Seminar-Adrenal Insuffieciency by Dr.Teshale K.-final.pptx

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ADRENAL INSUFFICIENCY
Presenter: Dr.Teshale K.(IMR2)
Moderator: Dr. Kibret E(Consultant Internist
and Endocrinologist)
21/2/18

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OUTLINE
 Historical back ground
 Anatomy and development of adrenal gland
 Overview of adrenal steroid biosynthesis
 Definition and Epidemiology of AI
 Etiology
 Clinical Manifestation
 Diagnosis
 Management
 prognosis
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HISTORICAL BACK GROUND
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ANATOMY AND DEVOLOPMENT OF
ADRENAL GLAND
 Adrenanl Gland - A pyramidal structure weighing 6-11gm, lie
on superior pole of kidneys.
 Composed of 2 functionally distinct major parts:
Adrenal cortex
Adrenal medulla- Synthesizes and releases
catecholamines.
 In the development of Adrenal gland cells forming the
Adrenal cortex orignates from intermediate mesoderm that
derive the Urogenital ridge at 4th week of gestation.
 Neural crest cells migrate to the adrenal gland at 9th weeks of
gestation.
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ADRENAL STEROIDS
BIOSYNTHESIS
 Cholesterol is the precursor adrenal steroidogenesis.
 Steroidogenesis involves the concerted action of
several enzymes, including a series of cytochrome
P450 enzymes.
 Classic endocrine feedback loops are in place to
control the secretion of both hormones.
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EFFECT OF GLUCOCORTICOID
 Cortisol 95% is bound to cortisol-binding globulin or
albumin, and 5% circulates as free cortisol.
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REGUALTION MECHANISM
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ADRENAL INSUFFICIENCY
 Adrenal insufficiency is defined by inadequate
production adernocortical hormones to meet the
physiologic needs.
 Adrenal insufficiency is classified :
 Primary AI
 Secondary AI
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EPIDEMIOLOGY OF AI
 The prevalence of well-documented, permanent AI is
5 in 10,000 in the general population.
 Hypothalamic-pituitary origin of the disease
prevalence of 3 in 10,000
 Primary AI has a prevalence of 2 in 10,000.
 Adrenal insufficiency due to exogenous
glucocorticoid treatment is much more common.
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1. PRIMARY ADRENAL
INSUFFICIENCY
 Primary-AI termed as Addison’s disease.
 It is a rare disease with a reported prevalence of about 100
to 140 cases per million and an incidence of 4:1 000 000
per year in Western societies
 Primary AI is defined by the inability of the adrenal cortex
to produce sufficient amounts of glucocorticoids and
mineralocorticoids.
 PAI is a severe and potentially life-threatening condition
due to the central role of these hormones in energy, salt,
and fluid homeostasis.
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1.1 AUTOIMMUNE ADRENAL
INSUFFICIENCY
 In high- income countries, 80% to 90% of patients with PAI
have autoimmune adrenalitis.
 It can be isolated, or seen as part of an autoimmune
polyendocrine syndrome.
 Antibodies most often to the 21-hydroxylase enzyme, detectable
in the serum of more than 90% of recent-onset patients.
 The cumulative risk of developing autoimmune Addison
disease in the presence of 21- hydoxylase antibodies was 39%,
somewhat higher in males, with median follow-up of 10 years.
 Approximately 50% of patients with Addison disease exhibit
an autoimmune polyendocrinopathy.
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1.2 INFECTIOUS ADRENALITIS
 Infectious diseases represent the most common cause
of primary adrenal failure worldwide, with generalized
tuberculosis being the most frequent single cause.
 All the clinically important fungi except Candida can
also cause AI.
 The most common is histoplasmosis, followed by
blastomycosis ,coccidioidomycosis, and
cryptococcosis.
 AIDS late stage – CMV ,MAC , fungi , Kaposi
sarcoma.
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1.3 ADRENAL INFILTRATION
 PAI was reported in 12.4% of patients with
bilateral adrenal metastases, and
in 20% of patients with bilateral metastases and
adrenal mass size greater than 4 cm.
Tumors that are commonly associated with AI are
cancers of the lung, kidney, stomach, colon, and
breast, as well as melanoma and lymphoma
Other rare couse Amyloidosis , hemochromatosis
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1.4 ADRENAL HEMORRHAGE
 Necrosis of the adrenals due to intra-adrenal hemorrhage
should be considered in any severely sick patient with the
following Risk factors.
 meningococcal septicemia
 Anticoagulant use
 trauma, hemorrhagic shock, sepsis, extensive burns, or
during adrenal vein sampling
 Antiphospholipid syndrome
• Typically, the patient will complain of back pain followed the
first signs and symptoms of AI without the usual
hyperpigmentation.
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1.5 GENETIC DISORDERS

Congenital adrenal hyperplasia
 autosomal recessive disease ,with inborn errors of steroidogenesis.
 Due to gene mutations affecting are the cytochrome P450 enzymes
21- hydroxylase, 11β- hydroxylase, and 3β- hydroxylase
dehydrogenase and, less often, 17α- hydroxylase/17,20-lyase,
cholesterol desmolase,
 Over 95% of cases of CAH have 21- hydroxylase deficiency with
varying degrees of deficiency of cortisol and aldosterone
synthesis, elevations of ACTH, and consequent excess adrenal
androgens.
 21-hydroxylase deficiency is the most common cause of AI in
children
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CONT…
 Adrenoleukodystrophy(ALD)
 is typically a disease of children
 rapidly progressive central demyelination .
 progressive failure of steroid-secreting cells
(adrenal and gonadal failure)
 elevated VLCFAs
 confirmation -Mutation analysis
 only autologous bone marrow transplantation
appears to be effective.
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CONT…
 Adrenomyeloneuropathy(AMN)
 disease of young adults
 slowly progressive mixed motor and sensory peripheral
neuropathy associated with UMNL
 progressive failure of steroid-secreting cells (adrenal
and gonadal failure)
 elevated VLCFAs
 Confirmation -Mutation analysis
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CONT…
 Congenital adrenal hypoplasia
 An X-linked disorder
 Caused by mutations in the genes encoding the
transcription factors SF-1 (NR5A1) and DAX-1
(NR0B1) that play a crucial role in adrenal
development
 Present with salt-losing PAI in infancy (60%) or
childhood (40%), followed by hypogonadotrophic
hypogonadism secondary to abnormal development
of both the hypothalamus and the pituitary.
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2. SECONDARY AI
 Secondary AI implies
 pituitary etiology
 hypothalamic etiologies
 Glucocorticod induced
 The prevalence of central hypoadrenalism is 125 to 280 per
million.
 It occurs in up to one-third of patients with pituitary disease.
 the most common reason is ACTH suppression by exogenous
glucocorticoid treatment.
 isolated ACTH deficiency is rare, and the diagnosis is
difficult to make.
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GLUCOCORTICOID-INDUCED- AI
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CONT…
 At least 1% of the population use chronic
glucocorticoid therapy as anti-inflammatory and
immunosuppressive agents.
 It is the most common form of adrenal insufficiency
globally, as up to 1% to 3% of the adult population is
prescribed glucocorticoid therapy.
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CONT…
 A meta-analysis of the risk of developing biochemical
glucocorticoid-induced adrenal insufficiency stratified by
glucocorticoid route of administration showed pooled
percentages of
 4.2% for nasal administration,
 48.7% for oral use
 52.2% for intra-articular administration.
 The risk also varied when stratified for
 dose (low dose 2.4% to high dose 21.5% ) and
 longer treatment duration (1.4% for<28 days) to 27.4%
for >1 year.
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CONT…
 Suppression of the HPA axis is an inevitable effect
of chronic exogenous glucocorticoid therapy.
 Glucocorticoids suppress HPA axis activity.
 Prolonged corticotropin deficiency results in atrophy
of the adrenal cortex and decreased ability to
produce cortisol.
 Any glucocorticoid dose above the physiologic daily
dose equivalent can potentially lead to suppression
of the HPA axis.
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CONT…
 The degree and persistence of HPA axis suppression
after cessation of glucocorticoid therapy are
dependent on overall exposure and other factors .
 Recovery of the HPA axis ranges from 9 to 12
months.
 Any route of administration has the potential of HPA
axis suppression.
 Duration of glucocorticoid therapy to pose risk for
adrenal insufficiency-3-4 weeks, or greater.
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CONT….
 Physiologic daily dose equivalent: Daily glucocorticoid
dose equivalent to average daily cortisol production .
 hydrocortisone 15-25 mg
 prednisone or prednisolone,4-6 mg
 Methylprednisone 3-5 mg
 dexamethasone 0.25-0.5 mg
 Endogenous production of cortisol is estimated to be 9-10
mg/day.
 The above mentioned doses are based on an estimate of
bioavailability.
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CONT…
 Concomitant therapies can augment potency and adrenal
suppression.
 The coadministration of inhaled fluticasone with
medications that suppress its clearance by inhibition
of CYP3A4 is associated with adrenal suppression
(e.g., ritonavir)
 Co-prescriptions of agents that do not affect
glucocorticoid clearance but have affinity for the GR
are also associated with adrenal suppression.
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CONT…
 All patients receiving long-term therapy with corticosteroids
should be treated in a similar fashion to patients with chronic
ACTH deficiency; they should carry steroid cards and be
offered steroid alert bracelets or necklaces.
 In the event of an intercurrent stress (e.g., infection,
surgery), supplemental steroid cover should be given.
 During recovery from suppression and without replacement
therapy, patients may experience symptoms of glucocorticoid
deficiency.
 To avoid these symptoms, steroids should be cautiously
withdrawn over a period of months
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OPIOID- INDUCED HPA AXIS SUPPRESSION
 Suppression of the HPA axis may follow opioid receptor
stimulation affecting hypothalamic CRH production.
 Low cortisol and sex steroids potentially add to the
disability associated with long-term opioid use.
 Adrenal insufficiency appears to be related to the
cumulative opioid exposure (dose and duration) and
may be diagnosed in 9% to 15% of patients taking
chronic opioids.
 Adrenal crisis has been reported in opioid-induced AI.
 Recovery of adrenal function may occur following the
cessation of opioids.
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HYPOADRENALISM DURING CRITICAL
ILLNESS
 Functional adrenal insufficiency.
 Inappropriately low cortisol levels can be seen
during critical illness with a structurally normal HPA
axis (relative AI).
 Severe illness causes decreased cortisol-binding
proteins, leading to an increase in the ratio of free to
bound cortisol.
 Free cortisol correlates more closely with illness
severity
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DIAGNOSIS OF ADRENAL
INSUFFICIENCY
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CLINICAL FEATURES OF AI
 Patients with primary adrenal failure usually have both
glucocorticoid and mineralocorticoid deficiencies.
 In contrast, those with secondary adrenal insufficiency
have an intact RAA system.
 This accounts for differences in salt and water balance
in the two groups of patients, which in turn result in
different clinical presentations.
 The most obvious feature that differentiates primary
from secondary hypoadrenalism is skin pigmentation
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INVESTIGATIONS
1. Morning plasma cortisol
 An early-morning serum cortisol level of less than
5 μg/dL is considered highly probable for AI.
 Morning cortisol concentrations greater than 10
μg/dL indicate a very low likelihood of AI.
 Basal cortisol should be taken as soon as possible
after waking because serum cortisol
concentrations fall by 30 nmol/L (1.2 μg/dL) per
hour between 7:00 am and 12:00 pm.
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CONT…
2. Corticotropin
When combined with an early-morning cortisol
measurement, corticotropin concentrations help
determine the type of adrenal insufficiency.
 normal reference range,15 -65pg/Ml
 >100 pg/mL in primary AI
 <20 pg/mL in Secondary AI.
.
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CONT…
3.Dehydroepiandrosterone Sulfate/DHEAS,DHEA
 In PAI, all adrenocortical steroid levels are low
(including DHEA and DHEAS).
 In secondary AI and glucocorticoid-induced adrenal
insufficiency, low or low normal levels of DHEAS.
 Because DHEAS circulates in high concentrations
and has a long half-life (7-10 hours), DHEAS serves
as an accurate predictive marker of hypothalamic-
pituitary-adrenal axis impairment.
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ASSESS ADEQUACY OF FUNCTION OF
THE HPAAXIS
1. ACTH Stimulation Test
 The most widely used dynamic test to assess adrenal function
and has higher sensitivity in primary AI
 Standard of care test for cortisol deficiency.
 The corticotropin (standard 250 mcg or low-dose 1 mcg) can
be given intravenously (IV) or intramuscularly with cortisol
measured baseline and 30 and 60 minutes after corticotropin.
 Cortisol levels >18 mcg/dL exclude primary AI and severe
chronic secondary AI.
 A normal cortisol response to cosyntropin renders AI
extremely unlikely.
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CONT….
2. Insulin Tolerance Test (ITT )
 IV insulin (0.1 to 0.15 U/kg) is given with glucose and
cortisol is measured at 0, 30, 45, 60, 90, and 120 minutes.
 Hypoglycemia of <45 mg/dL with neuroglycopenic
symptoms is essential-activation of the HPA axis.
 Normal response is a cortisol >20 mcg/dL ,at any time
during the test.
 Contaraindicted in IHD , CVD ,epilepsy, or severe
hypopituitarism .
 Needs specialized set up.
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CONT…
3. Overnight metyrapone test
 Its drug which inhibit 11B-hydroxyalse which converts
deoxycortisol to cortisol.
 alternative to ITT to diagnose secondary AI.
 30 mg/kg (maximum, 3 g) metyrapone is given at midnight,
and plasma cortisol and 11-deoxycortisol are measured at 8
am the following morning.
 an intact HPA axis
 ACTH levels rise andpeak 11-deoxycortisol value greater
than 7 μg/dl.
 Cortisol decreased
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CONT…
 Adrenal Autoantibody Tests antibodies against enzyme 21-
hydroxylase
 Serum 17-Hydroxyprogesterone is the cornerstone of diagnosis
of 21- hydroxylase deficiency
 Very Long Chain Fatty Acids for ALD or AMN
 Imaging
 Imaging of the adrenals is needed in cases of primary adrenal
insufficiency where a nonautoimmune etiology is considered
likely
 Clinical suspicion of hemorrhage, infection, infiltration, or
neoplastic disease exists, abdominal CT should be performed.
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OTHER INVESTIGATIONS
 RFT, LFT , TFT
 Serum electrolyte
 renin and aldosterone concentration
 Chest radiography ,gene expert
 pituitary MRI
 CT-guided adrenal biopsy
 other Autoantibodies
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MANAGEMENT OF AI
 ADRENAL CRISIS
 Adrenal crisis is a life-threatening state caused by
insufficient levels of cortisol.
 It requires immediate treatment with parenteral
glucocorticoids and isotonic fluid administration.
 Adrenal crisis denotes an episode of acute adrenal
insufficiency and should be considered in any patient with
shock.
 Acute adrenal crisis is characterized by severe hypotension
refractory to vasopressors.
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CONT….
 In addition patients commonly present with
nonspecific signs and symptoms including nausea,
vomiting, anorexia, fever, fatigue, weakness, and
confusion or loss of consciousness.
 If adrenal crisis is suspected, treatment should be
initiated immediately.
 Adrenal crisis occurs in patients with both primary
and secondary adrenal insufficiency,
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CONT…
 Uncommon in patients with adrenal insufficiency due
to prolonged administration of exogenous
glucocorticoids.
 Reported stressors include acute infection, especially
GI infection; surgery; extreme physical activity; acute
severe injury or burns; and cessation of chronic
glucocorticoid replacement.
 Infections are the most common precipitants.
 Clinical data evaluating the management of adrenal
crisis are limited.
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LONG-TERM REPLACEMENT
THERAPY
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CONT…
 Glucocorticoid replacement
 The aim of long-term therapy is to give
replacement doses of hydrocortisone to mimic
the normal cortisol secretion rate .
 Most patients are adequately treated usually
15–25 mg/day in divided doses.
 Doses are usually given on awakening, with a
smaller dose at 3 to 6 pm, but some patients feel
better with three-times-a-day dosing.
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CONT…
 Cortisol deficiency is a feature of primary and central
adrenal insufficiency, so any form of adrenal insufficiency
requires glucocorticoid replacement therapy.
 Hydrocortisone is the preferred glucocorticoid For most
patients with adrenal insufficiency.
 usually administered in two or three daily divided doses to
better mimic the circadian pattern of endogenous cortisol
secretion, with an early morning peak and a bedtime nadir .
 When hydrocortisone therapy is unavailable, the short-
acting agent cortisone acetate is a reasonable alternative.
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CONT…
 In a typical twice-daily regimen, approximately two-thirds of
the total daily dose is taken in the morning and one-third in
the afternoon.
 Three times daily regimens entail decreasing doses in the
morning, midday, and late afternoon (eg, HC 10, 5, and 2.5
mg taken at 7:00 AM, 12:00 PM,and 4:00 PM, respectively).
 The initial HC dose should be titrated as needed based on
clinical monitoring for evidence of under- or over treatment.
 The ideal dose is the lowest total daily dose that alleviates
symptoms of cortisol deficiency.
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CONT…
 Cortisone acetate is a short-acting glucocorticoid and is a
reasonable alternative is available in 25mg tablets.
 CA has a slightly delayed onset of action as it needs to be
activated to HC by hepatic 11b –hydroxysteroid
dehydrogenase (HSD) type 1.
 Similar to HC , CA are taken in two or three divided doses,
with the first dose upon awakening and the last dose
approximately 4–6h before bedtime
 If a longer-acting glucocorticoid is used for replacement
therapy, It is prefered the intermediate-acting agent
prednisolone.
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CONT…
 CYP3A4 is the key drug metabolizing enzyme affecting HC
clearance and concomitant administration of several drugs
can affect HC efficacy.
 Plasma ACTH and serum cortisol are not useful parameters
for glucocorticoid dose adjustment.
 Therefore, monitoring of glucocorticoid replacement
predominantly relies on clinical assessment.
 Patients should be assessed at least once every three months
early after diagnosis and during dose titration and at least
once annually after a stable replacement regimen is
established.
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CONT….
 Symptoms and signs of over-replacement are
 weight gain, insomnia
 peripheral oedema
 increase BP
 under-replacement is characterized by
 lethargy, nausea, poor appetite,weight loss
 increased pigmentation t
 In cases in which malabsorption is suspected, serum or
salivary cortisol day curve monitoring may be useful to
guide dosing.
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CONT…
2. Mineralocorticoid replacement
 Mineralocorticoids are vital for maintaining blood
pressure, and water and electrolyte homeostasis.
 Almost all patients with primary adrenal insufficiency
require mineralocorticoid replacement
 Initiate dose and treatment of chice is fludrocortisone
0.05 to 0.1 mg daily
 For individuals taking hydrocortisone or cortisone
acetate, generally choose an initial dose of
fludrocortisone 0.05 mg daily
 For individuals taking prednisolone, prednisone, or
dexamethasone, start fludrocortisone 0.1 mg daily.
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CONT…
 Patients are advised to eat sodium salt and salty foods
without restriction and to avoid potassium-containing salts
 The amount of fludrocortisone required is related to
individual fluid and electrolyte intake/losses.
 Patients on treatment needs both clinical and biochemical
assessments to assess the adequacy of mineralocorticoid
replacement therapy.
 Assessments done at least every one to three months
during treatment initiation or dose adjustments
 at least annually in individuals on stable replacement
regimens.
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CONT…
 Mineralocorticoid replacement is evaluated clinically by
asking the patient about
I. Salt cravings , lightheadedness, nausea or muscle
cramping
II. Measuring blood pressure in the supine and standing
positions,heart rate to assess for postural hypotension
 Hypertension and edema are signs of excessive
mineralocorticoid replacement
 Biochemical monitoring includes measurement of the
serum sodium, potassium, and creatinine concentrations
and PRA
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CONT…
 Fludrocortisone under replacement is common, and
 Sometimes compensated for by over replacement of
glucocorticoids, and possibly predisposes patients to
recurrent adrenal crises.
 Diuretics and drugs that affect blood pressure and
electrolytes might interact with fludrocortisone and may
require dose adjustments.
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CONT….
3. Adrenal androgen replacement
 In selected females with adrenal insufficiency,
androgen replacement therapy may be beneficial
 We suggest a trial of DHEA treatment in females with
adrenal insufficiency who have significant symptoms
of
Depression or anxiety,
Low libido or energy, or
 Impaired sense of well-being despite optimized
glucocorticoid and mineralocorticoid.
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CONT…
 For females who opt for a trial of androgen replacement therapy,
should typically start DHEA 25 to 50 mg once daily in the
morning and
 Adjust the dose based upon the serum DHEA concentration,
clinical response, and occurrence of adverse effects.
 Clinical benefits, if they occur, should be evident by six months
of therapy If no DHEA therapy is should discontinued
 Because the long-term effects of DHEA or testosterone
replacement therapy in patients with PAI are not known, such a
regimen should be used with caution.
 Common androgenic side effects of DHEA therapy in women
include oily skin, hirsutism, acne, and increased sweating and
odor
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CIRCUMSTANCES REQUIRING
GLUCOCORTICOID DOSE ADJUSTMENT
 Cortisol secretion normally increases with physiologic
stressors including illness and surgery.
 For patients with adrenal insufficiency, such circumstances
require transient increases in glucocorticoid doses to
prevent adrenal crisis.
 Few data are available to guide these dose adjustments,
which are generally based on stress physiology and clinical
experience.
 Glucocorticoid dose increases are not usually needed for
psychological stress (eg, anxiety or depression) or
moderate exercise
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STEROID REPLACEMENT DURING
PHYSICAL ACTIVITY
 PAI patients undergoing regular, accustomed and time-
limited physical activity do not generally need to make a
dose adjustment.
 In the face of unaccustomed, intense or prolonged exercise,
however, an increase in HC and salt intake may be necessary.
 For running a race, such a marathon, an extra 5 mg of HC
can be taken before the race.
 In hot conditions or during intense activity, additional fluid
and salt intake should be taken to replace sweat losses.
 However, there are no systematic studies of replacement
therapy during strenuous physical activity.
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STEROID REPLACEMENT IN
PREGNANCY
 For pregnant individuals, hydrocortisone is preffered
glucocorticoid replacement therapy.
 During early pregnancy, the patient's usual glucocorticoid
replacement dose is continued.
 monitoring for evidence of glucocorticoid over- or
undertreatment at least once every trimester.
 In the third trimester, most patients require an increase in
the HC dose of approximately 20 to 40 percent. .
 Most patients require this increased dose of HC due to the
progressive rise CBG.
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CONT…
 Serum progesterone has anti-mineralocorticoid effects,
and hence, the fludrocortisone dose may often need to
be increased during late pregnancy.
 So clinical and serum electrolytes as the best means for
dosage monitoring.
 During delivery, a bolus parenteral dose of 100 mg of
HC should be given at the start of labor and followed
by 150 to 200 mg daily administered in divided doses
every six to eight hours.
 The oral dose should be doubled for 24–48 h postpartum
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PREVENTION OF ADRENAL CRISIS
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GUIDELINES FOR FOLLOW-UP OF PATIENTS
WITH PRIMARY ADRENAL INSUFFICIENCY
 Annual follow-up
 The management of PAI patients includes regular
medical examinations to evaluate the
I. Biological condition of the patients,
II. The dosage of the replacement therapy and
III. Quality of life.
 The goal is to obtain good appetite, stable weight, full
professional activity and/or housekeeping, and normal
sexual activities
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CONT…
 The annual consultation should include questions regarding.
 family relationships and professional duties, self-esteem and
possible complaints due to PAI.
 Questions about the quality of the daily replacement therapy,
self-medication during inter-current illness and previous
adrenal crises are very important to avoid such events in the
future.
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SCREENING FOR ASSOCIATED
CONDITIONS
 Continuous surveillance for other autoimmune
disorders is necessary. ,
 Annual screening.
 Thyriod function test and TPO antibody
 HbA1C
 CBC and B12-level
 Itransglutaminase 2 autoantibodies and total IgA)
symptomatic pateient
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PROGNOSIS
 After being diagnosed with adrenal insufficiency,
 starting steroid treatment,
 being informed about the risk of and treatment for
adrenal crisis,
 patients with adrenal insufficiency generally have
very good quality of lifeand are capable of working,
participating in sports, and traveling.
 However, adrenal crisis can occur unexpectedly with
concurrent illness or trauma and can lead to critical
illness or death if not promptly treated with high
doses of glucocorticoids and other supportive therapy.
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REFFERENCES
 Williams text book of endocrinology 15th
edition
 Harrison 22st
edition
 Up to date 2025
 European Society of Endocrinology and Endocrine
Society Joint Clinical Guideline: Diagnosis and Therapy
of Glucocorticoid-induced Adrenal Insufficiency 2024
 Diagnosis and Treatment of Primary Adrenal
Insufficiency: An Endocrine Society Clinical Practice
Guideline 2024
 Adrenal_Insufficiency_in_Adults_A_Review_JAMA,_20
25
21/2/18

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Seminar-Adrenal Insuffieciency by Dr.Teshale K.-final.pptx