MRCP Part 1 and 2- Blog that helps you to pass your MRCP !!

Toxoplasmosis for MRCP

2011-12-18T05:38:00.000Z

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)

2011-05-22T15:35:00.000+01:00

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

2011-04-09T16:17:00.000+01:00

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

2011-02-20T07:46:00.000Z

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!

2011-02-02T15:48:00.000Z

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

2011-01-19T16:59:00.000Z

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

2011-01-12T09:13:00.000Z

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

2011-01-09T00:17:00.000Z

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

2011-01-04T08:19:00.005Z

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!!

2010-12-31T06:14:00.001Z

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

2010-12-17T10:03:00.004Z

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

2010-12-17T09:46:00.003Z

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

2010-11-16T10:41:00.003Z

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

2010-10-25T06:36:00.002+01:00

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

2010-10-20T05:37:00.002+01:00

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!!

Please join NOW to help PassPACES to improve!

Tumour Lysis Syndrome in MRCP

2010-10-18T08:30:00.004+01:00

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)

2010-04-18T16:06:00.002+01:00

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)

2010-04-11T05:49:00.003+01:00

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!

Multiple Myeloma in MRCP

2010-02-27T07:15:00.004Z

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!

Rosiglitazone in MRCP

2010-01-21T15:55:00.002Z

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!

Pass MRCP PACES in One Attempt

2009-12-19T06:31:00.005Z

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Bartter's and Gitelman's Syndromes

2009-12-06T13:32:00.005Z

Bartter's and Gitelman's Syndromes in MRCP

I hate syndromes because I always can't remember them well. My Professor once said, clinicians term something as syndrome when they do not know much about an illness.

Having said that, some syndromes are important for your MRCP,I am going to talk about Bartter's and Gitelman's syndrome.

First fact to remember, Bartter's syndrome is an disorder of transport in the medullary thick ascending limb of Henle.

Second fact to remember, Bartter's syndrome is an illness resembles patients chronically takingloop diuretcs that inhibit activity of Na-K-2Cl co transporter.

Third fact to remember- they do not have hypertension.

So, what will happen to you if you chronically take frusemide?

Easy- you get hypokalemia and alkalosis and hypercalciuria- therefore leading to nephrocalcinosis. You might not be able to explain hypercalciuria but just remember that. Therefore, patients with Bartter's syndrome get hypokalemic metabolic alkalosis. ( as compared to hypokalemic metabolic acidosis in Renal tubular acidosis)

If you are interested to read more about ROMK ( renal outer medullary potassium channel), try to search the net! ( not important in your MRCP!)

As for Gitelman's syndrome, it is an disorder of distal convulated tubule, it is an variant of Bartter's syndome with similar biochemical abnormalities except Gitelman's syndrome has hypocalciuria as compared to hypercalciuria in Bartter's syndrome and hypomagnesimia in Gitelman's syndrome. ( Bartter's syndrome has normal Magnesium Level)

MRCP Past Year Question

A 15-year-old girl is referred to clinic complaining of generalised muscle weakness, fatigue and polyuria. Her blood pressure in clinic is measured at 90/74 mmHg. Investigations:

Serum sodium 127 mmol/l
Serum potassium 3.0 mmol/l
Serum urea 7.2 mmol/l
Serum creatinine 110 umol/l
Serum chloride 92 mmol/l (NR 97-108 mmol/l)
Serum bicarbonate 34 mmol/l (NR 22-28 mmol/l)
82 mmol/l (NR 0.8-1.1 mmol/l)
Urine sodium 160 mmol/l (NR 40-130 mmol/l)
Urine calcium 8.0 mmol/24hr (NR 2.5-8.0 mmol/24hr)
Which of the following is the most likely diagnosis?
Available marks are shown in brackets

1 ) Addison's disease
2 ) Bartter's syndrome
3 ) Laxative abuse
4 ) Liddle's syndrome
5 ) Thiazide diuretic abuse

What is the answer??

How to pass your Part 1 and 2?

2009-12-04T01:40:00.003Z

How to pass your MRCP Part 1 and 2?

Today I am going to talk something different. No hard facts to learn today, just relax and listen to my 5-cent advice that can help you to pass your MRCP Part 1 and 2.

First of all, I think Part 1 is more difficult to pass because candidates seldom do in basic sciences questions. I will advise you to read more about basic sciences when you sit for your part 1. Anyway, there are a few strategies to pass both your Part 1 and 2.

1) Correct way to study

I must say that the fatest way to remember your facts is trying to answer past years questions. When you try to do these questions, read around the topic and learn more facts about a topic. You will be suprised how fast you can master a topic.

2) Correct books to buy

Buy the correct books to study. It is difficult to tell which book to buy but remember that a good book gives your relevant and important facts to remember not high-end useless not exam-orientated facts!

3) Be systematic and disciplined

You will never pass if you are not disciplined enough, always divide your time, let say you have another 10 months before your exam, divide your time like 1 month to study endocrinology, another month to study respiratory etc. Finish all the topics before your examination!

4) Always discuss with your friends

If you do not understand a topic, always discuss with your friends who are sitting the exam together. You will be suprised how easy he/she might answer your questions. There is an old Chinese saying, when there are 3 persons together, you ceratinly can learn new things from one of them!

5) Answer all your questions

During your exam, answer all your questions, no negative marking, you have 20% chance of get it right even though you know nothing. If you randomly answer 5 questions, you will get one right!!

Hope this piece of informations helps!

Pseudohypoparathyroidism in MRCP

2009-11-07T15:30:00.003Z

Pseudo- or pseudopseudohypoparathyroidism in MRCP

Before we understand any disease start off with pseudo-, we must understand the disease without the prefix of pseudo first. Therefore, before talking about pseudohypoparathyroidism, we must understand hypoparathyroidism first.

OK, I think it is easy, hypoparathyroidism just means you do not have enough parathyroid hormone. However, in order for you to understand the clinical and biochemistry features of hypoparathyroidism, you need to know the functions of parathyroid hormone.

Parathyroid hormone is important in calcium metabolism in human. Just remember that your parathyroid hormone will be released if there is hypocalcemia. Various mechanisms will be activated to bring back your calcium level to normal level such as,

1) increasing bone mineral dissolution, thus releasing calcium and phosphorus,

2) increasing calcium absorption but phosporus excretion by kidney,

3) enhancing calcium and phosphorus absorption from the gut,

Therefore, you anticipate patients with hypoparathyroidism to have hypocalcemia and hypophosphatemia.

OK, now you know the basic, pseudohypoparathyroidism just means patients with this disease actually do not have low level of parathyroid hormone ( that's why it is termed pseudo-) but they have the biochemical features of hypoparathyroidism.

How could that be possible? It is possible when your body/tissue does not respond to parathyroid hormone. The most common type of pseudohypoparathyroidism is type 1a, Albright's hereditary osteodystrophy, which is associated with short stature, round facies, obesity and brachydactyly.

As for pseudopseudohypoparathyroidism, it is easy patients have features of pseudohypoparathyroidism but biochemically, they are totally normal!

Just read a bit more how to have the diagnosis of these 2 conditions from your text book although I think it is not so important!

Cryoglobulinemia in MRCP

2009-10-13T13:44:00.003+01:00

Cryoglobulinemia in MRCP

Frankly speaking, I thought cryoglobulinemia is not an important topic when I was sitting for my MRCP until recently I learned from my friend that actually it is a very popular topic in Part 1 and 2.

There are a few important salient points to remember for your MRCP.

( Rash on lower extremities typical of cutaneous small-vessel vasculitis due to cryoglobulinemia secondary to hepatitis C infection.- Photo from eMedicine)

1) Cryoglobulin just means proteins that become insoluble in low temperature. Therefore, it is understandable that this leads to thrombosis and hyperviscosity leading to Raynaud Phenomenon.

2) There are 3 types of cryoglobulinemia according to Brouet classification- Type I, II, III. Just remember Type I is simple and Type II and III are mixed cryoglubulinemia.

3) Just main causes of Type I include lymphoproliferative disorders (eg, multiple myeloma, Waldenström macroglobulinemia). Type II and III causes are chronic inflammatory diseases such as chronic liver disease, infections (chronic HCV infection), and coexistent connective-tissue diseases (SLE, Sjögren syndrome). Mixed cryoglobulinemia is rarely associated with lymphoproliferative disorders.

4) Remember the common presentation of cryoglobulinemia is Meltzer triad, ie, purpura ( skin manifestation), arthralgia, and weakness ( neuropathy).

5) However, renal involvement is common too- the commonest type is membranoproliferative GN.

Sound easy right? I always remind my friends, if during your MRCP, they give you a case of patient with renal involvement ( proteinuria), skin rash and joint pain- always remember 2 possible diagnosis- SLE and of course cryoglobulinemia!!

Addison Disease in MRCP (2)

2009-09-27T06:38:00.004+01:00

Addison Disease in MRCP (2)

I strong believe that Addison Disease is a difficult diagnosis to make in clinical medicine. Anyway, there are a few points to remember if you are sitting for your MRCP,

1) The commonest cause of Addison disease is autoimmune in origin ( about 70%). Antibodies to 21-hydroxylase are commonly found.

2) There is long list of other causes, however, always remeber that it may be associated with infection ( especially tuberculosis) and autoimune polyglandular deficiency, therefore always look for other endocrine deficiency if you pick up Addison disease in a patient.

3) I think the common scenario they give you in your MRCP is a patient with chronic fatigue ( sometimes chronic diarrhoe) with the following abnormalities,

a) hyponatremia and hyperkalemia ( I hope you know the reason behind this!)
b) hypoglycemia
c) hypotension
d) pigmentation ( remember your ACTH??)- look at mucosal and palmar creases. A popular MRCP PACES short case!!

( Picture source:pathmicro.med.sc.edu)

It is easy to make a diagnosis, your adrenal should secrets cortisol if stimulated by ACTH, therefore, if your body fails to secrets cortisol to a certain level after ACTH ( synacthen test), that it means you have adrenal insufficiency ( Addison disease)

About the treatment, of course if patient comes in with crisis, treat accordingly and later put patient glucocorticoid therapy and if possible find out the underlying cause!

Other than Medicine

2009-09-24T14:43:00.004+01:00

Other than Medicine

I am very......very sorry being quiet for months!! As I progress to another stage of my life, I suddenly realize that there are other important matters other than medicine.

I hope you bear with me because this post has nothing to do with MRCP and medicine.

Yes, I am so happy that I have my second baby, some of you might know that besides medicine, I enjoy a lot of hobbies, I like programming, investing, travelling and of course sleeping.

One afterenoon in my new hospital, I sat down in one of the corner near my hospital and spent 5 min with myself and started to think what I want to do with my life.

For the last 8 years, I spent most of my time in hospital and I worked very hard , after seeing lives and deaths everyday, I actually do not know my destiny. A few years back, there was only one aim in my life- passing my MRCP, but now, what's next??

I feel a lot of us just work everyday and give the patients most of our times, I remember clearly my last holiday with my wife was actually 4 years ago!! Both of us just work and work again because we are so worried that we might not have enough money to raise our kids and for our retirement!

Just want to share with all of you, look beyond, MRCP is just a stop in your life, you have more things to do after your MRCP. Even though you do not pass your MRCP, don't be upset, you might have other better things to do in life than medicine!

Poisoning in MRCP(IV)

2009-01-04T09:30:00.002Z

Poisoning in MRCP(IV)- Methanol/ ethylene glycol

As I told you many months ago, there are many causes of metabolic acidosis you have to remember if you plan to sit for your MRCP.

When I was a medical student, my lecturer told me that when a young patient comes to hospital with shortness of breath ( air hunger) and you do an ABG showing metabolic acidosis, you must always consider 3 important diagnosis- 1) Diabetic ketoacidosis , 2) salicylates oberdose ,3 ) Ethanol/ ethylene glycol poisoning.

OK, although methanol is a component of shellacs, varnishes, paint removers and copy machine fluid, it is not uncommon to find it in some alcohol drinks produced illegally. For ethylene glycol, it is used commonly as coolant and preservative and also found in polishes and detergens.
A few important facts to remember for your MRCP Part 1 and 2,

1) Methanol can cause retina injury leading to blindness ( eye manifestations can happen as early as 15-20 hours post ingestion)

2) Ethylene glycol poisoning usually has 3 distinct clinical phases- first stage- CNS effects ( first 12 hours), second stage- cardiopulmonary effects ( CCF, ARDS etc) and third stage- renal effects- ARF.

3) Acute management include gastric lavage and correct the metabolic acidosis. Remember also that haemodialysis can be employed to fasten removal of the toxic metabolites.

4) Folinic acid can be used to protect against ocular toxicity of methanol whereas thiamine are administered to drive metabolism of ethlylene glycol to non-toxic metabolism.

Let me illustrate to you a MRCP question,
A 23-year gentleman is admitted to the A+E due to nausea and vomitting. On examination, he is dehydrated with GCS=14/15. Blood pressure on arrival= 90/60. Blood investigations sent in A+E reviews the following,

Salicylates level= normal

Na=134

K=5.1

BU=10

Creatinine= 100

ABG ( on 2L oxygen supplement)

PH=7.20

HCO3=12

PaO2=100 mmHg

PaCo2=21 mmHg

What further test you would like to order?

A) Random blood sugar B) CXR C) CT brain D) AXR E) Blood lithium level

So, do you know the answer??

Acromegaly in MRCP

2008-11-18T14:47:00.000Z

Acromegaly in MRCP

Acromegaly is always a popular case in MRCP PACES but I think it is an important endocrine illness as well in MRCP Part 1 and 2.

OK, acromegaly is an endocrine disorder with excessive growth hormone, I think everyone knows about that. The name ‘acromegaly’ comes the Greek words for “extremities” and “enlargement,” reflecting one of its most common symptoms—the abnormal growth of the hands and feet. It is easy to diagnose acromegaly in paediatrics patients ( because patients will present with gigantism) however, sometimes you might miss acromegaly in adult group.

Acromegaly is a popular case in MRCP PACES short station. However, for MRCP Part 1 and 2, common questions will be as below,

1) Ways to diagnose acromegaly

Always remember that you need OGTT first and later to confirm with Growth Hormone level. You may need to check insulin-like growth factor 1 (IGF-1). MRI brain is useful as well!

2) Picture test

They like to show you a picture and ask you about the diagnosis. I think no one should fail this because YOU SHOULD NEVER miss acromegaly in your life.

3) Symptoms and signs of acromegaly

Remember that patients may just present with hypertension or diabetes. And of course do not forget about loss of libido as well!

OK, about the treatment – just remember surgery or medical- classes of drug to be used-somatostatin analog and GH receptor antagonist

Hypercalcemia in MRCP(2)

2008-10-21T15:03:00.000+01:00

Hypercalcemia in MRCP(2)

As a medical student many years ago, I remembered I have to memorize a lot of medical mnemonics. It is easy to remember how a patient with hypercalcemia presents to hospital, just remember this sentence,

“ STONES, BONES, ABDOMINAL MOANS, AND PSYCHIC GROANS”

Let me explain these symptoms briefly,

1) Stone-

I think it is rather straightforward, high calcium in the blood also translates high calcium in the urine, therefore you are prone to get stone. Besides that, patients with hypercalcemia also easily get dehydration because they might have polyuria due to nephrogenic diabetes insipidus.

2) Abdominal moans-

Hypercalcemia leads to constipation, abdominal colic and pancreatitis.

3) Bones-

You get bone pain because there is increased in bone resorption/ breakdown due to tumour ( causing pathological fracture) or hyperparathyroidism.

4) Psychic groans-

I can’t explain this, hypercalcemia can cause psychosis, confusion etc. You have to remember it!!But I think all the electrolyte imbalances can cause some kind of mental problems.

About the treatment of hypercalcemia, I think it is not so important to remember, anyway, remember the following strategies,
1) Rehydration

2) Steroids

3) Calcitonin

4) Biophosphonates

5) Plicamycin

6) Dialysis

7) And of course, treat the underlying cause!!

However, just want to remind all of you, there are a few causes of hypercalcemia that you might can’t explain the mechanism involved but they are important. These causes are thyrotoxicosis, Addison’s disease and acromegaly.

If you can explain the mechanism involved, please share with other readers!!

Hypercalcemia in MRCP (1)

2008-10-08T14:54:00.002+01:00

Hypercalcemia in MRCP

As a houseofficer many years ago, I remember that there are two electrolytes that are frequently encountered during clinical practice- Potassium and Calcium.

We have discussed a lot about Potassium, I am going to talk about Calcium metabolism today and of course talk more about hypercalcemia.

It is pretty easy to remember, the only pool of calcium in our body is bone. Although tiny amount of calcium is being absorbed through the gut ( affected by Vitamin D), maintenance of normal calcium level in serum ( 2.2-2.6) greatly depends on exchange of Calcium between extracellular fluid and bone.

It is easy to remember that if we have low calcium level, our body will try to do the followings to increase calcium level in the serum,

1) Increase Calcium absorption from the gut
2) Increase bone resorption in the bone so that more calcium can be released to the serum
3) Reduce Calcium excretion from the kidney

The main organ that regulates these is parathyroid hormone. You can think of causes of hypercalcemia into a few big groups as below,

1) Bone problem
It is easy to understand this, when there is increased bone destruction, of course you calcium level is high. Therefore, any malignant disease either primary or secondary that leads to bone destructions can cause hypercalcemia.

2) Vitamin D problem
As I said before, Calcium absorption from the gut is mainly affected by Vitamin D, therefore, Vitamin D toxicity or granulomatous diseases ( such as Sarcoidosis or tuberculosis) can cause hypercalcemia.

3) Parathyroid hormone
Of course, when you have high parathyroid hormone ( primary and secondary), you calcium level is high but remember that secondary hyperparathyroidism may have normal or even low Calcium level.

4) Others
Some other rare causes such as Familial hypocalciuric hypercalcemia, milk alkali syndrome, immobility etc.

Immunosuppressive Drugs (1)

2008-09-20T08:57:00.001+01:00

Immunosuppressive Drugs- Cyclosporin

Sorry for the long absence from my blog. I just shifted to my new house and had to live without broadband for almost 3 months.

OK, today I am going to talk about cyclosporin ( prototype of calcineurin inhibitor) because this drug change the landscape we look at solid organ transplantation. It was discovered in 1971 and subsequently approved for use in 1983.

I do not think you care about the history. The more important topics you want to know are popular questions in MRCP, here are the popular questions,

1) Drug Interacations

Since cyclosporin is metabolised in the liver by cytochrome P-450, there are a lot of drug that can induce/inhibit this enzyme causing low/high cyclosporing level in the blood. Fo the mneumonics of enzyme inducers/inhibitors, you can read my previous blog. Remember that grape juice inhibit the cytochrome P-450!! ( ALL-TIME POPULAR MRCP QUESTION!!)

2) Side effects

This topic is ver popular if you get a case of kidney transplant in MRCP PACES, common side effects are,

Tremor
Hypertension
Gum hypertrophy
Electrolyte imbalance
Nephrotoxicity

I will talk more about immunosuppressive drugs in my future blogs!!

Guillain Barre syndrome in MRCP

2008-07-21T15:07:00.000+01:00

Guillain Barre syndrome in MRCP

There are only a few common neurology problems that are popular in MRCP. One of them is Guillain Barre syndrome and I think I will try to highlight some salient points about this condition.

First thing to remember about this condition is we always term any medical problem a syndrome when we do not understand fully about it.

GBS was first described in 1859 by Landry. Guillain Barre syndrome is a type of acute inflammatory demyelinating peripheral neuropathy mainly involving the motor modality.

Although it may involve sensory or autonomic modality, classically you will be given a question involving motor neuropathy in MRCP.

GBS is believed to result from autoimmune humoral- and cell-mediated responses to a recent infection or any of a long list of medical problems.

Second lesson to be learned if you are sitting for MRCP is patient with GBS usually come to the hospital after viral or bacterial infection. The common infections associated with GBS are Campylobacter jejuni , Haemophilus influenzae, Mycoplasma pneumoniae, and Borrelia burgdorferi and influenza. Therefore patients usually have gastrointestinal and respiratory illness before the onset of GBS.

Patient with unilateral foot drop

Patients usually come with ascending weakness and some of them may complain numbness over the extremities.The classical physical signs are bilateral foot drop with loss of reflexes. However, remember some rare variants involving cranial nerves may be seen ( Miller-Fisher),patients may present with facial weakness mimicking Bell palsy, dysphagia, dysarthria, ophthalmoplegia, and pupillary disturbances.

Patients with GBS will usually die because of autonomic dysfunction with cardiac dysrhythmias or respiratory muscle involvement.
How to diagnose GBS, you have to do lumbar puncture, classically you will find elevated CSF protein. However, you may want to do nerve conduction study ( a delay in F wave), if you are suspecting Miller-Fisher, anti-GQ1b may be present.
How to monitor your patient’s respiratory function, monitor their Forced vital capacity.

Treatment is giving IV Immunoglubulin!

Liver Cirrhosis in MRCP

2008-05-05T15:35:00.000+01:00

Liver Cirrhosis in MRCP

I came across a lot of liver cirrhosis cases during my housemanship. I remember a patient who actually came to medical ward almost every month for theraupeutic peritoneal tapping.
Liver cirrhosis just means the liver is irreversibly destroyed by fibrosis and degeneration of the hepatocytes. Actually, it should be a pathology diagnosis, however we always can diagnose this by physical signs and ultrasound alone.
There are a few important points for you to remember if you are sitting for your MRCP Part 1 and 2, I would summarize these points as below,

1) Causes of liver cirrhosis
The causes of liver cirrhosis greatly depend on where you are working. If you work in Western countries, alcohol is always the number one cause. However, chronic hepatitis will be top in the list if you live in Asia. For your MRCP, there are three more causes you need to remember- cryptogenic ( idiopathic), Budd-Chiari syndrome and haemochromatosis. I talked about haemochromatosis before, please read about it.

2) Clinical signs of chronic liver disease
If you are studying for your MRCP PACES, then you will know that there are more than 20 signs for stigmata of chronic liver disease. However, remember a few important ones such as jaundice, spider naevi, gynaecomastia, testicular atrophy, leuconychia, finger clubbing.......etc

3) Investigations
First you must try to find out the underlying cause, second you must prognosticate your patient. Child’s criteria is the important criteria to remember. The mnemonic to remember- BAPA + E( BAPA means ‘father’ in Malay language)- Bilirubin level, Ascites, PT ( INR) and Albumin level and encephalopathy.

4) Complications of liver cirrhosis
Patients usually die because of upper GIT bleeding. However, they are bought to hospital because of hepatic encephalopathy. Remember all the precipitating of hepatic encephalopathy.

5) Treatment of liver cirrhosis
Almost all are supportive, liver transplantation provides cure but almost not done in this part of the World. However, always prevent hepatic encephalopathy and minimize the risk of UGIB. Do yearly monitoring to look for liver cancer.

Gyanecomastia for MRCP

2008-04-28T17:16:00.000+01:00

Causes gyanecomastia for MRCP

I was asked by a medical student about gyanecomastia today during my ward round.
I think it is important during your MRCP Part 1 because it is a popular question. OK, before talking about the causes, let us define what gyanecomastia is. Gyanecomastia just means male breast enlargement.

It is certainly abnormal for male to get breast enlargement, however, you may be suprised that I divide gyanecomastia into physiological and pathological gyanecomastia.

You heard me right, there are times in a male life that he can get breast enlargement abd it is totally physiological!

Man gets gyanecomastia when they are newborn, adolescents (puberty) and they are old!
Causes of pathological gyanecomastia are enormous, however there are only a few big groups,

1) Drug related
I always remember a few important ones, they are cimetidine, ranitidine ( H2 antagonists), spirolactone, digoxin and of course estrogen or drug that makes you less masculine.

2) Certain tumours
Popular ones are brochogenic carcinoma, testicular tumour and HCG producing tumours

3) Congenital
Popular syndromes are Klinefelter syndrome, Kallman syndrome

4) Systemic illness
Popular systemic illnesses are chronic liver disease and in certain chronic kidney disease.

Chronic Myeloid Leukemia in MRCP

2008-04-10T15:20:00.000+01:00

Chronic Myeloid Leukemia in MRCP

Chronic Myeloid Leukemia (CML) is always a popular differential diagnosis in your MRCP PACES examination if you encounter massive hepatosplenomegaly during your abdominal short case.

CML is one of the 4 disorders ( besides polycythamia rubra vera, essential thmrobocythemia and myelofibrosis) termed as myeloproliferative disorders.

The term myeloproliferative disorders describes a group of conditions characterized by clonal proliferation of one or more haemopoietic components in the bone marrow and in many cases, the liver and spleen.

OK, patients usually present the following ways,

1) abdominal pain and distention because of massive hepatoslpenomegaly
2) bleeding tendency due to platelet dysfunction
3) features of anaemia
4) gout or renal impairment due to hyperuricaemia ( because of excessive purine breakdown)
5) some rare symptoms such as priapism ( this is the only cause of priapism I can remember during my medical school time because there was no Viagra yet at that time!!)

I think if you see a case of CML during your MRCP PACES, you must know how to come to a diagnosis of CML, basically, you can do the following,

1) You always find very high total white cell count when you do full blood count. I remember when I was a house-officer, I encountered a patient who were well and had a TWC of 150,000!!
2) Neutrophil alkaline phosphatase ( NAP) score is low!! ( Remember this well because it is a popular question in MRCP. Also remember diseases that have low NAP score!)
3) Chromosomal study- Remember that you usually find Philadelphia Chromosome which is a translocation of chromosome 9 and 22. ( This is the hottest exam question in MRCP and also your final MBBS!!)
4) Bone marrow is hypercellular with granulopoitic predominance.

5) Peripheral blood film may show various stages of granuloiesis including promyelocytes, myleocytes, metamyelocytes and band and segmented neutrophils

When I was a house officer, I remember that my consultant used a lot of hydroxyurea to treat CML. However, currently imatinib ( Gleevec) which is a tyrosine kinase inhibitor has become the first line treatment for CML.

Hyperkalemia in MRCP (2)

2008-03-22T03:57:00.000Z

Hyperkalemia in MRCP (2)

OK, if you are currently working in any hospital around the world, you certainly agree with me that hyperkalemia always disturbs you a lot. I remember that when I was a house officer many years ago, I was once called by staff nurse because she was worried that patient may collapse simply because his Potassium level was 5.4!

I think the general principles of treating hyperkalemia are simple,

First,

You have to act fast to avoid cardiac arrhythmia.

Second,

To shift the Potassium back to the cell ( intracellular) from extracellular ( plasma) if possible.

Third,

To reduce total body Potassium

Fourth,

AND of course, find out the underlying cause of hyperkalemia.

I will not discuss how aggressive you want to treat hyperkalemia and I think it is a judgment call. Anyway, I would be certainly very worried if the Potassium level is more than 6.5 and there is ECG changes. ( Learn about hyperkalemia associated ECG changes, it is a popular question in MRCP).

So, treatment of hyperkalemia can be outlined as below,

I think the very first step to take is to stabilize the heart by giving Calcium gluconate or Calcium chloride. You may want to open your physiology book to learn the mechanism how Calcium acts.

Then ,of course, you want to try to shift back the Potassium back to the cell by giving insulin and glucose. In Malaysia, the combination of insulin, glucose and Calcium therapy in treating hyperkalemia is termed as cocktail regime!

You can also use beta agonist to shift the Potassium back to the cell. Another useful strategy is bicarbonate infusion. Remember, acidosis causes hyperkalemia, therefore alkalosis corrects hyperkaelmia.
Another strategy you may want to try is giving patient cation exchange resin. However, remember that the effect is not immediate, therefore, you have to use previous various strategies to bring down the Potassium level promptly.

Anyway, I must say the most powerful way of treating your hyperkalemia is haemodialysis!!

Hyperkalemia in MRCP (1)

2008-03-13T13:56:00.001Z

Hyperkalemia in MRCP – Part 1

Electrolyte imbalance is an important topic in MRCP and I think Potassium is the single most important electrolyte in our bodies.

If you are a house officer, I think the commonest electrolyte abnormality you will see in medical ward is hypo/hyperkalemia.

Today, we will discuss about hypokalemia. Before we talk further about causes of hyperkalemia and how do we manage this, we have to learn about basic physiology.

First fact to remember, potassium is mainly intracellular, the concentration of K is about 150mmol/L of H2O inside the cell as compared to about 5 mmol/L outside the cell ( in plasma). Therefore, to maintain this concentration, our body depends greatly on Na-K ATPase channel ( this channel transport 3 Na out of the cell for each 2 K it transports in), however , you must always remember there are H-K ATPASE in specific organs such as kidneys for similar purpose.

Potassium is mainly excreted in kidney although a small proportion is excreted through GIT.

OK, let us talk about causes of hyperkalemia, I can divide them into either increased load, reduced excretion and increased release from cells ( Remember? Potassium is mainly intracellular!)

1) Reduced excretion
Chronic kidney disease ( Potassium is mainly excreted via kidney )
Mineralcorticoid deficiency ( learn the effect of mineralcortiocid on Na-K channel, you will understand)
Some drugs ( especially ACEI/ARB, heparin, potassium sparing drug)

2) Increased load
Overzealous Potassium supplement
Transfusion of blood

3) Increased release from cell
Any causes leading to major cell breakdown such as tumour lysis sundrome, tissue necrosis, rhabdomyolysis
Acidosis ( Remember I told you about H-K pump!!)
Beta blocker

OK, I will talk about management of hyperkalemia in my next post.

Hyperthyroidism in MRCP

2008-02-16T01:18:00.002Z

Hyperthyroidism in MRCP

Hyperthyroidism is the commonest endocrine problem you will see during your practice either you are in endocrine unit or general medicine.

Therefore, I think you must learn hyperthyroidism well and it is commonly asked in your MRCP/USMLE examination as well.

Common causes of hyperthyroidism are Grave’s disease, toxic multinodular goiter and toxic nodule (adenoma). You will most probably seeing mostly Grave’s disease as the cause of your patient’s hyperthyroidism especially among younger female patients.

Anyway, first thing to remember in your MRCP, there are a lot of drugs that can cause hyperthyroidism and two commonly asked drugs are Lithium and amiodarone. I have talked about amiodarone in my previous post. Learn this drug hard because it is important and a popular drug in your exam.

OK, to learn about the signs and symptoms of hyperthyroidism, it is rather logicaland easy to remember. It is an important metabolism hormone, therefore when there is an increased level of thyroid hormone, everything in your body is increased- your heart rate, your metabolism rate, your gut peristalsis etc. Therefore, you anticipate patient to compliant palpitation, weight loss and diarrhoe. Depending on whether patient has Grave’s disease, you may get some eye symptoms and signs.

However, as a medical student before, I remember that everything in hyperthyroidism is increased except patients have reduced power ( proximal myopathy) and female patients may have less/reduced menses ( amenorrhoea). Remember as well urticaria can develop in hyperthyroidism.

Another thing to remember, a lot of young patients with hyperthyroidism have a lot of symptoms but always older patients with hyperthyroidism appear to be ‘silent’ ( no symptoms) and they always present with just atrial fibrillation or symptoms suggesting heart failure.

One lesson to be learned here, always check patient’s thyroid function if you can’t find out the underlying cause of patient’s heart failure especially among older patients.

Learn how to interpret thyroid function test ( easy, T3 or T4 is high with low TSH suggest hyperthyroidism), however, remember the side effects of anti-thyroid drugs.
Two important side effects to remember- agranulocytosis and skin rash. It is your duty to check patient full blood count after you start them on anti-thyroid drugs because patient may later come to you’re A+E with leucopenic sepsis due to carbimazole!

Prolactin in MRCP

2008-01-23T13:48:00.000Z

Prolactin in MRCP

I always enjoyed studying endocrinology during my medical school time. One of my old professors said, endocrinology is straight forward and logical. Our body is designed in a way when our hormone level is high, there will be a negative feedback and vice versa. Our bodies try to maintain a normal level of all hormones so that we can function normally.

A trick to remember when you study endocrinology, you must understand normal physiology so that you can understand each hormone clearly and not just memorize them by hard.

OK, today, we will start to learn the first hormone- prolactin. Why prolactin?It is rather interesting that we know prolactin is important for females because it helps in milk production but its function in males remains a mystery!

I think there are a few important facts about prolactin that always asked in your MRCP!

Fact 1:

All hormones in pituitary glands are up regulated by another hormone in hypothalamus ( positive feedback) except prolactin. This means that prolactin production will be inhibited by another hormone prolactin inhibiting hormone ( PIH) from hypothalamus. Remember that PIH is dopamine, therefore your dopamine agonist such as bromocriptine is used to suppress prolactin and thus milk production. ( And also remember that due to its dopaminergic effects, bromocriptine is used in Parkinson’s disease).

Whereas drugs which as anti-dopamin effect such as metoclopramide is used to stimulate prolactin production and it is always used in O+G for post partum mothers if they have problems in milk production.

Fact 2:

You do not believe it, prolactin is a stress hormone. As a medical student, I always do not understand why God created prolactin as stress hormone. Anyway, prolactin level can be measured if you want to differentiate a true seizure from pseudo-seizure because its level is high after an epileptic fit.

Fact 3:

When there is a non-secreting tumour in pituitary causing damage to the stalk, you anticipate secretion of all hormones from pituitary to be reduced ( because positive feedback from hypothalamus) but prolactin level is high because there is no negative feedback from hypothalamus.

Fact 4:

One of the commonest causes of hyperprolactinoma and galactorrhoea is drug-induced and it is due to Phenothiazines!!

Benign Intracranial Hypertension in MRCP

2008-01-11T15:23:00.000Z

Benign Intracranial Hypertension in MRCP

I always remember that benign intracranial hypertension is a popular topic in MRCP Part 1 and 2. Recently, my wife was studying her FRACGP and I noticed that BIH is one the hottest topics as well.

Since this illness is so popular and important, I think we should spend sometime talking about BIH today.

OK, why we say intracranial hypertension is benign?? When there is intracranial hypertension, we anticipate there will be some problems inside our craniums, however, if there is presence of intracranial hypertension without any obvious intracranial mass or enlargement of ventricles or hydrocephalus, we term the illness as BENIGN ( it won’t kill you!!) intracranial hypertension.

There are a few facts to remember for BIH,

Fact 1:

Remember that majority of patients are young female who are obese and usually in your MRCP, they will give you an example of an obese lady with acne. Why acne?? I always wondering when I was a medical student. After struggling for many years, I finally understood this. The reasons are, some anti- acne actually cause BIH such as teteracycline, Vitamin A and drugs that can precipitate acne formation such as steroid also lead to BIH!!

Fact 2:

Although we were taught that papilloedema is an emergency if patient has headache. Remember that patient with BIH has headache and papilloedema ( although rarely they might have blurring of vision and seizure) but it is benign and the brain imaging and CSF are normal.

Fact 3:

Since patient with BIH is always a young female patient, you must put sagittal sinus thrombosis as your differential diagnosis. This is because you also anticipate young ladies are prone to get autoimmune disease especially SLE and they are usually on oral contraceptive pills and these put the ladies at risk of developing sagittal sinus thrombosis.

Fact 4:

Treatment is easy, stop the drug and weight reduction but you may use loop diuretics or acetazolamide.

Example of question:

A 22-year-old obese woman presented with an 8-week history of headaches, pulsatile tinnitus and transient visual loss on standing lasting a few seconds. She had otherwise been well with no history of note. She took the oral contraceptive pill and had been taking this for the last 6 months and used salbutamol inhalers on an occasional basis for her asthma which she had from childhood. She also took vitamin Asupplements which she bought over the counter for her general health. On examination, the only abnormality of note was bilateral papilloedema. MRI brain and MR Venogram are normal. Lumbar puncture showed an opening pressure of 38, normal protein, glucose, and cells.. What is the most likely diagnosis?

1 )Herpes simplex encephalitis

2 )Intracranial hypertension secondary to vitamin A

3 )Malignant meningitis

4 )Sagittal sinus thrombosis secondary to OCP

5 )Sagittal sinus thrombosis secondary to SLE

2008-01-08T15:10:00.000Z

Drug in MRCP-Phenytoin

Although some of you may be not so familiar about phenytoin especially for those who are practicing medicine in developed countries. I think this is because there are so many new antiepileptic drugs available in the market now.

Actually, phenytoin is the oldest non-sedative antiepileptic drug introduced in 1938!!
I think it is not so important for you to understand how phenytoin acts because I myself never understand it when I was a medical student myself many years ago.

In MRCP examination, there are a few important facts that you must always remember.

Fact 1 : Drug metabolism/binding

Remember that phenytoin is mainly bound to protein. Therefore, when there is hypoalbuminemia, there is decreased protein binding- results in a decrease in total plasma concentration of drug but not the free concentration.

Therefore a lot of doctors tend to increase the drug dosage to maintain total drug levels in the therapeutic range- leading to toxicity.

Besides that remember that hepatic enzyme induction and inhibition also alter its drug level.

Although phenytoin is mainly metabolized in liver, its metabolites are excreted in kidney, therefore, renal failure may precipitate toxicity.

Fact 2: Side effects

As I remember as a medical student, there are two interesting side effects of phenytoin- gum hypertrophy ( Look out the photo at http://www.passpaces.com/ ) and generalized lymphadenopathy. However, remember that acute toxicity of phenytoin also leads to cerebellar signs!!

Fact 3: Cardiac complications

Since phenytoin alters Na, K and calcium conductance, it can cause cardiac arrhythmia, therefore always put patient on cardiac monitor if you suspect toxicity.

Also remember that chronic use of phenytoin can lead to Vitamin D metabolism abnormalities and osteomalacia.

Happy New Year!!

2007-12-31T14:57:00.000Z

Happy New Year 2008

For those who will be sitting MRCP Part 1 and 2 in 2008, good luck and YOU CAN DO IT!!

Make a resolution today and hope 2008 will be a happy year for everyone!!

Wilson's Disease in MRCP

2007-12-18T14:27:00.000Z

Wilson’s Disease in MRCP

Actually, after practicing medicine for 6 years, I have seen only a case of Wilson’s disease. I have a patient with liver cirrhosis and after intensive investigations ( which include autoimmune screening, viral hepatitis screening, etc etc), no cause was found.

No doctor actually could find out the underlying cause of her liver cirrhosis and attributed that to cryptogenic liver cirrhosis. Later she developed tremor and was diagnosed to have Wilson’s disease after 5 years under our hospital follow up.

Anyway, I think it is a difficult disease to diagnose and I hope to discuss more about this illness today.

First thing to remember in your MRCP, Wilson’s disease is an autosomal recessive disorder involving copper metabolism. In normal subjects, ingested copper mostly will be absorbed and transported to the liver. In the liver, copper is incorporated into an alpha-2-globulin to form caeruloplasmin. Caeruloplasmin is the transport protein for copper and necessary for biliary excretion.

For patients with Wilson’s disease, there is defective intrahepatic caeruloplasmin formation. This leads to increased body and tissue copper level due to biliary excretion failure. However, urinary copper excretion is increased to compensate for defective biliary excretion.

OK, that’s the theory part of Wilson’s disease, you can think of copper as iron, when there is overload of copper in the body, it will be deposited in various organs in the body. However, remember five major organs/tissues that are frequently asked in your MRCP,

1) Brain- this can cause Parkinsonism and always remember that Wilson’s disease is one the most important differentials if you have a young patient with Parkisnonism.
2) Eye- Remember, in MRCP, they like to ask about Kayser-Fleischer rings ( although I never seen one in my life!)

3) Liver- this can lead to hepatitis, liver cirrhosis and even hepatocelular carcinoma.
4) Joints- patients can present with polyarthritis.

However, remember that you may not understand this but just remember the fact that patient with Wilson disease can have haemolysis anaemia and renal tubular acidosis and they might have pigment gallstone.

Diagnosis can only be confirmed with liver biopsy ( high copper level), however, you can detect low caerulopalsmin and high 24 hour urinary copper level.

Treatment is easy- give penicillamine or trientine for life.

Peripheral Blood Film in MRCP(3)

2007-11-24T01:27:00.000Z

Peripheral Blood Film in MRCP (3)

OK,sorry for the long inactivity and quietness of this blog.

Today, we are going to learn a few more important blood films that are frequently asked in MRCP.

4) Megaloblastic anaemia

During your MRCP examination, they will always show a film with hypersegmented neutrophils. Remember that a normal neutrophil usually has 3-4 segments instead of 8 lobes as shown above!

5) Rouleaux Formation

I was always asked by my lecturer during my second year medical school the question about the abnormality you can detect in blood film for a patient with multiple myeloma. You notice that the RBC's here have stacked together in long chains. Learn more about Multiple myeloma because it is popular in your MRCP.

6) Filariasis

You can detect this only in thick blood film. Although it is almost extinct in UK, you can find this is tropics and subtropics. I always remember it as one of the causes of unilateral leg swelling during my medical school.

Unilateral leg swelling

MRCP Question Bank

2007-11-01T08:05:00.000Z

MRCP Question Bank

Just relax, today we are going to try a few MRCP questions and I hope that you would try to answer all the questions first before looking at the answers at the end of this post.

1)
45 year old female presents with abdominal pain,depression, constipation, polyuria and thirst. Over the last 4 months she has become increasingly aware of tiredness and arthralgia since being diagnosed with hypertension and has been treated with ramipril 2.5 mg daily. Physical examination proves to be entirely normal except for a blood pressure of 162/94 mmHg. Her investigations are as follows:
Haemoglobin 14 g/dl
White cell count 7 x 109/l
Platelets 200 x 109/l
Sodium 148 mmol/l
Potassium 4 mmol/l
Chloride 105 mmol/l
Bicarbonate 28 mmol/l
Urea 8 mmol/l (NR 2-8)
Creatinine 105 umol/l (NR 50-100)
Calcium corrected 3.14 mmol/l (NR 2.2-2.6)
Parathyroid hormone 17 pmol/l (normal range 0.9-5.4)
Bilirubin 16 umol/l (NR 0-18)
ALT 10 IU/l (NR 10-40)
AST 17 IU/l (NR 10-40)
Alkaline phosphatase 130 IU/l (NR 50-100)
What is the diagnosis?
1) Depresseion
2) Primary hyperparathyroidism
3) Chronic renal failure
4) Secondary hyperparathyroidism
5) Bone metastasis due to underlying tumour

2)
A 55 year old male with a 12 year history of diabetes mellitus presents for annual review. He is currently receiving gliclazide at a dose of 80 mg twice daily. Examination reveals a pulse of 76 beats per minute regular and a blood pressure of 152/90 mmHg. Fundal examination reveals bilateral hard exudates. He has loss of vibration sensation in to the ankles but all pulses are palpable.
Investigations reveal the following:
Urine microalbumin = present
Plasma sodium138 mmol/l
Potassium3.8 mmol/l
Urea10.2 mmol/l
Creatinine160 µmol/l
Glucose12.1 mmol/l
HbA1c9.5%
Cholesterol5.5 mmol/l
Triglycerides2.8 mmol/l

Which of the following measures would you adopt to improve this patient's prognosis is?
1 ) ACE inhibitor
2 )Beta-blocker
3 )Increased dose of gliclazide
4 )Add insulin
5 )Aspirin

3)
A 22 year old female presents in the 21th week of pregnancy with profound tiredness and anxiety. Examiantion reveals a tremor, a pulse of 100 beats per minute and a soft bruit heard over the thyroid gland.
Thyroid function tests show a free T4 of 32.9 pmol/l (NR 9.8 - 23.1) and a TSH of 0.04 mu/l (NR 0.5 - 4).
Which of the following treatments would you select for this patient?
1 )Radioactive iodine therapy
2 )Carbimazole
3 )Lithium
4 )Propanolol
5 )Wait and see and repeat her thyroid function test again

4)
A 23 year old female presents with weight gain and a 4 month history of amenorrhoea. Examination reveals a BMI of 33 and mild hirsuitism. Relevant investigations reveal an oestradiol concentration of 1200 pmol/l (NR 130 - 800 pmol/l), a testosterone concentration of 2.8 nmol/l (NR less than 3 nmol/l), a prolactin concentration of 1500 mU/l (NR 50 - 450 mU/l),an LH of 1.2 u/l (NR 1.2 - 8 u/l) and a FSH of 1.5 u/l (NR 1.5 - 8 u/l).
What is the most likely diagnosis:
1) Prolactinoma
2) Polycystic ovaraian syndrome
3) Adrenal tumour
4) Pregnancy
5) Cushing syndrome

ANSWERS: 1) 2 , 2) 1 , 3) 2 , 4) 4

Hospital, hospital, hospital!!

2007-10-23T15:49:00.000+01:00

Hospital, hospital, hospital!!

Recently received an email from one of the readers of this blog asking me to write something about myself.

I also received another email from UK asking me to update this blog more frequently if possible. OK, OK......., certainly many doctors in a Malaysian public hospital will share with me the same feeling that while serving in a government hospital in Malaysia, you are mentally and physically prepared to be underpaid and overwork!

Today, there are 44 patients in my ward and three of them are critically ill. You can expect that you will never get enough ICU beds in hospital because there are simply too many patients in this country and too few beds!! I am running up and down of my ward and calling up other wards to beg for extra beds for my overflow patients.

We do not have enough beds not because we do not have enough hospitals but simply that our people just cannot afford to pay to go to private hospitals. There are more than 6 BIG private hospitals in Penang but these hospitals for the RICH only and of course, for those who have a medical card.

I do not know what the policy makers are having in their minds in this country. I anticipate that our country is going to be broke soon if we continue to practise subsidized healthcare system.

What I can see everyday in my hospital is our people are getting poorer and poorer although you may be bombared by news that our economy is great and we have produced the every first muslim astronaut in the World.

We need changes in our healthcare system. We have to make our healthcare more affordable for everyone and people can assess the healthcare system easily. No point if you say that we have the cheapest healthcare system in this World when large number of patients are clamped in a congested ward with limited numbers of staff nurses and doctors.

If we overwork and underpaid, we are providing sub-optimal care to our patients. And you can't expect our people to have first world mentality when they are getting third world salary!!

2007-10-04T15:06:00.000+01:00

Flow Volume Loops in MRCP

OK, if we talk about respiratory in MRCP, there are two important topics to learn before you decide to take your MRCP part 1 and 2. I think all MRCP candidates should learn by hard flow volume loop and spirometry because you will be expecting a lot MRCP questions about these two topics.

Today, we are going to learn about flow volume loop, a flow volume loop is produced by plotting flow on the y axis against volume on the x axis.

If a subject inspires rapidly from residual volume (RV) to total lung capacity (TLC) and then exhales as hard as possible back to residual volume, then a record can be made of the maximum flow volume loop.

1) Normal Flow Volume Loop

Normal. Inspiratory limb of loop is symmetric and convex. Expiratory limb is linear. Flow rates at the midpoint of the inspiratory and expiratory capacity are often measured. Maximal inspiratory flow at 50% of forced vital capacity (MIF 50% FVC) is greater than maximal expiratory flow at 50% FVC (MEF 50%FVC) because dynamic compression of the air-ways occurs during exhalation.

2) Obstructive disease ( asthma, COPD)

Although all flow rates are diminished, expiratory prolongation predominates, and MEF < MIF. Peak expiratory flow is sometimes used to estimate degree of airway obstruction but is dependent on patient effort.

3) Restrictive Disease ( interstitial lung disease)

The loop is narrowed because of diminished lung volumes, but the shape is generally the same as in nor-mal volume. Flow rates are greater than normal at comparable lung volumes because the increased elastic recoil of lungs holds the airways open.

You may find the graphs very confusing, just remember a few principles here,

1) In obstructive airway disease, due to airway obstruction, the PEF ( Peak expiratory flow rate) is lower than normal ( refer to above graph).

2) In restrictive lung disease, patient total lung capacity ( TLC) is compromised due to pathology ( such as fibrosis), therefore, you notice that, TLC in restrictive lung disease is smaller as compared to normal flow loop.

( One thing to remember, the value of X axis of the flow loop get smaller toward the right!!)

Source:
1) The Merck Manual

MRCP Questions

2007-09-19T15:06:00.000+01:00

MRCP Questions

Recently came across a few popular MRCP Part 2 questions. You may want to give these questions a try before looking at the answers at the end of this post.

1) A 58-year-old man with diabetes finds that the vision in one eye is blurred when he reads, but not at other times. The most likely diagnosis is:

A : Macular oedema
B : Floaters
C :Cataract
D :Glaucoma
E :Stroke.

2) A 22-year-old woman notice that her right eye vision has become blurred over the last three days and she can now see very little with it. The fundus (see image) shows:

A : papilloedema.
B : grade IV hypertensive retinopathy.
C : normal appearance.
D : optic disc swelling probably due to an acute optic neuropathy.
E : central retinal artery occlusion.

3) What does this optic fundus show?

A : Proliferative diabetic retinopathy
B : Background diabetic retinopathy
C : Grade III hypertensive retinopathy
D : Branch retinal vein occlusion
E : Central retinal vein occlusion

Answers:

1) A 2)D 3) B

New Drugs in MRCP- Rituximab

2007-09-11T14:20:00.000+01:00

New Drugs in MRCP- Rituximab

I am going to talk about another –ximab drug today-Rituximab. If you are currently working in a haematology unit, Rituximab is not a stranger to you because I think haematologists are the ones who use this drug most.

As Infliximab, Rituximab ( Trade name: Rituxan) is also a chimeric monoclonal antibody , it was first approved in 1997 for the treatment of lymphoma and it has become a standard treatment for aggressive lymphoma. As you might remember during your medical time that CHOP is the standard treatment for lymphoma but currently the treatment of choice it is R-CHOP! (CHOP stands for Cytoxan, Hydroxyrubicin (Adriamycin), Oncovin (Vincristine), Prednisone/Prednisolone.)

Besides lymphoma, remember that Rituximab is also useful for the treatment of Rheumatoid arthritis, autoimmune haemolysis, idiopathic thrombocytopaenia purpura, Evans syndrome and SLE ( Systemic Lupus Erythematosis). Rituximab is a unique therapy that works selectively by depleting CD20+ B cells.

The side effects of Rituximab is quite similar to Infliximab.

Check out more about this drug HERE!

New Drugs in MRCP-Infliximab

2007-09-03T13:41:00.000+01:00

Infliximab in MRCP

I learned pharmacology about 10 years ago. If you are one of few doctors that studied pharmacology many years ago, you might find some drugs that being asked in MRCP that you never come across before. I will talk about a few new drugs that are rather common and popular in MRCP that you might have not studied during your medical school.

The first drug is Infliximab ( Trade Name: Remicade) Infliximab is known as ‘ chimeric monoclonal antibody’ that blocks tumour necrosis factor alfa ( TNF alfa). You might come across the word ‘chimera’ in movies such as ‘Relic’ which means monster.

In Greek mythology, the Chimera is a monster, depicted as an animal with the head of a lion, the body of a she-goat, and the tail of a dragon (sometimes it has multiple heads).

In medicine, a chimera is an animal that has two or more different populations of genetically distinct cells that originated in different zygotes.

The first thing you need to know about Infliximab is its indications. Infliximab has been approved by the U.S. Food and Drug Administration for the treatment of psoriasis, pediatric Crohn's disease, ankylosing spondylitis, Crohn's disease, psoriatic arthritis, rheumatoid arthritis, and ulcerative colitis.

You must know that infiximab is classified as immunosuppressive drug, therefore always watch out for infections ( such as tuberculosis- always asked in MRCP. Always screen for possible latent TB before starting the drug!), blood disorders ( bone marrow suppression), cancers ( such as lymphoma) and allergic reaction.

Be careful if you want to start Infliximab in patients with heart failure and chronic viral hepatitis due to possibility of reactivation!

Peripheral Blood Film in MRCP(2)

2007-08-18T11:11:00.000+01:00

Peripheral Blood film in MRCP(2)

I told you a few basic terms used in haematology in my previous post. Today, I will talk about a few common and popular blood films that are commonly asked in MRCP Part 1 and 2.

1) Sickle Cell disease

( Blood film of sickle cell, polychromasia and target cell)

By far, I think this the most popular blood film in MRCP. Remember that patients with sickle cell may present with bone pain ( due to bone necrosis), osteomyelitis, leg ulcers or even iron overload. Remember that it is one of the important causes of chronic haemolysis anaemia, therefore, you might find pallor with jaundice in patients with Sickle Cell Disease. However, remember that you may not find splenomegaly ( although you anticipate splenomegaly in patients with chronic haemolysis) because there is a possibility of splenic infarct!!

( Patient presents with painful bony infarction)

2) Thalassemia

This disease needs no further explanation. I have seen so many Thalassemic patients during my paediatric posting when I was a medical student.

Look at the following blood film,

( Blood film showing hypochromic, microcyctic red cells)

You may be given a photo of patient with classical thalassemic facies and you are expected to know about types of Thalassemia, chromosome involved and complications!

3) Malaria

OK, if you are living in UK or Ireland, you may not seen a case of malaria in your whole life. However, malaria is endemic in tropical countries including Malaysia and Thailand. You may still remember that there are various species of Plasmodium such as P.falciparum, P.vivax and P.ovale. Anyway, remember that in your MRCP, they always show you the ring form!

Infectious Disease in MRCP- Leptospirosis

2007-08-07T15:34:00.000+01:00

Infectious Disease in MRCP-Leptospirosis

OK, I told you before a few common infections which are popular in MRCP examination. These infections include HIV, Tuberculosis, Infective endocarditis. Today, we are going to discuss another common infection which is popular if you are sitting MRCP Part 1 and 2 examination.

Yes, Leptospirosis is important because it is the most wide spread zoonosis caused by Gram-negative organism Leptospira interrogans. It is harboured by wide varities of animals but mainly by rats. Therefore, anyone exposed and has contact with animals, animal products ( like rats’ urine) or soil/water contaminated with leptospiras may get the infection.

Recreational activities like swimming, rafting, canoeing in contaminated rivers/lakes may expose someone to leptospiras.

Signs and symptoms of Leptospirosis

Always remember that patients always go through biphasic course during the illness. Phase 1 ( about 1 week) is considered as febrile/septicaemic phase where patients experience with high fever and non specific symptoms such as myalgia, headache, diarrhoea, arthralgia. ( symptoms that are common in viral infections)

During the second phase (4- 30 days), patients go through what is considered as immune phase where they may have aseptic meningitis, acute renal failure,pulmonary haemorrhage, myocarditis, liver failure ( therefore you may find jaundice) and ARDS.

Investigations

Always check FBC, LFT ( ALT usually mildly elevated), CK which may be raised due to carditis or muscle break down.
Remember that Leptospira can be cultured from blood or CSF during the first week of illness and from urine from 2-4 weeks of illness ( popular question in MRCP). However, diagnosis is usually confirmed by serology.

Complications
Acute renal failure ( common during immune phase), ARDS, DIVC

Treatment

IV penicillin or ceftrixaone or doxycyline for mild disease.

Pulmonary Embolism in MRCP

2007-07-25T14:10:00.000+01:00

Pulmonary Embolism in MRCP

I saw a case of suspected Pulmonary Embolism today, therefore, we will talk about PE today in our MRCP blog today.

I think that Pulmonary Embolism is important not just because you are sitting for MRCP Part 1 and 2 but also as a clinician in everyday practise because it is often missed and not treated.

As defined in Wikipedia, Pulmonary embolism (PE) is blockage of the pulmonary artery (or one of its branches) by a blood clot, fat, air, amniotic fluid, injected talc or clumped tumor cells. By far the most common form of pulmonary embolism is a thromboembolism, which occurs when a blood clot, generally a venous thrombus, becomes dislodged from its site of formation and embolizes to the arterial blood supply of one of the lungs.

However, when we talk about venous thromboembolism, always remember that there are three aspects you must always remember when blood clots inside a vessel. It can be due to either alterations in blood flow, factors in the vessel wall and factors affecting the properties of the blood--- these three factors are well known as Virchow's triad.

Remember that PE usually occurs due to embolism from a blood clot from the lower limb and predisposing factors for deep vein thrombosis is the most popular questions asked in MRCP.

It is easy to remember that there are two major risk factors predispose you to have thrombosis, either inherited or acquired, always suspect inherited causes if young patients present with thromboembolic events and there is presence of family history. Just remember that some inherited causes like Protein C,S, anti-thrombin deficiency and Factor-V Leiden mutation.

But put more emphasis on acquired causes because they are the more important and commoner causes for thromboembolic events, remember the mnemonics below,

EMBOLISM
E- Extra causes- inherited causes
M-Malignancy
B- Baby ( Pregnancy)
O- Oral Contraceptive pill
L- Large- obesity ( maybe lead you to immbolity)
I- Immune disease-Antiphospholipid
S-Surgery
M- Mobility ( immobilization)

Patients with PE usually present with SOB, haemoptysis, chest pain and even sudden death.

There are various investigations can be done to diagnose PE, however, remember you may find Westermark sign ( localised pulmonary oligaemia) in CXR and classical ECG finding ( S1QIIITIII) . Although you seldom see these in clinical practice, I do not understand why these questions are alwyas asked in your MRCP.

However, in 1995 Wells et al suggested a scoring system to diagnose PE and if you are sitting for MRCP PACES, learn this criteria hard!!

The treatment is easy, use heparin and give them warfarin for at least 6 months.

ECG in MRCP(3)

2007-07-14T07:01:00.000+01:00

ECG in MRCP(3)

I have covered common MRCP questions about ECG in my previous 2 posts, today, we are going to talk about heart block, there are two main type of heart block, AV ( atrio-ventricular) block and intraventricular block. We will talk about AV block today. As you might remember as a medical student, there are three subtypes of AV block, namely first, second and third degree heart block.

First degree heart block
It is easy to pick up in your ECG, normal PR interval is 0.12-0.20s, if PR interval is more than 0.2s, it is considered as first degree heart block.

Note: Always remember that shortened PR interval occurs in WPW syndrome!

Second degree heart block

There are two types of second degree heart block,

a) Classical “Wenckebach” ( Mobitz type 1) where the PR interval gets longer (by shorter increments) until a nonconducted P wave occurs. The RR interval of the pause is less than the two preceding RR intervals, and the RR interval after the pause is greater than the RR interval before the pause.

b) Mobitz type 2- For this heart block, AV block the PR intervals are constant until a nonconducted P wave occurs. ( as below ECG)

Third degree heart block

Easy to remember, complete AV dissociation

Blood Film in MRCP(1)

2007-05-25T09:04:00.000+01:00

Peripheral Blood Film in MRCP(1)

Certainly before your MRCP Part 1 and 2, you need to know a very important topic in haematology, you are right, many candidates have the tendency to go to the examination without knowing anything about blood film.

You must know a few popular blood films in MRCP, before we proceed to revise a few important blood films, I think you must remember these useful terms here,

1) AniSocytosis- Variation in Size.
2) Poikilocytes- Variation in shaPe
3)

Basophilic stippling of RBCs is seen in lead poisoining, thalassemia and other dyserythropoetic anaemias

( Image over the left with arrow)

4) Blasts- Nucleated precursors cells
5) Howell Jolly bodies- Nuclear remnants seen in in RBCs especially in post splenectomy
6) Leukaemoid reaction- A marked reactive leucocytosis
7) Left shift- Immature white cells seen in circulating blood
8) Right shift- Hypersegmented polymorphs ( Image below)

9) Rouleaux formation- Red cells stack on each other
10) Target cells RBCs with central staining, a ring of pallor and an outer rim

Spondyloarthropathies in MRCP (2)

2007-05-03T04:34:00.000+01:00

Spondyloarthropathies in MRCP (2)

I talked about Spondyloarthropathies ( Ankylosing spondylitis) in my previous post. In MRCP Part 1 and 2, there are a few more conditions you should know because these conditions are very popular.

1) Reiter’s syndrome

Remember the triad of conjunctivitis, urethritis and arthritis. This was described by Hans Reiter in 1916.

Reactive arthritis is triggered following enteric or urogenital infections. Reactive arthritis is associated with human leukocyte antigen (HLA)–B27, although HLA-B27 is not always present in an affected individual.

Bacteria associated with reactive arthritis are generally enteric or venereal and include the following:, Salmonella typhimurium, Salmonella enteritidis, Streptococcus viridans, Mycoplasma pneumonia, Cyclospora, Chlamydia trachomatis, Yersinia enterocolitica, and Yersinia pseudotuberculosis.

Remember that always suspect this in young patients who come in with large mono- or oligoarthritis especially knee pain.

Other features of this syndrome include Keratoderma blenorrhagica

( a popular image in MRCP, brown, aseptic abscesses on soles and palms)), iritis, mouth ulcers, enthesopathy ( plantar fascitis, Acgilles tendinitis) and aortic regurgitation ( rare)

You may do imaging such as , however, Plain radiography - May show no abnormalities early in the disease

Asymmetric, oligoarticular, and more common in the lower extremities pattern of joint involvement
Juxta-articular osteoporosis in acute episodes of arthritis - Erosions have indistinct margins and are surrounded by periosteal new bone.
Spinal pattern - Unilateral or bilateral sacroiliitis, asymmetric paravertebral comma-shaped ossification involving the lower thoracic and upper lumbar vertebrae

Treatment: bed rest and NSAID

2) Psoriatic arthropathy

Kindly visit PassPACES.com for further discussion

3) Enteropathic spondylitis

Always suspect this if patient has bowel symptoms ( diarrhoe and weight loss) and large mono- or oligo-arthropathy. However, remember as well that peripheral arthritis ( small joints) may be involved but it is rare!

Basic Anatomy in MRCP(II)

2007-04-07T15:40:00.000+01:00

Basic Anatomy in MRCP (II)

I have covered the first six cranial nerves in my previous post, today we are going to talk about another a few interesting points about the first six cranial nerves that are frequently asked in MRCP.

1) Correlation of third cranial nerve with pupil size is an important topic to study. Generally, if you can still remember as a medical student, isolated third nerve palsy is always divided into either a 'medical' or 'surgical' third nerve palsy. As you can remember from my previous post, I told you that third nerve palsy should cause patient to have dilated pupil due to its parasympathetic component.

A COMPLETE third nerve plasy ( Above patient - right third nerve palsy) should have:

i) Dilated pupil (mydriasis)
ii) Ptosis
iii) Deviation of eye laterally and downward ( due to unopposed actions of lateral rectus and superior oblique)

However, you may encounter a patient with third nerve palsy having ptosis and deviation of eye laterally and downward but without dilated pupil. This is what we call as 'medical' third nerve palsy. 'Surgical' third nerve palsy is usually due to compression of the nerve (e.g. by tumour, posterior communicating or posterior cerebral artery aneurysms) results in an acute total (painful) third nerve palsy with a dilated unreactive pupil. Pupillary dilatation occurs early when the nerve is compressed since sympathetic nerve fibres that innervate the iris are carried on the outside of the nerve bundle. Pupillary sparing is characteristic of third nerve lesions caused by infarction in patients with diabetes mellitus and hypertension.

2) Isolated 6th nerve palsy is possible and commonly found in patient with increased intracranial pressure. It is termed as ' False localizing sign' because actually you can’t localize any location at the brain that causing this palsy if you observe only isolated 6th nerve palsy. It occurs only to 6th cranial nerve in increased intra cranial pressure because of its long course intracranially and makes it prone to compression when there is an increased pressure inside the skull.

Arterial Blood Gas in MRCP (2)

2007-03-11T11:23:00.000Z

Arterial Blood Gas in MRCP (2)

In my last post, I talked about Metabolic Acidosis and respiratory acidosis. Today I will cover metabolic alkalosis and respiratory alkalosis.

Take it easy because these two conditions are rare in your MRCP examination.

1) Metabolic alkalosis

The only one time you will be see metabolic alkalosis in your clinical practice is after patient has severe prolonged vomiting (especially in pyloric stenosis). This is because our gastric juice is acidic, where there is excessive loss of acid from our stomach, we turn alkalosis. You notice PH↓ and HCO3↑. You body may compensate by keeping more CO2 therefore there is a possibility that in your ABG, PaCO2↑

2) Respiratory Alkalosis

This is commonly seen in your clinical practice especially in A+E department but it is not an emergency. You usually see young ladies come to A+E complaining of shortness of breath but it is actually due to hyperventilation ( may be due to anxiety or not). However, never always assume that young ladies have hyperventilation when they complain to you that they are breathless. My old professor always told me that because some young ladies may also have pulmonary embolism ( due to risk factor of taking oral contraceptive pill or underlying autoimmune disease) when they are breathless. Therefore, always do an ABG if you are in doubt.

MRCP candidates always worried because in MRCP Part 1 and 2 examinations, they may show combination of abnormalities. There is always one rule to remember, if you can’t explain the abnormalities, always suspect this possibility.

Let me illustrate to you a case, let say a diabetic patient is admitted to you’re A+E due to cough and fever for 1 week and his CXR shows pneumonia. His ABG result is as below,

PH=7.2
HCO3=10
Random blood sugar = high
PaCO2=7 kpa
PaO2= 8kpa

Ok, from these first three results, we notice that this patient has metabolic acidosis ( PH↓, HCO3↓) and it is most probably due to diabetic ketoacidosis because the sugar is high as well. However, you will anticipate the PaCo2 to be low ( due to air hunger) but in this case the PaCO2 is high as well, you can’t explain that ( this is not a normal physiological respond) but from logical thinking, you know that this is a combination of metabolic and respiratory acidosis! ( Patient’s lung is also failing due to severe pneumonia and it is unable to compensate for the metabolic acidosis!)

Arterial Blood Gas in MRCP(I)

2007-02-22T12:16:00.000Z

Arterial Blood Gas in MRCP (I)

Recently I received an email from a MRCP Part 1 and 2 blog reader about ABG interpretation in MRCP. I share with him the same feeling that ABG interpretation is important in MRCP as well as your daily clinical practice.

Our blood PH is closely regulated in a tight range around 7.4±0.05 so that our body can function properly. As you might remember during your secondary school time, enzymes function in certain PH range and will be damaged by acidic or alkaline environments.

Although a lot of candidates ( and a lot of house officers) tend to make various mistakes in ABG interpretation. I would like to give a few simple rules to remember so that you will not make any more mistakes in future,

1) There are two important organs in our body which control our body PH- lung and kidney.
2) Carbon dioxide is an acidic gas, therefore, in acidic environment ( due to various insults), our body ( the lung) tends to compensate by exhaling out more CO2 ( therefore, patient tends to hyperventilate) and vice versa.
3) HCO3 is alkaline and its level is mainly regulated in our kidney.
4) PH=7.4 is normal, if PH less than 7.35 is acidic and more than 7.45 is alkaline.
5) Remember other normal values, normal HCO3=22-28 mmol, PaO2 more than 10.6 kpa ( 1kPa=7.6mmHg), PaCO2=4.7-6.0 kPa ( 35-45mmHg)

OK, for you to interpret ABG results correctly, follow these simple steps,

1) Read the PH first, if PH<7.35, it is acidosis, if it is more than 7.45, it is alkalosis.
2) Once you know whether it is acidosis or alkalosis, you must determine eithet it is respiratory or metabolic, I find two useful parameters to look at, HCO3 and PaCO2.

Let me show you a few examples,

1) Metabolic Acidosis

I still think this is the commonest and most important acid-base balance disorder you will find in your MRCP and daily clinical practice. Read the causes for metabolic acidosis in my previous post.

However, in daily practice, you commonly find metabolic acidosis in uraemia ( chronic kidney disease patient) , diabetic ketoacidosis, salicylates poisoning and lactic acidosis.

Therefore, in metabolic acidosis, you will find PH↓, HCO3↓ and PaCO2↓, it is easy to understand, in metabolic acidosis, our body cannot conserve HCO3, therefore the level of HCO3 is low, however, for our body to compensate ( try to push up PH level), we will hyperventilate to blow out more CO2 ( because CO2 is acidic), therefore, patient will hyperventilate in metabolic acidosis. (air hunger)

You must remember that there are two types of metabolic acidosis- reduced anion gap and normal anion gap ( normal anion gap=8-16 mmol) metabolic acidosis, I have covered this topic in my previous post.

MRCP Question

A 16-year old girl is admitted to your ward from A+E department due to vomiting and abdominal pain. She has no known medical problems and denies taking any illegal drugs.

On examination, you noticed she is dehydrated, blood pressure=90/50, pulse rate=120 and her abdomen is soft. Below are her blood results,

Full blood count
Total white 16,000 ( Normal 4000-11,000)
Hb=12.3
Plt= 235,000

K= 3.2
Creatinine= 110
Na= 131
Cl=100

ABG ( on room air)
PH=7.21
HCO3= 12
PaO2= 12.2 kPa
PaCO2=2.5 kPa

Q: What is the diagnosis?
For the above ABG result, you know that the patient has metabolic acidosis and she presents with history of vomiting and abdominal pain, the first provisional diagnosis you should think of as a SHO is diabetic ketoacidosis!

2) Respiratory Acidosis

This is the second commonest acid-base balance problem you will see in your daily practice. Patients develop this because he/she is unable to blow out CO2 in the lung leading to accumulation of CO2 and respiratory acidosis. Therefore, our body will try to compensate by keeping more HCO3 via the kidney to buffer the acidosis. However, you must remember that kidney works somehow slower than the lung, therefore in acute respiratory acidosis (acute CO2 retention), you may find the HCO3 level is normal but in chronic CO2 retention ( such as in CAPD/COAD or chronic lung disease patients), the HCO3 level tends to be high.

This remembers me when I was a medical student where my lecturer liked to ask me way to help clinicians to differentiate COAD/COPD from asthma by looking at ABG results.

If you are a SHO on call in chest ward, a patient comes in with acute breathlessness and you notice he/she has rhonci all over the lung, you will most probably find the following ABG if you put patient on oxygen supplement,

PH ↓, PaO2 ↑, PaCO2↑ ( Respiratory acidosis)

For COAD /COPD, since that patients may have chronic CO2 retention, you will notice the HCO3 level tends to be high but in asthmatic patients, since it is an acute asthmatic attack that leads patient to have acute CO2 retention, you may find the HCO3 level to be normal ( kidney needs sometime to conserve HCO3, therefore in acute CO2 retention, the HCO3 level may be normal)

However, I must warn you that this rule is only for your reference only, there is no 100% in clinical medicine but I find this rule rather useful in daily practice.

I will talk about metabolic and respiratory alkalosis in my next post!

Happy Chinese New Year!

2007-02-18T11:46:00.000Z

Happy Chinese New Year!

For all MRCP Part 1 and 2 blog readers, Happy Chinese New Year! May your wish comes true this year!

Addison's Disease in MRCP

2007-02-13T13:12:00.000Z

Addison’s disease in MRCP

OK, today I am going to talk about one condition which is important in two ways, Addison’s disease is an important endocrine condition because,

1) It is a popular condition in your MRCP examination,
2) It is important clinically because the mortality is high if you do not pick it up fast in clinical practice especially if patients present with acute Addison's crisis!

Adrenal insufficiency can be due to dysfunction of the adrenal gland itself ( primary- Addison’s Disease) or due to disordered pituitary or hypothalamus function ( secondary)

I think we will cover Addison’s disease today and you can forget about secondary Adrenal insufficiency because it is rather rare.

Addison’s disease refers to primary failure of the adrenal gland leading to loss of production of glucocorticoids and mineralcorticoids.

Causes of Addison’s disease

1) Always remember that it is mainly due to autoimmune adrenalitis and it is associated with Polyglandular autoimmune syndrome. ( Never get yourself confused this with Multiple Endocrine Neoplasia, MEN)
Remember as well that you may find antibodies against the 21-hydroxylase enzyme in 90% of autoimmune cases.

2) Tuberculosis

3) Distant metastasis

Signs and symptoms

As I remember as a medical student, there are 3 main medical causes( non-surgical causes) of abdominal pain, of course Addison’s disease is one of them. The other two are Diabetic ketoacidosis and intermittent Porphyria. ( Always remember this and later you will realize that it is very common for your friends in A+E missing diabetic ketoacidosis simply because patients present with abdominal pain)

Other symptoms include lethargy, nausea and vomiting, dizziness.

Important signs to look for are
1) hyperpigmentation ( it is a popular case in MRCP PACES as well) and I hope you know the reason behind this.
2) postural hypotension
3) loss of body hair ( due to reduced production of androgen)

Investigations
Remember the important clues to look for are
1) Low Sugar
2) Low Sodium
3) High Potassium
------- SSP. Patient may present with fever as well.

Diagnosis

Synacthen test. I think you do not need to know the details and the values. Just know the principles, in normal people, cortisol level will increase significantly after synacthen ( ACTH) stimulation but for Addison’s disease, since there is primary failure of adrenal gland, it will not be stimulated to produce more cortisol after synacthen.

Management

Remember that acute Addsison’s crisis is a medical emergency and it is usually due to prolonged adrenal suppression secondary to exogenous drugs such as steroids.

For chronic Addison’s disease, supplement patients with glucocorticoid ( hydrocortisone) and mineralcorticoid ( fludrocortisone)

Tips for MRCP

You may give a case in your MRCP Part 2 where you are given some electrolytes imbalances in a patient who presents to A+E due to abdominal pain.

ECG in MRCP(2)

2007-02-01T01:41:00.000Z

ECG in MRCP(2)

In sinus rhythm, we know that every P wave is followed by QRS, you must learn hard the following conditions that do not give you sinus rhythm,

1) Atrial fibrillation

This is the commonest condition being asked in MRCP, I have covered this in my previous post.

2) Atrial flutter

Always described as “ Saw-Tooth” ECG in medical textbook. The atrial activity is usually between 250-350 beats /min and there is sually 2:1 or 3:1 block. Causes for atrial flutter are similar to atrial fibrillation as well as the management.

3) Ventricular tachycardia

Defined as three or more successive ventricular extrasystoles at a rate more than 120/min. Remember than VT has a wide QRS complex. Causes of VT include
a) Ischaemia to the heart
b) Hypo-or hyperkl\alaemia
c) Long QT interval ( a very popular question in MRCP, I will cover this in depth in my future post)
d) Cardiomyopathies

4) Torsades des pointes

Actually it is a type of ventricular tachycardia with a varying axis. It often happens after heart attack but can be due to drugs and other causes of prolonged QT interval.

5) Ventricular fibrillation

This rhythm needs immediate cardioversion. Usually happens after a hear attack

Important Tips for MRCP,

It is often difficult to differentiate an SVT with abberant ventricular conduction from VT ( both also have wide QRS complexes), however always remember in clinical practice, always assume VT if you are in doubt and treat accordingly because VT is commoner and life threatening. However, following features suggest SVT with abberant blocks,

1) No fusion or capture beats
2) Presence of P waves associated with ORS
3) Classical RBBB and LBBB ORS morphology
4) ORS <0.14s

5) Same QRS morphology as in sinus rhythm

6) Normal axis

Basic Anatomy in MRCP (I)

2007-01-23T14:48:00.000Z

Basic Anatomy in MRCP (I)

Anatomy was a hell for me when I was a medical student. There is no trick to be good in anatomy except you have a good memory. Luckily, there are not so many questions about anatomy being asked in MRCP Part 1. I will try to cover basic anatomy in a few posts and I hope the information provided in this blog will be useful for you to answer your MRCP questions.

OK, today I will try to cover the first 6 cranial nerves today and I will try to give you a few popular questions in MRCP.

Refresh your memory first and remember all 12 cranial nerves ,

Nerve I, Olfactory nerve- just remember that it is for smell

Nerve II ( Optic) and Nerve III ( Occulomotor) are important nerves to remember,

There are a few common questions asked in MRCP about these two nerves,

a) Remember that Optic nerve is for vision and you must always remember the visual fields , it is important in your MRCP Part1,2 as well as in MRCP PACES

b) Remember your afferent fiber for your pupillary reflex is your optic nerve and your efferent fiber is Occulomotor ( therefore occulomotor nerve is a parasympathetic fiber)

c) Remember that other components of Occulomotor nerve ( besides its parasympathetic function in constricting pupil) are motor components supplying all extraocular muscles except lateral rectus and superior oblique. It also supplies levator palpebrae superoris.

Therefore, a complete third nerve palsy gives,
i) Dilated pupil (mydriasis)
ii) Ptosis
iii) Deviation of eye laterally and downward ( due to unopposed actions of lateral rectus and superior oblique)

SO…….., one very,very important formula to remember in eye movement is (LR6SO4)3, lateral rectus is supplied by sixth nerve (abducent nerve) and superior oblique is supplied by fourth nerve (Trochlear nerve) and others are supplied by third nerve ( Occulomotor)

You will be surprised that we have learned 5 nerves out of first six cranial nerves, the fifth cranial nerve is trigeminal nerve, just remember that its sensory component supplying the facial sensory dermatomes ( One popular question in MRCP is they will show a patient with shingles over the face and you are expected to know what sensory component of trigeminal nerve is involved!)

New MRCP Sites

2007-01-19T12:54:00.000Z

New MRCP Sites

For those who are preparing for MRCP Part 1 and 2, I want to recommend you to visit the following sites which are written by Dr Osama Amin. Although I do not know him personally, I think he has done an excellent job to provide FREE information for those who are sitting for MRCP exams. I think he has similar intention as me----hoping that all of you can pass your MRCP if you really study hard!

1) Neurology for MRCP Mocks
2) Neurology for MRCP Blog

Good luck!

Infective Endocarditis in MRCP

2007-01-08T12:17:00.000Z

Infective Endocarditis in MRCP

Today I would like to discuss about infective endocarditis which is defined as infection of the endothelial surface of the heart. It is a common condition asked in MRCP!A heart valve is always involved but the infection may develop on a septal defect or on the mural endocardium.

Generally, it is useful to classify endocarditis into these three subtypes,

1) Native valve endocarditis- endocarditis develops in native valves. Patients developing native valve endocarditis usually have valvular heart lesion. Common valvular heart lesions that prone patient to get endocarditis include mitral valve lesions ( incompetence and stenosis), aortic valve lesions ( incompetence and stenosis)

2) Endocarditis in Intravenous Drug Abusers- usually IVDUs develop right heart endocarditis ( Tricuspid Valve) due to direct septic emboli to the right heart from peripheral vein.

3) Prosthetic Valve Endocarditis- Endocarditis develops in prosthetic valves. It is easier for you to remember the causative organisms if you divide Prosthetic valve endocarditis into early or late. For early onset Prosthetic valve endocarditis ( onset of symptoms within 2 months post valve replacement), the causative agent is mainly S.epidermidis. Late onset Prosthetic valve endocarditis usually happens post instrumentation in patients with prosthetic valve.

Signs and Symptoms of Infective Endocarditis

Patients may present with fever, lethargy ( may be due to anemia), unexplained weight loss, chest pain, confusion

Always remember about stigmata of infective endocarditis- Janeway lesion ( non- tender), Osler’s nodes (tender), splinter haemorrhages, Roth Spots and petechiae( due to septic emboli)
Splenomegaly
Murmurs
Clubbing
Fever

(A-splinter haemorrhage, B-Conjunctival petechiae, C-Osler's node, D-Janeway's Lesion)

( There is a criteria for you to diagnose Infective Endocarditis known as Durack’s criteria, you do not need to know about the details, however, remember that the two major criteria are positive isolation of organisms from blood culture and evidence of endocardial involvement on ECHO)

Investigations
Full blood count- raised TWC and anemia ( normocystic, normochromic), raised ESR
Haematuria may be present in 50% of cases
Blood culture ( remember that you may need CO2 culture for fastidious HACEK organisms-Haemophilus, Actinobacillus,Cardiobacterium,Eikenella and Kingella)

Complications
Mainly due to septic emboli- the emboli can go to brain, spleen, liver, lung leading to abscess formation. In the heart, infective endocarditis can cause valvular failure, heart block and prosthesis failure!

Treatment
Prolonged IV antibiotics ( up to 4-6 weeks) , usually combination of IV penicillin + gentamycin.
Surgery is indicated if development of fungal endocarditis, valve dehiscence, heart block, valve ring abscesses, failure of medical treatment!

Tips for MRCP
1) Remember patients with what valvular heart lesions need antibiotics prophylaxis before invasive procedures. Click here to find out more!

2) Remember what do you mean by invasive procedures, click here to learn more!

Happy New Year 2007!

2007-01-01T03:27:00.000Z

Happy New Year to MRCP Blog Readers !!

Hi, Happy New Year to all and for those who are sitting MRCP soon, good luck! I would like to wish all of you " Happy New Year" and hope that 2007 will be a wonderful year for everyone. I started MRCP Part 1 and 2 blog 6 months ago and I really like to thank all of you for reading this blog.

Anyway, while sufing the internet,besides learning about medical knowledge, I hope that all of you can get some benefits out of it. I want to introduce to you about AGLOCO. Do you realise how valuable we are?Advertisers, search providers, and online retailers are paying billions to reach you while you surf. Howmuch of that money are you getting? Zilt, so far that is........ZERO!
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Here is why I would like you to consider joining:
1. AGLOCO pays you, as an Internet user, your fair share of the value created while you surf.

2. The AGLOCO's free software puts you in control of what arrives on your screen and what data you allow outsiders to collect.

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Thanks

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ECG in MRCP(1)

2006-12-26T13:25:00.000Z

ECG in MRCP(1)

Today I am going to give you a few examples of abnormal ECGs that are commonly asked in MRCP. However, remember a few basic facts first. Look at a normal ECG first!

1) Heart axis- if I and II are both ‘positive’, axis is normal.
2) If every P wave is followed by ORS, then it is sinus rhythm.
3) Normal PR interval is 0.12-0.20 sec.
4) Normal ORS width is less than 0.12s, if it is more than more than 0.12s, it suggests conduction defects.
5) QT interval- From QRS start to end of T wave. Usually QTc is used and it equals to QT interval divided by square root of RR interval. Normal value:0.35-0.43. ( I try to remember as 0.33-0.43, it is a popular question in MRCP Part 1 about causes of prolonged QT interval!)
6) ST segment: either elevation or depression implies infarction or ishaemia.

OK, today I am going to talk about abnormal heart axis. There are two types of abnormal axis either left axis deviation or right axis deviation.

1) Right axis deviation- You will know it if Lead I is negative.

Causes: All pathology causing right ventricular hypertrophy or strain such as cor pulmonale, pulmonary embolism.

2) Left axis deviation- You will notice this if Lead II and III are negative.

Causes: Left ventricular hypertrophy or strain. Such as hypertension, aortic stenosis.

Merry Christmas and Happy New Year

2006-12-21T13:16:00.000Z

Merry Christmas and Happy New Year

To all readers of this blog, I would like to express my heartfelt gratitude to all of you for being so supportive to this blog. I promise I will try to make this blog better and provide more useful MRCP tips to all of you!

" Merry Christmas " and " Happy New Year"

Make a wish now and hope you can pass your MRCP in 2007!!

Hyperparathyroidism in MRCP

2006-12-01T14:27:00.000Z

Hyperparathyroidism in MRCP

OK, today we are going to discuss an important topic in endocrinology in MRCP, we are going to talk about hyperparathyroidism.

Hyperparathyroidism just means high levels of circulating parathyroid hormone. You must remember that there are three types of hyperparathyroidism, primary, secondary and tertiary.

1) Primary hyperparathyroidism
It is simple, there is no reason ( such as low Calcium level) for the raised parathyroid hormone. It is usually due to problems occurring to the parathyroid gland itself. Causes are adenoma, parathyroid hyperplasia or carcinoma.

2) Secondary hyperparathyroidism
Parathyroid gland is stimulated to secrete more parathyroid hormone due to some underlying reason such as low calcium because of renal failure, Vitamin D deficiency.

3) Tertiary hyperparathyroidism
After prolonged stimulation, the parathyroid gland becomes autonomous and secrets parathyroid hormone without any feedback mechanism

I hope to discuss more about primary hyperparathyroidism today because clinically, we see secondary and tertiary hyperparathyroidism mainly in renal failure patients.Therefore, they are not so important in your MRCP Part 1 and 2!

Presentation of Hyperparathyroidism

As you might still remember as a medical student, parathyroid hormone's main function is to mobilize calcium from bone ( therefore leading to hypercalcemia) and increase urinary phosphate excretion, therefore patients with primary hyperparathyroidism usually present with symptoms due to hypercalcemia.

Remember this old mnemonic:' bone,stones, abdominal groans and psychic moans'!
Other presentations include dehydration ( due to increased diuresis, the reason? Check your book now!), thirst, confusion and myopathy.

Clinical Signs

Not thing much to see and examine unless you get a patient with a very big adenoma or carcinoma. However, always look for associated endocrine neoplasia associated with hyperparathyroidism in MEN ( Multiple Endocrine Neoplasia) I and II such as hypertension ( due to phaeochromocytoma), features of acromegaly due to pituitary adenoma.

Investigations

Raised calcium with ALP
Urine calcium excretion is raised
Xray may show osteitis fibrosa cystica,pepper-pot skull and subperiosteal resorption

Plasma PTH- inapproriately raised! (of course!)

Treatment
Removal of the gland
Indications for operation ( American NIH consensus)
1) markedly elevated calcium (>3mmol)
2) impaired renal function
3) renal stones
4) nephrocalcinosis
5) reduced BMD
6) substantially elevated urinary calcium excretion (>10mmol/24h)

Tips for MRCP

1) remember to suspect MEN every time you diagnose primary hyperparathyroidism

Haematology in MRCP(2)-Sickle Cell Disease

2006-11-18T09:41:00.000Z

Haematology in MRCP(2)-Sickle Cell Disease

Sickle Cell Disease
Sickle cell disease is an inherited blood disorder that affects red blood cells. It is a type of hereditary haemoglobin disorder where valine has been substituted for glutamic acid at position 6 of haem beta chain, caused by a point mutation. You must remember that Sickle Cell Disease (SCD) is inherited in a Mendelian recessive manner. Therefore patients with two Sickle genes (SS) or carry one S gene but with concomitant Beta Thalassemia ( SB) are affected.

This disease is common in peoples of Equatorial African ancestry.

Clinical Presentations

Remember that all clinical features are due to two main features of the disease- haemolysis and vaso-occlusive crisis. You must understand that HbS is insoluble in the dexoygenised form and they have a shorter life span due to increased fragility, therefore causing chronic haemolysis ( similar to Thalassemia). The red blood cells with HbS also tend to aggregrate and cause thrombosis, this will leads to tissue infarction. Remember that the vaso-occlusive crisis tends to be precipitated by HADI ( hypoxia, acidosis,dehydration and infection)

Clinical features due to haemolysis

Anemia
Gallstone
Bone marrow enlargement
( these features also occur in Thalassemia patients)

Clinical fatures due to vaso-occlusive crisis

Bone pain- may cause vascular necrosis

Humerol head avscular necrosis

Leg ulcers
Genito-urinary- priapism
Cerebral-stroke
Spleen- initially may cause splenomegaly due to extra medullary haemopoiesis ( due to anemia) but later splenic infarct and hyposplenism. Patients tend to have capsulated bacteria infection and Salmonella osteomyelitis.
Chest-acute chest pain
( remember that these are all due to thrombotic events)

Physical Signs
Patients tend to be pale with jaundice. Hepatomegaly may be present. Look for chronic leg ulcers.

Investigations

Full blood count- low Hb with features suggesting haemolysis such as increased reticulocyte counts
LFT- increased bilirubin and AST
Peripheral blood film- sickled cells
Haemoglobin electrophoresis- to determine variant haemoglobin
X-ray- to look for vascular necrosis if patients present with joint pain.

Management

During sickle crisis ( oxygen, analgesia, rehydration)
Long term management
- prophylactic penicillin for prevention of penumococcal infection,
- management of anemia, however be careful about secondary iron overload due to multiple transfusions
- folate supplements

Tips for MRCP

1) Always suspect Sickle Cell Disease if a patient has anemia and chronic leg ulcers.

Haematology in MRCP-Polycythaemia

2006-11-08T12:27:00.000Z

Haematology in MRCP(1)- Polycythaemia

I am going to talk about a few important topics that are frequently asked in haematology, MRCP. The first topic that I want to talk about is polycythaemia.

Polycythaemia or erythrocytosis is defined as an increased concentration of red cells, usually with a corresponding increase in hemoglobin level.

I find the following classification of polycythaemia useful and easy to remember.

There are two main types of polycythaemia- Relative polycythamia ( pseudopolycythaemia) or absolute polycythaemia ( true polycythaemia).

Relative polycythaemia means that the absolute red cell counts are normal but due to haemoconcentration because of decreased plasma volume, patient’s haemoglobin is raised. This can be due to any kind of dehydration, however, there is a popular condition often asked in MRCP, it is an obscure condition of unknown origin known as Gaisbock’s syndrome (stress polycythaemia). It is a kind of relative polycythaemia.

For true polycythaemia, the absolute red cell counts are raised and it can be subdivided into either primary ( without obvious reason) or secondary ( with an underlying reason). For primary cause, the most important disease you must learn is polycythaemia rubra vera which I will cover in my future post. For secondary polycythaemia, the haemoglobin can be raised appropriately ( due to increase physiological need) or inappropriately.

There are three common tumours that cause secondary polycythaemia- namely renal cell carcinoma, hepatoma and hemangioblastoma ( very popular question in MRCP!). As for the examples of appropriate secondary polycythaemia, the causes are easy to remember because patients with all these conditions are hypoxia chronically, therefore they need an increase haemoglobin level to survive!

Cardiac Catheterization in MRCP(3)

2006-10-31T12:46:00.000Z

Cardiac Catheterization in MRCP (3)

Today I am going to talk about the last part of this important topic- Cardiac Catheterization in MRCP. In my previous two posts, we have learned about some common cases concerning cardiac catherization in MRCP. I am going to show two more cases here,

Case 1:

Coarctation of the aorta

This is an easy case!There is a steep systolic gradient between the left ventricle and the femoral artery; the gradient is calculated as 190 – 150 = 40 mmHg. Therefore the diagnosis is Coarctation of the aorta.

Case 2:

Tetralogy of Fallot

You notice a combination of pressure and oxygen saturation abnormalities. The abnormalities are,

i) Step-down in oxygen saturation between LA and LV, indicating right to left shunt at the level of the ventricles, therefore there is presence of VSD.
ii) Pulmonary stenosis: there is an 89 mmHg gradient across the pulmonary valve (RV systolic – PA systolic).
iii) RVH: Right ventricular pressures are high and there is a right to left shunt, as indicated by the oxygen saturations

Hope you find this information useful. Remember, in MRCP examination, you may be given the result of a cardiac catheterization and asked about the correct physical signs of a patient. In other type of question setting, you maybe given some important physical signs and the examiners want you to find the correct cardiac catheterization results.

Poisoning in MRCP(III)

2006-10-23T14:51:00.000+01:00

Poisoning in MRCP (III)-Tricyclic Antidepressants

The third serial of this topic- poisoning in MRCP, I am going to talk about tricyclic antidepressants. Examples of tricyclic antidepressants are amitriptyline, imipramine, doxepin etc.It is a common case scenario you would see during your internship/ housemanship. The reason is simple, doctors prescribe tricyclic antidepressants for patients with depression and these patients tend to use drugs for suicide.

As you might remember, tricyclic antidepressants help depressed patients through inhibition of reuptake of noradrenaline or serotonin in the brain, however, there are a few other effects of tricyclic antidepressants that explain its side effects,

1) it has central and peripheral anticholinergic effects
2) it causes depression of cardiac contractility
3) it slows down intraventricular and artrioventricular conduction ( cardiac conduction)
4) it causes CNS toxicity such as agitation, confusion , coma and seizures

Symptoms of Toxicity

Remember that all these symptoms are due to cardiac toxicity and anticholinergic effects of tricyclic antidepressants.

Cardiac toxicity
Cardiac arrhythmias, supraventricular or ventricular arrhythmias leading to hypotension, pulmonary oedema, therefore patients may present palpitation and breathlessness

Anticholinergic toxicity ( autonomic toxicity)
Dry mouth, urinary retention, dilated pupils, constipation and hyperreflexia

CNS toxicity
Seizures ( may cause severe metabolic acidosis), coma, confusion

Treatment

Gastric lavage
Continuous cardiac monitoring is mandatory
IV Sodium Bicarbonate may be useful to maintain arterial PH if patients develop severe metabolic acidosis
DC shock may be needed, however, anti-arrhythmias are contraindicated
Fluid resuscitation if hypotension
Haemodialysis is not useful.

Tips for MRCP
1) Remember that if you see a patient with dilated pupils, confusion and cardiac arrhythmias , always consider tricyclic antidepressants.

Rheumatology Questions in MRCP

2006-10-21T02:47:00.000+01:00

MRCP Rheumatology Questions

Let's us take a break and look at some of common rheumatology questions in MRCP,

1) A 30 year gentleman was admitted to ward due to history of backpain for 3 months. He denied small joints pain and history of family members having the same problem. There was no history of dysuria and red eye.Below is his X-ray. What is the diagnosis?

1) Ankylosing Spondylitis
2) Riter’s syndrome
3) Psoriatic arthropathy
4) Enteropathic spondylitis
5) Seronegative Rheumatoid arthritis

2) This gentleman presents with swollen joint and fever.

What is likely to be found on microscopy of aspirated synovial fluid?

1 )Bipyramidal crystals that exhibit strong positive birefringence under polarised light
2 )Gram positive cocci in clusters
3 )Needle-shaped crystals that exhibit strong negative birefringence under polarised light
4 )Rhomboid crystals that exhibit weak positive birefringence under polarised light
5 )Small, non-birefringent crystals visible only under electron microscopy

3) A 30 year-old man is admitted to casualty with a 24 hour history of a painful and swollen right knee. He denies any previous history of joint problems. Over the last two days, he has also noticed redness and soreness in both eyes. He has returned from a business trip to Kuala Lumpur a fortnight ago.
On examination, his temperature is 38.5°C. His eyes are red. His right knee is hot, swollen and tender to palpate. No other joint appears to be affected.
Investigations:
Hb 12.9 g/dl
WBC 14.0 x 109/l
Platelets 200 x 109/l
ESR 75 mm/h

Blood cultures
No growth after 48 hours

Urinalysis
No blood, glucose or protein detected

Knee x-ray
Soft tissue swelling around left knee
What is the most likely diagnosis?

1 )Gout
2 )Gonococcal arthritis
3 )Reiter's syndrome
4 )Rheumatoid arthritis
5 )Viral arthritis

4) Which of the following statements are correct regarding this patient's condition?

1 )It occurs more commonly in men
2 )Rheumatoid factor is positive in >90% of cases
3 )It is associated with an erosive arthritis
4 )Raynaud's phenomenon is a feature in ~10%
5 )It is associated with a reduced transfer factor

5) A 22 year old lady presents with typical erythema nodosum. She has a low grade fever and bilateral ankle arthritis but no other symptoms and has no medical history. There is no history of travel abroad and she is on no medication. Which of the following would be the most appropriate investigation for this patient?

1 )Barium enema
2 )Chest x-ray
3 )ESR
4 )Upper GI endoscopy
5 )Viral titres

Get your answers here!

Cardiac Catheterization in MRCP(2)

2006-10-10T11:25:00.000+01:00

Cardiac Catheterization in MRCP (2)

In my previous post, I talked about a few important examples of cardiac lesion that give you abnormal oxygen saturation, today I am going to give you a few important cardiac lesions ( mainly valvular lesions ) that will give you abnormal pressure during cardiac catheterization.

Before we proceed , remember the normal cardiac pressure and oxygen saturation

Case 1: Mitral Stenosis

Look at the following cardiac catheterization result of a 40-year old lady

The diagnosis is mitral stenosis, you notice a few abnormal results here,

i) The catheter data show a gradient across the mitral valve (LA pressure – LV end diastolic pressure) .Remember that usually LA pressure equals to LV end systolic pressure; you can use the PCWP as a surrogate for LA pressure. In this case the gradient is 26-6 = 20 mmHg.
ii) There is also evidence of right ventricular hypertrophy, with markedly elevated RV pressures due to secondary pulmonary hypertension.

Case 2: Aortic Stenosis

A 65- year old lady was admitted to hospital due to syncopal attack, below is the cardiac catheterization results.

There is a systolic gradient of 81 mmHg across the aortic valve (LV systolic pressure – aortic systolic pressure), indicating severe aortic stenosis. Remember that hypertrophic cardiomyopathy also presents with a similar result, howeve, patients tend to be younger!

Case 3: Aortic regurgitation

This is an easy case, you notice a wide pulse pressure ( aorta :150/40), therefore the diagnosis is aortic regurgitation.

I would talk about a few more cases in my last post.

AIDS Defining Conditions in MRCP

2006-10-07T11:36:00.000+01:00

AIDS Defining Conditions in MRCP-Kaposi's Sarcoma

I talked about AIDS/HIV three months ago in my blog. Today, we are going to revisit this common disease again because it is a very popular disease asked in MRCP.

There are a few simple facts to remember about HIV,

1) It is a retrovirus ( Family: Retroviridae) . HIV is completely dependent upon CD4 cells for replication and survival.
2) HIV leads to a progression fall in T-helper cells ( CD4) and a failure of T-cell proliferation.
3) HIV infection can be divided into 3 stages- acute seroconversion ( patients usually present with viral-like fever) , intermediate stage ( asymptomatic) and advanced stage ( AIDS)

Advanced stage of HIV (AIDS) is defined when the patient’s CD4 counts drop below 200 /cmm.

When our CD4 drops below 200, we are prone to get all kinds of rare infections ( opportunistic infections) which are uncommon in immune competent hosts.

There are a few AIDS defining conditions that are commonly asked in MRCP examination, these conditions are,

1) PCP
2) Toxoplasmosis
3) Cytomegalovirus
4) Kaposi’s Sarcoma
5) Cryptococcus meningitis
6) Extrapulmonary tuberculosis and atypical mycobacterium
7) Non-Hodgkin’s lymphoma

and others, however, I think these are the most important diseases you must learn.

About PCP, I think I have covered adequately in my previous post. Today I am going to talk about Kaposi’s Sarcoma (KS),

OK, this disease was considered to be very rare before the era of AIDS. It mainly affects elderly men of Mediterranean or Jewish heritage, organ transplant patients, or young adult African men. KS was named for Dr Moritz Kaposi who first described it in 1872.

In patients with AIDS, this tumuor tends to develop in the tissues below the skin surface, or in the mucous membranes of the mouth, nose, or anus. It is always described as raised blotches or lumps that may be purple, brown, or red. Sometimes the disease causes painful swelling, especially in the legs, groin area, or skin around the eyes. KS is caused by a herpes virus called Human Herpes Virus 8 (HHV-8).

However, KS is rare among Asian patients with AIDS as compared to Western patients.
In the skin, KS may not have to be treated if there are only a few lesions. Skin lesions can be:

Frozen with liquid nitrogen,
Treated with radiation,
Cut out surgically,
Injected with anti-cancer drugs or interferon alpha

A few photos of KS are shown below,

Tips for MRCP,
1) Remember that you may not only see KS occurs at skin but also mucous membrane

Spondyloarthropathies in MRCP (1)

2006-10-03T12:59:00.000+01:00

Spondyloarthropathies in MRCP (1)

This is a group of disorders with following characteristics, ( remember that spondyloarthropathies are popular questions in MRCP.

1) they are seronegative ( Rheumatoid factor negative)
2) usually larger joints are involved such as knees, ankles and sacro-iliac joints
3) if peripheral joints are involved, they are usually asymmetrical
4) characteristic articular features include enthesitis ( inflammation at sites of tendon insertion),dactylitis and scaroilitis.
5) strong association with HLA-B27

The arthropathies that are under this group are,
1) Ankylosing spondylitis
2) Reiter’s syndrome
3) Psoriatic arthropathy
4) Inflammatory Bowel athropathy ( Enteropathic arthritis)

Today I am going to talk about Ankylosing Spondylitis, it is a common short case as well if you are sitting for MRCP PACES, find more discussion at PassPACES.com

Clinical Presentations

Back pain and stiffness, usually happens during the third decade
Peripheral joint pain ( less common )
Uveitis

Physical Signs

Reduced spine movement and chest expansion
‘Question mark’ posture
Anterior uveitis
Anemia of chronic disease
Aortic regurgitation murmur
Achilles tendinitis
Apical fibrosis

Investigations

Sacro-iliac joints involvement

Spine xray- loss of lumbar lordosis, Bamboo spine ( calcification in anterior and posterior spinal ligaments)
Enthesitis
HLA-B27 positive ( about 90%)

Treatment

NSAID, NSAID, NSAID + physiotherapy
Disease modifying drugs have no effect on central disease ( spine) and maybe useful in peripheral disease ( peripheral joints involvement!)

Tips for MRCP,

1) They may show a spine x-ray or pelvic xray with classical history of ankylosing spondylitis, remember how to look for Bamboo spine and sacro-iliac joint involvement!

Poisoning in MRCP(II)

2006-09-26T15:14:00.000+01:00

Poisoning in MRCP (II)-Salicylates

In the second serial of this topic- poisoning in MRCP, I am going to talk about salicylates poisoning. It is an important topic in MRCP Part 1 and 2 as well as in your clinical practice. The reason is simple, salicylates can be obtained easily because it can be found in aspirin .You certainly know many patients are on aspirin if you go to ward everyday and at one time, some doctors even suggested to put aspirin in our tap water!

Before we discuss common presentations of a patient with salicylates poisoning, we must know the pathophysiology of salicylates overdose. Salicylates stimulate the respiratory centre initially and cause respiratory alkalosis. However, salicylates also interfere with carbohydrate metabolism and lead to accumulation of lactic acid and lead to metabolic acidosis.

Symptoms of Toxicity ( ASPIRIM)

Acute renal failure- symptoms of acute renal failure
Salicylism- deafness, tinnitus, vomitting
Pulmonary edema or cerebral edema (confusion)
Increased temperature
Respiratory alkalosis- hyperpnoea
GI disturbances and haemorrahge
Metabolic acidosis

Signs of toxicity

Air hunger ( due to metabolic acidosis)
Hyperpnoea ( due to respiratory alkalosis)
Remember that initially, there is respiratory alkalosis but later patient will have metabolic acidosis

Interactions

Increases anticoagulation effect
Low dose of aspirin precipitates gout

Treatment

Gastric lavage
Forced alkaline diuresis
Haemodialysis is indicated in severe cases

Hope you know how to answer your MRCP questions about salicylates after this post!

Common Mistakes Candidates Make in MRCP

2006-09-23T14:23:00.000+01:00

Common Mistakes Candidates Make in MRCP

OK, today I am not going talk about medicine but I would like to highlight to you a few common mistakes candidates make when preparing for thier MRCP,

1) I need at least one year or even more to prepare for MRCP Part1 and 2, but the fact is if you have a proper plan to study, you only need 5-6 months to cover every important topic.

2) I need to study a lot of books to know every fact, but the truth is you only need to stick to one good medical book. The trick is to do as many BOF as possible so that you know your weakness. Spend more time on your weak topics!

3) I need to take long leave to study their books. Medicine is always best learned beside your patients. If you see a SLE case today, go back and learn everything about SLE and find all BOFs about SLE and answer them!

4) I need to sit many times to pass the exam. You only need one attempt to pass MRCP if you prepare early and build up your confidence.

5) I must pay to get BOFs from the net, but the fact is there are a lot of sites out there which provide your free BOFs, just visit these sites and answer all these questions.

6) I must be very smart to pass MRCP, not quite, all my friends who pass their MRCP actually were not smart students when they were in medical schools.

Poisoning in MRCP(1)

2006-09-19T14:14:00.000+01:00

Poisoning in MRCP(1)-Lithium

For those who recently sat for thier Part 1, good luck to all of you and hope for the best!You can do it!
" There is always hope !"

My friend sat for his MRCP Part 1 in Singapore recently. He said that questions asked in MRCP are getting more difficult to answer now. I would like to talk about poisoning today. There are a few important subtopics you must remember when learn about common drugs which are asked in MRCP.

1) Common symptoms and signs when there is poisoning.
2) Possible antidotes.
3) Drugs interactions
4) Whether the drug can be cleared by dialysis ( very important fact to remember!)

Today, I am going to talk about Lithium. If I can still remember, this drug was asked in my MRCP Part 1 in 2003.

Introduction:

Lithium is used as mood stabilizer and can be used as a treatment for acute mania/hypomania. It has a narrow therapeutic range ( <1mmol).>Symptoms for toxicity (LITHIUM!!)

- Loose motion
-Impaired vision
-Tremor
-Hypothyroidism symptoms
-Increased thirst ( polydypsia)
-Urine output increased ( polyuria)
-Muscle weakness/metallic taste

Signs for toxicity

-hyper-reflexia
- ataxia/dysarthria
-Confusion/fits

Interactions

NSAID, Thiazide, Phenothiazide, pheytoin and methyldopa increase lithium toxicity

Treatment

No specific antidotes but dialysis may be indicated!

Lung Cancer in MRCP

2006-09-13T14:06:00.000+01:00

Lung cancer in MRCP

Lung cancer ( bronchial carcinoma) is a very popular topic in MRCP exam. The reason is quite simple, lung cancer is always among the top three cancer killer in males throughout the world. Cigarette is thought to be the major cause of lung cancer. There are a few important facts about lung cancer you must know,

1) There are 5 major subtypes of lung cancer

OSLAA- Oat cell ( small cell), squamous cell, Large cell , adenocarcinoma and alveolar cell carcinoma.
Small cell lung cancer is usually the commonest type you will see in your clinical practice. Other subtypes can be put under as non-small cell lung carcinoma.

2) There are three main complications of lung cancer

The complications can be either it is due to local spread of the disease, distant metastasis or paraneoplastic syndrome. Remember that Para-neoplasic complication is frequently asked in MRCP! The most popular question asked is about Eaton-Lambert syndrome!

3) Absolute contraindications for surgical intervention are presence of distant metastasis, malignant pleural effusion, FEV1<0.8ll,other>

Clinical presentations

Classical symptoms include loss of weight, loss of appetite, cough, haemoptysis or symptoms due to underlying Para- neoplastic syndromes.

Physical signs

The physical signs can be divided according to type of complication as mentioned above.

Local spread of disease- pleural effusion, recurrent laryngeal nerve palsy ( hoarseness of voice) , superior vena cava obstruction

Distant metastasis- bony tenderness, hepatosplenomegaly

Paraneoplastic syndrome- Cushing’s syndrome, clubbing+/- hypertrophic pulmonary osteoarthropathy. (HPA)

Paraneoplastic syndrome

There are a few main presentations that you must always remember,

a) Endocrine

SIADH, Ectopic ACTH ( especially in small cell)
Hypercalcaemia- ( in squamous cell)
Carcinoid-like syndrome…… etc, etc ( Make sure your remember these four!)

b) Neurology
Remember Eaton- Lambert(EL) and how to differentiate from Myasthenia gravis.
Remember that in EL syndrome,
- usually affect proximal limbs and trunks, ocular and bulbar rarely affected
- hyporeflexia
- repeated muscle contraction may lead to increased muscle strength
( Source: Oxford Handbook of clinical medicine)

c) others- HPA, clubbing, some very rare skin lesions ( occasionally asked in MRCP PART 1 such as Erythema gyratum repens, dermatomyositis, acanthosis nigricans)

Investigations
The most important investigation- CXR but definite diagnosis may only be made after bronchoscopy, lymph node biopsy or even CT-guided biopsy.

Treatment

Small cell is usually not operable on presentation, chemotherapy may be useful
For non- small cell cancer, surgical resection if possible

Cardiac catheterization in MRCP

2006-09-10T15:49:00.000+01:00

Cardiac catheterization in MRCP

I found questions about cardiac catheterization are always very challenging in MRCP Part 2 exam. When I sat for my Part 2 three years ago, they would usually show you the pressure and saturation from a cardiac catheterization and ask you what the underlying cardiac lesion is, however, I notice that recently they have switched the way of asking this type of question. They prefer to give you a case with important physical signs and ask you to choose the correct cardiac catheterization results.

Anyway, start form basic first, remember the normal and pressure of each cardiac chamber as below,

Left heart
Aorta-------120/80 ( pressure)---------98% (saturation)
LV----------150/5-10------------------98%
LA--------------------------------------98%

Right heart
RA------------0-8 (mean pressure)-----74%
RV-----------15-30/0-8----------------74%
PA-----------15-30/3-12---------------74%
SVC-------------------------------------74%
IVC-------------------------------------70%
PCWP--------1-10 ( mean)

There are two main groups of questions in MRCP, either a saturation or pressure problem, we would talk about saturation problem first today.
I would give you a few examples and explain to you the underlying cardiac lesions,

Case 1:

---------------Pressure mmHg --Saturation%
Right heart
SVC ------------------5-------------- 72
RA -------------------6-------------- 76
RV----------------- 25/0-5 ----------76
PA -----------------25/10----------- 77

Left heart
LV ---------------140/0-12---------- 97
Aorta --------------140/75 -----------97

You notice that the saturation at the superior vena cava is 72% and increases to 76%, if you remember your anatomy, blood from SVC would go to right atrium (RA) and the saturation should be the same ( see above image again), therefore , there must be presence of mixture of blood from more oxygenated blood from left atrium and right atrium. Yes, you are right, the diagnosis is atrial septal defect!

Case 2:

----------------Pressure (mmHg) ----Oxygen saturation (%)
SVC--------------- - ---------------------72
RA ------------------7--------------------72
RV----------------- 50/12----------------86
PCWP-------------- 16 ------------------- -
LV -----------------90/12----------------96
Aorta ---------------100/50---------------97

This question is easy, you notice there is a sudden increase in oxygen saturation from RA to RV, therefore, there must be mixture of blood over RV and LV, the diagnosis is Ventricular septal defect( VSD).

Case 3:

-------------------Pressure (mmHg)------ Oxygen saturation (%)
IVC -------------------------------------------60
RA ---------------------20---------------------66
RV--------------------- 100/20---------------- 67
PA ---------------------100/30---------------- 67
LV ----------------------100/10 ---------------70
Aorta-------------------- 105/80---------------70

This case is more complicated, however, stay calm, apply basic principles. You notice that there is an increase of oxygen saturation form IVC to RA ( sounds like it is an atrial septal defect). However, you notice that RV’s pressure is high and even equals to that of LV’s. Another abnormality you notice is the saturation of LV and aorta is low ( as compared to more than 95% in normal subjects). So…… the diagnosis is Eisenmenger’s syndrome secondary to ASD.

Case 4:

----------------------------Pressure (mmHg) --------Oxygen saturation (%)
Superior vena cava ----------------------------------------77
RA -----------------------------6--------------------------78
RV -------------------------------------------------------- 78
PA ---------------------------50/20----------------------- 86
PCWP--------------------------16-----------------------------
LV--------------------------120/11------------------------96
Aorta------------------------- 130/60----------------------97

This case is simple, you notice there is high pressure present over Pulmonary artery with sudden increase in oxygen saturation, therefore mixture of blood must be present over the pulmonary artery. Yes, you are right, you are dealing with Patent Ductus arteriousus.

Ok, that is enough for today, we have learn about cardiac lesions that give you abnormal oxygen saturation during cardiac catheterization, I would talk more about valvular heart lesions that give your abnormal pressure during cardiac catheterization in future posts.

Paget’s disease of bone in MRCP

2006-09-08T14:33:00.000+01:00

Paget's disease of bone

Disease of unknown origin. There is increased bone turnover due to an increase in bone osteoclast activity , which leads to increased osteoblast activity. Increased bone remodeling leads to bone enlargement, deformity and weakness.

Clinical presentations

Usually bone pain, bone deformity and deafness

Physical signs

You may notice bone deformity and warm bones. Rare in patients less than 40 years old. Rare as well in tropical countries.

Investigations

I notice that a lot of candidates have problems interpreting Calcium, phosphate, ALP in various conditions, I find this the following table useful,

Bone disease calcium Phosphate ALP
Paget’s Normal Normal ^^
Myeloma ^/Normal Normal unless fracture
Osteomalacia down down ^
Osteoporosis Normal Normal normal
Bone metastasis ^ ^/ normal ^

( It is even more confusing for hyperparathyroidism, I would cover that in future post)

Remember that level of ALP reflects osteoblast activity, therefore, if there is no new bone formation, ALP level would not be raised. This also explains ALP is high in growing children! On the other hand, level of urinary hydroxyproline reflects osteoclast activity, when there is breakdown of bone, the level would be raised.

Diagnosis

Based on typical x-ray appearance and raised AP with normal Calcium and phosphate

Coarse trabeculation and bony expansion

Complications

Nerve/ cord compression
Osteogenic sarcoma
Heart failure ( high output)

Treatment

Bisphosphonates is the treatment of choice. It inhibits bone resorption ( osteoclast activity) . It is also used in management of hypercalciamia especially in bone metastasis and osteporosis!

Tips for MRCP

Remember that patients with Paget's disease always have a raised ALP with normal calcium and phosphate !

Genetics in MRCP

2006-09-03T15:38:00.000+01:00

Today I am going to tell you a few genetics conditions which are commonly asked in your MRCP PART 1.

1) Autosomal dominant inheritance
- generally ‘ structural-type’ disorders

a) adult polycystic kidney disease
b) myotonic dystrophy
c) Elers-Danlos and Marfan’s syndrome
d) Hereditary haemorrhagic telangiectasia
e) Huntingtons chorea
f) Intestinal polyposis
g) Neurofibromatosis
h) Otesogenesis imperfecta
i) Tuberous sclerosis

2) Autosomal Recessive inheritance
- generally ‘metabolic type’ disorders

a) Infantile polycystic kidney
b) Alfa1-antitrpsin deficiency
c) Cystic fibrosis
d) Most inborn errors of metabolism ( galactosaemia, glycogen storage diseases etc)
e) Haemoglonbinopathies ( sickle cell disease and thalassaemias)
f) Wilson’s disease
g) Friedreich’s ataxia

3) Sex-linked dominant inheritance

a) Vitamin D risistnact rickets

4) Sex-linked recessive inheritance

a) G6PD deficiency
b) Haemophilia A and B
c) Lesch-Nyhan syndrome
d) Immunodeficinecies- agammagobulinaemia

However, there are a few types of muscular dystrophies you should remember,

Duchenne - X linked recessive
Becker -X linked recessive
Limb girdle -Autosomal recessive
Facio-scapulo-humerol -Autosomal dominant

Tips for MRCP

Remember how to interpret a family tree, it is the commonest way how genetics of above disoredrs are asked in MRCP!

Gout in MRCP

2006-08-31T00:56:00.000+01:00

GOUT IN MRCP

I saw this patient during my clinic follow up recently, so I am going to discuss with you about gout today. Gout is commoner than you think. Gout is due to deposition of uric acid crystals in joints. Certain joints are commonly involved such as first toe, ankle and small joints of hands.

Chronic tophaceous gout with tophi!

Clinical Presentations

There are a few possible manifestations of gout. These are,
a) asymptomatic hyperuricemia
b) acute arthritis
c) chronic arthritis
d) chronic tophaceous gout

Physical signs

You may find swollen and tender joint if patient has acute arthritis, you must always consider septic arthritis as your differential diagnosis. Patient may also present to you with chronic tophaceous gout as I have shown you as the images above.

Precipitating Factors for Acute Attack

There are a few precipitating factors for you to get acute attack of gout. These factors are,
a) Trauma
b) Drugs such as diuretics, aspirin ( always a popular question in MRCP, remember hat only low dose of aspirin precipitates gout)
c) Copious consumption of alcohol
d) Dehydration
e) Surgery
f) Infection
g) Food high in Purines
h) Induction chemotherapy for certain cancers such as leukemia

Treatment

Pharmacological and non-pharmacological treatments are available.
a) Diet and lifestyle changes
b) Drugs such as Allupurinol, Probenecid. Remember that allupurinol interacts with Azathioprine and cyclophosphamide and increases the toxicity of these cytotoxic drugs ( VERY popular question in MRCP!)

Gout Vs Pseudogout

Remember that pseudogout is acute arthritis resulting from the release of calcium pyrophosphate ( deposited in the bone and cartilage) into the synovial fluid.
Gout /Pseudogout

More severe and short lasting / less severe and longer lasting
Usually first toe involved/ mainly the knee
Negatively birefringent/ Positive
Needle shape crystal / Rhamboishape
No calcium deposition / Ca deposition on X ray

Tips for MRCP

1) Remember that allupurinol also can cause Steven Johnson syndrome!
2) Related post, click here!

Popular Drugs in MRCP (7)

2006-08-30T14:14:00.000+01:00

Popular Drugs in MRCP- Methotrexate

Today I am going to discuss with you with another popular drug in MRCP. Methotrexate (MTX) is a folic antagonist and also a dihydrofolate reductase inhibitor with potent immunosuppressive activity.

MTX is used in a lot of autoimmune diseases such as Rheumatoid arthritis , vasculitis such as Wegener’s granulomatosis. Certain types of cancer and even in ectopic pregnancy!

Common side effects

Nausea, vomiting
Mucosal ulcer
Hepatotoxicity
Lung fibrosis

Remember that other drugs that can cause lung fibrosis are amiodarone,bulsuphan, bleomycin, nitrofurantoin, hydralazine.

Tips for MRCP

1) Side effect of MTX that is commonly asked in MRCP is lung fibrosis and hepatotoxicity.

Good Luck To All!

2006-08-29T11:27:00.000+01:00

Good Luck!

Hi, For those who are sitting for their MRCP (UK) and MRCP (Ireland) Part 1 soon, good luck to all of you! You can do it, just remember to have a good sleep before your exam and stay calm in the examination hall!

Rheumatoid Arthritis in MRCP

2006-08-26T08:31:00.000+01:00

RHEUMATOID ARTHRITIS

RA is a type of autoimmune disease mainly involving joints. It leads to chronic inflammation of joints. However, candidates must remember that it is a multi-system disease that might involve other organs as well such as skin, eye , lung and cadiovascular. More female are affected with a ratio of 3:1.

Clinical Presentations

Majority of patients present with small joints pain. However, patients may have systemic symptoms such as fever, weight loss and fatigue.
Some patients may have eye symptoms such as red , painful eye ( due to scleritis and episcleritis)
There is possibility of lung fibrosis
Patients may have neurological deficits due to alanto-axial subluxation or mononeuritis multiplex.

Physical signs

Classical hand deformities are Z deformity, Swan neck , Boutonniere deformity, to learn more click www.passpaces.com/issue1.html
Lung fibrosis

Diagnosis

Diagnosis can be made based on American Rheumatism Association Criteria:
1) Morning stiffness >1 hour for 6 weeks or more
2) Swelling of at least 3 joints for 6 weeks or more
3) Swelling of wrist, MCP,PIP joints for 6 weeks or more
4) Symmetrical joints pain for 6 weeks or more
5) Subcutaneous nodules
6) +ve RF
7) Classical X ray appearance ( periarticular osteopenia)

Four or more out of seven criteria above, the diagnosis can be made

Investigations

Rheumatoid factor (RF)- however this is not specific, it can be positive in normal population ( false postive)
FBC- anaemia- Remember 4 causes of anaemia in RA- Chronic illness, Felty syndrome, Drug-induced (anaemia due to UGIB, secondary to gold, methotraxate)
Xray- lung ( fibrosis), hand, cervical ( subluxation)

Treatment

Disease modifying drugs such as sulphasalazine, methotraxate, gold
Latest drugs such as etanercept and infliximab- popular questions in MRCP, click here to learn more!

Tips for MRCP

1) Remember the side effects of drugs used to treat RA including etanercept and infliximab!

Sarcoidosis in MRCP

2006-08-25T11:40:00.000+01:00

SARCOIDOSIS

Sarcoidosis is always a popular question in respiratory section in MRCP. It was first described by a London surgeon-dermatologist, Dr. Jonathan Hutchinson in 1877. The doctor described the findings of a 50 year-old man who had large purple skin plaques on the hands and feet and a 64-year-old woman with large purple patches on her face and arms. You must remember that Sarcoidosis is a multisystem disease with unknown origin, however, in MRCP, two popular systems which are frequently asked are skin and lung.

Clinical Presentations

Usually asymptomatic, however patient may have constitutional symptoms such as fever, malaise and weight loss. Majority of patients have respiratory symptoms such as cough and shortness of breath.
Popular skin condition ( always asked in MRCP) associated with sarcoidosis is Erythema nodusom. Pateints may have arthralgia or bone pain.
Eyes-painful eyes, dry eyes
Other-dry mouth, hepatomegaly

Investigations

They would usually show show you a CXR in MRCP
Remember that 90% of CXRs have bilateral hilar LN enlargement. More advanced case may have diffuse fibrosis!

ESR-raised
Serum Calcium-raised
Serum ACE-raised
Lung function test may show obstructive changes

Diagnosis

Diagnosis can be made by lung biopsy-granuloma! Remember that serum ACE is not specific nor sensitive.

Treatment

The main treatment for sarcoidosis is prednisone. Prednisone is a corticosteroid, or anti-inflammatory drug. Sometimes it is used with other drugs. Sometimes other corticosteroids are used.

Tips for MRCP

1) If you are asked about a patient with painful skin lesions over shin area with dry cough, always think of sarcoidosis.

2) A patient with high calcium level and dry cough , think of sarcoidosis although there is possibility of lung cancer with bone metastasis!

MRCP Part 1-Mock Exam (2)

2006-08-21T11:16:00.000+01:00

MRCP Part 1 Questions

Here are some questions for MRCP Part 1, take the test and look at the answers later!

1)Ostium secundum ASD is associated with
A tricuspid regurgitation
B left bundle branch block
C fixed splitting of the second heart sound
D onset of atrial fibrillation in the second decade
E early onset of heart failure in the second decade

2)A 34 year old male presents with episodes of breathlessness on exertion. Examination reveals a loud P2 and fixed splitting of the second sound. Which of the following may be responsible for these signs?
1 ) Maternal chicken pox infection 2 ) Maternal thalidomide therapy
3 ) 47 XXY karyotype 4 ) Homocystinuria 5 ) Excess maternal alcohol consumption

3)A 35-year-old healthy woman has a faint systolic murmur on physical examination. An echocardiogram is performed, and she is found to have a bicuspid aortic valve. In explaining the meaning of this finding to her, the most appropriate statement is that?

1 ) An aortic valve replacement is eventually likely to be required.
2 ) Other family members are likely to have the same condition
3 ) She should be treated with a cholesterol-lowering agent
4 ) The problem resulted from past injection drug usage
5 ) This is one manifestation of an underlying autoimmune disease process

4) A 24-year-old woman develops infective endocarditis involving the aortic valve. She receives a porcine bioprosthesis because of her desire to have children and not to take anticoagulantmedication. After ten years, she must have this prosthetic valve replaced. Which of the following pathologic findings in the bioprosthesis has most likely led to the need for replacement?
1 ) Calcification with stenosis
2 ) Dehiscence
3 ) Infective endocarditis
4 ) Strut failure
5 ) Thrombosis

5) The following can cause bradycardia: EXCEPT
A hypothermia B hypothyroidism C severe anaemia D subdural haematoma E shock

6)The following are recognised causes of reversible dilated cardiomyopathy:- EXCEPT
A alcohol B Selenium deficiency C Acromegaly D Lead poisoning E Coxsackie virus

7) Which of the following concerning congenital heart disease is correct?
1 ) ASD is the commonest malformation at birth
2 ) congenital complete heart block is usually associated with Anti-Ro antibodies in the mother 3 ) Ebstein's anomaly is associated with maternal exposure to lithium carbonate
4 ) Hypoplastic left heart syndrome is characterised by a large, dilated left ventricle
5 ) Osteogenesis imperfecta is associated with aortic stenosis

8) Coarctation of the aorta is: EXCEPT
A usually congenital but may be aquired
B recognised by absent or delayed femoral pulses
C a common cause of heart failure in infancy but an uncommon cause of hypertension in adults D associated with an increased incidence of an aortic bicuspid valve
E a cause of left to right shunting of blood

9)A 65-year-old woman, a heavy smoker for many years, has had worsening dyspnoea for the past 5 years, without a significant cough. A chest X-ray shows increased lung size along with flattening of the diaphragms, consistent with emphysema. Over the next several years she develops worsening peripheral oedema. BP 115/70 mmHg. Which of the following cardiac findings is most likely to be present?
1 ) Constrictive pericarditis 2 ) Left ventricular aneurysm 3 ) Mitral valve stenosis
4 ) Non-bacterial thrombotic endocarditis 5 ) Right ventricular hypertrophy

10)Increased pulmonary vascular markings on chest x-ray are a recognized feature of:
A Pulmonary stenosis
B Mitral stenosis
C Persistent ductus arteriosus
D Primary pulmonary hypertension
E chronic constrictive pericarditis

11) A 59-year-old man who was active all his life develops sudden severe anterior chest pain that radiates to his back. Within minutes, he is unconscious. He has a history of hypertension, but a recent treadmill test had revealed no evidence for cardiac disease. Which of the following is the most likely diagnosis?
1 ) Acute myocardial infarction
2 ) Group A streptococcal infection
3 ) Pulmonary embolus
4 ) Right middle cerebral artery embolus
5 ) Tear in the aortic intima

12)Low T waves on an ECG are seen in:
A hyperkalaemia B hypercalcaemia C athletes D pericardial effusion E myelodysplasia

13)A 56 year old male with left ventricular systolic dysfunction was dyspnoeic on climbing stairs but not at rest. The patient was commenced on ramipril and frusemide.
Which one of the following drugs would improve the patient's prognosis?
1 ) Amiodarone 2 ) Amlodipine 3 ) Bisoprolol 4 ) Digoxin 5 ) Nitrate therapy

14) A 70-year-old male is referred by his GP for management of recently diagnosed congestive heart failure. The patient has a history of poorly controlled hypertension. Over the last three months he has been aware of deteriorating shortness of breath, fatigue, and orthopnea. Over the last month he had been commenced on Digoxin (62.5 micrograms daily), Frusemide (80 mg daily), and amiloride 10 mg.
On examination he has a pulse of 96 bpm regular, a blood pressure of 132/88 mmHg. His JVP was not raised, he had some scattered bibasal crackles on auscultation with a displaced apex beat in the anterior axillary line, 6th intercostal space. Auscultation of the heart revealed no murmurs and he had peripheral oedema to the mid tibia.
Investigations showed: electrolytes normal serum urea concentration 17 mmol/l (NR 2-8 mmol/l) creatinine 175 micromol/l (NR 55-110) Serum digoxin 0.7 ng/mL {therapeutic: 1.0-2.0}
One month previously his urea had been 11 mmol/l and creatinine 110 micromol/l. An ECG reveals left ventricular hypertrophy and Chest X-ray shows cardiomegaly and calcified aorta.
What is the most appropriate next step in management?
1 ) Add an ACE inhibitor to the current regimen
2 ) Add atenolol at a dose of 25mg daily
3 ) Increase digoxin to 0.25 mg daily
4 ) Increase frusemide to 80 mg twice daily
5 ) Maintain on current therapy.

15)A 17-year-old woman loses consciousness while out jogging one afternoon, as she has done for many years. She is taken to Accident and Emergency, where a chest X-ray, CT brain scan, FBC, and biochemistry are all normal. Over the next year, she develops mild dyspnea and fatigue. There are several episodes of pre-syncope. After another syncopal episode, she is referred to a cardiologist who orders and ECG that shows changes of left ventricular hypertrophy and broad Q waves. An echocardiogram reveals left ventricular and septal hypertrophy, small left ventricle, and reduced septal excursion. The septum has a "ground glass" appearance. She then dies suddenly and unexpectedly. The microscopic appearance of the septum with trichrome stain reveals myofiber disarray. Which of the following conditions is she most likely to have had?

1 ) Diabetes mellitus 2 ) Hypertrophic cardiomyopathy 3 ) Rheumatic heart disease 4 ) Systemic lupus erythematosus 5 ) Viral myocarditis

16) A 78 year old female is referred by her GP with high blood pressure. Over the last three months her blood pressure is noted to be around 180/80 mmHg. She has a body mass index of 25.5kg/m2, is a non-smoker.There are no features to suggest a secondary cause for her hypertension. Which of the following is the most appropriate treatment for her blood pressure?

1 ) Alpha-Blocker 2 ) Angiotensin Converting Enzyme (ACE) Inhibitor 3 ) Angiotensin Blocker 4 ) Beta-blocker 5 ) Calcium channel blocker

17) Infective endocarditis rarely occurs with:
A mitral valve prolapse B patent ductus arteriosus C bicuspid aortic valve D atrial septal defect E mitral stenosis

18) A 60-year-old man presents with an inferior MI and receives thrombolysis. 4 hours following initial presentation he becomes acutely breathless. His ECG demonstrates sinus tachycardia (rate 108bpm) with T wave inversion inferiorly. His ST segments are normal. On examination his JVP is elevated at 5 cm. Chest was clear to auscultation. Following 80 mg of Frusemide he deteriorates. His BP is now 80/60 and his urine output over the last 2 hours is 5 mls. What is the best investigative measure?

1 ) Arterial Blood Gases 2 ) Central Venous Pressure Monitoring 3 ) Chest X-Ray 4 ) Echocardiography 5 ) Pulmonary Capillary Wedge Pressure Monitoring

19) The following are true regarding mitral stenosis:
A it is not tolerated well in pregnancy
B there is characteristically a low wedge pressure
C in AF, the opening snap disappears
D loud murmurs if valve is high calcified
E Doppler U/S is usually inaccurate in determining severity

20) The following are recognised features of pulmonary embolism: EXCEPT

A long PR interval on the electrocardiogram
B decreased left atrial pressure
C pulmonary hypertension
D collapse of the affected lung segments
E necrosis of lung tissue

Find your answers here!

Primary Biliary Cirrhosis in MRCP

2006-08-20T09:03:00.000+01:00

Primary Biliary Cirrhosis (PBC)

PBC is an autoimmune disease. It is characterized by progressive inflammmation and destruction of of the small bile ducts within the liver. In the long run, it can lead to liver cirrhosis and PBC is one of the important causes of liver cirrhosis among female patients. ( 90% of PBC patients are female!)

Clinical Presentations
Usually asymptomatic but later due to biliary obstruction, patients tend to have pruritus and jaundice. Patients may present late with symptoms of liver cirrhosis such as upper GI bleeding or abdominal distention ( ascites)

Physical signs
Hepatosplenomegaly, Jaundice, scratch marks, xanthelasma, clubbing or other signs suggesting associated autoimmune diseases. Click here to see xanthelasma!

Associations
Autoimmune diseases such as Sicca syndrome, thyroiditis, RA, SLE

Investigations
I think the single test that can give a clue of PBC is LFT- you would notice markedly high ALP with raised bilirubin, IgM may be raised.
ANA may be positive
Diagnosis can be made by detecting antimitochondrial antibody. Specificity of the M2 subtype is 95-99%
Liver biopsy shows granulomas

Treatment
symtomatic relief of pruritus by cholestyramine.
Ursodeoxycholic acid may be useful
Cochicine may be used to slow down the progression
Immunosuppresants such as steroid, methotrexate may be useful
The only cure- liver transplantation

Tips for MRCP
1) Remember that if a lady has jaundice and very high ALP with pruritus, suspect PBC

Tuberous Sclerosis

2006-08-17T13:39:00.000+01:00

Tuberous Sclerosis in MRCP

There are a few conditions that are commonly asked in MRCP Part 1 and 2. These conditions include Tuberous sclerosis (TS), Neurofibromatosis..... etc. I am going to talk about TS today.
TS was discovered in the 1880's by a French physician named Bourneville. Remember that it is an autosomal dominant disease!

There are a few important features of TS, these include,

Facial angiofibroma
periungual fibromas
Hypopigmented macules
Shagreen patch (connective tissue nevus)
Multiple retinal nodular hamartomas
Subependymal nodule ( can be picked up in CT scan as calcification)
Subependymal giant cell astrocytoma
Cardiac rhabdomyoma, single or multiple
Lymphangiomyomatosis
Renal angiomyolipoma

Questions commonly asked in MRCP are photo-based questions, remember these photos.....
1) Periventricular calcification

2) Clinical features of TS

See more photos at www.passpaces.com

Tips for MRCP

1) A patient with recurrent seizure and CT scan shows calcification. Remember TS!

Popular Drugs in MRCP (6)

2006-08-16T13:20:00.000+01:00

Rosiglitazone

Rosiglitazone is a popular drug asked in MRCP examination. It is an aanti-diabetic drug from the thiazolidinedione class. Its mechanism of action is by activation of the intracellular receptor class of the peroxisome proliferator-activated receptors (PPARs), Rosiglitazone is ofter referred as 'insulin sensitizer' because it makes the body cells become more sensitive to insulin and remove more glucose from blood.

Indication for Rosiglitazone

Type 2 Diabetes mellitus. It is usually used alone or combined with metformin

Common side effects

It can cause mild to moderate oedema and should be avoided in acute heart failure or severe heart failure patients.
Possibility of liver impairment
Diarrhoe
Headache
Hypo or hyperglycaemia

Common Interaction

Gemfibrozil increases the concentration of rosiglitazone in the blood by reducing its breakdown. Therefore, gemfibrozil may increase the side effects of Rosiglitazone!

Tips for MRCP:
1) Remember about the side effects of Rosiglitazone.

Multiple Myeloma

2006-08-14T11:33:00.000+01:00

Multiple Myeloma in MRCP

Multiple Myeloma (MM) is a very important disease in haematology, MRCP. It is frequently asked and there are various clinical presentations in MM. Candidates must know that the malignant cells ( proliferation of plasma cells) are from bone marrow and not cortex of the bone ( as compared to osteosarcoma or scondary deposits of distant tumour to boen cortex). The monoclonal plasma cell line produces immunoglobulin which is abnormal and leads to suppression of normal immunity.

Clinical Presentations

Remember this mnemonic CRAB
Calcium abnormality - increased calcium level due to enhanced osteoclastic activity. Patients can present with confusion, dehydration, polyuria or even abdominal pain.
Renal impairment. Patients can present with tiredness
Anaemia ( due to suppression of bone marrow)- symptoms of anaemia
Bony abnormality- lytic lesions in almost 60-70%- bony pain

Physical Signs

Usually no hepatosplenomegaly but you may notice pallor, dehydration or bony tenderness.

Investigations

Monoclonal gammopathy ( usually Ig G- as compared to Waldenstrom's Macroglubinaemia which has increased Ig M)
Bone Marrow shows more than 30% plasma cells
Skeletal survey shows mutiple osteolytic lesions ( Candidates must remember that ALP of patients may be normal except there is presence of bone fracture)
ESR usually very high

Treatment

Thalidomide- Remember this drug in your medical student books? Thsi drug was usd extensively many years ago for insomnia and morning sickness for pregnant mothers but it was later found to be teratogenic. ( Remember your medical books with photo of babies without upper and lower limbs?)
However, current trials show it effectiveness against MM. Click here to learn more!

The latest drug- bortezomib!

Tips for MRCP
1) Suspect MM if patient has anaemia, renal impairment, high ESR and Calcium level.

MRCP Part 1 Questions (2)

2006-08-11T01:05:00.000+01:00

Hope you find these neurology questions useful..........

1) A 26-year-old male presents with 2 days history of diplopia and unsteadiness. 2 weeks ago he suffered from viral fever. Examination reviews that there is complete opthalmoplegia, areflexia and gait ataxia. Which of the following blood tests is the most likely to confirm the diagnosis?
1 ) Acetylcholine receptors antibodies
2 ) Anti GM1 antibodies
3 ) Anti GQib antibodies
4 ) Anti Topoisomerase antibodies
5 ) Anti purkinje cell antibodies

ANSWER: 3

2) A 40-year-old woman is referred with a two-week history of difficulty walking . On examination, there was distal limb weakness and the power is 3/5. Tendon reflexe was absent over ankle and the plantar responses were flexor.There was no sensory loss. What is the most likely diagnosis?
1 ) polymyositis
2 ) cervical cord compression
3 ) Guillain-Barré syndrome
4 ) myasthenia gravis
5 ) poliomyelitis

ANSWER: 3

3) A 50 year old female is admitted with progressive weakness following a flu-like illness. Which of the following would exclude Guillain-Barre Syndrome as the diagnosis?
1 ) Autonomic dysfunction
2 ) Elevated protein on CSF examination
3 ) Evidence of muscle wasting
4 ) Ophthalmoplegia
5 ) Sensory involvement

ANSWER: 5

4) A 15 year old girl presents with Guillain-Barre syndrome. Her weakness continues to worsen after admission to hospital and she complaines of shortness of breath. Which of the following should be used to monitor her?
1 ) arterial blood gases
2 ) chest expansion size
3 ) FEV1/FVC ratio
4 ) PEFR
5 ) vital capacity

ANSWER: 5

5) Which of the following clinical manifestations suggests Guillain Barré Syndrome?
1 ) Weakness beginning in the arms
2 ) Asymmetrical involvement of distal muscles
3 ) Bulbar involvement in about 50% of cases
4 ) Brisk tendon reflexes
5 ) Normal CSF protein

ANSWER: 3

6)A 43-year-old woman develops a progressive, ascending motor weakness over several days. She is hospitalized and requires intubation with mechanical ventilation. She is afebrile. A lumbar puncture is performed with normal opening pressure and yields clear, colorless CSF with normal glucose, increased protein, and cell count of 5/microliter, all lymphocytes. She gradually recovers over the next month. Which of the following conditions most likely preceded the onset of her illness?
1 ) Ketoacidosis
2 ) Staphylococcus aureus septicemia
3 ) Systemic lupus erythematosus
4 ) Viral pneumonia
5 ) Vitamin B12 deficiency

ANSWER: 4

7)Common features of normal pressure hydrocephalus are EXCEPT:
A papilloedema
B The opening pressure for lumbar puncture is normal
C gait apraxia
D incontinence
E cognitive impairment

ANSWER: B

8)A 60 year-old man presents with a 2 month history of progressive confusion, gait disturbance, and urinary incontinence. Examination reveals gait ataxia. CT brain done is as follow, lumbar puncture reveals normal CSF pressure and constituents. Which one of the following managements steps is likely to be most helpful?

1 ) CSF drainage via repeated lumbar puncture
2 ) EEG
3 ) Intracranial pressure monitoring
4 ) MRI brainstem
5 ) Serum B12 and folate levels
ANSWER: 1

9)A 75-year-old man presented with an unsteady gait. He was noted to be becoming impaired with his memory and agitated at nights. His GP started an antidepressant. He was incontinent of urine. He was a heavy smoker and had lost 2 stones in weight over 2 months. His blood sugar was 10 mmol/l.
Which is the next best investigation?
1 ) CT Head
2 ) CXR
3 ) Arterial Blood gas
4 ) Thyroid function test
5 ) Blood Calcium level

ANSWER: 1

Guillain-Barré Syndrome

2006-08-09T14:23:00.000+01:00

Guillain-Barré Syndrome in MRCP

This is a popular disease in MRCP part 1 and 2. In part 2, question about GB syndrome would be asked based on CSF interpretation.
GB is an acute polyneuropathy mainly affecting motor neuron. It is usually demyelinating type. Patient usually presents after recent viral/bacteria infections.

Trigerring Agents

Campylobacter jejuni ( usually cause diarrhoe)
CMV
EBV
HIV
mycoplasma species

Clinical Presentations
Acute onset of leg weakness and ascends to the upeer limbs. Peripheral numbness is possible.

Physical Signs
Lower motor lesion of both lower limbs ( sensory loss is distal and minimal)
Papilloedema
Autonomic dysfunction ( may lead to cardiac arrhytmia and death)
Cranial nerves involvement ( Miller Fisher variant- ophtalmoplegia with ataxia)

Investigations
For Miller Fisher, autoantibody GQ1B can be present.
CSF ( Cerebral spinal fluid ) shows high protein
Nerve conduction shows demyelinating pattern
Remember that to monitor patient ( in case of respiratory muscles involvement), you should monitorthe FVC ( spirometry) NOT Peak Expiratory Flow Rate (PEFR)

Treatment
IV Immunoglobulin. Plasma exchange can be considered.

Tips for MRCP:
1)If the weakness lasts longer than months, always consider CIDP ( chronic inflammatory demyelinating polyneuropathy.)
2) Major cause of death in patients with GBS is due to autonomic dysfunction and cardiac arrhytmia!

Journey to MRCP

2006-08-08T11:50:00.000+01:00

I came across this saying while surfing the net.....

Success is a journey, not a destination. The doing is often more important than the outcome.
Hope that candidates who did not make it for the recent Part 1 and 2 know that even most your consultants have to struggle a few times to pass their MRCP!

Normal Pressure Hydrocephalus

2006-08-07T12:27:00.000+01:00

Normal Pressure Hydrocephalus in MRCP

Normal pressure hydrocephalus (NPH) is hydrcephalus with normal intracranial pressure. You must remember that majority of patient has no identifiable cause for NPH. It usually happens in elderly patients.

Clinical Presentations

Triad of GUD
Gait disturbances, Urinary incontinence and Dementia.

Investigations

Picture source: e-medicine (arrow- dilated ventricles)

All investigations would be normal except CT/MRI head show non-obstructive hydrocephalus. PET scan mayshow hypometabolism.

Treatment

Ventricular shunting or lumbar puncture drainage of CSF

Tips for MRCP

1) Popular questions in MRCP are interpretation of CT brain, an elderly demented patient with urinary incontinence.
2) Remember that NPH is one of the important differential diagnosis of dementia!

Autoimmune Hepatitis

2006-08-06T07:18:00.000+01:00

Autoimmune Hepatitis in MRCP

I must tell you that this is a very important topic in MRCP gastroenterology. Besides that, it is rather common in your dily practice if you are attached to the gastroenterology unit. It is an autoimmunedisease with unknown aetiology. Usually questiosn about autoimmune hepatitis would be asked in Part 2and you are expected to know how to interpret liver function test and autoantibody profiles.Patients are usually young ladies.

Clinical Presentations

Patients usually come to you with jaundice and right hypochondrium pain. One important pointto remember about autoimmune hepatitis is that it is commonly associated with other immune diseasesuch as Sjoren's syndrome, Renal Tubular acidosis etc...

Clinical Signs

Patients may have chronic stigmata of chronic liver disease. You may find hepatosplenomegaly. If patient is on treatment, then you would find signs suggesting Cushing's syndrome. Patient mayend up with liver cirhosis and features of hypersplenism.

Investigations

Liver function test reveals increased bilirubin and ALT levels. Autoantibodies that may be positive include ANA ( up to 79-80%), Anti-smooth muscle antibodies, Anti-LKM-1 antibodies and anti-mitochondrial anti-bodies ( rarer in autoimmune hepatitis, you find this more common in primary biliary cirrhosis). Liver biopsy shows PIECEMEAL NECROSIS ( as above slaid)

Treatment

Steroid and steroid sparing agent such as Azathioprine, LIVER TRANSPLANT