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Year 4 Med > CCT > Flashcards

CCT Flashcards

1
Q

What are the 4P’s of personalised medicine?

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

How much adrenaline should be given in anaphylaxis?

A

500mcg IM 1:1000 units

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3
Q
  • 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?

A

Carpal tunnel

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4
Q

Carpal Tunnel causes wasting of what?

A

THENAR emminence

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5
Q

Examination signs of carpal tunnel syndrome?

A

Thenar wasting
Weakness of thumb abduction
+ Phalens and Tinnels

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6
Q

Carpal tunnel causes:

A
  • idiopathic
  • pregnancy
  • oedema e.g. heart failure
  • lunate fracture
  • rheumatoid arthritis
  • Acromegaly - bilateral cause
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7
Q

Management of carpal tunnel?

A

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

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8
Q

What are the causes of hypovolaemic hyponatraemia?

A

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

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9
Q

What are the causes of euvolaemic hyponatraemia?

A

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

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10
Q

What are the causes of hypervolaemic hyponatraemia?

A

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

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11
Q

What tests are required to confirm/exclude SIADH?

A

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.

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12
Q

What is the management for hypovolaemic hyponatraemia?

A

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

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13
Q

What is the management for euvolaemic hyponatraemia due to SIADH?

A

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

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14
Q

What is the management for euvolaemic hyponatraemia due to hypothyroidism?

A

The management for euvolaemic hyponatraemia due to hypothyroidism is levothyroxine.

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15
Q

What is the management for hypervolaemic hyponatraemia?

A

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

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16
Q

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

A

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

17
Q

SIADH is what type of hyponatraemia?

A

Euvolaemic

18
Q

Management of SIADH?

A

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
19
Q

ADH aka

A

vasopressin

20
Q

What does ADH do?

A

ADH stimulates water reabsorption from thecollecting ductsin the kidneys.

21
Q

Common cause of SIADH?

A

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

22
Q

Urine findings in SIADH

A

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

23
Q

Symptoms of hyponatraemia

A
  • Headache
  • Fatigue
  • Muscle aches and cramps
  • Confusion
  • Severe hyponatraemiacan cause seizures and reduced consciousness
24
Q

Read short list of SIADH causes:

A
  • 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
25
Q

How are SIADH investigations approached?

A

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 showeuvolaemia. U+Es will show a hyponatraemia. Urine sodium and osmolality will be high.

Other causes of hyponatraemia need to be excluded:

  • Negativeshort synacthen testto excludeadrenal insufficiency
  • No history of diuretic use
  • No diarrhoea, vomiting, burns, fistula or excessive sweating
  • No excessive water intake
  • Nochronic kidney diseaseoracute kidney injury
26
Q

What type of cancer is associated with SIADH?

A
  • Small cell lung cancer

Also:
- Pancreatic cancer
- Prostate cancer
- Thymoma
- Lymphoma

27
Q

What is CPM?

A

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

28
Q

Read summary of symptoms and management of CPM

A

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 asspastic quadriparesis,pseudobulbar palsy andcognitive and behavioural changes. There is a significant risk of death.

Preventionis essential as treatment is onlysupportiveonceCPMoccurs. A proportion of patients make a clinical improvement but most are left with some neurological deficit.

29
Q

What are the two types of diabetes insipidus?

A
  • A lack ofantidiuretic hormone(cranial diabetes insipidus)
  • A lack ofresponsetoantidiuretic hormone(nephrogenic diabetes insipidus).
30
Q

Function of ADH and where it acts!

A

ADH stimulates water reabsorption from thecollecting ductsin the kidneys.

31
Q

What is primary polydipsia?

A

Primary polydipsiais when the patient has a normally functioning ADH system but drinks excessive amounts of water, leading to excessive urine production (polyuria). This is notdiabetes insipidus.

32
Q

Explain the presentation of diabetes insipidus:

A

With diabetes insipidus, the kidneys are unable to reabsorb water and concentrate the urine, leading to:

  • Polyuria(excessive amounts of urine)
  • Polydipsia(excessive thirst)
33
Q

Read common causes of nephrogenic diabetes insipidus:

A

Nephrogenic diabetes insipidusis when the collecting ducts of the kidneysdo not respondtoADH. It can beidiopathic, without a clear cause, or it can be caused by:

  • Medications, particularlylithium(used inbipolar affective disorder)
  • Genetic mutationsin theADH receptor gene(X-linked recessive inheritance)
  • Hypercalcaemia(high calcium)
  • Hypokalaemia(low potassium)
  • Kidney diseases(e.g., polycystic kidney disease)
34
Q

Explain the production of ADH:

A

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

35
Q

CF treatment for allergic bronchopulmonary aspergillosis

A

Oral glucocorticoids are the treatment of choice for allergic bronchopulmonary aspergillosis

Year 4 Med (28 decks)

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