Happy New Year to all MRCP Blog readers! May 2011 become the year for you to pass your MRCP Part 1 and 2!!
Friday, December 31, 2010
Friday, December 17, 2010
Liddle's syndrome in MRCP
Liddle's syndrome in MRCP
I must say that there are a few genetic renal transport disorders which are popular in MRCP part 1 and 2. These are Bartter's syndrome, Gitelman's syndrome and of course Liddle's syndrome.
Liddle's syndrome is one of the rare causes of secondary hypertension. For you to understand better, you must know that our body maintains fluid balance mainly by controlling sodium homeostasis. However about 25000 mmol of sodium is being filtrated from our kidney everyday and it is crucial that majority of the sodium is being reabsorped from the tubule.
Although collecting duct is only responsible for 1-2% of total sodium reabsorption, it is the major site for our body to control the fluid status because it is the only site that is sensitive to our body hormone ( aldosterone)
I must say that there are a few genetic renal transport disorders which are popular in MRCP part 1 and 2. These are Bartter's syndrome, Gitelman's syndrome and of course Liddle's syndrome.
Liddle's syndrome is one of the rare causes of secondary hypertension. For you to understand better, you must know that our body maintains fluid balance mainly by controlling sodium homeostasis. However about 25000 mmol of sodium is being filtrated from our kidney everyday and it is crucial that majority of the sodium is being reabsorped from the tubule.
Although collecting duct is only responsible for 1-2% of total sodium reabsorption, it is the major site for our body to control the fluid status because it is the only site that is sensitive to our body hormone ( aldosterone)
Sodium is mainly being reabsorped via Sodium channel ( ENAc) at collecting duct. When aldosterone binds to mineralcorticoid ( MR) receptor, more ENac will be synthesized and more sodium will be reabsorped and more pottasium being excreted ( that explaines why primary aldosteronism patients have hypertension and hypokalemia)
Liddle's syndrome is just a genetic disorder when the ENac is activated all the time and sodium reabsorption is enhanced leading to hypertension and hypokalemia.
Hypokalemia and Hypertension
Hypokalemia and Hypertension
We are always reminded that when a patient is diagnosed to have hypertension, the possibility of secondary hypertension must be entertained especially for young patients.
There are various clues that can lead us to suspect a patient might have secondary causes and one of them is hypokalemia.
Therefore, if you find a patient with hypertension and hypokalemia, always think of the following diagnosis,
1) Renal Artery stenosis or renin secreting tumor ( RAS)
2) Liddle's syndrome
3) Adrenal hyperfunction- can be due to adrenal ademona/carcinoma leading to hyperaldosteronism
4) Licorice usage or syndrome of apparent mineralcorticoid access ( SAME)
And one of the popular question in MRCP is how to differentiate these four conditions!!
It is quite easy if we know how renin angiotensin aldosterone ( RAA) system works. It is summarised as the following image,
We are always reminded that when a patient is diagnosed to have hypertension, the possibility of secondary hypertension must be entertained especially for young patients.
There are various clues that can lead us to suspect a patient might have secondary causes and one of them is hypokalemia.
Therefore, if you find a patient with hypertension and hypokalemia, always think of the following diagnosis,
1) Renal Artery stenosis or renin secreting tumor ( RAS)
2) Liddle's syndrome
3) Adrenal hyperfunction- can be due to adrenal ademona/carcinoma leading to hyperaldosteronism
4) Licorice usage or syndrome of apparent mineralcorticoid access ( SAME)
And one of the popular question in MRCP is how to differentiate these four conditions!!
It is quite easy if we know how renin angiotensin aldosterone ( RAA) system works. It is summarised as the following image,
For RAS or renin secreting tumour, you will have high renin and high aldosterone. For aldrenal hyperfunction, patients have high aldosterone level but normal renin.
As for Liddle's syndrome and SAME, I will try to explain a bit deeper next time!
Tuesday, November 16, 2010
Pancytopenia for MRCP
Pancytopenia for MRCP
Recently I saw a patient with pancytopenia in my ward. A 24-year old ESRF gentleman on CAPD for the past 4 years ( with primary disease of SLE) came to us with fever and joint pain. Full blood count showed a Hb of 4.5, TWC of 1.2 and Plt count of 45.
As we all know, bone marrow produces red cell, white cell and platelet. Pancytopenia just means a condition with reduction of all these three cell types.
It is always interesting to find the underlying cause for pancytopenia and I always try to remember the causes as the following order,
1) Inability for production/Infiltration of bone marrow
- Certainly one of the commonest cause is leukaemia, however, you have to always bear in mind the possibility of aplastic anemia. In older patients, always consider the possibility of bone marrow infiltration by tumour due to secondaries. Severe folic and Vitamin B12 also can cause pancytopenia but frankly speaking, I have never encountered one in my life!
2) Consumption
- although the production in the bone marrow is normal, all these cells can be broken down ( consumed) in the periphery. This can happen either in the spleen ( due to hypersplenism) or in circulation because of autoimmune respond ( due to underlying autoiimune disease)
3) Drugs
- certain drugs or even some infections can cause bone marrow suppression leading to pancytopenia. Popular drugs include choramphenicol, azathioprine ( especially used with allupurinol). Various infections can lead to pancytopenia but always remember about Parvovirus b 19.
Back to our patient, he actually has azathioprine induced pancytopenia. However, pancytopenia due to SLE should be entertained as well!
The worrying thing about pancytopenia is of course managing the neutropenic sepsis if it occurs. My patient actually developed neutropenic sepsis and he was treated with broad spectrum antibiotics. His cell counts improved after azathioprine was stopped.
Recently I saw a patient with pancytopenia in my ward. A 24-year old ESRF gentleman on CAPD for the past 4 years ( with primary disease of SLE) came to us with fever and joint pain. Full blood count showed a Hb of 4.5, TWC of 1.2 and Plt count of 45.
As we all know, bone marrow produces red cell, white cell and platelet. Pancytopenia just means a condition with reduction of all these three cell types.
It is always interesting to find the underlying cause for pancytopenia and I always try to remember the causes as the following order,
1) Inability for production/Infiltration of bone marrow
- Certainly one of the commonest cause is leukaemia, however, you have to always bear in mind the possibility of aplastic anemia. In older patients, always consider the possibility of bone marrow infiltration by tumour due to secondaries. Severe folic and Vitamin B12 also can cause pancytopenia but frankly speaking, I have never encountered one in my life!
2) Consumption
- although the production in the bone marrow is normal, all these cells can be broken down ( consumed) in the periphery. This can happen either in the spleen ( due to hypersplenism) or in circulation because of autoimmune respond ( due to underlying autoiimune disease)
3) Drugs
- certain drugs or even some infections can cause bone marrow suppression leading to pancytopenia. Popular drugs include choramphenicol, azathioprine ( especially used with allupurinol). Various infections can lead to pancytopenia but always remember about Parvovirus b 19.
Back to our patient, he actually has azathioprine induced pancytopenia. However, pancytopenia due to SLE should be entertained as well!
The worrying thing about pancytopenia is of course managing the neutropenic sepsis if it occurs. My patient actually developed neutropenic sepsis and he was treated with broad spectrum antibiotics. His cell counts improved after azathioprine was stopped.
Monday, October 25, 2010
Hemoglobinuria or myoglobinuria
Hemoglobinuria and myoglobinuria
I always confused these two conditions when I was a medical student. Now let me make these conditions as simple as possible.
Hemoglobinuria just means presence of hem in the urine whereas myoglobinuria means presence of myoglobin in the urine. Both can cause acute kidney injury due to pigment nephropathy.
Remember that both can cause a false positive in urine dipstick for RBC. Patients with both these conditions produce tea coloured urine. However myoglobinuria may be differentiated from hemoglobinuria by performing a series of simple tests.
-Myoglobinuria is brown, and often only a few RBCs are present in the urine.
-Hematuria produces a reddish sediment in spun urine samples.
-Red or brown urine with a negative dipstick result for blood indicates a dye in the urine.
-Hemoglobin produces a reddish or brown coloration in the spun serum, whereas myoglobin does not discolor the serum.
-CK levels are markedly elevated in myoglobinuria.
Another common question in MRCP- if you notice red to brown urine with negative dipstick, there are only a few possibilities- bladder analgesic phenazopyridine or a variety of other medications, certain food dyes, the ingestion of beets in susceptible subjects, porphyria and hydroxocobalamin for the treatment of cyanide intoxication.
Question in MRCP
A 17 year old male with glucose-6-phosphate dehydrogenase deficiency presents with tiredness and is noticed to
be jaundiced. These features have developed since he developed a mild chest infection one week ago. Which one
of the following is the most likely haematological finding?
be jaundiced. These features have developed since he developed a mild chest infection one week ago. Which one
of the following is the most likely haematological finding?
1 ) Haemoglobinuria
2 ) low mean cell volume
3 ) Positive direct antiglobulin test
4 ) Reduced reticulocyte count
5 ) Spherocytes present on blood film
2 ) low mean cell volume
3 ) Positive direct antiglobulin test
4 ) Reduced reticulocyte count
5 ) Spherocytes present on blood film
Answer: 1
Wednesday, October 20, 2010
Vasculitides in MRCP
Vasculitides in MRCP
Let me makes this topic a very simple one, you just to know two conditions in this topic- Wegener Granulomatosis and Chrug- Strauss Disease.
Anyway, before we zoom in into these two conditions, I think candidates need to know this topic as a whole, vasculitis just means inflammation of blood vessels with reactive damage to the wall which can lead to downstream ischemia and necrosis.
Classification of vasculitis is depending on the size of vessel involved. You might want to know more about Chapel Hill Classification- either big vessel, medium or small vessel.
However, I do not think you need to know all these conditions- for MRCP candidates- big vessels vasculitis, you need to know Giant cell arteritis, medium size vasculitis- you need to know polyarteritis nodosa and small vessel disease- of course you MUST know Wegener Granulomatosis (WG) and Churg-Strauss Disease ( CS)
I will talk about Giant cell arteritis and polyarteritis nodosa next time and for today, we will put emphasis on WG and CS.
Since both involve small vessels, multiple organs can be involved, however, just remember the following similarities and differences between these two conditions.
Both of WG and CS can cause pauci immune glomerulonephritis and the classical finding is cresentric GN on biopsy
Both can be ANCA positive but WG is mainly c-ANCA and CS is mainly p-ANCA
WG patients usually have upper respiratory airway problem and can be misdiagnosed as nasopharygeal carcinoma or tuberculosis.
For CS, patients might present with asthma and usually has eosinophilia.
Yes, you are right, that’s all you need to know!!
Let me makes this topic a very simple one, you just to know two conditions in this topic- Wegener Granulomatosis and Chrug- Strauss Disease.
Anyway, before we zoom in into these two conditions, I think candidates need to know this topic as a whole, vasculitis just means inflammation of blood vessels with reactive damage to the wall which can lead to downstream ischemia and necrosis.
Classification of vasculitis is depending on the size of vessel involved. You might want to know more about Chapel Hill Classification- either big vessel, medium or small vessel.
However, I do not think you need to know all these conditions- for MRCP candidates- big vessels vasculitis, you need to know Giant cell arteritis, medium size vasculitis- you need to know polyarteritis nodosa and small vessel disease- of course you MUST know Wegener Granulomatosis (WG) and Churg-Strauss Disease ( CS)
I will talk about Giant cell arteritis and polyarteritis nodosa next time and for today, we will put emphasis on WG and CS.
( Wegener Granulomatosis patients usually go to see an ENT surgeon first!!)
Since both involve small vessels, multiple organs can be involved, however, just remember the following similarities and differences between these two conditions.
Both of WG and CS can cause pauci immune glomerulonephritis and the classical finding is cresentric GN on biopsy
Both can be ANCA positive but WG is mainly c-ANCA and CS is mainly p-ANCA
WG patients usually have upper respiratory airway problem and can be misdiagnosed as nasopharygeal carcinoma or tuberculosis.
For CS, patients might present with asthma and usually has eosinophilia.
Yes, you are right, that’s all you need to know!!
Please join NOW to help PassPACES to improve!
Monday, October 18, 2010
Tumour Lysis Syndrome in MRCP
Tumour Lysis Syndrome in MRCP
OK, this is a popular problem you see during your internship if you are working in an oncology ward. Remember that it is a MEDICAL EMERGENCY!
Tumor lysis syndrome (TLS) describes a condition with significant clinical and lab abnormalities caused by rapid and massive tumor cell death. Occurring either spontaneously or after chemotherapy. Therefore, it is quite logical to get this in patients with very high tumour load ( such as leukemia or lyphoma with very high white cell load)
You always encounter this syndrome post chemotherapy and always suspect this if patient develops acute kidney injury and hyperkalemia post chemotherapy.
Due to massive cell lysis, you will anticipate patients to have hyperkalemia, high phosphate and high uric acid with low Calcium.
Sometimes, patients might just present with seizure or cardiac arrthymias.
The pathogenesis of acute kidney injury is not so important for MRCP Part 1 and 2. Anyway you might get some ideas from the photo below,
OK, this is a popular problem you see during your internship if you are working in an oncology ward. Remember that it is a MEDICAL EMERGENCY!
Tumor lysis syndrome (TLS) describes a condition with significant clinical and lab abnormalities caused by rapid and massive tumor cell death. Occurring either spontaneously or after chemotherapy. Therefore, it is quite logical to get this in patients with very high tumour load ( such as leukemia or lyphoma with very high white cell load)
You always encounter this syndrome post chemotherapy and always suspect this if patient develops acute kidney injury and hyperkalemia post chemotherapy.
Due to massive cell lysis, you will anticipate patients to have hyperkalemia, high phosphate and high uric acid with low Calcium.
Sometimes, patients might just present with seizure or cardiac arrthymias.
The pathogenesis of acute kidney injury is not so important for MRCP Part 1 and 2. Anyway you might get some ideas from the photo below,
About the amanegement, it is easy, the principles are below,
1) Adequately hydrate patient to prevent cystals formation
2) Prevent/minimize uric acid formation by giving allupurinol or rasburicase.
and of course sometime, you might need to dialyse the patient.
Sunday, April 18, 2010
MRCP Mock Exam (2)
MRCP Mock Exam (2)
More questions......
Question 1:
A 45-year-old man presented with diplopia, dysarthria and difficulty with swallowing. Over the next few days he developed weakness of the upper and lower limbs. On day 4 he was unable to walk unaided. He denied any sensory symptoms or bladder disturbances. His previous medical history is unremarkable. He is a non-smoker, does not drink alcohol excessively. He does not take any drugs .
On examination he was apyrexial. His general medical examination was normal. His higher mental function was unremarkable. There were no signs of meningism. Cranial nerve examination showed bilateral dilated and fixed pupils. He had binocular diplopia but
no obvious ophthalmoplegia. He was dysarthric with weak cough. His vital capacity was 3.15 standing and 2.00 lying flat. He had lower motor neuron tetraparesis of power 3/5. He was hyporeflexic with normal sensation. He was unable to walk unaided.
Blood tests including FBC, U+Es, LFTs, TFTs, Ca, Autoantibody screen, ESR,
CRP were normal. ECG and CXR were unremarkable. CT brain was normal. Nerve conduction studies and EMG were normal.
What is the most likely diagnosis?
1 ) Guillain Barre Syndrome
2 ) Lyme disease
3 ) Myasthenia gravis
4 ) Botulism
5 ) Vasculitis
Question 2:
A 75 year-old woman presents with a two month history of episodic loss of vision in her right eye. Her ECG was normal and carotid ultrasound reveal a 50% stenosis of the right internal carotid artery What is the most appropriate treatment for this patient?
1 ) Aspirin
2 ) Carotid endarterectomy
3 ) Dipyridamole
4 ) Prednisolone
5 ) Warfarin
Question 3:
A 70 year old woman presented with a history of pancreatitis and persistent diarrhoea. She also gave a history of osteoporosis and had had a deep vein thrombosis. Which one of the following drugs will become less effective after she starts taking Cholestyramine to relieve intolerable itching?
1 ) Aspirin
2 ) Folic Acid
3 ) Thiamine
4 ) Vitamin D
5 ) Warfarin
Question 4:
A 55 year old female presents with episodic sweats and tremors which are are relieved by glucose. She has gained approximately 6 kg in weight of late and drinks approximately 10 units of alcohol weekly. Her investigations show normal Full Blood Count, Normal Urea and electrolytes and a fasting plasma glucose concetration of 4 mmol/l (3-6). What is the most appropriate investigation for this patient?
1 ) 72 hour fast
2 ) CT scan of pancreas
3 ) EEG
4 ) Insulin and C-peptide concentration
5 ) Oral glucose tolerance test
Question 5:
A 33 year old female is admitted with erythema multiforme and erythematous lesions of the mouth and eyes.
Which one of the following drugs may account for her presentation?
1) Diazepam
2 ) Fluoxetine
3 ) Mebeverine
4 ) Oral contraceptive
5 ) Sulphasalazine
Answers to the above questions: 4,1,4,1,5. Got 100%?
More questions......
Question 1:
A 45-year-old man presented with diplopia, dysarthria and difficulty with swallowing. Over the next few days he developed weakness of the upper and lower limbs. On day 4 he was unable to walk unaided. He denied any sensory symptoms or bladder disturbances. His previous medical history is unremarkable. He is a non-smoker, does not drink alcohol excessively. He does not take any drugs .
On examination he was apyrexial. His general medical examination was normal. His higher mental function was unremarkable. There were no signs of meningism. Cranial nerve examination showed bilateral dilated and fixed pupils. He had binocular diplopia but
no obvious ophthalmoplegia. He was dysarthric with weak cough. His vital capacity was 3.15 standing and 2.00 lying flat. He had lower motor neuron tetraparesis of power 3/5. He was hyporeflexic with normal sensation. He was unable to walk unaided.
Blood tests including FBC, U+Es, LFTs, TFTs, Ca, Autoantibody screen, ESR,
CRP were normal. ECG and CXR were unremarkable. CT brain was normal. Nerve conduction studies and EMG were normal.
What is the most likely diagnosis?
1 ) Guillain Barre Syndrome
2 ) Lyme disease
3 ) Myasthenia gravis
4 ) Botulism
5 ) Vasculitis
Question 2:
A 75 year-old woman presents with a two month history of episodic loss of vision in her right eye. Her ECG was normal and carotid ultrasound reveal a 50% stenosis of the right internal carotid artery What is the most appropriate treatment for this patient?
1 ) Aspirin
2 ) Carotid endarterectomy
3 ) Dipyridamole
4 ) Prednisolone
5 ) Warfarin
Question 3:
A 70 year old woman presented with a history of pancreatitis and persistent diarrhoea. She also gave a history of osteoporosis and had had a deep vein thrombosis. Which one of the following drugs will become less effective after she starts taking Cholestyramine to relieve intolerable itching?
1 ) Aspirin
2 ) Folic Acid
3 ) Thiamine
4 ) Vitamin D
5 ) Warfarin
Question 4:
A 55 year old female presents with episodic sweats and tremors which are are relieved by glucose. She has gained approximately 6 kg in weight of late and drinks approximately 10 units of alcohol weekly. Her investigations show normal Full Blood Count, Normal Urea and electrolytes and a fasting plasma glucose concetration of 4 mmol/l (3-6). What is the most appropriate investigation for this patient?
1 ) 72 hour fast
2 ) CT scan of pancreas
3 ) EEG
4 ) Insulin and C-peptide concentration
5 ) Oral glucose tolerance test
Question 5:
A 33 year old female is admitted with erythema multiforme and erythematous lesions of the mouth and eyes.
Which one of the following drugs may account for her presentation?
1) Diazepam
2 ) Fluoxetine
3 ) Mebeverine
4 ) Oral contraceptive
5 ) Sulphasalazine
Answers to the above questions: 4,1,4,1,5. Got 100%?
Sunday, April 11, 2010
MRCP Mock Examination (1)
MRCP Mock Examination (1)
Hi, sorry for the long absence from this blog, these MRCP questions are the questions provided by Ahmed Hakim in his site.
Question 1:
60-year-old woman presented with 3 months history of diplopia and blurred vision of left eye. She denied any pain or other neurological symptoms. Her previous medical history is unremarkable. She smokes 20 cigarettes per day and drinks alcohol in moderation. Her general medical examination is normal. Her visual acuity on the right is 6/6 and on the left 6/36.
There is left partial ptosis and mild proptosis with conjunctival injection. The left pupil is smaller than the right but reacting normally to light. There is some limitation of abduction of the left eye. Fundoscopy showed a pale left optic disk. The left corneal reflex is reduced.
The remaining of the neurological examination is normal. Routine blood tests including FBC, U+Es, LFTs, TFTs, Ca, Creatine kinase, autoantibody screen were normal. ECG, CXR were unremarkable. Slit lamp examination was normal. Intra-ocular pressures were within normal range.
Where is the most likely cause of her symptoms?
1 ) Cavernous sinus
2 ) Superior orbital fissure
3 ) Orbital apex syndrome
4 ) Optic chiasm
5 ) Brain stem
Question 2:
A 72 year old male is being treated for hypertension, gout, Gastro-oesophageal reflux and has a three year history of type 2 diabetes. He takes a variety of medications. His general practitioner is concerned after requesting U+Es on this patient which reveal:
Serum Sodium 138 mmol/l
Serum Potassium 4.4 mmol/l
Serum Urea 12.8 mmol/l
Serum Creatinine 162 micromol/l
Of the following drugs that he takes, which one's dose does NOT need to be reduced for this patient?
1 ) Allopurinol
2 ) Gliclazide
3 ) Lansoprazole
4 ) Lisinopril
5 ) Metformin
Question 3:
A 16 year old girl is seen in clinic as she is concerned due to areas of hair loss on the scalp. Past medical history includes atopic eczema and she has a number of depigmented areas on her hands. What is the most likely diagnosis?
1 ) Alopecia areata
2 ) Hypothyroidism
3 ) Seborrhoeic dermatitis
4 ) SLE
5 ) Trichotillomania
Question 4:
A 17 year old male with glucose-6-phosphate dehydrogenase deficiency presents with tiredness and is noticed to be jaundiced. These features have developed since he developed a mild chest infection one week ago. Which one of the following is the most likely haematological finding?
1 ) Haemoglobinuria
2 ) low mean cell volume
3 ) Positive direct antiglobulin test
4 ) Reduced reticulocyte count
5 ) Spherocytes present on blood film
Question 5:
A 32 year-old man presented to hospital with a four week history of progressively worsening dyspnoea on exertion. He also complained of a non-productive cough. Over the two days preceeding admission the patient had become breathless at rest and was started on oral co-amoxiclav by his general practitioner.
On examination he was febrile 38°C and looked unwell. Candida was noted on the tonsilar pillars. No wheeze or crackles were heard in his chest. His chest radiograph is shown. Oxygen saturation was 95% on room air, but fell to 85% following about of coughing. Arterial blood gases show pO2 of 59 mmHg.
What treatment shold be given?
1 ) Co-amoxiclav + clarithromycin
2 ) Co-trimoxazole + prednisolone
3 ) Vancomycin + ceftazidime
4 ) Cefuroxime + metronidazole
5 ) Benzylpenicillin + flucloxacillin
Question 6:
A 52 year old female presents with blistering of the hands and arms which deteriorates during the summer. She was otherwise well and drinks approximately 20 units of alcohol weekly. Examination of her skin revealed erosions and scarring on the backs of her hands and forearms and some mild hirsutes.
Which one of the following is the most likely diagnosis?
1 ) Acute intermittent porphyria
2 ) Erythropoietic protoporphyria
3 ) Pemphigoid
4 ) Porphyria cutanea tarda
5 ) Subacute lupus erythematous
OK, now mark your marks, the answers to above questions are 3,3,1,1,2,4.
I will try to upload more questions soon.
Check out the latest PassPACES ebook offer!
Hi, sorry for the long absence from this blog, these MRCP questions are the questions provided by Ahmed Hakim in his site.
Question 1:
60-year-old woman presented with 3 months history of diplopia and blurred vision of left eye. She denied any pain or other neurological symptoms. Her previous medical history is unremarkable. She smokes 20 cigarettes per day and drinks alcohol in moderation. Her general medical examination is normal. Her visual acuity on the right is 6/6 and on the left 6/36.
There is left partial ptosis and mild proptosis with conjunctival injection. The left pupil is smaller than the right but reacting normally to light. There is some limitation of abduction of the left eye. Fundoscopy showed a pale left optic disk. The left corneal reflex is reduced.
The remaining of the neurological examination is normal. Routine blood tests including FBC, U+Es, LFTs, TFTs, Ca, Creatine kinase, autoantibody screen were normal. ECG, CXR were unremarkable. Slit lamp examination was normal. Intra-ocular pressures were within normal range.
Where is the most likely cause of her symptoms?
1 ) Cavernous sinus
2 ) Superior orbital fissure
3 ) Orbital apex syndrome
4 ) Optic chiasm
5 ) Brain stem
Question 2:
A 72 year old male is being treated for hypertension, gout, Gastro-oesophageal reflux and has a three year history of type 2 diabetes. He takes a variety of medications. His general practitioner is concerned after requesting U+Es on this patient which reveal:
Serum Sodium 138 mmol/l
Serum Potassium 4.4 mmol/l
Serum Urea 12.8 mmol/l
Serum Creatinine 162 micromol/l
Of the following drugs that he takes, which one's dose does NOT need to be reduced for this patient?
1 ) Allopurinol
2 ) Gliclazide
3 ) Lansoprazole
4 ) Lisinopril
5 ) Metformin
Question 3:
A 16 year old girl is seen in clinic as she is concerned due to areas of hair loss on the scalp. Past medical history includes atopic eczema and she has a number of depigmented areas on her hands. What is the most likely diagnosis?
1 ) Alopecia areata
2 ) Hypothyroidism
3 ) Seborrhoeic dermatitis
4 ) SLE
5 ) Trichotillomania
Question 4:
A 17 year old male with glucose-6-phosphate dehydrogenase deficiency presents with tiredness and is noticed to be jaundiced. These features have developed since he developed a mild chest infection one week ago. Which one of the following is the most likely haematological finding?
1 ) Haemoglobinuria
2 ) low mean cell volume
3 ) Positive direct antiglobulin test
4 ) Reduced reticulocyte count
5 ) Spherocytes present on blood film
Question 5:
A 32 year-old man presented to hospital with a four week history of progressively worsening dyspnoea on exertion. He also complained of a non-productive cough. Over the two days preceeding admission the patient had become breathless at rest and was started on oral co-amoxiclav by his general practitioner.
On examination he was febrile 38°C and looked unwell. Candida was noted on the tonsilar pillars. No wheeze or crackles were heard in his chest. His chest radiograph is shown. Oxygen saturation was 95% on room air, but fell to 85% following about of coughing. Arterial blood gases show pO2 of 59 mmHg.
What treatment shold be given?
1 ) Co-amoxiclav + clarithromycin
2 ) Co-trimoxazole + prednisolone
3 ) Vancomycin + ceftazidime
4 ) Cefuroxime + metronidazole
5 ) Benzylpenicillin + flucloxacillin
Question 6:
A 52 year old female presents with blistering of the hands and arms which deteriorates during the summer. She was otherwise well and drinks approximately 20 units of alcohol weekly. Examination of her skin revealed erosions and scarring on the backs of her hands and forearms and some mild hirsutes.
Which one of the following is the most likely diagnosis?
1 ) Acute intermittent porphyria
2 ) Erythropoietic protoporphyria
3 ) Pemphigoid
4 ) Porphyria cutanea tarda
5 ) Subacute lupus erythematous
OK, now mark your marks, the answers to above questions are 3,3,1,1,2,4.
I will try to upload more questions soon.
Check out the latest PassPACES ebook offer!
Saturday, February 27, 2010
Multiple Myeloma in MRCP
Multiple Myeloma in MRCP
Multiple myeloma is always an interesting disease to diagnose because patients might just present to you with acute kidney injury! My university lecturer told me once, when an elderly patient comes to see you with kidney failure with no previous medical history, you must always look for multiple myeloma or drug induced ( especially NSAID!)
Another interesting fact about Multiple myeloma is Urine Bence Jones protein. I still remember during medical school time, lecturer always asked us about how to differentiate Urine Bence Jones protein from proteinuria at bed side, I hope you all know the way!
Urine Bence Jones is named after Henry Bence Jones, a famous British physician and chemist. In 1848, he was cited as the driving force for the investigation of an unusual chemical analysis discovered in the urine of a patient with myeloma in a paper titled "On the microscopical character of mollities ossium" (mollities ossium was the name for myeloma, which at the time was thought of as a bone disease based on the osteolytic bone metastases which resulted).
As for you, remember that Multiple myeloma patients always present with hypercalcemia, osteolytic bone lesions ( bone pain) and classical bone marrow findings ( proliferation of plasma cell in bone marrow). Patients might present with polyuria because hypercalcemia is one of the causes for nephrogenic diabetes insipidus!
Thursday, January 21, 2010
Rosiglitazone in MRCP
Rosiglitazone in MRCP
Rosiglitazone is one of the popular drugs commonly asked in MRCP Part 1. It is an anti-diabetic drug and a member of thiazolidinediones group.
The mechanism of action of rosiglitazone is through activation of the intracellular receptor class of the peroxisome proliferator-activated receptors (PPARs), specifically PPARγ. Rosiglitazone is a selective ligand of PPARγ and has no PPARα-binding action.
For MRCP, side effects of Rosiglitazone is a popular topic to be asked. Just remember these side effects,
1) Higher incidence of fracture
There is a greater incidence of fractures of the upper arms, hands and feet in female diabetics given rosiglitazone compared with those given metformin or glyburide.The information was based on data from the ADOPT trial.
2) Higher incidence of Cardiovascular event?
It was a great debate about this a few years back. I think if you are given 2 options- fracture or CVS event, choose fracture because no one will disagree with you!
3) Macular Odema
A possible side effect.
Remember, Rosiglitazone should not be used in patients with overt heart failure!
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