Adrenal Insufficiency Flashcards

1
Q

What are the causes of primary adrenal insufficiency (Addison’s Disease)?

A

1) Autoimmune adrenalitis: most common cause of Primary A-I (80-90%)

2) Infectious adrenalitis
- TB (calcified adrenals): 2nd most common cause
- Opportunistic infections in HIV e.g. CMV

3) Bilateral adrenal haemorrhage i.e. Waterhouse-Friderichsen Syndrome (in meningococcemia)
4) Genetic disorders such as CAH
5) Bilateral adrenalectomy

6) Drug-induced (etomidate, antifungals e.g. ketoconazole)
- Recall: this is the medical therapy for cushing’s!

7) Infiltrative
- Metastasis
- Lymphoma
- Amyloidosis
- Haemochromatosis

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2
Q

What are the causes of Secondary/ Central Adrenal Insufficiency i.e. decreased ACTH production?

*note that mineralocorticoid production remains INTACT as it is controlled by RAAS axi

A

Chronic exogenous glucocorticoid use from TCM, Hospital etc

  • Chronic use causes negative feedback to decreased endogenous ACTH production 🡪 shutting down this axis
  • Hence sudden reversal of chronic medications + acute insult will lead to ADDISONIAN CRISIS
  • Hypopituitarism

Trauma / Radiation

  • Surgery (eg: Trans-Sphenoidal Surgery)
  • Macroadenomas
  • Sheehan’s Syndrome causing Pituitary Apoplexy
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3
Q

What are the clinical features of primary adrenal insufficiency?

A

↓ Aldosterone

  • HypoTN / Orthostatic
  • HypoNa
  • HyperK
  • NAGMA: HyperK 🡪 rTA

↓ Cortisol

  • LOW, LOA, Lethargy
  • Depression
  • GI S/E: N&V, Diarrhoea
  • HypoTN / Orthostatic
  • Hypogly
  • HypoNa

↓ Androgens
(Females only)
- Loss of libido
- Loss of axillary and pubic hair

↑ ACTH: Hyperpigmentation of areas that are not normally exposed to sunlight (e.g., palmar creases, mucous membrane of the oral cavity)

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4
Q

What are the clinical features of secondary adrenal insufficiency?

A

↓ Cortisol

  • LOW, LOA, Lethargy
  • Depression
  • GI S/E: N&V, Diarrhoea
  • HypoTN / Orthostatic
  • Hypogly
  • HypoNa

↓ Androgens
(Females only)
- Loss of libido
- Loss of axillary and pubic hair

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5
Q

What is the most important triad to recall 1st as a clinical presentation of adrenal insufficiency?

A
  • Hypotension
  • Hyponatraemia: because of loss of ACTH suppression by cortisol
  • Hypoglycaemia: since cortisol is a counter-regulatory hormone
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6
Q

What is the investigations to work out hypocortisolism?

A

1) 8 am cortisol
- Random cortisol in urgent situations/ or start dexamethasone
- Note binding of cortisol to albumin / CBG (can be falsely low cortisol values if albumin low)

2) Serum ACTH – Differentiates primary and secondary cause

3) Standard short Synacthen test (250mcg) im/iv aka cosyntropin test
- To assess the function of Adrenals w ACTH stimulation: Serum cortisol is measured before SST, 30th min after, & 60th minute after (0, 30, 60 min)

4) Complications
- Capillary Blood Glucose: Hypoglycaemia
- Blood pressure: Hypotension
- Plasma Renin & Aldosterone levels: for hypoaldosteronism
- Total testosterone + SHBG: for Hypoandrogenism (in females)
- Renal panel & U/E/Cr: Hyponatraemia (since cortisol serves to ↓ ADH release via -ve feedback)
+/- Hyperkalaemia

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7
Q

What are the investigation results if Pri Hypocortisolism?

A

↑ ACTH, Suboptimal Synacthen Stimulation

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8
Q

What are the investigation results if Acute Sec Hypocortisolism?

A

↓ ACTH, Optimal Synacthen Stimulation

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9
Q

What are the investigation results if Chronic Sec Hypocortisolism?

A

ACTH, Suboptimal Synacthen Stimulation

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10
Q

What is the further workup for primary adrenal insufficiency?

A

Screen for adrenal antibodies and other autoimmune diseases e.g., Hashimoto thyroiditis, pernicious anemia, type 1 DM

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11
Q

What is the further workup for secondary adrenal insufficiency?

A

If secondary

  • MRI brain
  • TRO Exogenous Steroid Use
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12
Q

What is the management of a patient with adrenal insufficiency?

A

Hydrocortisone (given because short acting)

  • If PRIMARY Hypocortisolism: 10mg on waking, 5mg at noon, 5mg at 5pm
  • If SECONDARY Hypocortisolism: 10mg on waking, 5mg at 5pm

Aldosterone replaced in primary AI (not secondary): 50-100 μg fludrocortisone / day

Sex steroids (for woman- woman’s choice )

  • Androgen replacement helps to reduce libido and improve QoL
  • However generally we DO NOT REPLACE

No need to replace adrenalinesince medulla function is NOT affected in both 1’ & 2’ A-I

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13
Q

How much hydrocortisone should the patient take if they are sick?

A

Mild-moderate illness (eg: runny nose, sore throat) <39 degrees 🡪 2x dose for 3 days till mild illness is over

Severely unwell >39 degrees 🡪 Please come to hospital for parenteral steroids

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14
Q

What are the side effects of fludrocortisone?

A

If excessive replacement – HTN, HypoK (S&S of weakness, Polyuria)

If insufficient – Hypotension, Postural Hypo, HypoNa, HyperK

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15
Q

What are the S/E of overtreatment of adrenal insufficiency

A
  • Endocrine: weight gain, worsening/ new onset of DM
  • GI: dyspepsia, PUD
  • Psych: confusion, irritiability, suicidal thoughts
  • MSK: osteoporosis, proximal myopathy
  • opthal: glaucoma and cataracts
  • CVS: oedema, HTN, electrolyte abnormalities
  • Skin: thinning of skin and delayed wound healing
  • Immunosuppresion: Increased risk of infection
  • Irreversible growth suppression in children and young people
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16
Q

What is the S/E of under treatment of adrenal insufficiency

A

Weight loss, fatigue, N&V, postural dizziness

Hypoglycaemia, Hyponatremia

If hypoaldosteronism – Hyperkalaemia, NAGMA

17
Q

What are the precipitating factors of Addisonian crisis?

A
  • Acute infection
  • Trauma, surgery
  • Missed medication
18
Q

What are the clinical features of an addisonian crisis?

A
  • Shock
  • Weak, confused 🡪 Drowsy/Comatose (AMS)
  • Hypoglycaemia
  • Hyponatraemia
  • Hyperkalaemia
  • Metabolic Acidosis
  • Weight loss ± abdominal pain (mimics Peritonitis)
19
Q

What is the Mx of an addisonian crisis?

A

Investigations

  • Bloods for cortisol and ACTH
  • Check potassium & ECG

Immediate hydration and correction of hypoglycemia

  • Administration of 2-3L IV saline or 5% dextrose in isotonic saline with frequent hemodynamic monitoring
  • Note: the “pressor” for Addisonian crisis is Bolus Hydrocortisone ↓

Correct cortisol

1) High-Dose IV Hydrocortisone
- 100 mg IV hydrocortisone BOLUS STAT
- Followed by 100–200 mg hydrocortisone INFUSION over 24 hours via: Continuous Infusion in D5% (serves as both hydration + corrects Hypoglycaemia) OR IM / IV hydrocortisone 25 -50 mg QDS
2) No need for mineralocorticoid acutely:
- High dose hydrocortisone (>50 mg/day) has mineralocorticoid effect.
- Only when subsequently lowering of Hydrocortisone dose + transition from IV to PO 🡪 loss of mineralocorticoid effect 🡪 we then add on Fludrocortisone.

Investigate and treat underlying cause

Once Stabilized:

  • Gradually taper the IV dose 🡪 change to PO regime
  • Add on Fludrocortisone once dosage <50mg/day
20
Q

When will there be an overlap of hypothyroidism and adrenal insufficiency? What are the considerations when prescribing hydrocortisone?

A

Both may co-exist due to:

  • AI Adrenalitis & AI Thyroiditis
  • Panhypopituitarism

Hydrocortisone replacement is to be given BEFORE thyroxine replacement in patients with concomitant hypothyroidism. Because Thyroxine can increase the body’s need for cortisol and drive the person into further hypocortisolism if not careful

21
Q

What is the mechanism in which hydrocortisone replacement unmask previous DI?

A
  • Hypoadrenalism 🡪 hypotension 🡪 triggers greater ADH (Vasopressin) release
  • In pt w/ undiagnosed DI: Hypoadrenalism drives up ADH to physiological levels
  • Hence on replacement of cortisol, ADH returns to sub-physiological levels