Toxoplasmosis for MRCP

Toxoplasmosis for MRCP

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

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

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

Cerebral toxoplamosis- usually multifoci!

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

Hypercalcemia in MRCP(II)

Hypercalcemia in MRCP (II)

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

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

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

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

Pamidronate- A bisphosphonate

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

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

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

Heparin Induced Thrombocytopenia

Heparin Induced Thrombocytopenia

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

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

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

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

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

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

Multiple Sclerosis in MRCP

Multiple Sclerosis in MRCP

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

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

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

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

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

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

MRI is always helpful in making the diagnosis.

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

Happy Chinese New Year!

Happy Chinese New Year!

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

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

RBBB in MRCP

RBBB in MRCP

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

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

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

1) Normal variant

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

3) Congenital heart disease especially atrial septal defect

4) Myocardium ischemia, myocarditis etc.

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

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

Whipple's Disease in MRCP

Whipple's Disease in MRCP

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

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

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

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

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

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

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Iron Deficiency Anemia

Iron Deficiency Anemia


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

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

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

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

Iron Metabolism for MRCP

Iron Metabolism For MRCP

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

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

There are a few important fact to remember for MRCP,

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

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

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

How about for iron absorption?

You can remember this process by the following picture,

A few important facts to remember,

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

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

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