Making the most of your first two years of medicine

"It is unfortunately common experience that respiratory physiology learned in the preclinical years proves to be an incomplete preparation for the clinical field. Indeed, the emphasis of the preclinical course seems, in many cases, to be out of tune with the practical problems to be faced after qualification and specialization. Much that is taught does not apply to man in the clinical environment while, on the other hand a great many physiological problems highly relevant to the survival of patients finds no place in the curriculum. It is hoped that new approaches to the teaching of medicine may overcome this dichotomy and that, in particular, much will be gained from the integration of physiology with clinical teaching."

John F Nunn - Preface to Nunn's Applied Respiratory Physiology First Edition
(a classic reference that is still used in the Anaesthetic Primary exam)

An inordinate amount of effort is expended in grasping the biomedical sciences in the initial years of medical training. It is equally a pity that much of it is ignored in the latter years (much to the detriment of the student’s clinical abilities). Yet, I often tell junior residents that most clinical problems can be solved with knowledge that was acquired in the first two years of their medical course. A few fundamental concepts from exposure to barely a hundred medical conditions combined with a systematic approach to assessment can provide enough raw information to produce a reasonable differential diagnosis, investigative strategy and management plan for the majority of patients.

Students could be forgiven to think that these prior experiences are not applicable to patient care. Often the way that biomedical knowledge is learnt and assessed is different to how it is formulated and applied in the clinical context. It is reinforced by the fact that most clinicians will not deliberately revisit biomedical concepts to provide an explanation of their observations or thought processes. Students are assumed to possess the requisite knowledge and readily apply them in the clinical setting. But often this connection can be difficult to make. At the University of Pennsylvania School of Medicine, a solution has been to formally reintroduce a biomedical component during the latter clinical years of study. However, this could be an onerous and unnecessary burden in the short time frame of a Graduate entry program. A similar effect could be achieved if the student incorporates a few simple routines into their study schedule.

Here are ten common ways where combining pre-clinical and clinical knowledge will enable students to maximise the effectiveness of their learning and accelerate their transition to clinical practise:

1) Understanding the patho-physiological mechanisms underlying cardinal symptoms and signs allows you to narrow down a differential diagnosis


The common symptom of dyspnea encompasses a huge ranges of possibilities that can be quickly narrowed down by considering the patho-physiology.

Broadly, these include disorders of gas exchange and acid-base balance (registered by chemoreceptors, changes in lung mechanics (detected by mechanoreceptors), and pulmonary irritants (by lung chemoreceptors).

Reviewing abnormalities in gas exchange with pulse oximetry identifies pulmonary pathologies altering the alveolar-arterial gradient through physiological shunt e.g. pneumonia

Increased work of breathing can be due to resistive or obstructive work. Obstructive work may be evident clinically e.g. wheeze or objectively e.g. spirometry. Further clinical information helps to discriminate the difference between asthma or COAD.

A similar algorithmic approach can be applied to any number of conditions ranging from hypotension, jaundice, renal failure or vertigo using basic concepts in circulatory physiology, bile production, glomerular function or vestibular neurophysiology respectively.

2) Appreciating anatomical relationships allows one to incorporate all diagnostic possibilities


Whilst cardiac causes for chest pain are an important consideration, other causes need to be also entertained. A few screening questions from the review of symptoms or past medical history may implicate another structure causing the pain e.g. lung - cough, sputum, haemotypsis, recurrent or chronic respiratory illness, venous thrombo-embolic disease; upper GI tract - regurgitation, reflux, dysphagia, odynophagia, dyspepsia, peptic ulcer disease; hepato-biliary - jaundice, gallstones disease. The responses will prompt the doctor to perform a more detailed evaluation of alternative(s).

A similar method can be applied to head, abdominal or limb pain.

3) Understanding neuro-anatomical pathways provides useful information in localising pathology.

The complexity of sensory pathways can produce pain distant from the source or alter its perception.


Pathology arising from the embyrological foregut, midgut and hindgut has a typical sensory distribution to the upper, mid and lower abdomen respectively. Hence right colic diverticulitis will cause lower abdominal pain.

Sub-phrenic pathology resulting in irritation of the phrenic nerve and shares similar spinal cord segments to parts of the upper limb resulting in shoulder tip pin.

Pathology involving the visceral organs and pleura or peritoneum causes dull, poorly localised pain. However, when the disease process reaches the parietal structures, the pain becomes more sharp and localised, heralding a new phase of the disease. Thus anginal pain is dull whilst pericarditis is sharp. The initial peri-umbilical dull pain of appendicitis that localises to the right iliac fossa is first due to inflammation of the organ itself, followed by peritoneal irritation as the disease extends trans-murally.

4) Understanding the manifestations of disease can be inferred from knowing the normal structure (anatomy) and function (physiology) of the organ or system affected.

Disease manifests can itself in three ways:

a) by the homeostatic response to the organ / organ system e.g. chronic hypertension > pathologic hypertrophy > cardiomegaly on CXR ; haemorrhagic shock > tachycardia, pallor;

b) loss of organ function e.g. biliary duct obstruction > jaundice;

c) impaired homeostatic responses e.g. autonomic neuropathy > disordered baroreceptor reflex > postural hypotension; anti-mitotic drugs > depletion of white bloods cells > susceptibility to infection

Acknowledging this distinction prevents us treating the compensatory response e.g. tachypnea rather the complication e.g. hypoxia

5) The chronology suggests the pathology

Each general pathological process has common themes in aetiology, pathogenesis, natural history and complications. These map to a typical chronological development in the patient's history.


Atheromatous disorders follow a long asymptomatic history of risk factors such as diabetes or smoking before the symptoms of ischaemia develop. The features of vascular occlusion or disruption and infarction occurs within seconds of the the onset of the complication. Neoplasia begins an initially indolent course years after the inciting event but may transition to a more aggressive form in its latter stages, acute infection occurs within days or a several weeks of exposure to the microbiological agent.

The timing of the aetiological factors and changing pace of clinical features provides important clues to the likely problem.

6) Pathology (and diagnosis) is related to the sequence of events

Diagnosis cannot be achieved purely by fulfilling a list of diagnostic criteria. Their order and cadence is equally important


If a patient complains of ischaemic-sounding chest pain and rapid palpitations, at least two formulations could be obtained. Palpitations preceding chest pain for several minutes, may be interpreted as a primary arrhythmic event leading to poor diastolic filling, reduced cardiac output and rate-related cardiac ischaemia. Initial chest pain suggests an acute ischaemic event precipitating an abnormal electrophysiological alteration of the heart leading to arrhythmia. The difference in pathophysiology warrants different treatments and initial approaches to evaluation.

7) The pathology determines both the likely test and treatment

The assessment and management of different pathological process e.g. vascular, infection/inflammation, neoplasia and immune-mediated tend to have common themes.


Atheromatous disease requires vascular imaging either by ultrasound or contrast angiography. Treatment involves vasodilators, surgical or radiologic revascularisation. Thrombo-embolic disease demands urgent treatment via mechanical or pharmacological techniques to remove clot.

Infection is evaluated by clinical manifestations of inflammation e.g. redness, fever, pain and swelling associated with raised inflammatory markers e.g WCC, CRP and identification of an offending agent through microbiological cultures and serological techniques.

Solid neoplasia is identified via tumour markers, imaging and tissue biopsy. Following this the treatment broadly falls under one or more of the following modalities: surgery, chemotherapy and/or radiation therapy.

8) The known natural history, chronology and presence of complications determines the urgency of treatment

Timely and appropriate referral is in important part of efficient use of health services. Disabling or rapidly progressive disease requires urgent hospitalisation e.g. acute ischaemia, infection with septicaemia. Asymptomatic though gradually lethal conditions require more rapid evaluation but still can be achieved in the community with early specialist referral e.g. uncomplicated malignancy. Undifferentiated disease following a fairly stable may require extensive investigation over many weeks before a diagnosis is reached e.g. chronic joint pain, chronic renal failure

9) Surgery corrects disordered anatomy (surgical pathology)

Procedures can be used to repair and reconstruct destructive and compressive lesions (e.g. neoplasia, fractures) operforation and obstruction to hollow viscus (e.g. complications of stomach ulcers) and blood vessels (e.g. atherosclerotic and thrombosed arteries, aneurysms); restore organs to normal anatomical planes (e.g. hernias), remove abnormal communications (e.g. fistulas), or drain abnormal collections (e.g. haemothorax, subdural haematomas).

10) Pharmacology is just reversal of disordered physiology

Pharmacological treatment manipulates physiologic targets and homeostatic mechanisms to compensate for the derangements caused by disease. Knowing the mechanism of action of the drug and its target receptor and combining that with knowledge from physiology, one can infer its possible clinical uses, side effects, interactions and contraindications.


Beta2-adenergic antagonists can reduce blood pressure by reducing cardiac contractility, decrease heart rate in some tachyarrhythmias or treat chronic glaucoma by reducing aqueous humour production. The extension of these actions result in hypotension or bradycardia. Beta2 antagonism on the peripheral vasculature may exacerbate claudication. Interaction can occur with medications that also reduce cardiac rate and contractility e.g. calcium channel blockers. Effects on bronchial smooth muscle tone caution its use in obstructive airways disease such as asthma and COAD.

Studying medicine in a four year program can be an intense and exhausting experience and students are at real risk of burnout and exam fatigue. In a graduate entry program, the pre-clinical component is often presented in highly compressed format and there is little time to revisit information before the new challenges of clinical work are confronted. But logical application of this knowledge enables the clinician to be a more thorough and methodical diagnostician and directs her to gather and integrate much more useful information than a haphazard approach based on randomly rote learned facts, recent clinical recollections or incomplete pattern recognition. This knowledge should be frequently revisited throughout your clinical career so that it can consolidate the observations that you make at the bedside.

Dr. Derek Louey is a Senior Emergency Physician at Flinders Medical Centre and offers weekly tutorials to first and second year medical students on clinical integration and reasoning for the academic year.