MERRY CHRISTMAS AND HAPPY NEW YEAR
The year is coming to an end. Year 3 Medicine Posting Rotation 3 will commence on 4 January 2010. Hope our efforts will bear fruit 100% this time
Thursday, December 24, 2009
Wednesday, December 2, 2009
Friday, November 27, 2009
STUDENTS' MISCONCEPTIONS - II
Most of the students suffer from a poverty of words when they write a few lines in MEQ. In olden times there were real essay questions, where the student had to write a few pages properly arranged in paragraphs. Later due to the labour and hardship involved in marking, it was changed to MEQ. Although it is named modified essay question, there is hardly any element of essay in it. It's always 'listing' or 'stating' or maximum 'briefly explain' or 'outline'. Even then students fail to express well. Marks are lost because of improper expression even when the student seems to know the answer.
This is true especially when the question is of neurology. Sides and sites are very important here. Imagine the examiner's dilemma when the student writes facial palsy and not mention the side, or just upper motor neurone lesion without the exact site or side.
Some of expressions and misconceptions are evident in the recently finished MEQ.
Thrombolytics and fibrinolytics for secondary prevention of stroke
Syncope due to high blood pressure
LMN lesion progressing UMN lesion in a case of stroke due to worsening of the brain lesion
Transient loss of consciousness due to stroke
Carotid bruit produced by turbulence at aortic valve - (IT IS NOT CALLED BRUIT BUT RADIATING MURMUR)
Anticoagulants such as aspirin and clopidogrel
Postural syncope secondary to systemic hypertension
High pressure due to LV hypertrophy leads to systemic hypertension causing hypervascularity leading to systolic bruit up to the neck at the carotid artery - WHAT AN APPALLING CONCEPT!!
Unable to close eye interpreted as due to III nerve palsy - JUST THE REVERSE
Site of lesion above anterior horn cell of the spinal cord, left side of the head
Heaving apex beat and loud A2 due to RV hypertrophy and pulmonary hypertension
Ischaemic stroke at upper motor neurone
Diuretic to treat diabetes and postpone nephropathy
Finger biting in epilepsy
Transient LOC due to ischaemic stroke
EEG to confirm hypoperfusion of the brain
Neck bruit indicating turbulence in the aorta
This is true especially when the question is of neurology. Sides and sites are very important here. Imagine the examiner's dilemma when the student writes facial palsy and not mention the side, or just upper motor neurone lesion without the exact site or side.
Some of expressions and misconceptions are evident in the recently finished MEQ.
Thrombolytics and fibrinolytics for secondary prevention of stroke
Syncope due to high blood pressure
LMN lesion progressing UMN lesion in a case of stroke due to worsening of the brain lesion
Transient loss of consciousness due to stroke
Carotid bruit produced by turbulence at aortic valve - (IT IS NOT CALLED BRUIT BUT RADIATING MURMUR)
Anticoagulants such as aspirin and clopidogrel
Postural syncope secondary to systemic hypertension
High pressure due to LV hypertrophy leads to systemic hypertension causing hypervascularity leading to systolic bruit up to the neck at the carotid artery - WHAT AN APPALLING CONCEPT!!
Unable to close eye interpreted as due to III nerve palsy - JUST THE REVERSE
Site of lesion above anterior horn cell of the spinal cord, left side of the head
Heaving apex beat and loud A2 due to RV hypertrophy and pulmonary hypertension
Ischaemic stroke at upper motor neurone
Diuretic to treat diabetes and postpone nephropathy
Finger biting in epilepsy
Transient LOC due to ischaemic stroke
EEG to confirm hypoperfusion of the brain
Neck bruit indicating turbulence in the aorta
Sunday, November 22, 2009
STUDENTS' MISCONCEPTIONS
I was struck by some of the glaring misconceptions I encountered while going through the MEQ/SAQ scripts of the just completed end of posting exam of Y3M at Sibu. I would share and help clear some of these misconceptions harbored by some of year 3 students. WHAT THE STUDENTS WROTE ARE GIVEN IN CAPITAL LETTERS and my explanations in sentence case.
LUMMBAR PUNCTURE (LP) CAN CAUSE STROKE / HERNIATION OF SPINAL CORD: Stroke is not a complication of LP, there is no logic in this answer. LP can cause herniation of the brainstem or uncus through the foramen magnum. Spinal cord starts below the foramen magnum so no question of herniation of spinal cord.
OGTT TO DIAGNOSE ACROMEGALY: Glucose load is used to suppress GH secretion. In acromegaly glucose load will not be able to suppress the GH secretion. This test should be called GH suppression test using glucose. OGTT is used to diagnose diabetes.
SUDDEN STEROID WITHDRAWAL CAN CAUSE END STAGE RENAL FAILURE: Where do you get this idea from?
PREDNISOLONE FUNCTIONS AS AN NSAID: NSAID means non-steroidal anti inflammatory drugs and prednisolone is a steroid, so no sense in this statement.
EPILEPSY DESCRIBED AS TWITCHING OF MUSCLES: Twitching of muscles might be used to describe fasciculation or myoclonus, but not convulsion. Epilepsy is diagnosed when patient has repeated seizures without a known cause. A generalized convulsion with loss of consciousness is termed seizure.
TRANSIENT LOSS OF CONSCIOUSNESS (LOC) ATTRIBUTED TO CAROTID STENOSIS: Consciousness is maintained by the reticular activating system situated in the brainstem. Loss of blood supply to this area - supplied by the vertebrobasilar system (posterior circulation) can sometimes cause LOC. A unilateral cerebral lesion does not cause LOC. Cerebral lesion has to be bilateral and massive to cause LOC. The usual way in which a cerebral stroke causes LOC is by herniation of brain substance through the tentorium cerebelli leading to compression of the vital structures in the brainstem.
INABILITY TO CLOSE AN EYE ATTRIBUTED TO PARALYSIS OF LEVATOR PALPABRAE SUPERIORIS (LPS) SUPPLIED BY CRANIAL NERVE VII (FACIAL NERVE): This shows the poor antomical background of the student. First of all LPS is not innervated by CN VII, but by CN III (Occulomotor) and its action is to elevate the upper eyelid. Paralysis of LPS will cause ptosis of the eyelid. Eye closure involves orbicularis occuli, innervated by CN VII. A lower motor neurone lesion of CN VII will cause ipsilateral inability to close the eye. An upper motor neurone lesion will spare the upper part of the face, including the orbicularis occuli. Remember the UMN fibers innervating the right facial nerve nucleus come from the left cerebral cortex and vice verse.
NECK BRIUT IS DUE TO HIGH CARDIAC OUTPUT DUE TO HYPERTENSION: A bruit results from turbulent flow through a stenosis in an artery. It can also occur when there is excessive blood flow through the thyroid gland in hyperthyroidism or through a malignant tumour like hepatocellular carcinoma or an arterio-venous fistula. The confusion may be related to the flow murmur created by high flow through pulmonary / aortic valve. Hypertension does not cause high cardiac output. Increased vascular tone is what increases the blood pressure. Increased stroke volume in aortic regurgitation can increase the systolic pressure. Hypertension does not increase cardiac output.
LOUD AORTIC SECOND SOUND (A2) IS DUE TO HIGH CARDIAC OUTPUT: A2 is produced by the closure of the aortic valve. If there is increased pressure in the systemic circulation, it will close more forcefully causing a loud A2, so it is found in hypertension. A2 is softer in aortic stenosis. There is no loud A2 when cardiac output is increased. S1 can be loud when there is hyperdynamic circulation.
FASTING PLASMA GLUCOSE OF 6.8 mmol/L IS A BIT LOWER THAN NORMAL (7 mmol/L) AND 2 HOUR POST GLUCOSE PLASMA GLUCOSE OF 11.0 IS ALSO LOWER THAN NORMAL (11.1). SO THE PATIENT IS HYPOGLYCAEMIC: The student has apparently taken the plasma glucose level diagnostic of diabetes as the normal level and anything below that as hypoglycaemia. On the contrary, a FPG of 5.6 and 2-hr Post glucoe plasma glucose level of 7.8 and above (but less than 11.1) should be considered abnormal - prediabetes or impaired fasting glucose / impaired glucose tolerance. Prediabetes also carries higher risk of coronary artery disease.
LOWER MOTOR NEURONE (LMN) LESION DUE TO STROKE: Stroke being a vascular lesion either in the brain or brainstem, the only LMN lesion it can cause is that of the cranial nerve nuclei originating in the brainstem. There is no LMN lesion of the limbs in any stroke. Students often attribute the hypotonia and hyporeflexia of limbs found in the acute stages of stroke to LMN lesion. There is no basis for this. The typical features of spasticity and hyperreflexia and clonus may take a day or two to manifest. It is still upper motor neurone lesion from day one.
NUCLEAR VII NERVE PALSY TERMED AS BELL'S PALSY: Bell's palsy is also a LMN lesion of the VII cranial nerve, but it is not a nuclear lesion. It is a lesion outside the brainstem before the nerve emerges from the skull.
DYSARTHRIA ATTRIBUTED TO SPEECH CENTRE LESION: Dysarthria is difficulty in articulation of words with no problem in the language function. Patient can still think normally, form words and write if the power in the hand muscles are adequate. Dysarthria is purely due to weakness of the muscles involved in articulation - tongue, face, palate, pharynx. Cranial nerve lesions V, VII, X, XII will affect articulation and cause dysarthria. On the other hand, speech centre lesions cause dysphasia (aphasia) – abnormality in reception or expression of language. Of course a lesion causing dysphasia can also be associated with weakness of cranial nerves. So it is possible for dysphasia to be associated with dysarthria. But dysarthria can be without dysphasia.
HYPERTROPHIC CARDIOMYOPATHY SECONDARY TO HYPERTENSION:Cardiomyopathy is essentially idiopathic. Hypertension is not a cause of cardiomyopathy. Left ventricular hypertrophy can occur in hypertension and it is entirely different from hypertrophic obstructive cardiomyopathy, which is not associated with hypertension.
MANY STUDENTS WROTE HYPOGLYCAEMIA AS A CAUSE OF TRANSIENT LOSS OF CONSCIOUSNESS: This is beyond my understanding. First of all hypoglycaemia has to be very severe to cause loss of consciousness. It is called hypoglycaemic coma. It is a fatal condition unless reversed by glucose given intravenously to raise the plasma glucose level to normal. There is no chance of hypoglycaemic coma getting back to normal spontaneously. Then how can it be the cause of transient loss of consciousness??
ASPIRIN LYSES EMBOLUS: Neither aspirin nor any other antiplatelet agent (clopidogrel, ticlopidine, dipyridamole) would lyse a embolus. Clots can be lysed using throbolytic agents (fibrinolytic agents) like streptokinase, tPA. The function of antiplatelet agents is to inhibit platelt adhesion and chances of thrombosis - only prophylactic effect.
POSTERIOR CIRCULATION STROKE CAUSING DYSPHASIA: Speech centres are are supplied by middle cerebral artery, not by posterior cerebral artery.
MANY STUDENTS RECOMMENDED USE OF tPA AND STREPTOKINASE FOR SECONDARY PREVENTION OF STROKE: This arises from lack of understanding of the terms primary prevention, secondary prevention and treatment. Primary prevention is done by taking measures to prevent the risk factors in order to avoid developing a disease. If you already have the disease, then applying measures (including drugs)to prevent another attack of the same disease is called secondary prevention. Treatment includes measures taken to abort the manifestations of the disease when it has already occurred. Streptokinase and tPA are thrombolytic agents used to lyse a clot (treatment. Secondary prevention measures include antiplatelet agents, antihypertensives, antidiabetics, statins etc.
MICTURITION AND COUGH WILL DECREASE VENOUS RETURN TO HEAD AND CAUSE SYNCOPE: The student seems to know that cough and micturition can cause syncope, but unable to explain the mechanism. First of all, there is no question of venous return to the head. Venous blood returns to the right chambers of the heart. A paroxysm of cough and straining (for micturition in the elderly men with prostatic enlargement)for any purpose will increase intrathoracic pressure (as well as intraabdominal pressure). Increased intrathoracic pressure will prevent venous return to the right cardiac chambers from the systemic veins, which will lead to a fall in cardiac output as well as blood pressure causing syncope.
SOME STUDENTS ARE UNABLE TO PERCEIVE THAT A SINGLE LESION CAN CAUSE A CROSSED PARALYSIS: Crossed paralysis means cranial nerve lesion on one side and limb weakness on the opposite side. This will not happen in a cerebral lesion because UMN fibers innervating cranial nerves and limbs cross to the opposite side at different levels in the brainstem. A lesion in the brainstem will destroy cranial nerve nuclei on the same side (their UMN fibers have already crossed over to innervate them) and cause limb paralysis on the contralateral side (as the pyramidal tract has not yet crossed). It crosses at the lower part of the medulla.
HEAVING APEX BEAT DUE TO RIGHT VENTRICULAR HYPERTROPHY(RVH) / RIGHT ATRIAL HYPERTROPHY): RVH will cause a left parasternal heave, not a heaving apex beat (it will be found in left ventricular hypertrophy. Right atrium forming apex beat is beyond imagination. Right atrium lies at the right cardiac border, far away from the apex.
To be continued
LUMMBAR PUNCTURE (LP) CAN CAUSE STROKE / HERNIATION OF SPINAL CORD: Stroke is not a complication of LP, there is no logic in this answer. LP can cause herniation of the brainstem or uncus through the foramen magnum. Spinal cord starts below the foramen magnum so no question of herniation of spinal cord.
OGTT TO DIAGNOSE ACROMEGALY: Glucose load is used to suppress GH secretion. In acromegaly glucose load will not be able to suppress the GH secretion. This test should be called GH suppression test using glucose. OGTT is used to diagnose diabetes.
SUDDEN STEROID WITHDRAWAL CAN CAUSE END STAGE RENAL FAILURE: Where do you get this idea from?
PREDNISOLONE FUNCTIONS AS AN NSAID: NSAID means non-steroidal anti inflammatory drugs and prednisolone is a steroid, so no sense in this statement.
EPILEPSY DESCRIBED AS TWITCHING OF MUSCLES: Twitching of muscles might be used to describe fasciculation or myoclonus, but not convulsion. Epilepsy is diagnosed when patient has repeated seizures without a known cause. A generalized convulsion with loss of consciousness is termed seizure.
TRANSIENT LOSS OF CONSCIOUSNESS (LOC) ATTRIBUTED TO CAROTID STENOSIS: Consciousness is maintained by the reticular activating system situated in the brainstem. Loss of blood supply to this area - supplied by the vertebrobasilar system (posterior circulation) can sometimes cause LOC. A unilateral cerebral lesion does not cause LOC. Cerebral lesion has to be bilateral and massive to cause LOC. The usual way in which a cerebral stroke causes LOC is by herniation of brain substance through the tentorium cerebelli leading to compression of the vital structures in the brainstem.
INABILITY TO CLOSE AN EYE ATTRIBUTED TO PARALYSIS OF LEVATOR PALPABRAE SUPERIORIS (LPS) SUPPLIED BY CRANIAL NERVE VII (FACIAL NERVE): This shows the poor antomical background of the student. First of all LPS is not innervated by CN VII, but by CN III (Occulomotor) and its action is to elevate the upper eyelid. Paralysis of LPS will cause ptosis of the eyelid. Eye closure involves orbicularis occuli, innervated by CN VII. A lower motor neurone lesion of CN VII will cause ipsilateral inability to close the eye. An upper motor neurone lesion will spare the upper part of the face, including the orbicularis occuli. Remember the UMN fibers innervating the right facial nerve nucleus come from the left cerebral cortex and vice verse.
NECK BRIUT IS DUE TO HIGH CARDIAC OUTPUT DUE TO HYPERTENSION: A bruit results from turbulent flow through a stenosis in an artery. It can also occur when there is excessive blood flow through the thyroid gland in hyperthyroidism or through a malignant tumour like hepatocellular carcinoma or an arterio-venous fistula. The confusion may be related to the flow murmur created by high flow through pulmonary / aortic valve. Hypertension does not cause high cardiac output. Increased vascular tone is what increases the blood pressure. Increased stroke volume in aortic regurgitation can increase the systolic pressure. Hypertension does not increase cardiac output.
LOUD AORTIC SECOND SOUND (A2) IS DUE TO HIGH CARDIAC OUTPUT: A2 is produced by the closure of the aortic valve. If there is increased pressure in the systemic circulation, it will close more forcefully causing a loud A2, so it is found in hypertension. A2 is softer in aortic stenosis. There is no loud A2 when cardiac output is increased. S1 can be loud when there is hyperdynamic circulation.
FASTING PLASMA GLUCOSE OF 6.8 mmol/L IS A BIT LOWER THAN NORMAL (7 mmol/L) AND 2 HOUR POST GLUCOSE PLASMA GLUCOSE OF 11.0 IS ALSO LOWER THAN NORMAL (11.1). SO THE PATIENT IS HYPOGLYCAEMIC: The student has apparently taken the plasma glucose level diagnostic of diabetes as the normal level and anything below that as hypoglycaemia. On the contrary, a FPG of 5.6 and 2-hr Post glucoe plasma glucose level of 7.8 and above (but less than 11.1) should be considered abnormal - prediabetes or impaired fasting glucose / impaired glucose tolerance. Prediabetes also carries higher risk of coronary artery disease.
LOWER MOTOR NEURONE (LMN) LESION DUE TO STROKE: Stroke being a vascular lesion either in the brain or brainstem, the only LMN lesion it can cause is that of the cranial nerve nuclei originating in the brainstem. There is no LMN lesion of the limbs in any stroke. Students often attribute the hypotonia and hyporeflexia of limbs found in the acute stages of stroke to LMN lesion. There is no basis for this. The typical features of spasticity and hyperreflexia and clonus may take a day or two to manifest. It is still upper motor neurone lesion from day one.
NUCLEAR VII NERVE PALSY TERMED AS BELL'S PALSY: Bell's palsy is also a LMN lesion of the VII cranial nerve, but it is not a nuclear lesion. It is a lesion outside the brainstem before the nerve emerges from the skull.
DYSARTHRIA ATTRIBUTED TO SPEECH CENTRE LESION: Dysarthria is difficulty in articulation of words with no problem in the language function. Patient can still think normally, form words and write if the power in the hand muscles are adequate. Dysarthria is purely due to weakness of the muscles involved in articulation - tongue, face, palate, pharynx. Cranial nerve lesions V, VII, X, XII will affect articulation and cause dysarthria. On the other hand, speech centre lesions cause dysphasia (aphasia) – abnormality in reception or expression of language. Of course a lesion causing dysphasia can also be associated with weakness of cranial nerves. So it is possible for dysphasia to be associated with dysarthria. But dysarthria can be without dysphasia.
HYPERTROPHIC CARDIOMYOPATHY SECONDARY TO HYPERTENSION:Cardiomyopathy is essentially idiopathic. Hypertension is not a cause of cardiomyopathy. Left ventricular hypertrophy can occur in hypertension and it is entirely different from hypertrophic obstructive cardiomyopathy, which is not associated with hypertension.
MANY STUDENTS WROTE HYPOGLYCAEMIA AS A CAUSE OF TRANSIENT LOSS OF CONSCIOUSNESS: This is beyond my understanding. First of all hypoglycaemia has to be very severe to cause loss of consciousness. It is called hypoglycaemic coma. It is a fatal condition unless reversed by glucose given intravenously to raise the plasma glucose level to normal. There is no chance of hypoglycaemic coma getting back to normal spontaneously. Then how can it be the cause of transient loss of consciousness??
ASPIRIN LYSES EMBOLUS: Neither aspirin nor any other antiplatelet agent (clopidogrel, ticlopidine, dipyridamole) would lyse a embolus. Clots can be lysed using throbolytic agents (fibrinolytic agents) like streptokinase, tPA. The function of antiplatelet agents is to inhibit platelt adhesion and chances of thrombosis - only prophylactic effect.
POSTERIOR CIRCULATION STROKE CAUSING DYSPHASIA: Speech centres are are supplied by middle cerebral artery, not by posterior cerebral artery.
MANY STUDENTS RECOMMENDED USE OF tPA AND STREPTOKINASE FOR SECONDARY PREVENTION OF STROKE: This arises from lack of understanding of the terms primary prevention, secondary prevention and treatment. Primary prevention is done by taking measures to prevent the risk factors in order to avoid developing a disease. If you already have the disease, then applying measures (including drugs)to prevent another attack of the same disease is called secondary prevention. Treatment includes measures taken to abort the manifestations of the disease when it has already occurred. Streptokinase and tPA are thrombolytic agents used to lyse a clot (treatment. Secondary prevention measures include antiplatelet agents, antihypertensives, antidiabetics, statins etc.
MICTURITION AND COUGH WILL DECREASE VENOUS RETURN TO HEAD AND CAUSE SYNCOPE: The student seems to know that cough and micturition can cause syncope, but unable to explain the mechanism. First of all, there is no question of venous return to the head. Venous blood returns to the right chambers of the heart. A paroxysm of cough and straining (for micturition in the elderly men with prostatic enlargement)for any purpose will increase intrathoracic pressure (as well as intraabdominal pressure). Increased intrathoracic pressure will prevent venous return to the right cardiac chambers from the systemic veins, which will lead to a fall in cardiac output as well as blood pressure causing syncope.
SOME STUDENTS ARE UNABLE TO PERCEIVE THAT A SINGLE LESION CAN CAUSE A CROSSED PARALYSIS: Crossed paralysis means cranial nerve lesion on one side and limb weakness on the opposite side. This will not happen in a cerebral lesion because UMN fibers innervating cranial nerves and limbs cross to the opposite side at different levels in the brainstem. A lesion in the brainstem will destroy cranial nerve nuclei on the same side (their UMN fibers have already crossed over to innervate them) and cause limb paralysis on the contralateral side (as the pyramidal tract has not yet crossed). It crosses at the lower part of the medulla.
HEAVING APEX BEAT DUE TO RIGHT VENTRICULAR HYPERTROPHY(RVH) / RIGHT ATRIAL HYPERTROPHY): RVH will cause a left parasternal heave, not a heaving apex beat (it will be found in left ventricular hypertrophy. Right atrium forming apex beat is beyond imagination. Right atrium lies at the right cardiac border, far away from the apex.
To be continued
Monday, November 16, 2009
Y3M QUIZ 3 - SOME EXPLANATIONS
The quiz 3 is yet to be marked. Marks will be published after the EOPE. Meanwhile read below. Some of the difficult items are explained here.
Skin is not the best place to look for the pallor of anaemia. Palms can be pale due to increased skin thickness. Look at mucous membranes to assess anaemia.
There is collapsing pulse in severe anaemia. Remember, the essential ingredients for collapsing pulse are: large stroke volume and leak back into LV or peripheral run off. In anaemia both these are fulfilled - large stroke volume and fast peripheral run off. Vasodilation leads to fast peripheral run off of the blood.
SOB is invariably present in anaemia as there is decreased O2 carrying capacity of the blood. The CVS and RS have to work harder to meet the demands of the tissues. Dyspnoea is usually experienced on exertion.
Angina will be worsened in anaemia. This is due to decreased O2 supply to the myocardium, also experienced during exertion.
Koilonychia is a late feature of iron deficiency. It first appears on toe nails. The nails will be brittle and easily breakable. Splenomegaly has nothing to do with iron deficiency anaemia. Dysphagia can be experienced - Plummer-Vinson syndrome - due to web formation in the oesophagus.
Thrombocytopaenia causes skin and mucous membrane bleeding, deep tissue bleeding is not a feature of ITP. It is usually seen in coagulopathies like haemophilia.
Spleen moves anteromedially on inspiration. It is superficial and not covered by intestines, so is dull on percussion. It is not ballotable - a differentiating feature from kidney. Friction rub on the spleen can be heard if there is splenic infarct.
In Dengue haemorrhagic syndrome, there is plasma leak into extravascular spaces leading to haemoconcentration and increase in haematocrit - significant when there is 20% rise in Hct. Hct will drop back when the patient is rehydrated. So a rise in Hct of 20% with treatment, is also significant.
Primary tuberculosis in immunocompetent individuals can go unnoticed. Advanced PTBs you usually find are all post-primary. The bacilli can remain dormant after the primary focus is healed. Post primary results from a reactivation of primary or a reinfection. Manifestations depend, again, on the immune status of the host. In HIV/AIDS, there is extensive TB - pulmonary as well as extrapulmonary. Miliary TB has no predilection for any particular lobe of the lung, it is seen as milletseed lesions all over the lungs, and also affecting other organs.
Enteric fever spreads by fecal-oral route. Humans are the only host for enteric fever, Salmonella. Leptospira comes through rodents' urine, usually found in ponds - not flowing water. The microbes can enter the body through mucosae. So, even washing face in pond water can be the source of infection.
Vertical transmission is from mother to foetus, usually occurs during the third trimester or peripartum in HIV. Also Hep B
There is no loss of tendon reflexes in meningitis. Plantar reflex may be bilaterally extensor, if the patient is unconscious. Flexing neck will be painful in mengitis - neck stiffness.
PUO - FUO is fever of three weeks' duration with no known cause after routine investigations and observation in the hospital. Antibiotics and some drugs also can cause fever - drug fever. Sometimes one needs to stop all medications to exclude this condition. Repeated physical examination is very useful as some signs may appear later in the course.
GORD is due to loss of tone of the lower oesophageal sphincter. Any posture or process that increases intraabdominal pressure will aggravate the symptoms - mainly heartburn. Some patients also get chronic cough due to acid getting into the respiratory tract. Treatment is mainly acid neutralizing drugs.
Jaundice affects all tissues. Bilirubin has special affinity for elastin in the sclerae, that is why sclera is the best place to look for jaundice. It is not only sclera that is jaundiced, it is the patient that is jaundiced.
Finger (digittal) clubbing is found in only 30% cases of cirrhosis. Palmar erythma is a possible sign of excess oestrogen leading to erythema. It is found in several other conditions including normal pregnancy, rheumatoid arthritis, thyrotoxicosis, etc.
Hepatitis A virus spreads through fecal contamination of water and food. Vertical transmission is known to occur in Hepatitis B. Loss of appetite is one of the earliest symptoms. Hep A does not lead to chronic infection. It usually subsides leaving life-long immunity in the host. Hep B and Hep C infection lead to chronic liver disease.
Skin is not the best place to look for the pallor of anaemia. Palms can be pale due to increased skin thickness. Look at mucous membranes to assess anaemia.
There is collapsing pulse in severe anaemia. Remember, the essential ingredients for collapsing pulse are: large stroke volume and leak back into LV or peripheral run off. In anaemia both these are fulfilled - large stroke volume and fast peripheral run off. Vasodilation leads to fast peripheral run off of the blood.
SOB is invariably present in anaemia as there is decreased O2 carrying capacity of the blood. The CVS and RS have to work harder to meet the demands of the tissues. Dyspnoea is usually experienced on exertion.
Angina will be worsened in anaemia. This is due to decreased O2 supply to the myocardium, also experienced during exertion.
Koilonychia is a late feature of iron deficiency. It first appears on toe nails. The nails will be brittle and easily breakable. Splenomegaly has nothing to do with iron deficiency anaemia. Dysphagia can be experienced - Plummer-Vinson syndrome - due to web formation in the oesophagus.
Thrombocytopaenia causes skin and mucous membrane bleeding, deep tissue bleeding is not a feature of ITP. It is usually seen in coagulopathies like haemophilia.
Spleen moves anteromedially on inspiration. It is superficial and not covered by intestines, so is dull on percussion. It is not ballotable - a differentiating feature from kidney. Friction rub on the spleen can be heard if there is splenic infarct.
In Dengue haemorrhagic syndrome, there is plasma leak into extravascular spaces leading to haemoconcentration and increase in haematocrit - significant when there is 20% rise in Hct. Hct will drop back when the patient is rehydrated. So a rise in Hct of 20% with treatment, is also significant.
Primary tuberculosis in immunocompetent individuals can go unnoticed. Advanced PTBs you usually find are all post-primary. The bacilli can remain dormant after the primary focus is healed. Post primary results from a reactivation of primary or a reinfection. Manifestations depend, again, on the immune status of the host. In HIV/AIDS, there is extensive TB - pulmonary as well as extrapulmonary. Miliary TB has no predilection for any particular lobe of the lung, it is seen as milletseed lesions all over the lungs, and also affecting other organs.
Enteric fever spreads by fecal-oral route. Humans are the only host for enteric fever, Salmonella. Leptospira comes through rodents' urine, usually found in ponds - not flowing water. The microbes can enter the body through mucosae. So, even washing face in pond water can be the source of infection.
Vertical transmission is from mother to foetus, usually occurs during the third trimester or peripartum in HIV. Also Hep B
There is no loss of tendon reflexes in meningitis. Plantar reflex may be bilaterally extensor, if the patient is unconscious. Flexing neck will be painful in mengitis - neck stiffness.
PUO - FUO is fever of three weeks' duration with no known cause after routine investigations and observation in the hospital. Antibiotics and some drugs also can cause fever - drug fever. Sometimes one needs to stop all medications to exclude this condition. Repeated physical examination is very useful as some signs may appear later in the course.
GORD is due to loss of tone of the lower oesophageal sphincter. Any posture or process that increases intraabdominal pressure will aggravate the symptoms - mainly heartburn. Some patients also get chronic cough due to acid getting into the respiratory tract. Treatment is mainly acid neutralizing drugs.
Jaundice affects all tissues. Bilirubin has special affinity for elastin in the sclerae, that is why sclera is the best place to look for jaundice. It is not only sclera that is jaundiced, it is the patient that is jaundiced.
Finger (digittal) clubbing is found in only 30% cases of cirrhosis. Palmar erythma is a possible sign of excess oestrogen leading to erythema. It is found in several other conditions including normal pregnancy, rheumatoid arthritis, thyrotoxicosis, etc.
Hepatitis A virus spreads through fecal contamination of water and food. Vertical transmission is known to occur in Hepatitis B. Loss of appetite is one of the earliest symptoms. Hep A does not lead to chronic infection. It usually subsides leaving life-long immunity in the host. Hep B and Hep C infection lead to chronic liver disease.
Friday, November 6, 2009
Yesterday I had the privilege of being part of a counseling mission embarked to rescue the four students who failed two postings one after the other in year 3 postings at Sibu.
The four students were interviewed by our psychiatrist and later interviewed by a high level team including our beloved dean, deputy dean academics, head of departments and coordinators. I was impressed and rather moved by the care and concern shown by the team members and the cordial atmosphere in which the whole event happened to be. The students were called one by one into the room and put at ease, and were asked to share freely about their problems and difficulties, weaknesses and strengths.
I am sure the four students would have gone back uplifted and motivated.
The current Y3M is approaching their end of posting exam starting on 17th November. It is their second posting and some of them have already failed their first posting - surgery. I earnestly hope none of the current batch would have the 'fortune' to experience such an interview by the high level team.
However, I wish the students appreciate the care and concern evinced by the UNIMAS medical faculty management, and the time and money they are willing to spend just to see that their students do their best and become valuable assets of Malaysia and the world.
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