I am back! Irritable Bowel Syndrome for MRCP

Yes you are quite right, irritable bowel syndrome is always a diagnosis of exclusion. Always think of other diagnosis than irritable bowel diagnosis if your patient has either the following one,

1) Age more than 50 years

2) Weight loss

3) Per rectal bleeding

4) Anemia

There are two major criteria  either Rome or Manning criteria. Usually patients will have symptoms for at least 3 months. There are three types of IBS- constipated predominant, diarrhoe predominant or mixed type.

Patients usually have very non specific abdominal pain, pain and discomfort which is related to defecation and constipation or diarrhoe.

Minimal Change Nephropathy

Minimal Change Nephropathy (MCN)

There are a few common questions for MRCP Part 1 and 2 about nephrology, minimal change nephropathy is one of them.

There are a few important facts to remember,

1) Minimal change nephropathy is the commonest cause of nephrotic syndrome in children as well as in adult. Another important cause of nephrotic syndrome in adult is Focal Segmental glomerulosclerosis.

2) Minimal change literally means the kidney biopsy of  MCN will be normal unless your have electron miscroscope which shows efficement of foot processes.

3) More than 90% will respond to steroid.

4) There are a few secondary causes of minimal change nepropathy causing nephrotic syndrome- Gold, penicillamine, tumour etc

If a patient with nephrotic syndrome patient comes in with severe abdominal pain, always think of

1) Renal vein thrombosis
2) Spontaneous bacterial peritonitis

Toxoplasmosis for MRCP

Toxoplasmosis for MRCP

I liked cat very much when I was young until I knew there is a disease called Toxoplasmosis. Duing my second year parasitology, when I knew that cat is the intermediate host for a parasite called Toxoplasmosis gondii, I promised myself I would never keep cat as pet anymore in my life. You can see the life cycle of this parasite as below,

For MRCP, just remember that only immunosuppressed patients manifest this illness as reactivation of a primary disease. It is pretty high chances that you are infected before ( general population has high sero conversion- meaning most of us was infected before) and usually we recover from primary infection with good prognosis.

For certain groups of patients especially those with AIDS and on long term immunosuppression ( such as post transplantation) patients, Toxoplamosis usually manifests as central nervous infection- and patients usually present with confusion, seizure  and headache ( with of without fever).

Cerebral toxoplamosis- usually multifoci!

For your MRCP examination, if a HIV patient is admitted with seizure and a CT scan film is shown, 95% of the time is Toxoplasmosis infection, however, you must be aware that another differential diagnosis is cerebral lymphoma!!

Hypercalcemia in MRCP(II)

Hypercalcemia in MRCP (II)

It has been almost 3 years ago when I last talked about hypercalcemia. I mentioned about common causes of hypercalcemia in my previous post. Today, I am going to talk about managing hypercalcemia in clinical practice.

Before this, I think we have to pick up hypercalcemia in daily clinical practice, although I would say most of the time, patients are asymptomatic, you must remember that classically, hypercalcemia leads to,

" groans, moans,bones,stones and psychiatric overtones"

However, I usually noticed they came in unspecific complaints- lethargy,fatigue but quite common they are dehydrated and developed acute kidney injury ( hypercalcemia is one of the major causes of nephrogenic diabetes insipidus and patients with hypercalcemia develop acute kidney injury may be due to dehydration and other factors as well- You may want to find out how hypercalcemia can lead to AKI)

Pamidronate- A bisphosphonate

I always remind my junior doctors that strategies to manage hypercalcemia are
1) To correct hypercalcemia
2) To find out the underlying cause

Various ways to reduce hypercalcemia, they are hydration, steroid, bisphosphonates and calcitonin and of course after treating the hypercalcemia, find out the underlying cause.

I would say that commonly I find that the major causes are either primary tumour ( especially multiple myeloma) or secondary malignancy due to metastasis to the bone!

Heparin Induced Thrombocytopenia

Heparin Induced Thrombocytopenia

Although I will think that thrombocytopenia is not such a common case in MRCP, it is certainly a very common scenario in clinical practice.

The best way to think about high/low level in clinical medicine is the remember logically how a subtance/ product is being produced and destroyed in the normal physiology.

Therefore, low thrombocytopenia can be due to 2 main causes- reduced production from the bone marrow or increased destruction in the periphery.

I will talk about HIT ( Heparin Induced Thrombocytopenia) today in this post.
If you ask who is prone to get HIT, then I think is the group of patients who is being exposed to heparin almost everday. Yes, you are right, these patients are End stage renal failure patients who are on regular haemodialysis.

There are 2 types of HIT- early and late stage HIT. Type 1 HIT refers to condition of thrombocytopenia developing 1-2 days after heparin usage. It is a non immune condition due to direct effect of heparin on platelet. It is usually self-limiting and the platelet count usually normalizes after continued heaprin usage.

For type 2 HIT, it is an immune condition that happens later, usually 4-10 days after usage and it is life-threatening. The only option you have is to stop heparin usage.

Multiple Sclerosis in MRCP

Multiple Sclerosis in MRCP

Yes, you are right, Multiple Sclerosis although is rather rare in Malaysia, it is certainly not unusual in Western countires and certainly a popular question  in MRCP!
I will try to mentione a few important for those who are sitting for MRCP soon.

Multiple sclerosis is an autoimmune demyelinating disease affecting the central nervous system-brain and the spinal cord.

Since Mutiple Sclerosis ( MS) can affect any part in the central nervous system, patients with MS can present in diverse ways. However, 2 clincal syndromes that are popular in MRCP is acute transverse myelitis and Optic neuritis.

Patients with acute transverse myelitis usually have acute paralysis of lower limbs with sensory level ( upper motor neuron signs) with or without autonomic symptoms- urinary/bowel incontinence.

For patients with Optic neuritis, usually one eye is involved and patients may get blurring of vision or even visual loss!

For you to diagnose MS, you can follow the Poser criteria. You can click here to learn more. For you, I think you need to remember only this - you need 2 sites ( central nervous system) involvement at 2 different times ( 2 attacks) to make the diagnosis.

MRI is always helpful in making the diagnosis.

As for the treatment, I think you just need to remember one of them is interferon!

Happy Chinese New Year!

Happy Chinese New Year!

Best wishes to all Chinese readers. May the year of Rabbit brings prosperity and wealth to all of you! And certainly hope all of you will pass your MRCP Part 1 or 2 in just ONE Attempt!!

I will try my best to help you all to pass!!

RBBB in MRCP

RBBB in MRCP

OK, Right bundle branch block ( RBBB) is certainly a favourite ECG finding your consultant would like to show you during grand round.

How to pick up RBBB? It is easy, always look for rsR pattern in lead V1 with prolonged QRS complex ( it can be normal in partial RBBB). Besides that, pick up the slurred S ( wide negative S) wave in V6.

Common question for MRCP exam, the causes for RBBB, just remember a few important causes below,

1) Normal variant

2) Increased  right ventricular pressure,especially in cor pulmonale and sometimes in pulmonary embolism.

3) Congenital heart disease especially atrial septal defect

4) Myocardium ischemia, myocarditis etc.

However, you must not miss Brugada syndrome which has quite similar ECG finding such as RBBB as showed below,

The right bundle branch block pattern seen in patients with this syndrome is not actually right bundle branch block but is a function of the unusual repolarization abnormality. The ECG shows ST-segment elevation in leads V1-V3, and patients are at risk for sudden cardiac death.

Whipple's Disease in MRCP

Whipple's Disease in MRCP

Yes, you are right, Whipple's disease is rare but not in your MRCP Part 1 and 2 examination. I myself never diagnosed Whipple's disease before but this illness is ceratinly a all time favourite in MRCP examination.

It is a rare, systemic infectious disease caused by the bacterium Tropheryma whipplei. First described by George Hoyt Whipple in 1907.

It is one of a important diffential diagnosis of malabsorption syndrome and mainly affect the small bowel. It is more common in those with HLA-B27

Although Whipple's disease primary leads to GIT syndrome ( diarrhoe,weight loss) but for MRCP, patients with Whipple's disease is usually illustrated with symptoms of joint pain!

The diagnosis- jejunal biospy with PAS staining.The macrophages stain strongly with PASand contain intracellular bacilli of the bacteria.

Treatment- prolonged antibiotics of penicillin,tetracycline,co-tromoxazole or chrolamphenicol.

.

Iron Deficiency Anemia

Iron Deficiency Anemia


In my last post, I talk about iron metabolism in MRCP, as you all know, iron is an important ingredient in heme synthesis. Therefore iron deficiency leads to anemia ( hypochromic,microcystic anemia) which is a type of anemia manifested by small red cells ( low MCV- mean corpuscular volume) and pale red blood cells ( low MCHC- mean cospuscular hemoglobin concentration).

Iron deficiency is diagnosed by diagnostic tests as a low serum ferritin, a low serum iron level, an elevated serum transferin and a high total iron binding capacity (TIBC).

So what causes iron deficiency anemia- yes, it is mainly due to chronic blood loss and the main cause worldwide is worms infestations! (hookworms, whipworms, roundworms). However, another reason for chronic blood loss is GIT bleeding, therefore, for anyone older than 50 years, always think of the possibility of GIT malignancy!

One thing to take note, Thalassemia minor also has the similar lab results as iron deficiency and you must always consider Thalassemia as your differential diagnosis in iron deficiency anemia!

Iron Metabolism for MRCP

Iron Metabolism For MRCP

Iron metabolism is always an interesting topic to discuss in MRCP. It is a very important topic to know in depth as well if you are preparing for MRCP Part 1 and 2.

To make this topic as easy as possible to answer, it is best illustrated as the picture below,

There are a few important fact to remember for MRCP,

1) Majority of iron in our body is contained in heme, which is the oxygen carrying molecules.

2)Some iron is bound as ferritin in cells of liver or hepatocytes. Therefore, high ferritin should also represent higher iron store, however, remember that ferrin is an acute phase protein. It is raised in acute/chronic inflammation.

3)Iron is also stored as a pigment called hemosiderin in an apparently pathologic process.

How about for iron absorption?

You can remember this process by the following picture,

A few important facts to remember,

1) Iron absorption occurs predominantly in the duodenum and upper jejunum.

2) Iron is best absorped in the form of heme and then Fe2+, therefore agents such as Vitamin C than can reduce Fe3+ to Fe2+ increases iron absorption.

3) Hepcidin role in iron metabolism is out of topic for MRCP but it is getting momentum in Nephrology field in explaining the reason behind functional iron deficiency.

Happy New Year!!

Happy New Year

Happy New Year to all MRCP Blog readers! May 2011 become the year for you to pass your MRCP Part 1 and 2!!

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)

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,

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!

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.

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?

1 ) Haemoglobinuria
2 ) low mean cell volume
3 ) Positive direct antiglobulin test
4 ) Reduced reticulocyte count
5 ) Spherocytes present on blood film

Answer: 1

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.

( 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!!

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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,

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.

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%?

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.
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