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

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