As with previous 'wars' after 'battles' these are just a few quick questions to see if your brain cells have retained the information provided in battles 2.1 and 2.2.
Jot down your answers then compare them to mine here
Question 1:
Name 6 drugs associated with drug-induced lupus
Question 2:
Name the 3 best tests for monitoring SLE activity.
Question 3:
What is libman-sacks?
Question 4:
Name 3 conditions associated with Jaccouds arthropathy
Question 5:
List as many side effects of amiodarone as you can manage
Click here for the answers
Sunday, 5 September 2010
MRCP revision battle 3.2: hypercalcaemia and hyperparathyroidism
Hypercalcaemia
Ah, hypercalcaemia, the classic 'stones, bones, abdominal groans and psychic moans'... and a favourite of MRCP questions.
So what are the causes?
The top 2 to consider are always MALIGNANCY and PRIMARY HYPERPARATHYROIDISM.
Once you've thought of those, think toxic COAT MISST paget...
Malignancy may be hinted at by other blood tests showing low albumin, chloride or an alkalosis.
Think of myeloma, the possiblity of boney mets and of tumours producing PTH-P.
For boney mets remember the brilliant 'bronchus, breast, byroid, brostate and bridney'
For PTH-P the main culprits are squamous cell lung carcinoma, breast and kidney.
Primary hyperparathyroidism is usually due to a single adenoma (85% of the time) and is covered more in the topic of that name below.
So on to the slightly more eoseritc possiblities.... TOXIC COAT MIIST PAGET
TOXIC = vit D or vit A toxicity
COAT = the endocrine causes; essentially any 'growth' hormone excess will increase calcium (GH/oestrogen/thyrotoxicosis/steroids) and COAT is a way to recall the important ones: cushings, acromegaly/addissons, thyrotoxicosis. Phaechromocytoma can occasionally be a culprit too.
MIIST = the random causes
Milk-alkali syndrome - treat with n.saline and loop diuretics
Iatrogenic - thiazides, lithium
Idiopathic infantile - supravalvular aortic stenosis (think of if 'elfin facies' are mentioned)
Sarcoid
TB/any granulomatosis disease (histoplasmosis, wegeners granulomatosis)
PAGETS - pagets disease of the bone does not normally cause raised calcium but will if the patient has been immobile for a long period.
Having considered the causes, lets take a step back and look at the 2 main 'characters' involved in calcium balance.
Firstly, theres vitamin D. Vit D is made from cholesterol, meaning that while meat-fans can get some of theirs from food vegetarians are reliant on their body making some (made in the skin with the aide of sunlight, making the UK's weather not ideal...)
Vit D affects calcium by:
- promoting GI absorption of Ca and phos
- promoting renal reabsorption of Ca and phos.
Unsuprisingly, its net effect is therefore to increase both calcium and phosphate.
The second 'character' is PTH. This affects calcium by:
- promoting renal reabsorption of calcium (and encouraging renal loss of phosphate)
- promoting osteoclast activity --> increasing both Ca and phos
- increasing Vit D hydroxylation - which indirectly increases GI calcium absorption
So, overall its net effect is to increase calcium and decrease phosphate.
Keep these bits in mind and when hypocalcaemia pops up they may come in handy again!
Hyperparathyroidism
PTH is released in response to decreased ionised calcium. It works in the way described above, causing a net increase in calcium and decrease in phosphate.
Primary hyperparathyroidism causes raised calcium, raised PTH, raised alk phos and low phosphate.
85% of the time it is a solitary adenoma, 15% of the time hyperplasia of all glands and <0.5% of the time a carcinoma.
Rarely osteitis fibrosa cystica can develop = bone marrow fibrosis and cyst formation due to severe reabsorption. This results in brown tumours, subperiostial erosions of distal phalanges and pepper-pot skull.
Secondary hyperparathyroidism is the 'good' form - this occurs when calcium is low as a compensatory mechanism, so biochemically the bloods will show low Ca, raised phosphate and raised PTH
Tertiary hyperparathyroidism is back into the 'inappropriate' catagory - it is seen after long term secondary hyperparathyroidism and is due to the parathyroid glands getting 'too big for their boots' and become hyperplasic/acting autonomously. Biochemically it causes raised calcium and very high PTH.
Phew well thats enough for one day... time for some chocolate!
Unless you're feeling up for testing what you remember from battle 2... if so click here
Ah, hypercalcaemia, the classic 'stones, bones, abdominal groans and psychic moans'... and a favourite of MRCP questions.
So what are the causes?
The top 2 to consider are always MALIGNANCY and PRIMARY HYPERPARATHYROIDISM.
Once you've thought of those, think toxic COAT MISST paget...
Malignancy may be hinted at by other blood tests showing low albumin, chloride or an alkalosis.
Think of myeloma, the possiblity of boney mets and of tumours producing PTH-P.
For boney mets remember the brilliant 'bronchus, breast, byroid, brostate and bridney'
For PTH-P the main culprits are squamous cell lung carcinoma, breast and kidney.
Primary hyperparathyroidism is usually due to a single adenoma (85% of the time) and is covered more in the topic of that name below.
So on to the slightly more eoseritc possiblities.... TOXIC COAT MIIST PAGET
TOXIC = vit D or vit A toxicity
COAT = the endocrine causes; essentially any 'growth' hormone excess will increase calcium (GH/oestrogen/thyrotoxicosis/steroids) and COAT is a way to recall the important ones: cushings, acromegaly/addissons, thyrotoxicosis. Phaechromocytoma can occasionally be a culprit too.
MIIST = the random causes
Milk-alkali syndrome - treat with n.saline and loop diuretics
Iatrogenic - thiazides, lithium
Idiopathic infantile - supravalvular aortic stenosis (think of if 'elfin facies' are mentioned)
Sarcoid
TB/any granulomatosis disease (histoplasmosis, wegeners granulomatosis)
PAGETS - pagets disease of the bone does not normally cause raised calcium but will if the patient has been immobile for a long period.
Having considered the causes, lets take a step back and look at the 2 main 'characters' involved in calcium balance.
Firstly, theres vitamin D. Vit D is made from cholesterol, meaning that while meat-fans can get some of theirs from food vegetarians are reliant on their body making some (made in the skin with the aide of sunlight, making the UK's weather not ideal...)
Vit D affects calcium by:
- promoting GI absorption of Ca and phos
- promoting renal reabsorption of Ca and phos.
Unsuprisingly, its net effect is therefore to increase both calcium and phosphate.
The second 'character' is PTH. This affects calcium by:
- promoting renal reabsorption of calcium (and encouraging renal loss of phosphate)
- promoting osteoclast activity --> increasing both Ca and phos
- increasing Vit D hydroxylation - which indirectly increases GI calcium absorption
So, overall its net effect is to increase calcium and decrease phosphate.
Keep these bits in mind and when hypocalcaemia pops up they may come in handy again!
Hyperparathyroidism
PTH is released in response to decreased ionised calcium. It works in the way described above, causing a net increase in calcium and decrease in phosphate.
Primary hyperparathyroidism causes raised calcium, raised PTH, raised alk phos and low phosphate.
85% of the time it is a solitary adenoma, 15% of the time hyperplasia of all glands and <0.5% of the time a carcinoma.
Rarely osteitis fibrosa cystica can develop = bone marrow fibrosis and cyst formation due to severe reabsorption. This results in brown tumours, subperiostial erosions of distal phalanges and pepper-pot skull.
Secondary hyperparathyroidism is the 'good' form - this occurs when calcium is low as a compensatory mechanism, so biochemically the bloods will show low Ca, raised phosphate and raised PTH
Tertiary hyperparathyroidism is back into the 'inappropriate' catagory - it is seen after long term secondary hyperparathyroidism and is due to the parathyroid glands getting 'too big for their boots' and become hyperplasic/acting autonomously. Biochemically it causes raised calcium and very high PTH.
Phew well thats enough for one day... time for some chocolate!
Unless you're feeling up for testing what you remember from battle 2... if so click here
MRCP revision battle 3.1: Hilar lymphadenopathy
Currently in a stint of antisocial long shifts so struggling to squeeze in revision, but have managed to squash a quick review of 3 topics in, all prompted by one question about a patient with bilateral hilar lymphadenopathy:
1) causes of bilateral hilar lymphadenopathy (sure that one wasn't a suprise)
2) hypercalcaemia (predictable, given topic 1)
3) hyperparathyroidism (an obvious progression from topic 2)
Causes of bilateral hilar lymphadenopathy
I like to try and remember these as a rhyming song:
"cancer, sarcoid and TB, lymphoma HIV.... and the other 5 are 2CHEAP2 to me... oh the joys of bilateral hilar lumphadenopathy..."
CHEAP = 2 Cs (CF, Churg Stauss), EAA, pneumoconiosis, phenytoin (2Ps)
Onwards to battle 3.2...
1) causes of bilateral hilar lymphadenopathy (sure that one wasn't a suprise)
2) hypercalcaemia (predictable, given topic 1)
3) hyperparathyroidism (an obvious progression from topic 2)
Causes of bilateral hilar lymphadenopathy
I like to try and remember these as a rhyming song:
"cancer, sarcoid and TB, lymphoma HIV.... and the other 5 are 2CHEAP2 to me... oh the joys of bilateral hilar lumphadenopathy..."
CHEAP = 2 Cs (CF, Churg Stauss), EAA, pneumoconiosis, phenytoin (2Ps)
Onwards to battle 3.2...
Subscribe to:
Posts (Atom)