Others CS-OSPE

Case 1:

A 19-year-old male admitted with acute onset generalized weakness for 1-day duration. He woke up with diffuse weakness; no anti-gravity strength in arms (he cannot lift an object; severe weakness), unable to get out of bed. Proximal > distal weakness; bilaterally symmetrical on both sides. He denied diplopia, dysphagia, dysarthria, facial droop, drooling, or change in level of consciousness.

PMH: Similar episode in Feb 2013, admitted to the local hospital for 4-5 days. Diagnosed with GBS (Guillain-Barre syndrome), treated with plasmapheresis, no LP/EMG. So the diagnosis was not confirmed.

O/E: Vitals stable. General physical exam unremarkable. Neurological exam Mental status: AAO * 4 Speech: Fluent with comprehension intact CN 2-12: PERRLA, EOM – full, normal facial sensation and symmetry,

Normal facial strength, hearing intact, equal palatal elevation, and tongue midline; so all cranial nerves were intact and normal. Motor: Power: 2+ ULL & LL Sensory: Intact DTX: Diminished Planter: Down going.

Test	Result
Hb	14.6
WBC	6.1
Plt count	215
Glucose	51 mmol/l
Sodium	143 mmol/l
Calcium	9.3 mg/dl
K	1.3 mmol/l
Magnesium	2.0 mg/dl
Chloride	110 mmol/l
Phosphorus	2.4
BUN	13
CK	493
Creatinine	0.83
Aldolase	15.7
free T3	3.8
free T4	0.9
TSH	2.082
Urine electrolytes	NAD

So what’s the problem here? This is a young man with a similar attack a year and a half ago, he has diffuse muscle weakness in upper and lower limbs, especially in the anti-gravity muscles.

Cranial nerves exam is normal, and there’s no diplopia; in other words, he does not have myasthenia gravis.

He does not have dysphagia or dysarthria, which means that the brainstem is normal. So someone can say that there’s no diplopia, dysphagia, dysarthria, then the brainstem is out.

So what’s the other differential diagnosis?

Is it in the central nervous system? Here all the cranial nerves are normal, there’s nothing wrong in the brain itself.

Is it in the peripheral nervous system? It’s a possibility; here, the reflexes are diminished, but the sensation is intact so the peripheral nerves are fine because you cannot have a pure motor weakness with peripheral nerves disease, and this patient has pure motor weakness.

Is it in the neuromuscular junction? Or is it in the muscle? If you look at the investigations of the patient, you can see that the potassium is very low and the CK is raised while all other investigations are normal.

This is not an uncommon case in Saudi Arabia, do you know about “Hypokalemic periodic paralysis”?

It’s a condition in which you get severe hypokalemia and complete paralysis of the whole body, and this condition usually occurs after consuming a good carbohydrate-rich meal; you eat a big meal and then you become flat.

But it still could be a Guillain-Barre syndrome; we didn’t ignore that completely, but the important thing here is to differentiate from is it a central nervous system or is it a peripheral nervous system or is it neuromuscular or is it in the muscle?

Here predominantly, the problem is the muscle weakness with intact all cranial nerves.

So the differential diagnosis:

1. Periodic hypokalemic paralysis.
2. Myasthenia gravis.
3. Guillain-Barre syndrome.

What disease(s) should be excluded? You should exclude:

1. Paraneoplastic syndrome.
2. …

It’s not a typical question, and you don’t have to answer it 100% here if you said it’s a generalized muscle weakness then you answered 50 – 60%.

Case 2:

A 76-year-old woman is admitted unwell with vomiting and is found to have low blood pressure. She had recently been given diclofenac for backache. Her blood results are:

Test	Result
Na+	137 mmol/l
K+	6.7 mmol/l
Urea	223 mmol/l
Creatinine	609 μmol/l
Cl-	95 mmol/l
HCO3-	24 mmol/l

So what are the abnormal results here? Potassium is very high, urea is also high, creatinine is also very high, so what’s the cause here? She’s vomiting??

The only history here is that she had a backache, and she was given diclofenac, which is a non-steroidal anti-inflammatory drug.

So which system, which part of the body affected the most? Which system is failing? It’s the kidney, of course, the kidney is gone.

This patient has an acute renal failure which happened abruptly, so what’s the cause?

She was given a drug, and it’s well known that non-steroidal anti-inflammatory drugs can cause acute tubular necrosis, interstitial necrosis, or acute renal failure, so it’s drug-induced renal failure.

We all agree that there are abnormal kidney function tests, so it’s the kidney and cannot be anything else.

So the question is “what’s the cause”? Whether underlying disease, drugs, SLE, I don’t care about that, but what I want not to miss is the abnormality of these findings.

So we say this is acute renal failure with high potassium, creatinine, and urea.

What’s the threat of life here? Which of these elements is a killer? Potassium, of course, as it’ll affect the heart; it’ll cause heart asystole and arrest, so the biggest concern here is the potassium.

So how to deal with that? Of course, calcium resonate is the correct answer, but how can you move the calcium from blood to the cells?

You also know that when you are treating a patient with DKA, you give potassium, why?

To enter the cell with the insulin, can you do the same here? Yes, you can give glucose, and that will move with insulin potassium from blood into the cells.

It’s a very serious risk here, so you can give insulin with glucose, you can give calcium resonate, which is a correct answer.

Anything else? Of course, you can do dialysis, it’s the easiest way. The important thing is that you be able to pick the abnormality as this is an easy question.

Case 3:

A 33-year-old female presented with malaise, joint discomfort, and a general feeling unwell. She was diagnosed with Graves’ disease four years ago and rendered euthyroid (she was treated and became normal) (Normal thyroid function). She had also suffered from celiac disease since her teens. She had no respiratory complaint. She had a recent chest X-ray which showed right pleural effusion of moderate size. Pleural aspiration was performed which showed:

Pleural fluid sample

Test	Result
Total protein	33.2 g/l
LDH	287 IU/l
pH	7.036
Microbiology	Nil seen
Amylase	65 U/l
Rheumatoid factor	557 IU/l

She is a young lady with a past history of 2 autoimmune diseases; Grave’s disease and celiac disease, so she is an autoimmune problem, maybe it’s not the answer here, but this is how to read the case scenario, it’s how to approach the problem.

Now, this patient is asymptomatic, and the chest X-ray was done routinely to discover the pleural effusion.

First of all, you must read this pleural effusion to know is it transudate or exudate? Here the protein is so high, so it’s exudate; also, LDH is so high, and it’s the most sensitive test for pleural effusion exudate.

So what’s the other abnormality here? It’s the rheumatoid factor; it’s very very high.

Now what’s the cause of this pleural effusion? She has joint pains, so rheumatoid arthritis is an excellent answer, anything else? Systemic lupus is also a 100% correct answer because she’s an autoimmune patient, and she’s a good case for SLE as well as for rheumatoid arthritis.

But rheumatoid arthritis here is more the correct answer because of the very high rheumatoid factor, in SLE, she may have a high rheumatoid factor as well, so the correct answer here is either SLE or rheumatoid arthritis, although nothing was given in the history.

Case 4:

A 45-year-old lady is complaining of generalized aches and pains for several months. She still is menstruating regularly. Her blood tests include the following:

Test	Result
Calcium	2.99 mmol/l
Phosphate	0.44 mmol/l
ALP	158 U/l
Albumin	41 g/l

What’s the abnormal here? This is high calcium. This is a 45-year-old lady with high calcium “moans, groans, and pains”; it’s a typical symptom of hyperparathyroidism.

Now what’s the cause of hypercalcemia?

1. Multiple myeloma, it’s very high calcium.
2. Sarcoidosis.
3. Malignancies in the body.
4. Metastasis in the bone or anywhere else.
5. Granulomatous diseases as TB.

So anyone who would say that he’ll treat it with phosphate I’ll accept that because you don’t know more than that.

Now, what essential test would you request? We have to look for a cause for high calcium.

If you suspect hyperparathyroidism, you do parathyroid hormone; if someone said I’ll do plasma Electrophoresis, it’ll be alright.

What I want to know from you have to give me one test, something which will lead to the cause.

Urgent Part 1

Case 1:

6 weeks ago, the patient came to us, and he had a painful lump on the skin of his leg which had resolved in 2 weeks’ time, and the investigations are:

• Normal full blood count.
• Normal sodium.
• Potassium is 2.8
• Chloride is 100
• Urea is 2.4
• Serum creatinine is 83
• Calcium 3.4

The first question is “what’s the abnormality in this chest X-ray?“. What do you see?

Student: The voice is not clear.

So you think that there’s some abnormal shadowing here and here, now anatomically what this area is called? It’s called the hilum of the lung.

So you have abnormal shadowing in the hilar region, and this could be what? What’s normally in this region? Lymph nodes, it’s the normal structure in the hilar area.

So now we have a young man who has bilateral lymph node enlargement in his hilar region of the lung.

The heart looks normal, the lungs are slightly… Because you can see the distance between the ribs in the left is more than the right, so it’s partially irritated??

The next question is: “what’s the most likely diagnosis of this lymph node enlargement on both sides”?

Student: Metastasis.

Metastasis, that’s a good answer because in chest X-ray, we can only make a comment on what’s it, and it could be a metastatic lesion, but what’s the commonest cause of bilateral lymph node enlargement? Lymphoma, it’s very common. Anything else?

You should think in pattern, could it be an infectious process? Could it be a granulomatous disease? Could this be a malignant disease?

Is there any infection that can do this? Of course, TB is the number one cause, it can present completely like this.

Any granulomatous diseases? Sarcoidosis, so here we have multiple answers to that.

So what’s the bilateral hilar lymphadenopathy cause?

1. Sarcoidosis.
2. Infections: TB, mycoplasma, fungal infections, and Intestinal Lipodystrophy (Whipple’s disease).
3. Malignancies: lymphomas, carcinoma, and mediastinal tumors.
4. Inorganic Dust diseases: silicosis and Berylliosis.
5. Extrinsic allergic alveolitis: Such as bird fancier’s lung disease; if you are exposed to birds, you may get this disease.

So the most common is infection and malignancies.

But what’s the most likely diagnosis in this case? This patient had a painful lump in the skin of his leg, what’s the painful lump in a patient with sarcoidosis or TB? Erythema nodosum.

So this patient has erythema nodosum, bilateral lymphadenopathy, and chest symptoms, so the number one diagnosis is sarcoidosis and then TB. But it’s okay to write this or that in the exam, it’s the same because, in the X-ray, we cannot differentiate.

Now look at the investigations; the potassium is 2.8, and calcium is 3.4, and it’s very high “hypercalcemia”, and what’s the commonest cause of hypercalcemia? Sarcoidosis is number one, malignancies, and metastatic disease.

And so you should read everything and put all pieces together, so the patient with chest symptoms, erythema nodosum, and hypercalcemia.

Erythema nodosum is not common with malignancies, so now we can exclude malignancies, so anybody will say lymphoma he’ll be incorrect.

Case 2:

I want to read this ECG for you, a 28-year-old lady presented with sharp chest pain which radiated to the trapezius and was versed in a supine position (she got better in the supine position), the pain lasted for hours.

So which chest pain with this ECG will be compatible?

Student: Angina.

Angina is a possibility, let’s see what’s the abnormal in this ECG, here there’s ST segment elevation; it’s very high in lead 1 and lead 2 while in lead 3 it’s slightly up but not markedly elevated.

But here, the ST segment elevation is not convex, so it’s not myocardial infarction; here, the ST segment elevation is more concave diffuse, so it’s Pericarditis.

MI and pericarditis have the same story, the same thing, but it’s convex in MI and concave in pericarditis.

So here’s ST segment elevation with concavity and tall T wave.

So what’s the likely diagnosis? Pericarditis.

But remember we cannot roll out MI completely because, on the base of ECG alone, we cannot exclude it, and so in the exam, any answer that’s nearly relevant will get marks but not as much as pericarditis.

So what’s the pericarditis? The causes:

1. Infections: commonest bacterial, TB is not very common now.
2. Systemic diseases like rheumatoid arthritis, SLE, rheumatic fever.

Rheumatic fever is by definition a pancarditis; they get pericarditis, myocarditis, and endocarditis, all of them together. 3. Liver failure. 4. Acute myocardial infarction

What’s the complication of acute MI which is commonly associated with pericarditis? The second common is dressler syndrome.

Pericarditis can be inflammation of the pericardium or fluid accumulation which can be transudate or exudate.

Now what’s the difference between the two? Which one is more abnormal?

This is a chest X-ray of the same patient, this looks more like a heart which means that the fluid has been taken out by pericardiocentesis, and so this is before pericardiocentesis and this is after.

Case 3:

A 26-year-old lady presented with muscle weakness, cramps, numbness, and tingling of her hands and feet, so this is very important “weakness of the muscles”, and she gets cramps too, this could be paresthesia or could be some nerve problem, but mostly it’s a muscle problem.

She was diagnosed with hypertension 4 years ago.

So hypertension in a young patient, what problem is that? In young hypertensives, it’s mostly a secondary cause of hypertension; they are not primary hypertensives.

So in any young patient with hypertension, it’s important to roll out the secondary causes.

So that’s the scenario here, and if you didn’t notice it, then you missed.

On examination:

• Pulse: 60/min.
• BP is high.
• Mild proximal weakness; it’s very important.

So we have a young hypertensive, treatment was given 4 years ago on treatment, muscle pain, and proximal weakness.

And the rest of the exam is normal.

Investigations:

• Normal full blood count.
• Normal sodium.
• Potassium is low. You must notice because, in the exam, you’ll be given a reference page but not with CBC, urea, creat. Potassium, sodium, and liver enzymes, but anything else other than that will be included.

Why am I saying that? Because each case scenario will have 2, 3, 4 questions; one will be “what are the abnormal laboratory findings?”

And so here we have low potassium.

• Bicarb normal range is 22 – 26, so this is abnormally high bicarb.
• Normal chloride.
• Normal urea.
• Creat. Is normal.
• Calcium 2.4
• Magnesium is normal.

In the chest X-ray, there’s no cardiomegaly, but ECG shows prolonged QT interval and U wave (which always comes after the T wave), and this is classically hypokalemia.

And so this patient has hypokalemia and high bicarb, what’s the cause of this patient’s hypokalemia? Which hypertension disease is always associated with hypokalemia? What are the drugs that cause hypokalemia? Diuretics such as thiazides and Lasix.

Now we have a young lady, hypertensive for 4 years with hypokalemia and proximal muscle weakness, and we want to know the disease that can cause this secondary hypertension.

Causes of secondary hypertension:

• Renal artery stenosis.
• Pheochromocytoma.
• Coarctation of the aorta.
• Primary hyperaldosteronism “conn’s syndrome”, it’s number one cause of secondary hypertension, and it causes high aldosterone, low potassium, and proximal muscle weakness.

What’s the cause of alkalosis? It’s because of the high bicarb.

What’s the further noninvasive investigation you recommend? As we said this is a case of aldosteronism “conn’s disease”, so we can look at the aldosterone level in the blood and for the suprarenal tumor, we can do MRI to the gland.

Read this ECG, this is typical hypokalemia; here’s T wave and U wave, normally you have a normal P wave and normal PR interval, normal QRS complex, and you have a rounded normal T wave, and sometimes you may find a U wave normally.

Look here in the hypokalemia, the PR interval is slightly prolonged, the ST segment is slightly down, shallow T wave and a very prominent U wave.

Case 4:

A 28-year-old man presented with a 6-month history of 4 kg weight loss, fever at night, and sweats.

Now the question is “describe the chest X-ray findings”.

Here on the right side, there’s a fluid level, then what’s the next step for diagnosis? Aspiration of the pleural fluid.

That’s correct, but which infection can cause weight loss with night sweats and fever? TB is number one, and it could be a malignancy also.

But this is not what I’m asking, if you said “pleural aspiration” correct; because you want to know whether it’s transudate or exudate, but when you do pleural aspiration, you can do pleural biopsy; it’s the same procedure at the same time, and you’ll find the diagnosis.

But a CT scan is correct, MRI is correct, culture is correct, they are all correct, but it’s half a mark only, not a full mark.

And the correct answer is pleural biopsy.

Case 5:

This is a bone marrow aspirate of a patient with multiple myeloma; describe the morphology of the cells.

What are these cells? What’s the classical cell of multiple myeloma? It’s called by the name of the cell, its plasma cell.

The plasma cell has a very huge nucleus which is eccentric always near the cell wall, it’s not a central nucleus unlike other cells.

And the other disease it can cause is “plasma cell leukemia” apart from multiple myeloma.

Case 6:

A 30-year-old woman presented with thirst, polyuria, and polydipsia, and there’s no past medical history of note, and the examination is normal.

In which condition you get polyuria and polydipsia? Diabetes, and it can be diabetes mellitus, and it can be diabetes insipidus.

Diabetes insipidus can be either central from the brain or from the kidney.

But until now, we cannot differentiate between insipidus and mellitus in this case; both diseases present with polyuria and polydipsia.

Investigations:

• Sodium is normal.
• Potassium is normal.
• Urea is normal.
• Plasma osmolality is normal; the normal is 275 ml/osm to 290 ml/osm.
• The patient is passing 8 liters of urine every day.

It can be diabetes insipidus, we cannot roll it out, but in diabetes insipidus, you produce a lot of ADH, and what will that do? It’ll retain the water and the osmolality will go high.

Simply there’s something that’s called “primary psychogenic polydipsia”; it’s a young lady drinking water too much.

Now how would you diagnose it? She’s passing 8 liters of urine every day; she’s drinking too much obsessively.

Because we can see that the osmolality is normal, and she’s not in the diabetic insipidus range either nephrogenic or central, and the glucose is normal, and she’s not a diabetic either.

And so she is not diabetes mellitus, and she is not diabetes insipidus, and she is drinking too much water.

Now how can you make a full diagnosis? If you said you’ll do ADH level, I’ll accept that because you want to roll out DI, but what’s the best test here?

It’s called a water deprivation test; we bring her here in controlled conditions and give her only that much of water and monitor the amount of urine she passes, and everything will change.

We can also use desmopressin; it has ADH-like action to see the function of the pituitary and the kidney axis.

Case 7:

Read this ECG now, there are only 3 leads here; lead 1, lead 2 and lead 3, nothing else.

First of all, see whether the complex is normal or not,… Voice is not clear, but PR interval, ST segment, T wave, QRS complex all appear normal to me.

What’s the rate here? It’s 45 beats/min, she’s almost heart block or it’s severe bradycardia.

So in ECG findings, there’s severe bradycardia with likely heart block.

Q1: Clinical features of vasculitis include:

1. Generalized lymphadenopathy.
2. Mononeuritis multiplex.
3. Enlarged thyroid.