Friday, October 31, 2008

Koebner phenomenon


I remember this sign very well since I was a medical student. When I was sitting for the MRCP exam, I was told that most candidates will get psoriasis as a case in Station 5. However, not all will get a 4/4. To get 4/4 you need to shine among your other colleagues who are taking the exam at the same time.
So, remember that when you see a patient with psoriasis, always look for this sign which will be at any place with a trauma or scar.
The Koebner phenomenon, also called the isomorphic response, refers to the appearance of lesions along a site of injury.
The next question is what lesions causes Koebner phenomeonon. You need to memorise these
1) psoriasis
2) lichen planus
3) warts
4) molluscum contagiosum
5) vitiligo
There are a few more which are not so common

Monday, October 20, 2008

MRCP Part 2a Written


This is a very good book for Part 2a Written. I won't be using it anymore. So, for those who are interested in this book, you can write to me at thienthienlim@gmail.com. I hope the person who is buying it would be sitting for the Part 2a Written as it is very useful for that part. Btw, you will only find this book out of Malaysia and I actually bought it in Singapore.

Sunday, October 12, 2008

Necrobiosis Lipoidica Diabeticorum



This patient has a sharply demarcated oval plaque over the shin. The lesion has shiny atrophic surface and a waxy yellow centre and brownish-red edges.
The diagnosis is necrobiosis lipoidica diabeticorum.

It is associated with diabetes
Differential diagnosis include
Granuloma annulare
Nodular vasculitis
Localised scleroderma/sarcoidosis

Treatment includes steroids(topical or local injection), severe cases can be treated with excision and skin grafting.

Other skin lesions in diabetics :
Diabetic dermopathy
Infective(Boils, candidiasis)
Foot/leg ulcers
Vitiligo
Fat atrophy/hypertrophy
Xanthomas
Acanthosis nigricans
Peripheral anhidrosis
Chlorpropamide alcohol flush

Hypocalcaemia

video

I am sure there are many medical students who have read about this over and over again but may not have seen it. I take this opportunity to share one of my patients who has hypocalcaemia secondary to Albright Hereditary Osteodystrophy(very very rare cause) and in paeds. Actually he is followed up in paeds and was incidentally admitted to my ward because of low calcium. I elicited Chvostek's sign in him and immediately treated his hypocalcaemia

Symptoms

Symptoms generally correlate with the magnitude and rapidity of the fall in serum calcium: mild hypocalcaemia (2.00-2.12 mmol/l) can be asymptomatic whereas acute symptoms of neuromuscular irritability can develop in the more severe form(<1.9>

  • Paraesthesia (usually fingers, toes and around mouth)
  • Tetany
  • Carpopedal spasm (wrist flexion and fingers drawn together)
  • Muscle cramps

Signs

  • Chvostek's sign (tapping over facial nerve causes facial muscles to twitch) Note: this may be present in some normocalcaemic individuals. (refer video)
  • Trousseau's sign (carpopedal spasm after inflating a BP cuff on the upper arm) (refer video)
  • Seizures
  • Prolonged QT interval which may progress to VF or heart block
  • Laryngospasm
  • Bronchospasm

With prolonged hypocalcaemia

  • Sub-capsular cataract
  • Papilloedema
  • Abnormal teeth
  • Ectopic calcification (for example, in basal ganglia may cause extrapyramidal neurological symptoms)
  • Dementia and confusion
Aetiology

Causes of true hypocalcaemia fall into two main classes:

With low PTH levels (hypoparathyroidism)

  • Parathyroid agenesis- alone or along with other abnormalities e.g. Di George syndrome
  • Parathyroid destruction- due to surgery, radiotherapy, infiltration by metastases or systemic disease
  • Autoimmune
  • Reduced parathyroid secretion - due to gene defects, hypomagnesaemia, neonatal hypocalcaemia (may be due to maternal hypercalcaemia), hungry bone disease (after parathyroidectomy), mutation in calcium-sensing receptor.

With high PTH levels (secondary hyperparathyroidism)

  • Vitamin D deficiency- due to nutritional lack, malabsorption, liver disease, receptor defects
  • Vitamin D resistance (rickets)- renal tubular dysfunction (Fanconi's syndrome) or receptor defect
  • PTH resistance - pseudohypoparathyroidism, hypomagnesaemia

Important other causes

  • Hyperventilation
  • Drugs- calcium chelators (citrate in blood transfusion); bone resorption inhibitors (bisphosphonates, calcitonin, plicamycin); drugs affecting vitamin D (phenytoin, ketoconazole), foscarnet
  • Acute pancreatitis
  • Acute rhabdomyolysis - usually in relation to crush injuries
  • Malignancy - tumour lysis(following chemotherapy) or osteoblastic metastases (most common in prostate and breast cancers)
  • Toxic shock syndrome

Commonest causes are hypoparathyroidism (frequently following surgery), vitamin D deficiency or abnormal metabolism, renal failure, hypomagnesaemia.
Hypocalcemia is extremely common in patients in hospital and correlates with the severity of their illness.3

Differential diagnosis

Serum phosphate Serum PTH Serum ALP Other
Renal failure Raised Raised Raised Raised creatinine
Hypoparathyroidism Raised Low/undetectable
Normal Vitamin D metabolites
Pseudohypoparathyroidism Raised Raised

Vitamin D deficiency or malabsorption Low Raised Raised Raised 25 (OH)D3 levels
  • Hypoalbuminaemia - correct for albumin
  • Consider drug therapy, malignancy, acute pancreatitis and rhabdomyolysis
Investigations
  • Is the patient really hypocalcaemic? (Ideally take fasting blood specimens, uncuffed -remove tourniquet after needle in vein, but before taking blood sample). Ensure use an adjusted calcium value
  • Exclude renal failure (check U&Es), acute pancreatitis (check amylase), rhabdomyloysis (check serum CK)
  • Estimate serum magnesium
  • Estimate serum PTH
  • Evaluate Vitamin D metabolism

Always assess the patient clinically. Patients vary: some may be symptomatic within the normal reference range since there are narrow individual ranges within the normal reference range.

Management

Acute hypocalcaemia

  • Treat where symptomatic (seizures, tetany) or at high risk of complications with a serum calcium <1.90>
  • Give calcium gluconate IV 10 ml (2.25 mmol) of calcium gluconate 10% by slow injection. Repeat as necessary or follow with infusion of calcium gluconate 10% infusion - 40 ml (9 mmol)/24 hours.
  • Monitor serum calcium concentrations regularly to judge response.
  • If likely to be persistent, give vitamin D by mouth.
  • If hypomagnesemic, necessary to correct magnesium level before the hypocalcaemia will resolve.
Extracted from http://www.patient.co.uk/showdoc/40001110/

Saturday, October 4, 2008

Bitemporal hemianopia


When I was in UK, I attended a PACES course. There were 3 patients whom I was asked to examine the visual fields and the findings were bitemporal hemianopia. They also had a scar as shown above. In fact, they had craniopharyngioma which has been operated via a transfrontal approach. You don't always get a clear scar like this in the exam. So, sometimes you have to look in between the hairs for the scar.

Where is the lesion ? Optic chiasm


If you are asked to examine the eyes,
1) Inspection for scars (transfrontal and transphenoidal)
2) Examine the visual acuity with a Snellen chart
3) Test the visual fields (you will find bitemporal hemianopia)
4) Check light reflex and look for RAPD(relative afferent pupillary light reflex or Marcus Gunn pupil), accomadation reflex
5) Check eye movements
6) Do a fundoscopy ( look for optic atrophy, particularly if there is RAPD)
7) Look for a medic alert bracelet
8) Look for other features of endocrinopathy eg acromegaly, Cushing's syndrome which should also have been picked up during inspection

The other causes of a chiasmal lesion include pituitary adenoma, meningioma, aneurysm, glioma