Endocrine

Question 1

A -What is the clinical range for Hypercalcaemia?

B- Range for
Mild ?
Moderate?
Severe?

Answer 1

Greater than 2.6mmol/l / 10.5mg/dl [Serum corrected calcium]

B - Mild (2.6-3)
Moderate (3-3.4)
Severe (3.4+)

Question 2

Name Causes for Hypercalcemia

B- 2 Most Common?

Answer 2

Primary Hyperthyroidism [MC]
Malignancy [MC] [Bone destruction]
Drugs - Vit D toxicity, Thiazide Diuretics
Granulomatous diseases- TB, Sarcodoisis
Renal disease,
Non-parathyroid endocrine diseases - Acromegaly, pheochromocytoma, Adrenal insufficiency
Familial hypocalciuric hypercalcaemia (Increase ca+ needed to regulate and inhibit PTH)
Immobility
Paget’s Disease

Question 3

Clinical Features of Hypercalcemia?

Answer 3

Bone pain, 
Osteoporosis, 
Fatigue, 
Confusion, 
Memory problems, 
Abdo Pain 
Constipation
N+V
Depression
Renal impairment/Colic

Symptoms can be non-specific.
Bones, stones, groans and moans (Bone pain, renal stones, abdo pain, psych symptoms)

Question 4

ECG Features of Hypercalcemia?

Answer 4

Short ST segment + QT segment
J waves (Osborn waves)
Wide T waves

Question 5

What does ionised calcium tell you?

Abnormal Level?

Answer 5

Above 1.3
>1.7 Severe
Less variation in the value - biologically active form

Guides you about the control of the parathyroid glands. When IC is low PTH is released ++

Question 6

Investigations for hypercalcaemia?

Answer 6

Bloods - Ca+, PTH, eGFR, Creatinine, Urea, Vit D, glucose, UE, FBC (haematocrit)

Urine- Excess CA + phosphate (Also polyuria+dypsia due to Neph DI)

CXR - ?Sarcoidosis
Ultrasound - Kidney/Chronic renal failure (Ca+ can precipitate in soft tissues, impairing function, possible stones also)

EXTRA - Serum Ca is influenced by serum albumin levels so important to check if these are abnormal also.

Question 7

Emergency Hypercalcaemia

TREATMENT Plan

Answer 7

1. IV 0.9% Nacl to dilute ca levels
2. Loop diuretic to increase ca excretion
3. Bisphosphonates to inhibit osteoclast activity (zolendronic acid)
4. Calcitonin to inhibit osteoclasts + enhance urinary ca excretion
5. Mobilise

Question 8

Where is calcium intake absorbed?

What is the distribution of Ca Intracellular/Extra?

Answer 8

Duodenum (Around 20%) - Rest is excreted by faeces.

98% Intracellular (Bones), 1% Extracellular (More than half is bound to albumin, rest is ionised).

Question 9

Lab Values for Hyper parathyroidism
A - Primary
B - Secondary
C - Tertiary

Answer 9

A - Ca (U), PTH (U/N), Vit D (U), Phosphate (D)
B - Ca (N/D), PTH (U), Vit D (D), Phosphate (U/D)
C - Ca (U), PTH (UUU), Vit D (D), Phosphate (U)

Question 10

What is the clinical picture for someone with primary aldosteronism?

Answer 10

AKA Conn's Syndrome (Adrenal adenoma cause) 
Muscle weakness,  Paraesthesia 
Tiredness, 
Headaches, 
Mood disturbances
Polyuria + Nocturia

• Generally unremarkable examinations, High BPs
• Bloods - Typical picture of High sodium, low potassium

Question 11

Define Primary aldosteronism?

Answer 11

Excess release of aldosterone from the adrenal cortex. (ZG)

Mineralocorticoid.
Common cause for secondary HTN (Unexplained HTN in young Pt)
Suppression of renin release (High ARR)

Question 12

3 Main Causes of Primary Aldosteronism?

Answer 12

Adrenal Adenoma
Idiopathic adrenal hyperplasia (Bilateral) [MOST COM-70%]
Others - Familial hyperaldosteronism, Adrenal carcinoma

Question 13

How and where does Aldosterone act?

Answer 13

Acts on renal collecting ducts increasing water and sodium retention (Na, H20. Cl) and excretes potassium in distal tubuals.

Released as part of the RAAS system
Angiotensinogen (Renin) - Ang 1 - (ACE) Ang 2- Aldosterone release.

Question 14

Investigations for someone with Primary aldosteronism?

Answer 14

UE - Na (U) , K (D)
ECG - Hypokalaemia (Widened PR-Int, Flattened T wave or inverted, ST depression, U-Waves)
ABG/VBG - Metobolic alkolosis?
Aldosterone:Renin Ratio(ARR) - High due increased levels of aldosterone suppresses renin (High Aldo: Low Renin)
Serum Aldosterone levels (>20ng/dl)

Extra tests for dianostics
Saline suppression test - No drop (Usually would see a drop in Aldosterone)
Captopril challenge test
Oral sodium loading test

Imaging/Venous sampling - Adrenal CT

Question 15

Management of Primary aldosteronism?

What are the main side effects of medical management?

Answer 15

Surgical
Resection/Adrenalectomy (Adrenal adenoma)
+ Spironolactone

Medical - Aldosterone antagonists (Spironolactone, Eplerenone)
ENaC Inhibitor - Amiloride (K+ sparring diuretic - Spiro sub)
Usually always given in cases of Idiopathic adrenal hyperplasia

Spiro S/E - Gynaecomastia, Rashes, Nausea

Question 16

What cells release renin from the kidneys?

Answer 16

Granular cells (Juxtaglomerular cells) of the juxtaglomerular apparatus.

Renin release is triggered by decreased renal perfusion, sympathetic stimulation, low sodium by sensed macula densa cells.

Question 17

Give some examples of secondary aldosteronism?

Answer 17

High Renin and High Aldosterone (ARR)

Renal vascular disease (e.g. fibromuscular dysplasia - narrowing of renal arteries)
Heart Failure
Nephrotic syndrome
Renin Producing Tumours

Question 18

What triggers should indicated looking for secondary cause of hypertension?

Answer 18

1. HTN and hypokalaemia (spontaneous or diuretic-induced)
2. Severe hypertension (sys > 150, dia > 100)
3. HTN resistant to treatment

4+ - HTN W/ Adrenal incidentaloma
Sleep apnea
Family history of early onset hypertension
Family history of early onset CVA
Primary aldosteronism affecting all 1st degree relatives with hypertension