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6th Year > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

What is primary adrenal insufficiency (Addison’s) , and what is the most common cause causes?

A

= when the adrenal glands have been damaged, resulting in reduced cortisol & aldosterone secretion.

  • Aetiology
    • Autoimmunity → most common
    • Infections → TB, CMV
    • Short-term steroid use
    • Trauma
    • Adrenal tumours
    • Surgical removal of the adrenal glands
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2
Q

What is secondary adrenal insufficiency, and what causes this?

A

= the result of inadequate ACTH stimulating the adrenal glands, causing low cortisol release.

  • Aetiology
    • Tumours → pituitary adenomas
    • Surgery to pituitary
    • Radiotherapy
    • Sheehan’s syndrome
    • Trauma
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3
Q

What is tertiary adrenal insufficiency? Describe the pathophysiology

A

= the result of inadequate corticotropin-releasing hormone (CRH) release by the hypothalamus.

  • Usually caused by patients taking long-term steroids (>3 weeks)
    • Suppresses the hypothalamus due to negative feedback → when the steroids are withdrawn, the hypothalamus does not wake up fast enough, meaning endogenous steroids are not adequately produced.
    • This is why we taper steroid use slowly
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4
Q

What are the symptoms of adrenal insufficiency?

A
  • Often very vague
  • Low cortisol
    • Fatigue → increases throughout the day
    • Muscle weakness & cramps
    • Weight loss
  • Low aldosterone
    • Dizziness & fainting
    • Thirst & craving salt
    • Abdominal pain
  • Low androgens
    • Reduced libido & sexual function
    • Depression
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5
Q

What are the signs of adrenal insufficiency?

A
  • Increased ACTH
    • Bronze hyperpigmentation of the skin, particularly in creases → ACTH stimulates melanocytes to produce melanin. Only in primary adrenal insufficiency.
  • Low cortisol
    • Low BMI → unintentional weight loss
  • Low aldosterone
    • Hypotension → postural drop
    • Tachycardia
  • Low androgens
    • Loss of axillary & pubic hair
  • Other signs, associated with other autoimmune disorders
    • Goitre → hashimoto’s thyroiditis
    • Vitiligo
    • Dermatitis herpetiformis → coeliac
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6
Q

What investigations are done for suspected adrenal insufficiency?

A
  • Hyponatraemia → key finding
  • Other potential blood findings
    • Hyperkalaemia
    • Hypoglycaemia
    • Raised creatinine & urea → due to dehydration
    • Hypercalcaemia
  • 9am cortisol → low, can be falsely normal
  • Autoantibodies may be present → adrenal cortex antibodies, 21-hydroxylase antibodies

Short Synacthen Test:

= the test of choice for diagnosing adrenal insufficiency, it is ideally performed in the morning.

  • Give a dose of synthetic ACTH (synacthen), checking the blood cortisol level before, 30 mins after, and then 60 minutes after
  • The Synacthen will stimulate healthy adrenal glands to produce cortisol → the level should at least double
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7
Q

What long-term management is given to someone with adrenal insufficiency?

A
  • Patient education, steroid card, ID tag, and emergency letter → ensure that steroid doses are not missed, and doubled during an acute illness.
  • Hydrocortisone → cortisol replacement
  • Fludrocortisone → aldosterone replacement
  • IM hydrocortisone given for emergencies
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8
Q

What is an adrenal crisis, and how does it present?

A

= an acute presentation of severe adrenal insufficiency where the absence of steroid hormones leads to a life-threatening emergency.

  • This may be the initial presentation of adrenal insufficiency or triggered by infection, trauma, or other acute illness in established adrenal insufficiency

Presentation:

  • Reduced consciousness
  • Severe weakness
  • Severe abdominal pain
  • Nausea & vomiting
  • Hypotension
  • Hypoglycaemia
  • Hyponatraemia
  • Hyperkalaemia
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9
Q

How is an adrenal crisis managed?

A
  • A-E approach
  • IM or IV hydrocortisone → 100mg, followed by an infusion or 6hrly doses
  • IV fluids
  • IV 5% dextrose
  • Careful electrolyte monitoring
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10
Q

What do the following results indicate on a radioisotope scan of the thyroid?
1. Diffuse high uptake
2. Focal high update
3. Cold areas

A
  1. Diffuse high uptake - graves
  2. Focal high update - toxic multinodular goitre, adenomas
  3. Cold areas - thyroid cancer
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11
Q

What is toxic multinodular goitre?

A
  • Due to the development of physiologically active nodules on the thyroid gland, which do not respond to TSH & continuously produce excessive thyroid hormones
  • Insidious onset & older patients compared with Graves.
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12
Q

What is De Quervains Thyroiditis?

A

= when a viral infection causes thyroiditis - presents with thyrotoxicosis initially and a painful neck lump/goitre

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13
Q

What are some signs specific to Graves disease?

A
  • Graves eye disease
    • Conjunctival injection
    • Aching at the back of the eye
    • Diplopia
    • Lid retraction
    • Lid lag
    • Exophthalmos → bulging of the eyes caused by Grave’s disease
      • Inflammation, swelling & hypertrophy of the tissue behind the eyeballs force them forward, causing them to bulge out of the sockets
  • Pretibial myxoedema
    • Waxy, oedematous appearance over the pre-tibial area
  • Thyroid acropachy
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14
Q

What do TFTs show for hyperthyroidism?

A
  • Primary (most common)→ low TSH, high T3/4
  • Secondary → high TSH, high T3/4
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15
Q

What medication can be given for symptomatic relief in hyperthyroidism?

A

Beta-blockers -> propranolol

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16
Q

How is hyperthyroidism treated first line (usually)?

A

Block & Replace:

  • Involves blocking the excess thyroid hormone production & replacing it with the correct concentration of exogenous thyroid hormones.
  • In most patients with Graves, a block & replace regime can induce remission.
  • Blocking → carbimazole
    • First line, taken for 12-18 months
    • Risks → acute pancreatitis, agranulocytosis
  • Replacing → levothyroxine
  • Propylthiouracil → 2nd line anti-thyroid. Small risk of severe liver reactions, including death.
17
Q

What are the rules which must be followed when giving radioactive iodine for hyperthyroidism?

A
  • Women must not be pregnant, breastfeeding, or become pregnant within 6 months of treatment
  • Men must not father children within 4 months of treatment
  • Limit contact with people after the dose, particularly children & pregnant women
18
Q

What is a thyroid storm (crisis)? How does it present, and how is it managed?

A

= a rare complication of thyrotoxicosis which involves excessive adrenergic activity, which can be life threatening.

Clinical Features:

  • Palpitations
  • Fever
  • Confusion/agitation
  • Seizures
  • Tachycardia
  • Nausea & vomiting
  • Abdominal pain

Management:

  • Admission for monitoring
  • Treat similar to any other thyrotoxicosis, but with some additional measures → fluid resuscitation, anti-arrhythmic medication
19
Q

What will show on TFTs with hypothyroidism?

A

Primary - high TSH, low T3/4

Secondary - low TSH, low T3/4

20
Q

What is myxoedema coma?

A
  • = a rare & life-threatening complication of hypothyroidism presenting with altered mental state, hypothermia, bradycardia, and hypoventilation.
  • Must be treated rapidly with thyroid replacement therapy, glucocorticoid therapy, and supportive measures.
21
Q

What is the definition of diabetes insipidus?

A

= a disease characterised by the passage of large volumes (>3L/24hrs) of dilute urine.

22
Q

What investigations are done for diabetes insipidus?

A
  • 24hr urine collection
  • Plasma glucose → rule out DM
  • U&Es → assess renal function, rule out electrolyte abnormalities
  • Simultaneous plasma & urine osmolality → low urine osmolality, high/normal serum osmolality
  • Urine specific gravity
  • Water deprivation test
23
Q

How does a water deprivation test work, and what do its results show?

A
  • Patient avoids all fluids for up to 8 hours before the test → urine osmolality is then measured.
  • If urine osmolality is low, then desmopressin is given → urine osmolality is then measured over the 2-4hrs following this.
  • In primary polydipsia → water deprivation will cause urine osmolality to be high, desmopressin does not need to be given.
  • In cranial DI → the patient lacks vasopressin. Initially urine osmolality remains low, but the kidneys will respond to desmopressin and then urine osmolality will go high.
  • In nephrogenic DI → the patient is unable to respond to vasopressin, so will remain low throughout.
24
Q

How is neurogenic/cranial diabetes insipidus managed?

A
  • Desmopressin to replace the endogenous deficit.
  • Check serum sodium osmolality every 1-3 months
  • Overdose results in hyponatraemia
25
Q

What are the common causes of SIADH?

A
  • Post-operative → after major surgery
  • Lung infection → atypical pneumonia & lung abscesses
  • Brain pathologies → stroke, TBI, intracranial haemorrhage, meningitis
  • Medications → SSRIs, carbamazepine
  • Malignancy → SCLC
  • HIV
26
Q

How does SIADH present?

A

Symptoms:

  • Mild hyponatraemia → nausea, vomiting, headache, lethargy, anorexia
  • Moderate hyponatraemia → muscle cramps, weakness, confusion, ataxia
  • Severe hyponatraemia → drowsiness, seizures, coma

Signs:

  • Decreased level of consciousness
  • Confusion
  • Seizures
  • Hypervolaemia → pulmonary oedema, peripheral oedema, raised JVP
27
Q

How is SIADH managed?

A
  • Hospital admission if symptomatic or severe (Na<125)
  • Treat any underlying cause
  • Fluid restriction
    • Temporarily used to increase sodium concentrations
    • 750-1000ml per day
  • Correct slowly to prevent osmotic demyelination syndrome & cerebral oedema → <10mmol/L in 24hrs.
  • Vasopressin receptor antagonists → tolvaptan
    • Block ADH receptors
    • Can cause a rapid rise in sodium, and are initiated by an endocrinologist with close monitoring.

6th Year (18 decks)

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