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??

Acromegaly in MRCP

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)

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)

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)

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

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

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.