ChemPath: Clinical Chemistry CPC

Question 1

Describe the effect of hypokalaemia on the myocardium.

Answer 1

Increases the myocardial irritability.

Question 2

Describe the cardiac consequences of plasma potassium being too high or too low.

Answer 2

• Too low - ventricular fibrillation (unstable membranes)
• Too high - asystole (ultimate stable rhythm)

K+ affects heart, Ca2+ muscles

Question 3

What is the difference between a Colles’ fracture and a Smith’s fracture?

Answer 3

• Colles’ - fracture caused by falling on an outstretched hand. The radial head will be displaced backwards (away from the palm).
• Smith’s - fracture caused by falling on a flexed wrist. The radial head will be displaced forwards (towards the palm)

Question 4

What is a Pott’s fracture?

Answer 4

Ankle fracture involving the tibia and fibula

Question 5

What would you expect to see on the urine dipstick of someone with subacute bacterial endocarditis?

Answer 5

Microscopic haematuria

Question 6

What is the physiological role of PTHrP?

Answer 6

• Our genome encodes a gene for PTHrP
• This is important in foetal life because it allows us to steal calcium from our mother to help form our skeleton

NOTE: PTHrP is also produced by the lactacting breast

NOTE: PTHrP stimulates cancer cells to invade bone

Question 7

Name and describe an eye sign of hypercalcaemia.

Answer 7

• Band keratopathy - calcium deposition across the front of the eye
• It is a feature of chronic hypercalcaemia (i.e. it will not be caused by hypercalcaemia of malignancy)

Only in longstanding unstreated primary hyperparathyroidism (cancer causing this would’ve killed you by now)

Question 8

What is a key difference between calcium stones and urate stones?

Answer 8

Calcium stones are radio-opaque

Urate stones are radiolucent

Majority are Ca2+

Question 9

List some complications of hypercalcaemia.

Answer 9

• Renal stones
• Pancreatitis
• Peptic ulcer disease
• Skeletal changes (osteitis fibrosa cystica - bone cysts) - only in longstanding low Ca2+

Symptoms - Stones, bones, abdominal moans, psychic groans

Question 10

List some risk factors for hypercalcaemia.

Answer 10

Family history

Dehydration

Hyperparathyroidism

Question 11

Which bacterium has a predilection to infect urinary tract stones?

Answer 11

Proteus mirabilis

Question 12

What are the main investigations used for urinary tract stones?

Answer 12

• CT-KUB
• Stone analysis
• Urine and serum biochemistry

Question 13

Most important test to distinguish between causes of hypercalcemia

Answer 13

PTH

If high Ca2+ with a non-parathyroid cause –> PTH should be 0 (i.e. completely suppressed)

NOTE: PTH could still be technically be within the normal range but in the context of a high Ca2+, PTH HAS TO BE suppressed fo it be a non-parathyroid cause e.g. cancer, sarcoidosis

Question 14

What are some management options for urinary tract stones?

Answer 14

• Lithotripsy
• Cystoscopy
• Lithotomy

Most stones pass themselves –> painful

Question 15

How can urinary tract stones be prevented?

Answer 15

• Drink more water
• Treat hypercalciuria (thiazides)
• Treat hypercalcaemia

NOTE: loop diuretics increase urine calcium

Question 16

At what point would you use emergency management of hypercalcaemia?

Answer 16

When serum calcium > 3 mmol/L or very unwell (e.g. dehydrated, confused, drowsy, seizures)

Question 17

Outline the emergency management of hypercalcaemia.

Answer 17

• IV access
• Insert catheter - to measure urine ouput
• 3-6 L 0.9% saline over 24 hours
• 1st litre should be given quickly (over 1 hour) to correct dehydration
• Elderly patients should also be given furosemide (to prevent pulmonary oedema)

Question 18

How are bisphosphonates used in managing hypercalcemia

Answer 18

Only used for hypercalcemia due to malignancy

• • Pamidronate (IV)
• Good at treating bone pain but takes at least 1 week to start working and gets incorporated into bone for a very long time

In primary hyperparathyroid –> bisphophonates will work (i.e. prevent bone resorption) –> but when adenoma is removed —> Ca2+ will not be regulated because the new bone created cannot be resorbed

Question 19

In which group of patients would you used dextrose rather than saline?

Answer 19

Liver failure - they have a tendency to retain salt

Question 20

Outline the treatment of non-emergency hypercalcaemia.

Answer 20

• Keep well hydrated
• Avoid thiazides (they reduce hypercalciuria but they increase plasma calcium concentration)
• Surgery –> parathyroid adnectomy

Question 21

What is minimally invasive parathyroidectomy?

Answer 21

• A technetium sesta MIBI scan shows a hyperactive parathyroid
• An USS is also performed and if the results of the sesta MIBI and USS are concordant, the whole neck does not need to be opened
• If they are not concordant, the surgeon will need to view all four glands and take out the largest one

Question 22

What feature may you see on an X-ray of the hands in a patient with primary hyperparathyroidism?

Answer 22

Cystic changes in the radial aspect

Question 23

What is a characteristic histological feature of long-standing undiagnosed hyperparathyroidism?

Answer 23

Brown tumours - they are multinucleated giant cells in the bone. The giant cells are activated osteoclasts.

Question 24

What is the mainstay of treatment of sarcoidosis?

Answer 24

Steroids

Question 25

How does sarcoidosis cause hypercalcemia

Answer 25

Macrophages in lung –> secrete 1-alpha hydroxylase

(Normally only produced by kidneys)

Rate-limiting step in producing calcitriol (active vitamin D)

Increased Ca2+ reabsorption in gut + kidney

Question 26

What is the histological hallmark of sarcoidosis?

Answer 26

Non-caseating granulomas

(present systemically)

Question 27

How does panicking affect serum Ca2+

Answer 27

hyperventilation –> alkalosis –> Ca2+ more adherent to albumin –> free Ca2+ falls –> hypocalcemia

Can exacerbate hypocalcemia if patient has carpopedal spams then panics

CATs go numb –> carpopedal spasm