominant feature)
– Fluid retention& HTN
– Glucose intolerance
– Steroid psychosis
• Absence of other features may be explained by more sudden
onset by acquired ACTH from tumor.
• F/M (1:1)

Complications of Cushing's if Untreated:

• DM
• HTN
• Osteoporotic fractures and avascular necrosis
• Infections
• Psychosis
 Screening Test
• Overnight dexamethasone suppression test
(1 mg at 11 pm, cortisol measured at 8-9 am)
Plasma cortisol> 50 nmol/L (Cushing’s syn.)
- High sensitivity (95%) but low specificity
Or
• 24 hour urine free cortisol increased above normal (3x)
- High sensitivity & specificity
Or
• Midnight plasma cortisol > 130 nmol/L
Midnight salivary cortisol > 5 nmol/L
- (100% sensitivity& 96% specificity)
 False Positives
• Severe depression
• Severe stress
• Estrogen (pregnancy or oral CP)
• Morbid obesity
False negatives
• Phenytoin/phenobarbital/rifampin
(accelerated metabolism of dexamethasone)
 Confirmatory Test
Low dose dexamethasone suppression test
• Dexamethasone 0.5 mg q 6 x 48 hours
- Plasma cortisol > 50 nmol/L (measured after
48 h)
- 97%-100% true positive
Or
• Measure urine cortisol during the last 24
hours (urine free cortisol >40 micrograms/d)
 Differential diagnosis 1
ACTH levels may distinguish:
– ACTH independent (adrenal or exogenous
glucocorticoids)
from
– ACTH dependent (pituitary, ectopic ACTH)
• ACTH independent- low ACTH to<5 pg/ml
• ACTH dependent-ACTH normal or high>15pg/ml
• In addition ectopic ACTH levels are usually 8x
higher than pituitary caused ACTH secreting
adenomas
 ACTH independent
• Unenhanced CT adrenals:
Bilateral micronodular or macronodular
adrenal hyperplasia or unilateral adrenal mass
 ACTH- dependent
Differential diagnosis 2
• MRI pituitary (not show an abnormality in up
to 40% of cases because of small tumors)
• CRH test (ACTH increase>40% at 15- 30 min &
cortisol > 20% at 45- 60 min after CRH 100 µg
IV)
• High dose DEX test (cortisol suppression > 50
% after q6h 2 mg DEX for 2 days)
❑ Positive (Cushing’s disease)

❑ Negative test (Ectopic ACTH)

❑ Equivocal
(Inferior petrosal sinus sampling)

❑ petrosal/ peripheral ACTH ratio > 2 at baseline,

> 3 at 2-5 min after CRH 100 µg i.v
Positive (Cushing’s disease)
Negative ( ectopic ACTH source)
In case of ectopic ACTH syndrome:
• High-resolution, fine-cut CT scanning of the
chest and abdomen for (lung, thymus, and
pancreas).
• If no lesions are identified, an MRI of the chest
for carcinoid tumors.
• Octreotide scintigraphy in some cases (ectopic
ACTH-producing tumors express somatostatin
receptors)
Inferior petrosal sinus sampling
 Treatment
❑ Transsphenoidal surgery
• Cushing’s Disease: Transphenoidal resection of pituitary
adenoma (cure in 70-80%). If recurs:
❖ Pituitary radio-therapy
❖ Stereotactic radiosurgery
❖ Bilateral adrenalectomy
❑ Medical therapy
- Control cortisol level pre-operatively
- Tumor can’t be located in ECTOPIC ACTH
- CA with metastasis
• Adrenal neoplasms: Resection.
• Ectopic ACTH: Resection if possible or bilateral adrenalectomy.
• Bilateral adrenal hyperplasia: May need adrenalectomies
(lifelong glucocorticoid and mineralocorticoid replacement).
 ‘Medical’ Adrenalectomy
• Ketoconazole (600 to 1200 mg/day) inhibits cortisol
synthesis by a direct action on the P450 cytochrome
enzyme
• Metyrapone, blocks the 11-ß hydroxylase enzyme
(exacerbates female virilization) 500mg tid.(max 6g)

• Mitotane(2-3 g/day)- adrenolytic agent, mainly for

adrenal CA, small dose for adenoma 500-1000mg/d.
• Aminoglutethimide (1g/day)
• Octreotide, major side effect is adrenal insufficiency,
therefore start at lowest dose and titrate
• In severe cases, etomidate (blocks 11βhydroxylase)by
low dose continuous IV infusion
 Pheochromocytoma
• At the end of this lecture, students should be
able to:
1. Define pheochromocytoma.
2. Recognize the etiology of
pheochromocytoma.
3. Describe the clinical features of
pheochromocytoma.
4. State the diagnosis and treatment of
pheochromocytoma.
 CASE SCENARIO
• A 47-year-old ma with no previous medical history presented
complaining of episodic headaches, sweating, palpitations,
and a tremor. The symptoms started a few years ago, have
become more frequent, and can last anywhere between a few
seconds to an hour.
• He does not have a history of serious illnesses,
hospitalizations, or trauma. He is not on any medications.
• On physical examination, vital signs showed:
BP of 168/96 mm Hg, PR of 116 beats per minute, RR of 20
breaths/min, and a temperature of 36.66°C.

1- Discuss the differential diagnosis

2- Discuss the management plan
• They may arise sporadically or be inherited as
features of MEN type 2.
• It is estimated to occur in 2–8 of 1 million
persons per year, and about 0.1% of
hypertensive patients have pheochromocytoma.
• The mean age at diagnosis is about 40 y.
• The "rule of tens" for pheochromocytomas
states that about:
10% are bilateral
10% are extra-adrenal
10% are malignant
 Etiology
• Well-vascularized tumors that arise from cells
derived from the sympathetic (e.g., adrenal
medulla) or parasympathetic (e.g., carotid
body, glomus vagale) paraganglia.
• They are catecholamine-producing tumors,
including those in extra-adrenal
retroperitoneal, pelvic, and thoracic sites
 Clinical Features
• Episodes of palpitations, headaches, and
profuse sweating are typical and constitute a
classic triad.
• These three symptoms in association with HT
(sustained or paroxysmal) make
pheochromocytoma a likely diagnosis.
• It can be asymptomatic for years, and some
tumors grow to a considerable size before
symptoms.
Other CF associated with pheochromocytoma:
• Anxiety and panic attacks, Pallor, Nausea,
Abdominal pain, Weakness, Weight loss,
Polyuria and Polydipsia, Constipation
Orthostatic hypotension, Dilated CMP,
Erythrocytosis, Elevated blood sugar,
Hypercalcemia.
• The dominant sign is hypertension
• Catecholamine crises can lead to HF, pulmonary
edema, arrhythmias, and intracranial
hemorrhage.
• During episodes of hormone release, patients are
anxious and pale, with tachycardia and
palpitations.
• These paroxysms last less than an hour and may
be precipitated by surgery, positional changes,
exercise, pregnancy, and various medications
(e.g., tricyclic antidepressants, opiates,
metoclopramide).
 Diagnosis
• Biochemical testing and localization of the tumor.
• Elevated plasma and urinary levels of
catecholamines and the methylated metabolites,
(VMA, metanephrines, and normetanephrines) are
the cornerstone for the diagnosis.
• Borderline elevation cause false positive result.
• Suppression test using clonidine may be valuable
(the measurement of plasma normetanephrine 3 h
after oral intake of 300µg clonidine).
• Abdominal CT or MRI, MIBG scintigraphy, Fluoro-
DOPA PET/CT.
(A) Anterior (left) and posterior (right) whole-body
images of 51-y-old woman with right adrenal tumor on
CT, confirmed as pheochromocytoma at surgery. (B)
Anterior (left) and posterior (right) whole-body images
of 28-y-old woman with paraganglioma metastatic to
bone.
A 54-y-old man with benign sporadic right adrenal pheochromocytoma (arrows). (A) PET
scan showing physiologic brain uptake; urinary excretion; and mild activity in blood pool,
cardiac wall, salivary glands, and gastrointestinal tract. (B) prominent uptake in spleen,
kidneys, liver, and pituitary; low-level uptake in salivary glands and thyroid; and prominent
normal left adrenal (arrowhead). (C) uptake in basal ganglia; low-level uptake in esophagus
and cardiac wall; normal left adrenal (arrowhead) and GIT; and excretion through kidneys
and bladder. (D) uptake in pheochromocytoma (arrow) (greater than liver level) and in
thyroid, despite blockade; mild uptake in pheochromocytoma (arrow) in liver.
 Treatment
• Complete tumor removal is the goal.
• Preoperative patient preparation is essential
for safe surgery.
• α- blockers (phenoxybenzamine) should be
initiated at relatively low doses (e.g., 5–10 mg
orally 3X/ day) and increased every few days.
• Good hydration is necessary to avoid
orthostasis.
• Adequate α- blockade generally requires 7 days,
with a typical final dose of 20–30 mg
phenoxybenzamine 3X/d.
• Oral prazosin or intravenous phentolamine can be
used to manage paroxysms while awaiting
adequate alpha blockade.
• Before surgery, BP should be below 160/90
mmHg.
• Beta blockers (10 mg propranolol 3-4 times daily)
can be added after starting alpha blockers and
increased as needed if tachycardia persists.
• Nitroprusside infusion is useful for intraoperative
hypertensive crises.
 CASE SCENARIO 1
❑ A 35-year old female is admitted to the ICU with fever,
chills, dysuria, diarrhea, marked dizziness, anorexia,
nausea, vomiting and abdominal pain for 4 days. On
examination:
❑ She is ill-appearing
❖ Temperature= 39C, PR= 98/minute
❖ BP= 100/70 mm/Hg/ supine position
❖ BP= 80/56 mm/Hg/ standing
❖ Abdominal exam shows mild diffuse tenderness.
❖ BUN= 25 mg/dl (n= 7-22), Cr.= 1.2mg/dl (n= 0.7-1.5)
❖ FBS= 60 mg/dl (n= 70-110)
She had a brain tumor removed 2 years ago and has
been on multiple hormone replacement medicines
since then, none of which have been taken for the past
3 days because of nausea.
 ADRENAL INSUFFICIENCY (AI)
Definition:
 There is a decrease in the secretion of cortisol and or
aldosterone.
 Variable presentation and potentially fatal.
 Prevalence of permanent adrenal insufficiency is 5 in 10,000.
CAUSES
Secondary (low ACTH) is the most common.
 Pituitary tumors (endocrine adenomas, rarely carcinoma).
 Mass lesions affecting the HP region (craniopharyngioma,
meningioma, metastases).
 Pituitary irradiation.
 Pituitary apoplexy/hemorrhage.
 Pituitary infiltration (TB, actinomycosis, sarcoidosis, Wegener's
granulomatosis, metastases).
 Chronic glucocorticoid excess.
 Combined pituitary hormone deficiency (CPHD).
 Congenital isolated ACTH deficiency.
Primary (high ACTH) Addison’s disease:
 Autoimmune (sporadic or polyglandular failure, APS1 and
APS2).
 Adrenal infection (TB, HIV, CMV, cryptococcosis,
histoplasmosis, coccidioidomycosis).
 Adrenal infiltration (Metastases, lymphomas, sarcoidosis,
amyloidosis, hemochromatosis).
 Bilateral adrenalectomy.
 Adrenoleukodystrophy (ALD).
 Adrenal hemorrhage (Meningococcal sepsis)
antiphospholipid syndrome.
Imparied Steriodiogensis
 CAH, Drugs (ketoconazole, etomidate, metyrapone etc)
 Epidemiology
 Addison’s disease is a rare and chronic disease.
 Prevalence of 2 in 10,000 per year.
 Usually effects 30-50 year-olds, but can be seen in all
ages.
 AI arising from suppression of the HPA axis as a
consequence of exogenous glucocorticoid treatment
occurs in 0.5–2% of the population in developed
countries.
 Clinical Features
 Signs and Symptoms Caused by
Glucocorticoid Deficiency:
 Chronic fatigue
 Weight loss, anorexia
 Myalgia, joint pain
 Hypoglycemia, Hyponatremia due to loss of feedback
inhibition of ADH release
 Anemia, eosinophilia and lymphocytosis
 Low blood pressure, postural hypotension
 Fever
 Slightly increased TSH (due to loss of feedback
inhibition of TSH release)
Signs and Symptoms Caused by
Mineralocorticoid Deficiency (Primary AI Only) :

❑Abdominal pain, nausea, vomiting

❑Dizziness, postural hypotension
❑Salt craving
❑Low BP, postural hypotension
❑Increased serum creatinine (due to volume
depletion)
❑ Hyponatremia
❑Hyperkalemia
 Signs and Symptoms Caused by
Adrenal Androgen Deficiency:
 Lack of energy
 Dry and itchy skin (in women)
 Loss of libido (in women)
 Loss of axillary and pubic hair (in women)
Other Signs and Symptoms:
 Hyperpigmentation (primary AI only) [due to excess
of pro-opiomelanocortin (POMC)–derived peptides]
 Alabaster-colored pale skin (secondary AI only)
(due to deficiency of POMC- derived peptides)
 ACUTE ADRENAL INSUFFICIENCY

❑More frequently observed in patients with

primary AI.
❑Postural hypotension may progress to
hypovolemic shock.
❑ AI may mimic features of acute abdomen.
❑May resemble neurologic disease, with
decreased responsiveness, progressing to
stupor and coma.
❑An adrenal crisis can be triggered by an
intercurrent illness, surgical stress, infection.
 DIAGNOSIS
 Determined by low level of adrenal hormone after
stimulation with synthetic ACTH hormone
(tetracosactide or short Synacthen test)
Short Test:
❑ 250 µg of cosyntropin i.m or i.v injection
❑ Blood cortisol levels 30- 60 min
(cortisol post cosyntropin is < 500 nmol/l)
❑ CBC, serum Na, K, creatinine, urea, TSH
For dDx:
Plasma ACTH, renin, S. aldosterone.
❑High ACTH, high PRA, low aldosterone (primary AI)
❑Low- normal ACTH, normal PRA and aldosterone
(secondary)
❑ Adrenal autoantibody
❑ Antibodies against (steroid secreting cells,
thyroid Ag, parietal cells, pancreatic cells)
❑ CBC to look for pernicious anemia
❑ Blood Ca and glucose
❑ CXR, U/S and X-ray of adrenals for TB
calcifications
❑ CT or MRI of adrenals for malignancies,
hemorrhage.
❑ HIV test
❑ Serum Na and K
❑ Tests for 17OHP and in men plasma VLCFA.
❑ MRI pituitary for hypothalamic pituitary mass.
 TREATMENT
❑ Replacement (always need glucocorticoid and
usually mineralcorticoid therapy).
❑ Cortisol orally 15 mg at morning and 5 mg at
evening
(1 mg hydrocortisone, 1.6 mg cortisone acetate, 0.2
mg prednisolone, 0.25 mg prednisone, and 0.025
mg dexamethasone).
❑ Doses change according to lifestyle, i.e. stress,
infection, or injury
❑ Have to carry emergency injection of
hydrocortisone and steroid card/bracelet
indentifying their condition.
❑ Monitor treatment by body w.t and BP.
❑ Mineralocorticoid replacement is by giving
fludrocortison 0.05- 0.1 mg/day
❑ Adrenal androgen replacement is an option in
patients with lack of energy, despite optimized
glucocorticoid and mineralocorticoid
replacement.
❑ It may also be indicated in women with loss of
libido.
❑ Replacement can be achieved by once-daily
administration of 25–50 mg DHEA. Treatment
is monitored by measurement of DHEAS,
androstenedione, and testosterone.
 CASE SCENARIO 2
A 32-year-old woman with known hypothyroidism is
admitted to hospital. Her BP is 86/53 mmHg and
her pulse 100 bpm. Investigations reveal:

Serum Na: 126 mmol/L (137-144)

Serum K: 5.8 mmol/L (3.5-4.9)
Serum glucose: 3.0 mmol/L (3.0-6.0)

❑What is the most likely diagnosis?

❑What is the most appropriate investigation to
confirm your diagnosis?
 ADDISONIAN CRISIS

❑Severe hypotension (shock)

❑Hyperkalemia
❑Hyponatremia
❑Hypoglycemia
❑Unexplained fever, diarrhea, vomiting
❑Could cause coma and death
❑Precipitated by infection, surgery or
intercurrent disease
 TREATMENT
❑ It is a medical emergency.
❑ IV fluid( normal saline 1L/h and 10% dextrose
followed by 4-6 L over 24h).
❑ Hydrocortisone 100 mg bolus then 100- 200 mg
over 24h (infusion or multiple injections) until GI
symptoms improve then start oral therapy.
❑ Mineralocorticoid replacement can be initiated
once the daily hydrocortisone dose has been
reduced to <50 mg.
❑ Treat precipitated cause.