Pass MRCP PACES in One Attempt

Pass MRCP PACES in ONE Attempt!

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Bartter's and Gitelman's Syndromes

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?

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

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

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)

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

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)

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??