CCT

Question 1

What are the 4P’s of personalised medicine?

Answer 1

1. Prediction and prevention of disease
2. Precise diagnosis
3. Targetted and personalised preventions
4. Participation of patients

Question 2

How much adrenaline should be given in anaphylaxis?

Answer 2

500mcg IM 1:1000 units

Question 3

• pain/pins and needles in thumb, index, middle finger
• unusually the symptoms may ‘ascend’ proximally
• patient shakes his hand to obtain relief, classically at night

= typical hx of what?

Answer 3

Carpal tunnel

Question 4

Carpal Tunnel causes wasting of what?

Answer 4

THENAR emminence

Question 5

Examination signs of carpal tunnel syndrome?

Answer 5

Thenar wasting
Weakness of thumb abduction
+ Phalens and Tinnels

Question 6

Carpal tunnel causes:

Answer 6

• idiopathic
• pregnancy
• oedema e.g. heart failure
• lunate fracture
• rheumatoid arthritis
• Acromegaly - bilateral cause

Question 7

Management of carpal tunnel?

Answer 7

Conservative 1st for moderate
Wrist splints for transient e.g pregnancy
Corticosteroid injections
Surgery - division of flexor retinaculum

Question 8

What are the causes of hypovolaemic hyponatraemia?

Answer 8

The causes of hypovolaemic hyponatraemia include burns, sweating, diarrhoea, vomiting, fistulae, and Addison’s disease.

Question 9

What are the causes of euvolaemic hyponatraemia?

Answer 9

The causes of euvolaemic hyponatraemia include the syndrome of inappropriate ADH release (SIADH) and hypothyroidism.

Question 10

What are the causes of hypervolaemic hyponatraemia?

Answer 10

The causes of hypervolaemic hyponatraemia include renal failure, heart failure, liver failure, and nephrotic syndrome.

Question 11

What tests are required to confirm/exclude SIADH?

Answer 11

The tests required to confirm/exclude SIADH include urea and electrolytes (while not on diuretics), urine and plasma paired osmolalities (while not on diuretics), urine sodium (while not on diuretics), urine dip, TSH, and cortisol.

Question 12

What is the management for hypovolaemic hyponatraemia?

Answer 12

The management for hypovolaemic hyponatraemia includes IV normal saline and treating the underlying cause.

Question 13

What is the management for euvolaemic hyponatraemia due to SIADH?

Answer 13

The management for euvolaemic hyponatraemia due to SIADH includes fluid restriction, ADH receptor antagonists, oral sodium and furosemide.

Question 14

What is the management for euvolaemic hyponatraemia due to hypothyroidism?

Answer 14

The management for euvolaemic hyponatraemia due to hypothyroidism is levothyroxine.

Question 15

What is the management for hypervolaemic hyponatraemia?

Answer 15

The management for hypervolaemic hyponatraemia includes fluid restriction and treating the underlying cause.

Question 16

What is the risk when correcting sodium faster than 12mmol/L/day?

Answer 16

Correcting sodium faster than 12mmol/L/day leads to a significant risk of central pontine myelinosis because of fluid shifts.

Question 17

SIADH is what type of hyponatraemia?

Answer 17

Euvolaemic

Question 18

Management of SIADH?

Answer 18

Management revolves around offloading this excess water:

1. Fluid restriction (up to 750ml/day) and treat underlying cause
2. ADH antagonists (e.g. tolvaptan, deomeclocycline)
3. Oral sodium and furosemide

Question 19

ADH aka

Answer 19

vasopressin

Question 20

What does ADH do?

Answer 20

ADH stimulates water reabsorption from thecollecting ductsin the kidneys.

Question 21

Common cause of SIADH?

Answer 21

Posterior pituitarysecreting too much ADH or the ADH may be coming from somewhere else, for example, asmall cell lung cancer.

Question 22

Urine findings in SIADH

Answer 22

The urine becomes more concentrated as less water is excreted by the kidneys therefore patients with SIADH have a “highurine osmolality” and “highurine sodium”.

Question 23

Symptoms of hyponatraemia

Answer 23

• Headache
• Fatigue
• Muscle aches and cramps
• Confusion
• Severe hyponatraemiacan cause seizures and reduced consciousness

Question 24

Read short list of SIADH causes:

Answer 24

• Post-operative from major surgery
• Infection, particularly atypical pneumonia and lung abscesses
• Head injury
• Medications (thiazide diuretics, carbamazepine, vincristine, cyclophosphamide, antipsychotics, SSRIs, NSAIDSs,)
• Malignancy, particularly small cell lung cancer
• Meningitis

Question 25

How are SIADH investigations approached?

Answer 25

In a way, SIADH is a diagnosis of exclusion as we do not have a reliable test to directly measure ADH activity. Clinical examination will show euvolaemia. U+Es will show a hyponatraemia. Urine sodium and osmolality will be high. Other causes of hyponatraemia need to be excluded: - Negative short synacthen test to exclude adrenal insufficiency - No history of diuretic use - No diarrhoea, vomiting, burns, fistula or excessive sweating - No excessive water intake - No chronic kidney disease or acute kidney injury

Question 26

What type of cancer is associated with SIADH?

Answer 26

- Small cell lung cancer Also: - Pancreatic cancer - Prostate cancer - Thymoma - Lymphoma

Question 27

What is CPM?

Answer 27

Central pontine myelinolysis (CPM) is also (and more accurately) known as “osmotic demyelination syndrome”. It is usually a complication of long term severe hyponatraemia (< 120 mmols/l) being treated too quickly (> 10 mmol/l increase over 24 hours).

Question 28

Read summary of symptoms and management of CPM

Answer 28

First phase: this is due to the electrolyte imbalance and the patient presents as encephalopathic and confused. They may have a headache or nausea and vomiting. These symptoms often resolve prior to the onset of the second phase. Second phase: this is due to the demyelination of the neurones, particularly in the pons. This occurs a few days after the rapid correction of sodium. This may present as spastic quadriparesis, pseudobulbar palsy and cognitive and behavioural changes. There is a significant risk of death. Prevention is essential as treatment is only supportive once CPM occurs. A proportion of patients make a clinical improvement but most are left with some neurological deficit.

Question 29

What are the two types of diabetes insipidus?

Answer 29

- A lack of antidiuretic hormone (cranial diabetes insipidus) - A lack of response to antidiuretic hormone (nephrogenic diabetes insipidus).

Question 30

Function of ADH and where it acts!

Answer 30

ADH stimulates water reabsorption from the collecting ducts in the kidneys.

Question 31

What is primary polydipsia?

Answer 31

Primary polydipsia is when the patient has a normally functioning ADH system but drinks excessive amounts of water, leading to excessive urine production (polyuria). This is not diabetes insipidus.

Question 32

Explain the presentation of diabetes insipidus:

Answer 32

With diabetes insipidus, the kidneys are unable to reabsorb water and concentrate the urine, leading to: - Polyuria (excessive amounts of urine) - Polydipsia (excessive thirst)

Question 33

Read common causes of nephrogenic diabetes insipidus:

Answer 33

Nephrogenic diabetes insipidus is when the collecting ducts of the kidneys do not respond to ADH. It can be idiopathic, without a clear cause, or it can be caused by: - Medications, particularly lithium (used in bipolar affective disorder) - Genetic mutations in the ADH receptor gene (X-linked recessive inheritance) - Hypercalcaemia (high calcium) - Hypokalaemia (low potassium) - Kidney diseases (e.g., polycystic kidney disease)

Question 34

Explain the production of ADH:

Answer 34

Made in the hypothalamus. Then secreted by the posterior pituitary.

Question 35

CF treatment for allergic bronchopulmonary aspergillosis

Answer 35

Oral glucocorticoids are the treatment of choice for allergic bronchopulmonary aspergillosis