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