Parkinsonism

Parkinsonism is when there is a triad of bradykinesia, resting tremors and rigidity. There are many causes of parkinsonism. The most commonly seen parkinsonism in the  undergraduate medical final examinations would be Idiopathic Parkinson's disease. 

However, not everyone presenting with Parkinsonism signs have Idiopathic Parkinson's Disease. Therefore students should be wary and mindful about offering the diagnosis of Idiopathic Parkinson's disease upon encountering patients with the above triad. Remember, Idiopathic Parkinson's is a clinical diagnosis and its aetiology is idiopathic i.e. cause is uncertain. Although it is a clinical diagnosis and lab and radiological workup is not required to make the diagnosis, it is also important to consider other differentials causing Parkinsonism signs especially if the patient has risk factors. 

One key feature of Idiopathic Parkinson's Disease is that it is asymmetrical. In the early stages of the disease, parkinsonism can be seen affecting one side of the body. As shown in the video above, this patient has resting tremors affecting his right hand. 

The video below shows bradykinesia affecting the right hand of the same patient. 

As the disease progresses over the years, it may affect the contralateral side of the body as well. However, the key feature remains and Parkinsonism signs would still be asymmetrical. As shown in the next video below, this elderly gentleman has advanced Idiopathic Parkinson's disease as well but take note that the frequency of tremors affecting one arm is different from the other arm. 

Anything that causes damage to the basal ganglia can result in Parkinsonism. For example stroke (vascular), demyelinating diseases, brain tumors, drugs or even metabolic disorders like Wilson's disease. It is good to revise about Parkinsonism as it is a common appearance for the medical examinations. 

CCE. 

 

Chronic Tophaceous Gout

This would be a short case discussion. 

This case is a male patient with multiple joint swellings affecting both upper limbs. The swellings seem to affect the DIPJ, MCPJ as well as wrists. What is also strikingly noticeable is the presence of multiple tophi over the joint swellings. It is not difficult to reach a conclusion of tophaceous gout. 

Tophi are usually found occuring over distal joints or tissues where temperatures are relatively "cooler". This will enable cystallization to occur. This tophi are usually found over distal finger or toe joints, ear pinna. In severe cases, tophi can even be found ocurring almost anywhere on the body as depicted above. 

The next step would be to look for the possible aetiology. Look for psoriatic rashes, polycythemia, hepatosplenomegaly and lymphadenopathies to suggest hematological malignancies.

Then, last but not least, look for complications of the disease itself. Look for sallow coloured skin, dialysis catheters, arteriovenous fistulas to suggest chronic kidney or end stage kidney disease either as a result of obstructive uropathy or chronic NSAID intake for gouty pains. Examine the abdomen for enlarged ballotable kidneys to suggest obstructive uropathy due to urolithiasis. Also look for complications of chronic steroid therapy e.g. Cushing syndrome, hypertension, hyperglycemia (many GP clinics prescribe steroids and NSAIDs to control gouty arthritic pains). 

Remember to apply the triad of diagnosis - aetiology - complications for any case you encounter regardless of short or long case examination. This guide will serve you well and assist you in approaching any case as complete as possible. 

The image above shows central obesity with striation over the anterior abdomen suggesting a Cushingoid appearance. Take note also that there are multiple hyperpigmented scars over the peri-umbilical region suggesting repeated injections likely insulin therapy thus suggesting this patient may have concomitant diabetes mellitus. This will further strengthen the suspicion of Cushing's syndrome. Also notice that there are multiple tophi over the anterior abdominal wall as well. 

Therefore it can be concluded that this patient has been suffering from chronic tophaceous gout for which he has been treated with chronic steroid therapy resulting in secondary Cushing's syndrome. 

Should this case appear for the examinations, the case can be approached from the aspect of gout or can be approached from the aspect of Cushing's syndrome from which the diagnosis of gout is expected to be offered as the underlying main problem. So students should be ready for any possibilities. 

For the long case examination involving a patient with gout, it would be sensible to approach gout from this perspective: 

Gout is due to hyperuricemia.

Hyperuricemia can accumulate due to increased production or decreased clearance. 

For increased production, ask about dietary purine intake, ask about lifestyle (alcohol), ask about cell hemolysis (can be from polycythemia, can be from large solid tumours, can be from hemolytic anemia), ask about tissue damage (burns, surgery, trauma) and last but not least genetic factors (so ask about family history). 

For decreased clearance, ask about dehydration, ask about medications e.g. ACE inhibitors or ARBs or diuretics or aspirin which impedes uric acid excretion and ask about underlying kidney diseases.

Lastly remember to apply the triad of diagnosis - aetiology - complications as well to make your history complete. 

CCE.

Tackling A Case Of Stroke For The Long Case Examination

As an undergraduate, you are highly likely to encounter a case of stroke in the medical examinations either in the long case format or short case format.

Making a diagnosis of stroke is not difficult.

So, how do you suspect a patient has had a stroke?

From history taking, the patient may provide information regarding weakness affecting one side of the body i.e a hemiparesis or a single limb i.e. a monoparesis. The patient may also have cranial nerve involvement, presenting with diplopia, ptosis, facial asymmetry or slurred speech. It is uncommon to get a patient with dysphasia or aphasia for the undergraduate exams as this will impede history taking and physical examination. Nevertheless, you may still encounter a patient with aphasia or dysphasia if there is a shortage of neurological cases for the exams.

The student will be expected to take necessary detailed history pertaining to the right sided hemiparesis e.g. onset of weakness, progression of weakness, and severity. From history taking it is difficult to determine if the patient has had an ischemic stroke or a hemorrhagic stroke. However, in general, if the patient complained of a sudden severe headache preceding or occurring concurrently with the hemiparesis, it is always good to exclude hemorrhagic stroke first. In real life practice, there are many cases of hemorrhagic stroke where the patient presents with just sudden onset of limb weakness without any headaches. The severity of the hemiparesis is not a good indicator to suggest an ischemic event or a hemorrhagic event. There are cases of basal ganglia hypertensive hemorrhages where the patient only has a mild hemiparesis of 3-4/5 whereas there are cases of left middle cerebral artery territory infarctions with dense hemiparesis of 0-1/5.

Once you have decided that the patient has a hemiparesis, you can make a diagnosis of a stroke. If the student has already decided that this presenting complaint is likely due to an ischemic stroke, then a reasonable differential diagnosis would be hemorrhagic stroke. It is also applicable vice versa i.e. if the provisional diagnosis is a hemorrhagic stroke, then the differential would be an ischemic stroke. Only a CT brain can confirm the diagnoses.

Remember to explore other possible differentials as well. Ask about prolonged headaches, constitutional symptoms to suggest a brain tumour. Ask about stepwise deterioration of neurology e.g. history of facial asymmetry 10 years ago, then history of numbness affecting left leg 7 years ago, then history of bladder incontinence 3 years ago etc. This may suggest a possibility of a demyelinating condition such as multiple sclerosis. Also ask about recent head injury or trauma which may suggest a intracranial hemorrhage causing the stroke like symptoms. And also ask about fever, rashes, photophobia, neck stiffness or altered behaviour to suggest intracranial infection e.g. meningitis or cerebral abscess.

Once the student has established the diagnosis and its differentials, the next step should be to explore the aetiology. From history, ask about risk factors for the stroke i.e. hypertension and its BP control, diabetes and its glycemic control, dyslipidemia and its lipid control, history of ischemic heart disease, history of cigarette smoking or chronic alcohol consumption/ abuse, connective tissue disorders (especially if the patient is young, explore regarding anti phospholipid syndrome), medication history (compliance to medications as well as whether patient is on anti-platelet therapy or anti-coagulation therapy) and history of head injury. It is also good to get a detailed family history regarding cardiovascular risk factors as conditions like diabetes, dyslipidemia, hypertension may run in families. Also explore regarding dietary habits – fast food, oily food, high salt diet, lots of processed foods etc. These aetiologies are supporting a diagnosis of ischemic/ hemorrhagic stroke. Remember to get history regarding aetiologies for the other differentials too if relevant to your patient. 

Next step would be to explore complications that may arise from the stroke. Ask about headaches, blurred vision which could indicate raised intracranial pressure. Also ask about fever, cough, dyspnoea and choking episode to suggest that the patient may have aspirated. Ask about seizures as post stroke patients have tendency for seizures. Ask about falls and physical injuries due to the physical limitations as a result of the stroke. Ask about cognitive impairment or change in consciousness (very unlikely to get a demented or delirious or confused patient in the exam setting!).

Last but not least, explore about the patients social history in more detail than usual. As stroke affects the patient’s life very significantly, it is also good to know the patient’s baseline functionality e.g. right or left handedness, occupation, breadwinner or not, living at home with whom, hobbies, staying in what sort of house (single storey versus multi storey and whether there is lift facility). All this will give a rough idea on how the stroke may impact the patient’s life once he is discharged from the hospital. The information obtained will help you plan for long term management. For example if the patient is the sole breadwinner of his family and he is no longer able to work, then you may offer referral to social welfare for assistance. Another example would be if the patient is right hand dominant and is a typist and loves to play tennis using his right hand and he just suffered a stroke with right hemiparesis, then he will benefit from occupation therapist referral to get him to adapt and learn to adjust using his left hand while awaiting right hand to recover with rehab (if at all possible). 

Once the above mentioned has been settled, the student should go on to complete the other components of history taking to ensure a complete history is taken e.g. drug history, allergy history, surgical history, etc.

For physical examination (from head to toe), 

Head:

Examine the Glasgow Coma Scale (GCS) and also orientation to time, place, person. Look for cranial neuropathy if it is suggestive from the history taking. Example, if the patient complained of facial asymmetry and slurred speech, then it is probably worth examining the facial nerve and the cranial nerves 9,10,12 properly. If upon general inspection there is eye deviation or ptosis, then a proper examination of the cranial nerves 3,4 and 6 is warranted. Otherwise it is unnecessary to do a FULL cranial nerve examination. Time is the limiting factor here! If the student managed to complete history taking within a short time frame, then perhaps when there is ample time, the student may still do a concise but full cranial nerve examination (The olfactory nerve is probably the least examined cranial nerve as it rarely appears for exams. So be smart when choosing which cranial nerve to examine). Look for risk factors for stroke: xanthelasma, arcus senilis, acanthosis nigricans (darkening and velvety like skin over the neck and flexure area). Also assess speech and nystagmus if history suggests cerebellar involvement. 

UL:

Finger prick marks for diabetes mellitus. Nicotine stain over the finger nails. Tendon xanthomas. Upper motor neuron (UMN) signs affecting the weak arm: hypertonia, hyperreflexia. And also quantify the weakness using the MRC scale 0-5. Also check sensory deficits. Remember to check cerebellar signs as well if not yet done as part of the CN assessment. Important to check the blood pressure using sphygmomanometer as well. 

LL: 

Check for UMN signs affecting the weak leg: hypertonia, hyperreflexia, clonus, upgoing Babinski response. Quantify the weakness using MRC scale. And check for sensory deficits. Cerebellar assessment is also important if not yet done for UL or CN assessment. However if while assessing CN and UL and no cerebellar signs were detected, then it is not necessary to do cerebellar assessment for LL. Last but not least, ask the patient to walk to assess gait (do this only if the patient is able to walk. Do not cause a fall which may injure the patient). 

CCE.

Diabetes Mellitus - How to Approach a Patient with Diabetes Mellitus in the Long Case Examination (Physical Examination)

Once you have completed the history taking, you will know which system to examine more thoroughly i.e. the system that correlates with the primary or chief complaint. For example, if the chief complaint was numbness in the feet, then a thorough examination of the lower limbs would be the next logical step. 

For the purpose of this blog, I'll list out the things required for examination in general. You may tailor the examination requirement based on the patient you've clerked in the exam. 

General Examination:

1. GCS - always good to assess this. An alternative is the orientation to time/ place/ person assessment. The patient's mental state is an important first assessment for a diabetic patient as such patients are prone to cerebral ischemia, neuroglycopenia, hyperglycemic complications e.g. HHS and even vascular-related neurocognitive impairments. 

2. If the patient has trouble remembering many facts during history taking, you may want to offer to do a Mini Mental State Examination (MMSE) at the end of the presentation to identify presence of and severity of cognitive impairment or dementia at the end of the patient's examination (however, this will not be possible in the real exam setting due to time constraints). 

3. General appearance - Acromegaly, Cushingoid, thyrotoxicosis as these conditions may predispose to development of DM or aggravate DM control. Also look out for skin changes e.g. pallor or sallow coloured skin to suggest presence of chronic kidney disease and rashes that may suggest presence of connective tissue disorders e.g. systemic lupus, psoriasis, systemic sclerosis etc. Do take note of the peripheral joints as well especially the fingers, toes and ankle regions for any deformities to suggest a chronic inflammatory arthropathy or gout. The earlier mentioned conditions may all be treated with steroids for a prolonged period of time resulting in hyperglycemia or steroid induced diabetes mellitus.

4. Accessories - intravenous drips, insulin syringe pumps, intravenous antibiotics, oxygen support, orthoses (ankle splints for foot drop or limb prosthesis), customised shoes for Charcot foot or walking aids. Also improtant to take note of presence of arteriovenous fistulas and dialysis catheters (internal jugular or femoral dialysisc atheters)

5. Eyes - at least a visual acuity assessment using a portable modified Snellen's chart and RAPD assessment for any retinal or optic disc abnormality. If there is RAPD detected, then the next assessment would be funduscopy for diabetic retinopathy if time permits.

6. CVS - look for displaced apex with murmurs, raised JVP and bibasal crepitations to indicate heart failure (coronary artery disase is a complication of long standing and uncontrolled DM)

7. Respi - examination of this system should be selective. Look briefly for evidence of fluid overload e.g. basal crepitations to suggest pulmonary oedema or stony dullness percussion note with reduced vocal resonance to suggest pleural effusion. 

8. Peripheral pulses especially the distal pulses e.g. dorsalis pedis,/ posterior tibialis pulses. This would be more relevant if the patient reports claudication pain during history taking. Auscultation of the carotid arteries for any bruit to indicate stenosis is also important if time permits. Do take note that uncontrolled diabetes mellitus may accelerate atherosclerosis changes along major arteries. 

9. Neurological examination - particularly the lower limbs. You may limit the neurological examination to information obtained during history taking. For example if the patient reports that he has history of right sided leg weakness, then perhaps it is sufficient to focus your neurological examination to the lower limbs only, while briefly screen through neurological examination of the upper limbs and cranial nerves. Conducting a full neurological examination as a routine assessment during long case examination can be challenging due to time constraints. The earliest sign of diabetic peripheral neuropathy is loss of vibration sense and loss of proprioception in the distal joints e.g. interphalangeal joints in the toes. Also look out for diabetic foot ulcers, calluses over bony prominences and trophic changes affecting the skin over the lower limbs which may strongly suggest presence of peripheral neuropathy. 

10. Abdominal examination - look for signs of lipohypertrophy or lipoatrophy to suggest repeated insulin injections. This can usually be found at the periumbilical region. If found, it would be important to highlight this finding during the case presentation as it will impact treatment outcome. Patients that fail to rotate the insulin injection sites adequately will have the above changes occurring and this will impair optimal insulin absorption and affect adequacy of glucose control. Look for Tenchoff catheters over the anterior abdominal wall to suggest patient has ESRF and is undergoing CAPD. Also look renal transplantation scars to suggest a history of diabetic kidney disease (renal transplant scars are usually J shaped and located at either right iliac fossa or left iliac fossa regions). It is also possible that immunosuppressive therapy post organ transplant be the aetiology for diabetes mellitus in such a patient. Do consider palpating the abdomen for an abdominal aortic aneurysm as well. 

11. Lastly, do steal some time to screen the patient's body for any cutaneous infections like carbuncles, furuncles. Look also for tinea infections affecting the skin flexures e.g. axillary, infra-mammary, groin area. In uncontrolled diabetics, skin infections may be extensive. 

CCE

Murmurs Made Easy

For the purpose of this post, I shall fast forward the examination of the heart to auscultation of the heart murmurs. 

We begin auscultation of the precordium by placing the stethoscope over the mitral area. 

A hand drawn picture of the anterior chest with the location of each valves

One very important step which is often overlooked or neglected by medical students is the instruction to the patient to breathe in and breathe out slowly. Personally, I would let my stethoscope to remain over each valve area for a total duration of 2 breathing cycles (i.e. breathe in-breathe out-breathe in-breathe out) before moving to the next valve area. 

Let us recap the basic physiological changes that affect murmurs during breathing. During inspiration, the increased thoracic cavity volume lowers intrathoracic pressure thus increases venous return to the right side of the heart. This will cause an increase in murmur intensity for tricuspid and pulmonary valve disorders. 

On the other hand, expiration reduces the thoracic cavity volume and thus increases arterial outflow from the left side of the heart. This will cause an increase in murmur intensity for mitral and aortic valve disorders. 

This basic concept is very important and will help guide you to eliminate and narrow down possible differentials for every murmur heard over any particular valve area as I will explain next. 

Let us begin at the mitral valve area. Place the diaphragm of the stethoscope over the mitral valve area. Regardless whether you hear any murmurs or not, I would encourage you to do the breathing manouvres for at least 2 breath cycles as mentioned above. If there are any soft murmurs, this manouvre will enhance or increase the murmur intensity. 

If there is a murmur heard over the mitral area, below are the possible causes:

1. Mitral regurgitation (MR)

2. Mitral stenosis (MS)

3. Aortic stenosis (AS)

4. Tricuspid regurgitation (TR)

5. Ventricular septal defect (VSD)

To help differentiate between the causes, here is how the breathing manouvre will help narrow down the diagnoses. 

If during inspiration, the murmur heard over the mitral area becomes louder, then it can be concluded that the murmur is actually originating from the neighbouring tricuspid valve. Therefore the murmur detected over the mitral valve can be ignored. The murmur will then be best heard over the tricuspid area after completing the mitral valve examination. 

If during expiration, the murmur heard over the mitral area becomes louder, then it can be concluded that the murmur is unlikely to originate from the tricuspid valve or VSD. Only 3 possibilities remain i.e. MR, MS or AS. To differentiate between the 3 possible source of the expiratory phase murmur heard over the mitral valve area, the student will need to time the murmur by palpating the carotid or radial pulse. If the expiratory murmur coincides with the diastolic phase, then the only diagnosis possible would be a MS murmur. Next step is to listen and verify that the murmur is indeed a mid diastolic murmur (MDM) of MS i.e. switching to the bell of the stethoscope and listening for the MDM with the patient lying left lateral.

If the expiratory murmur coincides with the systolic phase, then you have ruled out MS. So all that is left would be either MR or AS. To differentiate between this two, listen to the systolic murmur carefully and decide if its a pansystolic murmur (PSM) or an ejection systolic murmur (ESM). A PSM would classically have a soft S1 with the systolic murmur extending throughout systole. An ESM, on the other hand, would have a clearly heard S1 and the systolic murmur would be heard in mid systole. 

If it is a PSM, then the diagnosis would be a MR. This can be further confirmed by auscultating the axillae for radiation of the MR murmur. If it is a ESM, then the only diagnosis possible would be an AS murmur. An AS murmur can sometimes be heard all the way to the left axillae as well. This phenomenon is called the Gallarvardin phenomenon. 

If there no variation in the murmur intensity between inspiration and expiration, time the murmur by palpating the carotid or radial pulse. A systolic murmur that does not vary with inspiration or expiration heard over the mitral area can only be caused by a VSD. Once you have completed the mitral valve examination, confirm the earlier heard murmur which will be best heard over the lower left sternal edge. This will confirm the presence of a VSD. 

 

Over the tricuspid valve area, the same manouvres as above should be applied. If a PSM is heard over the tricuspid valve area, there are only 3 possibilities: a TR, a VSD or a loud MR. Remember, the chest cavity and specifically the heart isnt a very large structure. Therefore any loud murmur can practically be heard everywhere. If the PSM increases intensity during inspiration, the PSM is confirmed to be from the tricuspid valve i.e. a TR. If the PSM is louder during expiration, then the murmur is a radiation from the mitral valve i.e. a MR. But if the murmur does not change with either inspiration or expiration, then the PSM could be from a VSD. 

 

Over the pulmonary valve area, it is unusual to hear a PSM. But you could detect a ESM of pulmonary stenosis (PS). This is, however, uncommon for undergraduate examinations. An early diastolic murmur (EDM) of pulmonary regurgitation (PR) is even more rare. Both PS and PR murmurs will be louder during inspiration. Also, do look out for machinery or continuous murmurs near the pulmonary valve area. This may indicate presence of a Patent Ductus Arteriosus (PDA). The machinery murmur of a PDA is often heard over the upper left chest area just below the left clavicle. This area is often close to the pulmonary valve area.

Over the aortic valve area, it is also uncommon to hear a PSM. Look out for ESM of aortic stenosis (AS) and EDM of aortic regurgitation (AR). Both AR and AS murmurs will be louder during expiration. AR murmur can be further verified by presence of EDM which is best heard over the Erb's space or second aortic space over the left sternal edge with the patient leaning forward. AR murmurs are usually accompanied by other peripheral signs like Corrigan's sign (bilateral prominent carotid arterial pulsations), a collapsing pulse as well as wide pulse pressure. AS murmurs can sometimes radiate to both carotid arteries and this feature should be looked for and examined routinely in patients with AS murmurs. However, AS due to aortic sclerosis (degenerative cause) may not always have radiation to both carotids. The ESM murmur may be localised to the aortic valve area only. It is important to take note of this. In real life practice, the ESM of AS can sometimes be heard over the pulmonary valve area as well. This may confuse the unsuspecting student. However this confusion can be avoided when patient is asked to inspire and expire slowly. If the ESM heard over the pulmonary valve area is louder during inspiration as mentioned earlier, then the ESM is likely due to PS. If the ESM over the pulmonary valve area is louder during expiration, then the ESM is likely to originate from the neighbouring aortic valve i.e. an AS.

CCE.

Cushing's syndrome

Cushing's syndrome is a favourite appearance in the medical examinations. 

Often, the stem would be to "look and proceed". Often the diagnosis would be easily suspected. 

From head to toe, the clinical findings are as below:

1. Depression or psychosis

2. Cataracts

3. Acne

4. Rounded facies

5. Hirsuitism in females

6. Central obesity

7. Increased supraclavicular fat pads

8. Increase dorso-cervical fat pad

9. Acanthosis nigricans

10. Purple striae at anterior abdomen or axillary skin folds or thighs

11. Easy skin bruising

12. Osteoporosis

13. Diabetes mellitus (look for finger prick marks at finger tips, funduscopy for diabetic retinopathy changes)

14. Hypertension (offer to check patient's blood pressure using manual sphygmomanometer)

15. Hypogonadism (menstrual disturbances, impotence)

16. Proximal muscle weakness (myopathy)

17. Thin arms and legs

Once the diagnosis of Cushing's syndrome is made, investigations will be focused on determining the aetiology of Cushing's syndrome i.e ACTH-dependent (ACTH secreting pituitary tumours/ ectopic ACTH-secreting tumours) versus ACTH-independent (adrenal causes or exogenous steroid exposure). A differential of a person with Cushingoid appearance would be pseudo-Cushing's which can be seen with persons with obesity or chronic alcoholism.

CCE.

Diabetes Mellitus - How to Approach a Patient with Diabetes Mellitus in the Long Case Examination (History Taking)

Diabetes Mellitus (DM) is a common entity nowadays and therefore it should be well known by every healthcare practitioner particularly the clinicians. 

Similarly, diabetes mellitus is also a common appearance in the medical examinations. They may appear in various forms e.g.  target organ damage, complications related to treatment, as well as psychosocial issues surrounding the condition itself. 

For the undergraduate final examinations, students can expect to encounter cases where a patient presents with a particular complaint related to a target organ damage. For example the patient may present with numbness affecting the feet or even blurred vision affecting one or both eyes. The student is expected to get a competent and complete history pertaining to the presenting complaint as well as establish the diagnosis of diabetes mellitus and whether there are presence of other target organ damage occurring concomitantly with the presenting complaint.

So, let us refresh our memories with regards to diabetes mellitus and its complications.

Diabetes mellitus are broadly categorised into 2 types (for the undergraduate level, at least):

Type 1 - Autoimmune cause, due to premature loss of pancreatic beta islet cells

Type 2 - Acquired cause, usually due to insulin resistance as a result of increased adipocity, hormonal dysregulation etc.

There are other types as well e.g Maturity Onset of Diabetes in the Young (MODY), Gestational diabetes, Double Diabetes (mixture of both Types 1 and 2 in the same patient) etc. But those are for another topic and discussion as it can be complex. 

In general, the differentiating factor between Types 1 and 2 Diabetes Mellitus is age of onset. Type 1 typically occur in the young, usually pre adolescent age whereas Type 2 diabetes occur in adulthood (in general). However this distinctive factor is no longer clearcut and we are seeing younger patients with Type 2 diabetes due to lifestyle and the ever increasing waistline among youngsters. 

After tackling the presenting complaint, you can add the following information within the history of presenting illness (HOPI) segment. 

Enquire and explore regarding complications resulting from diabetes mellitus:

MACROVASCULAR:

• Coronary artery disease
• Ask about chest pains (categorise according to Canadian Cardiovascular Society classification), dyspnoea (categorise according to New York Heart Association classification), pedal oedema, orthopnoea, paroxysmal nocturnal dyspnoea etc
• Cerebrovascular disease
• Ask about facial assymetry, unilateral limb weakness, speech impairment, dysphagia, memory impairment (vascular dementia)
• Peripheral arterial disease
• Claudication pains, resting pains, digital cyanosis or gangrene

MICROVASCULAR:

• Retinopathy
• Ask about scotomas, blurred vision, floaters, visual field defects
• Nephropathy
• Ask about frothy urine, pedal oedema, facial puffiness, periorbital oedema, dyspnoea, uremia (nausea/ vomiting/ anorexia/ chest pains (pericarditis) / abdominal pains (uremic peptic ulceration)/ altered sensorium or seizures (uremic encephalopathy), dialysis, renal transplantation)
• Neuropathy - somatic and autonomic
• Ask about numbness affecting extremities especially the foot, pressure ulcers, digital gangrene, foot deformities, postural giddiness, recurrent vomiting (gastroparesis)
• Sexual dysfunction - erectile dysfunction (a sensitive issue due to the taboo among Asian customs, but if approached professionally and you are able to obtain information regarding this issue, many patient's will be grateful and of course, impress the examiners)

METABOLIC:

• Hyperglycemia
• Ask about polyuria, polydipsia, unintentional weight loss, nocturia (not to be mistaken with prostatism - diabetic polyuria have good amd large volume urine stream due to osmotic diuresis whereas prostatism nocturia have weak urine stream with the usual lower urinary tract symptoms e.g. terminal dribbling, hesitancy etc). 
• Diabetic ketoacidosis (DKA) or hyperosmolar hyperglycemic syndromes (HHS)
• Ask about symptoms of hyperglycemia plus dyspnoea (may suggest acidotic breathing), sweet fruity breath smell (ketone breath), altered sensorium (HHS) or involuntary limb movements (hemichorea hemiballismus due to HHS) ** diabetic emergencies will not appear for exams, rest assured 😏
• Hypoglycemia
• Ask about hand tremors, hunger pangs, diaphoresis, agitation/ anxiety/ restlessness, syncope and coma (unlikely to appear in the exams as you wont be able to clerk the patient!!) 

In the review of systems segment, can explore regarding any health problems from head to toe which may be the cause of diabetes mellitus e.g. connective tissue disorders e.g. SLE/  rheumatoid arthritis or chronic lung disease (asthma/COPD) (chronic steroid usage), acromegaly, Cushing's syndrome. If the patient is young, presence of concomitant connective tissue disease (s) may suggest an autoimmune cause of DM. 

In the family history segment, explore about strong family history of DM. 

For past medical history or surgical history segment, enquire about history of pancreatitis, pancreatic tumours or pancreatic surgery. Also about any pituitary tumour resection (pituitary Cushing's or Acromegaly), adrenal tumour (Adrenal Cushing's) resections. 

In the drug history section, can check with the patient regarding their medication list and compliance. Patients may know the medications they are on and the dosages. Alternatively, patients may be provided a prescription slip and will be instructed to show the medical student upon request. If there is element of non-compliance, be sure to enquire the reason behind the behaviour. Very often, the patient may inform of some adverse side effects as a result of taking that particular medication which causes the non-compliance. For example, the patient may be non-compliant to metformin because of bloating or frequent loose stools. 

Physical examination of the patient with diabetes mellitus requires a comprehensive approach from head to toe similar to history taking. There will be many areas to cover and therefore, it will be covered in the next post "Diabetes Mellitus - How to Approach a Patient with Diabetes Mellitus in the Long Case Examination (Physical Examination)". 

CCE. 

Chest Pains - Approach to a Patient with Chest Pain for the Long Case Examinations

Chest pain is a common exam question especially for the long case in undergraduate level exams. 

As in any scenario, usage of common sense is important and this will help you use time more effectively in the 60 mins designated for the long case exam. 

Differential diagnoses will depend on the anatomical location of the chest pain:

Skin:

Herpes zoster

• Fever, rash (usually in dermatomal location), history of varicella zoster infection, enquire about immune suppressed states: DM, malignancies, chronic steroid therapies or immune suppressive therapies 

Muscle:

Hematoma or soft tissue injury 

• history of chest wall trauma 
• Signs of external injuries: bruises, abrasions, deformities 
• Tender on palpation

Bone:

Costochondritis 

• recent exertion involving chest wall movement 
• Pain aggravated by thoracic wall movements (leaning forwards or backwards, rotatory movements, breathing in/ out movements)

Rib/ sternal fractures

• recent trauma to chest wall
• Chest wall deformities or signs of external injuries
• Chest spring will be positive over the fracture site 

Lung:

Pneumonia

• fever, cough, dyspnoea 
• Chest pain is usually described as pleuritic in nature nature 
• Usually associated with bronchial breathing and reduced breath sounds with coarse creps over the pain area 

Pneumothorax

• history of fever, cough, dyspnoea preceding or concurrent with pain onset 
• chest pain is usually described as sharp and sudden in onset for spontaneous pneumothorax
• history of recent chest wall trauma 
• history of pneumothorax 
• History of chronic lung disease 
• Look for chest tube scars or thoracotomy scars 
• Tall stature with long limbs suggestive of Marfanoid feature

Empyema

• Usually will have associated high grade fever, cough, dyspnoea
• Cough productive of purulent or blood stained sputum 
• Usually unwell appearance (septic looking)
• Chest pains due to empyema are usually pleuritic in nature
• Reduced chest expansion over the pain site 
• Reduced breath sounds with pleural effusion like findings 

Pleural effusion/ hemothorax

• similar to empyema except patient may be less septic looking on presentation
• the complaint may be more of dyspnoea or chest tightness as compared to chest pain
• may have other features of fluid overload: congestive heart failure, nephrotic syndrome, liver cirrhosis 
• Recent Chest wall trauma with evidence of external chest wall injury e.g. bruises, chest wall deformities, positive chest spring on palpation

Heart:

Angina

• pressing or crushing retrosternal chest pains (usually left sided) with typical radiation to i psi lateral shoulder or upper limbs and neck with associated diaphoresis, nausea, vomiting with/without syncope 
• History of similar attacks, or history of exertional angina 
• Risk factors: Age, family history of coronary artery disease, cigarette smoking, alcohol, DM, HPT, dyslipidemia, CKD

Dissecting aneurysm 

• usually present with back pains
• described as tearing pain
• History of high BP
• Check discrepancy in UL pulses
• Look for Marfanoid features 
• Look for new onset aortic valve murmurs
• Patient usually unwell 

Gastrointestinal tract:

GERD

• burning type retrosternal chest pains 
• May originate from epigastric region and extend superiorly to the throat 
• Assoc with acid or water brash
• May or may not have hoarseness or voice 
• Preceding heavy meals, spicy or oily foods 
• Usually symptoms have been ongoing for a long time 

FB 

• ask about bony fish meals or accidental or deliberate swallowing of any foreign bodies recently (if yes, you may need to explore suicidal tendencies and major depression). 

Spine:

Radiculopathies

• pain is usually circumferential ie radiating from the back around the sides to the front of the thorax. It is important to clarify this with patient so they may give you a clear description with regards to the nature and origin of the pain (on a personal note, I have encountered a case that was referred for chest pains suspecting to be unstable angina only to discover that the pain is actually from a collapsed thoracic vertebra due to TB spondylitis causing nerve root compression of the exiting thoracic spinal nerve). Radiculopathies can be caused by compression of the exiting spinal nerve root by a prolapsed intervertebral disc, a spinal cord tumour, paraspinal abscess or a collapsed vertebra as mentioned above, etc
• This type of pain may be aggravated by certain manouvres eg coughing, straining etc. 

Psychiatry:

Anxiety

• chest pains can be felt like a central anterior chest tightness sensation when experiencing a panic attack. It is usually accompanied by other supporting symptoms like feeling extreme fear, light headedness, palpitations, hand tremors, and the patient may or may not have a clear precipitating event or stressor. 

Major depression

• A depressed person may have multiple psychosomatic complaints. Pain may not necessarily be limited to the chest. Pain may also affect other body parts. Enquire about other depressive symptoms e.g. low mood, suicidal ideations, anhedonia, anorexia, etc. 

The list of chest pain aetiology mentioned above may seemed a lot and you may wonder if you will ever have time to explore each differential within the 60 min time frame. This is a valid concern. Therefore you need to be selective and use common sense and try narrow down the differentials based on the patient in front of you. As the clerking progresses, you’ll be able to gain more information to help you cross off the differentials one by one quickly. 

Lastly, practice makes perfect. So go out there and clerk many cases of dyspnoea. There are many such cases in the medical wards as it is a common presenting complaint. Happy learning. 

CCE. 

Right Eye Horner's Syndrome

This elderly male patient presented with chronic coughing associated with dyspnoea and weight loss. 

Examination noted partial ptosis of the right eye but no ophthalmoplegia.

Further examination of the eyes noted reduced pupil size over the right eye compared to the left eye. 

The left eye pupil size was normal.

A diagnosis of right Horner's syndrome was made. 

Respiratory examination noted bronchial breathing over the right lung apex with tracheal deviation to the contralateral side suggestive of a right pancoast tumour. 

Therefore the unifying diagnosis was Right pancoast tumour causing Right eye Horner's syndrome. 

CCE. 

Cranial Nerve 3 Palsy - Surgical CN3

The picture below shows a young girl with complete ptosis of the left eye. She presented with progressive and worsening ptosis affecting her left eyelid. At the same time, she reported having diplopia as well. 

Upon elevating her left upper eyelid, her left eyeball is displaced inferolaterally in neutral position. This finding is consistent with a left CN 3 (occulomotor) palsy. The eyeball is deviated in such a manner due to unopposed action of the left lateral rectus and left superior oblique muscles which are innervated by the left CN 6 (abducens) and left CN 4 (trochlear) nerves respectively. 

It is also important to take the opportunity to assess the left pupil size to determine the possible cause of her left CN 3 palsy. In this picture, it can be seen that her left pupil is dilated compared to the right pupil. This suggests that she may have a space occupying lesion compressing the CN3. In most cases, a cerebral aneurysm (particularly from the posterior communicating (PCOM) artery) need to be looked for. The pathogenesis of a dilated pupil in such a scenario is that an aneurysm arising from the PCOM artery compresses on the CN 3 putting pressure on, and damaging the parasympathetic nerve fibres that innervate the constrictor pupillae muscle that is responsible for pupillary constriction. These parasympathetic nerve fibres run on the surface of the CN 3, therefore when there is an external compression onto the CN3, the parasympathetic nerve fibres would be affected as well.

Once a surgical cause i.e. an aneurysm has been excluded, then a medical cause can still be possible. Bear in mind, the parasympathetic nerve fibres that innervate the constrictor pupillae muscle that is responsible for pupillary constriction is also supplied by tiny blood vessels called vasa nervorum. The vasa nervorum are equally susceptible to damage from medical diseases e.g. connective tissue disorders, diabetes mellitus, atherosclerosis etc like other arteries elsewhere in the body. Once the blood supply to the parasympathetic nerve fibres are disrupted, there will be ischemic damage followed by impaired parasympathetic nerve function resulting in a dilated pupil.

CCE.