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2a mid tier > Endo > Flashcards

Endo Flashcards

1
Q

What is the aetiology of secondary adrenal insufficiency?

A
  • Iatrogenic due to long-term steroid therapy

- Hypothalamic-pituitary disease resulting in decreased ACTH production

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2
Q

What is the pathophysiology secondary adrenal insufficiency?

A
  • Reduction in ACTH release causing decreased cortisol
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3
Q

What is the presentation of secondary adrenal insufficiency?

A
  • Vague symptoms of feeling unwell

- No skin hyperpigmentation

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4
Q

How many secondary adrenal insufficiency investigated?

A
  • ACTH level are low

- Mineralocorticoid production intact

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5
Q

How is secondary adrenal insufficiency managed?

A
  • Oral hydrocortisone

- Should recover if long-term steroids are slowly weaned off

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6
Q

What is the aetiology of hyperkalaemia?

A
  • Acute self-limiting occurs normally after vigorous exercise
  • Decreased exertion – AKI, drugs (ACEi, NSAID, potassium-sparing diuretics)
  • Redistribution (intra to extracellular) – diabetic ketoacidosis, metabolic acidosis, tissue necrosis
  • Increased load (potassium chloride, transfusion of stored blood)
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7
Q

What is the pathophysiology of hyperkalaemia?

A
  • When K+ levels in the blood rise, it reduces the difference in electrical potential between cardiac myocytes and the outside of cells
  • Decreased action potential threshold  abnormal action potentials and abnormal heart rhythms
  • Can result in VF and cardiac arrest
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8
Q

What is the presentation of hyperkalaemia?

A
  • Asymptomatic until K+ is high enough to cause cardiac arrest
  • Fast irregular pulse
  • Chest pain
  • Weakness
  • Light-headedness
  • Muscle weakness and fatigue
  • May be associated with metabolic acidosis therefore Kussmaul’s respiration (low, deep, sighing inspiration and expiration)
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9
Q

What are the differential diagnoses of hyperkalaemia?

A
  • Haemolysis
  • Contamination with K+ EDTA anticoagulant
  • Thrombocythaemia
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10
Q

How is hyperkalaemia investigated?

A
  • Serum K+ > 5.5mmol/L
  • Serum K+ > 6.5mmol/L = medical emergency
  • Progressive ECG abnormalities (tall, tented T waves, small P waves, wide QRS complex)
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11
Q

How was hyperkalaemia managed? (non-urgent and urgent management)

A

NON-URGENT – treat underlying cause, review meds (esp ACEi, NSAIDs), dietary K+ restriction, can give polystyrene sulfonate resin

URGENT – IV 10ml 10% calcium gluconate, soluble insulin, glucose, IV salbutamol

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12
Q

What is the aetiology of hypokalaemia?

A
  • Increased renal excretion (thiazide/loop diuretics, increased aldosterone secretion, exogenous mineralocorticoids, renal disease)
  • Reduced dietary K+ intake
  • Redistribution to cells (beta-agonists, salbutamol, acute MI)
  • GI losses (vomiting, severe diarrhoea, laxative abuse)
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13
Q

What is the presentation of hypokalaemia?

A
  • Usually asymptomatic
  • Muscle weakness
  • Cramps
  • Hypotonia
  • Hyporeflexia
  • Tetany (intermittent muscle spasms/ cramps)
  • Palpitations
  • Light-headedness
  • Arrhythmias
  • Constipation
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14
Q

How is hypokalaemia investigated?

A
  • Serum K+ < 3.5mmol/L
  • Serum K+ < 2.5mmol/L = medical emergency
  • ECG (flat/inverted T waves, increased QT, visible U waves, ST depression)
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15
Q

How is hypokalaemia managed? (initial management as well as management for mild and severe cases)

A
  • Identify and treat and underlying cause
  • Acute can self-resolve usually after stopping diuretics/ laxatives
  • MILD – oral K+ supplements (+ K+ sparing diuretic if on thiazide diuretic)
  • SEVERE – IV K+ cautiously
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16
Q

What is the aetiology of syndrome of inappropriate secretion of ADH?

A
  • Tumours
  • Pulmonary lesions
  • Alcohol withdrawal
  • Drugs (e.g. carbamazepine)
  • CNS causes (meningitis, tumours, head injury, SLE)
17
Q

What is the pathophysiology of syndrome of inappropriate secretion of ADH?

A

Continuous secretion of ADH despite plasma being very dilute, leading to retention of water (increased aquaporin-2 channels) and excess blood volume, therefore hyponatraemia

18
Q

What is the presentation of syndrome of inappropriate secretion of ADH?

A
  • Symptoms as a result of hyponatraemia
  • Varied and generic
  • Anorexia/ nausea and malaise
  • Weakness and aches
  • Reduced GCS, confusion and drowsiness
  • Fits and coma (later)
19
Q

How is syndrome of inappropriate secretion of ADH investigated?

A
  • Serum: low sodium, low plasma osmolality
  • Urine: high sodium, high osmolality
  • Normal renal, adrenal and thyroid function
20
Q

How is syndrome inappropriate secretion of ADH managed?

A
  • Treat underlying cause
  • Restrict fluid intake
  • Hypertonic saline is very symptomatic
  • Oral demeclocycline
  • Vasopressin antagonist (e.g. oral tolvaptan)
  • Salt and loop diuretic (e.g. oral furosemide)
21
Q

What is the aetiology of cranial diabetes insipidus?

A

idiopathic, congenital defects in ASH gene, hypothalamus disease, tumour, trauma, infiltrative disease

22
Q

What is the aetiology of nephrogenic diabetes insipidus?

A

hypokalaemia, hypocalcaemia, drugs, renal tubular acidosis, sickle cell disease, familial mutation of ASH receptor

23
Q

What is the general pathophysiology of diabetes insipidus?

A

Reduced ADH secretion or impaired response to ADH results in significant water losses and therefore dilute urine

24
Q

What is the main risk factor of diabetes insipidus?

A

Family history

25
Q

What is the presentation of diabetes insipidus?

A
  • Polyuria (15L in 24h)
  • Compensatory polydipsia (thirsty)
  • No glycosuria
  • Hypernatraemia due to more water loss than sodium loss (lethargy, thirst, weakness, irritability, confusion, coma, fits)
  • Can lead to dehydration
26
Q

What is the differential diagnosis of diabetes insipidus?

A
  • diabetes mellitus
  • hypokalaemia
  • hypercalcaemia
27
Q

How is diabetes insipidus investigated?

A
  • Urine volume measured to confirm polyuria
  • Check blood glucose to exclude DM
  • Water deprivation test
  • IM desmopressin to determine nephrogenic or cranial (concentrated urine in cranial)
  • MRI hypothalamus
28
Q

How is cranial diabetes insipidus managed?

A
  • Find the cause

- Synthetic ADH analogue e.g. oral desmopressin

29
Q

How is nephrogenic diabetes insipidus managed?

A
  • Treat cause (usually renal disease)
  • Thiazide diuretics (oral Bendroflumethiazide)
  • NSAIDS (ibuprofen)
30
Q

What is the aetiology of Addison’s disease?

A
  • Autoimmune adrenalitis
  • TB
  • Adrenal metastases
  • Long-term steroid use
  • Opportunistic infections in HIV
  • Adrenal haemorrhage
31
Q

What is the pathophysiology of Addison’s disease?

A
  • Destruction of entire adrenal cortex resulting in aldosterone, cortisol and androgen deficiency
  • Reduced cortisol leads to increased CRH and ACTH
32
Q

What is the presentation of Addison’s disease?

A
  • Lethargy, depression, low mood, low self-esteem
  • Anorexia and weight loss
  • Vitiligo
  • Nausea and vomiting
  • Tanned skin
  • Pigmentation of skin
  • Diarrhoea, constipation, abdominal pain
  • Impotence/ amenorrhea
  • Postural hypotension
33
Q

How’s Addison’s disease investigated?

A
  • Blood tests – hyperkalaemia hyponatraemia, , hypoglycaemia, hypoaldosteronism, low cortisol
  • Short ACTH stimulation test
  • Adrenal antibodies
  • AXR/ CXR if history of TB
34
Q

How was Addison’s disease managed?

A
  • If seriously ill, IV hydrocortisone, IV 0.9% saline, glucose infusion
  • Replace steroids with glucocorticoids or mineralocorticoids
  • IV hydrocortisone if in adrenal crisis ( = nausea, vomiting, abdominal pain, muscle cramps, confusion)

2a mid tier (10 decks)

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