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TCM TESTING CENTER
Clinical Sciences Exam-Review Questions


by Attilio P. D’Alberto

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Cardiovascular System:

1. Q. What are the three causes of cardiac chest pain?

A. Angina, Myocardial Infarction and Pericardial involvement.

Angina

Myocardial Infarction

Pericardial Involvement

Heartburn

1. Brought on by physical or emotional exertion,

2. Relieved by rest,

3. Usually retrosternal (behind the sternum),

4. Often worse after food or in cold winds,

5. Often relieved by nitrates,

6. Radiates to the left arm, back, neck, jaw and teeth,

7. Seldom lasts more than 15 minutes.

1. Lasts at least 30 minutes but more often hours (48hrs),

2. Usually a crushing, squeezing or constricting feeling,

3. Usually occurs during rest,

4. Radiates to the arms, back, neck, jaw and teeth,

5. Vomiting and sweating occur also.

1. Inflammation of the pericardium,

2. Caused by MI and infection,

3. Soreness,

4. Radiated to the left shoulder,

5. Worse on movement,

6. Worse when breathing in.

1. Scalding or burning sensation

2. Retrosternal

3. Radiates towards the throat

3. Worse on eating, bending + lying down

4. Relieved by Antacids

5. Accompanied by a Water Brash Reflex (reflex salivation in the mouth)

 

 

2. Q. What are the clinical presentations of ischaemic heart disease?

A. Ischaemic heart disease (angina pectoris or cardiac pain) is shown in the table below:

Signs

Symptoms

  1. Pain radiates to the arm (commonly on the left), and to the jaw and teeth.
  1. Chest pain and tightness.
  2. Breathlessness.
  3. Dizziness.
  4. Tiredness.
  5. Choking feeling in the throat.
  6. Discomfort after running, eating or in the cold wind.

 

3. Q. What questions would you ask a patient who presents cardiac pain?

A.

  1. Do you get pain in your chest on exertion?
  2. Whereabouts in the chest do you feel it?
  3. Is it worse in cold weather?
  4. Is it worse if you exercise after a big meal?
  5. Is it bad enough to stop you from exercising?
  6. Does is go away when you rest?
  7. Do you ever get similar pain if you get excited or upset?

 

4. Q. What are the causes of palpitations?

A.

  1. Extrasystoles.
  2. Paroxysmal atrial fibrillation.
  3. Paroxysmal supraventricular tachcardia.
  4. Thyrotoxicosis.
  5. Perimenopausal.

 

5. Q. Compare the JVP and the carotid pulse.

A. See the table below:

Jugular Venous Pulse (JVP)

Carotid Pulse

  1. The pulsation cannot be felt.
  2. Moves inside.
  3. See two movements for one heart beat.
  4. Increases when pressure is applied to the liver.
  5. Pressure increased by deep inspiration.
  1. The pulsation can be felt.
  2. Moves outside.
  3. Feel one movement for one heart beat.
  4. No change when pressure is applied to the liver.
  5. Breathing has no effect on the pulse.

 

6. Q. What is the major pathological reason for a general increase in JVP?

A.

  1. Right cardiac failure.
  2. Obstruction superior to the vena cava.
  3. Tricuspid reflux and stenosis (an abnormal narrowing of an opening or passageway in the body).
  4. Pulmonary embolism (a blockage of a pulmonary artery by a foreign matter): blocks pulmonary arteries thus blood on the right side cannot flow correctly causing a back-up of blood.

 

7. Q. What is the mechanism for the first heart sound?

A. The closure of the tricuspid and bicuspid valves.

 

8. Q. What is the mechanism for the second heart sound?

A. The pulmonary and aortic heart valves closing.

 

9. Q. What are thrills (systolic murmurs) and which anatomical structures of the heart are they associated with?

A. They are palpable murmurs implying an abnormality. Systolic (a heart contraction) thrills in the aortic area are due to aortic stenosis (an abnormal narrowing of an opening or passageway in the body), whereas at the apex a systolic thrill is due to mitral regurgitation. A diastolic (the heart at maximum relaxation) thrill is caused by mitral stenosis (a large amount of blood passing through a normal valve) caused by anaemia or hyperthyroidism (hyperactivity of the thyroid gland).

 

10. Q. What are heaves and what is the pathological mechanism for this and which part of the heart is involved?

A. Heaves are a thrusting impulse that is sustained and forceful and lifts the palpating fingers. It is found in patients with either hypertrophy (an increase in the size of an organ) of the cardiac muscle or dilatation (stretched) of the heart.

 

11. Q. What are the signs and symptoms of right and left heart failure?

A.

 

Right Heart Failure

Left Heart Failure

Signs

 

 

 

 

1. Peripheral oedema,

2. Raised JVP,

3. Congested Liver,

4. Ascites,

5. Triple rhythm,

6. Tachycardia,

7. Palpable right ventricle,

8. Central cyanosis,

9. Tricuspid regurgitation,

10. Systolic murmurs,

11. Enlarged heart.

1. Pallor,

2. Orthopnoea (person must sit or stand to breath easier),

3. Nocturnal dyspnoea (difficultly in breathing),

4. Wheezing in well-established left,

5. Basal crepitations (crackles),

6. Low blood pressure,

7. Cyanosis if severe,

8. Possible abnormal precordial (the region over the heart and lower part of the thorax) pulsation,

9. Enlarged heart (in chronic left ventricular failure),

10. Triple rhythm and fourth rhythm,

11. Tachycardia,

12. Pulsus (),

13. Oliguria (low urine output),

14. Heaves in apex area,

15. Systolic murmurs.

Symptoms

1. Swollen ankles,

2. Swollen flanks,

3. Breathlessness (dyspnoea),

4. Nausea.

1. Frothy and/or blood stained sputum.

2. Shortness of breath (dyspnoea),

3. Anxiety,

4. Wheezing,

5. Cold and clammy feet (peripheries).

 

12. Q. Review ECG readout.

A. Definitions:

Atrial tachycardia: rapid beating of the atria caused by abnormal automaticity, triggered activity or intra-atrial re-entry. The atrial rate is usually less than 200 bpm.

Atrial fibrillation (AF): a cardiac arrhythmia characterised by disorganised electrical activity in the atria accompanied by an irregular ventricular response that is usually rapid. It is associated with rheumatic heart disease, mitral stenosis, acute MI.

Atrial flutter (AF): a type of atrial tachycardia with rates from 230 to 380bpm.

Ectopic beats: an impulse that originates in the heart at a site other than the sino atrial node.

Ventricular ectopic beats: a premature beat originating from the ventricle.

Ventricular fibrillation (VF): a cardiac arrhythmia marked by rapid disorganised depolarisation of the ventricular myocardium. The condition is characterised by a complete lack of organised electric activity, aswell as ventricular contraction. Blood pressure falls to zero, resulting in unconsciousness. Death may occur within 4 minutes.

 

13. Q. What questions would you ask a patient who presents dyspnoea?

A.

  1. Do you have a respiratory illness? I.e. asthma, pulmonary oedema, etc.
  2. How long have you had breathlessness?
  3. Was it sudden? Pulmonary oedema (the accumulation of extravascular fluid in the lung tissues and alveoli) is sudden. Asthma, pneumonia (an acute inflammation of the lungs), pulmonary oedema, allergy is over a few hours. Pleural effusion (an accumulation of fluid in the spaces of the lungs) and carcinoma (a malignant epithelial neoplasm that tend to invade surrounding tissue) of the brochus/trachea is over days. COPD, cryptogenic (unknown cause) fibrosing alveolitis (severe allergic pulmonary reaction), non-respiratory disorders: anaemia (a decrease in blood levels), hyperthyroidism is over months or years.
  4. Is there any pain and if so does it move?
  5. Do you have any past history of breathlessness?
  6. Is there any family history of breathlessness?

 

14. Q. What questions would you ask a patient who presents palpitations?

A.

  1. Are they regular or irregular?
  2. Are you taking any medication?
  3. How long have you been experiencing these palpitations?
  4. Are there any other (associated) symptoms?
  5. How or when did it start?
  6. What is your diet, lifestyle (alcohol, smoking)?
  7. Do you have any chest pain?

 

15. Q. What questions related to family history would you ask a patient presenting with heart disease?

A.

  1. Is there any heart disease in your family?
  2. Are your parents still alive?
  3. Did they live to a good age?
  4. Do you know what they died from?
  5. Have you any brothers or sisters?
  6. Do any of them have a heart problem?

 

16. Q. Where should one look for peripheral and central cyanosis and what are their mechanisms?

A. The definition of cyanosis is a dusky blue discolouration of the skin. It is due to the presence of unoxygenated haemoglobin.

Peripheral cyanosis is due to vasoconstriction and stasis of blood in the extremities and increased oxygen extraction by peripheral tissue. It occurs in congestive heart failure, shock, exposure to cold and abnormal peripheral circulation.

Central cyanosis is present when the tongue and lips is cyanosed. It is caused by cardiac failure or respiratory disorders. The central cyanosis of pulmonary or cardiac failure is improved by breathing oxygen.

 

17. Q. What happens to the lungs when the pressure in the left atrium is very high? What is the cause of this raised pressure? What is the patient likely to complain of and what will you hear at the lung bases through the stethoscope?

A. Pulmonary oedema (the accumulation of extravascular fluid in the lung tissues and alveoli) has occurred due to an increase in pressure caused by fluid in the alveoli, therefore sputum will be bloody. You will hear on inspiration at the base of the lung a crackling sound. The patient will complain of dyspnoea (difficultly in breathing), paroxyenal nocturnal and orthopnoea (person must sit or stand to breath easier). The patient will have peripheral cyanosis (right side heart failure causes central cyanosis).

 

18. Q. List the three important factors influencing blood pressure?

A.

  1. Cardiac output: a decrease lowers the blood pressure whilst an increase raises blood pressure.
  2. Blood volume: anything lowering the volume such as haemorrhage, lowers blood pressure and anything raising the volume such as water retention increases blood pressure.
  3. Peripheral resistance: refers to the vascular resistance offered by the cardiovascular system opposing blood flow. An increase in arterial vasoconstriction causes a rise in blood pressure and an increase in vasodilatation results in a fall in blood pressure.

 

19. Q. List the major local and general causes of ankle swelling. In each case, indicate whether the swelling is likely to be unilateral or bilateral.

A.

Unilateral: local inflammation. DVT caused by an increase in hydrostatic (fluid) pressure. Embolism caused by fat in the vein.

Bilateral: Cardiac failure due to an increase in venous pressure. Kidney failure due to a decrease in albumen levels which control hydrostatic pressure. Also liver failure causes a lack of protein intake; lack of muscle contraction.

 

20. Q. List three common pathological situations which can displace the apex beat.

A.

  1. Cardiac enlargement: left or right ventricle hypertrophy (an increase in the size of an organ).
  2. Pneumothorax (collapse of a lung).
  3. Pleural effusion (an accumulation of fluid in the spaces of the lungs).

 

21. Q. Name some common physiological and pathological situations which cause a loud first heart sound.

A.

  1. Anaemia (a decrease in blood levels).
  2. Mitral stenosis (an abnormal narrowing of an opening or passageway in the body) due to rheumatic heart disease (damages to the heart muscle and heart valves caused by rheumatic fever).
  3. Valves becoming rigid and calcified.

 

22. Q. Name some common and physiological and pathological situations which causes a softer first heart sound.

A.

  1. Heart failure.
  2. Mitral valve regurgitation (the back flow of blood through a defective heart valve).
  3. Decreased output.
  4. Tachycardia.

 

23. Q. What is the mediastinum?

A. It is the central tissue mass that divides the thoracic cavity into two pleural cavities. It includes the aorta and other great vessels, the oesophagus, trachea, thymus, the pericardial cavity and heart, nerves, small vessels and lymphatics.

 

24. Q & A. Complete the following:

Blood returns to the heart via the INFERIOR VENA CAVA from the trunk and the limbs via the SUPERIOR VENA CAVA from the head and neck. The blood enters the RIGHT ATRIUM and passes through the TRICUSPID valve into the RIGHT VENTRICLE. The blood is then ejected through the PULMONARY VALVE into the PULMONARY TRUNK. From the lungs the blood passes via the PULMONARY VEIN to the left atrium where it is ejected through the BICUSIP (MITRAL) valve to the left ventricle for distribution to the rest of the body.

 

25. Q. Give two cardiovascular causes of clubbing.

A. Cyanotic congenital heart defect (an inborn heart defect that allows the mixing of unsaturated (venous) blood with saturated (arterial) blood to produce cyanosis) and infective endocarditis (affects the endocardium and heart valves and is characterised by lesions).

 

26. Q. What causes xanthelasmata?

A. Hyperlipidaemia (abnormal collections of lipids in the skin).

 

27. Q. What causes corneal arcus?

A. Hypercholesterolaemia (when greater than normal amounts of cholesterol are found in the blood).

 

 

Respiratory System:

1. Q. What can you find during inspection, palpation, percussion and auscultation for pneumonia, pneumothorax, chronic airway obstruction and fibrosis?

A.

 

Pathological Process

Mediastinal Shift

Chest Wall movement

Resonance / Fremitus

Percussion Note

Breath Sound

Added Sound

 

Pneumonia- Consolidation

No

Reduced

Increase

Dull

Bronchial

Crackles

 

Fibrosis:

Localised

 

Generalised

 

Yes

 

No

 

Reduced (one side)

 

Reduced (both sides)

 

Normal to Increase

 

Normal to Dull

 

Normal to Bronchial

 

Fine & Coarse Crackles

 

Collapse

Yes (towards)

Reduced

Decrease

Dull

Decrease

-

 

Pneumothorax

Yes (away)

Reduced

Decrease

Hyper-resonant

Decrease

-

 

Pleural effusion

Yes (away)

Reduced

Decrease

Dull

Decrease / absent

Pleural rub

 

 

2. Q. State four mechanisms that can lead to bilateral and unilateral reduction in chest wall movement?

A.

Bilateral:

  1. Reduced rib cage movement.
  2. Local lung fibrosis (the formation of scar tissue in the connective tissue of the lungs as a sequel to inflammation or irritation).
  3. Hyper-inflated lung (over inflated lung).
  4. Myasthenia gravis.

Unilateral:

  1. Pneumothorax (collapse of the lung).
  2. Pleural effusion (an accumulation of fluid in the spaces of the lungs).
  3. General lung fibrosis (the formation of scar tissue in the connective tissue of the lungs as a sequel to inflammation or irritation).
  4. Pneumonia (an acute inflammation of the lungs) (consolidated).

 

3. Q. What are dullness, resonance, hyper-resonance, collapse and consolidation?

A.

  1. Dullness: a dull sound produced by percussion of an organ or cavity of the body during a physical examination.
  2. Resonance: an echo or other sound produced by percussion of an organ or cavity of the body during a physical examination.
  3. Hyper-resonance: a high noted sound produced by percussion of an organ or cavity of the body during a physical examination.
  4. Collapse: reduced size of the lung.
  5. Consolidation: lung tissue becomes solid.

 

4. Q. State bronchial and vesicular breathe sounds. Draw a diagram to show this.

A. Vesicular breath sounds are normal sounds heard over the lung fields and have a rustling quality. Bronchial breath sounds however, are heard in the trachea and main bronchi and are transmitted to the chest wall. Bronchial breath sounds have a higher frequency and are harsher than normal breathe sounds. Below is a diagram illustrating their correlation with inspiration and expiration and their intensity.

 

5. Q. What are the changes in the pathology of pneumonia?

A.

  1. Congestion: fluids coming in.
  2. Red hepatisation: blood cells get in, fibrin, lung has a reddish colour.
  3. Grey hepatisation: fibrin. B cells try to be a grey colour.
  4. Resolution: Lungs become clean and normal, or
  5. Organisation.
  6. Abscess.

 

6. Q. State the differences between Type A (pink puffer) and Type B (blue bloater).

A.

Type A

Type B

  1. Always breathless.
  2. Not cyanosed/are thin.
  3. Associated with emphysema.
  4. Cough sputum are less common.
  5. Carbon dioxide levels in the blood are normal or low.
  1. Central cyanosed from hypoxia (inadequate oxygen at the cellular level).
  2. Bloated from right sided heart failure.
  3. Features of chronic obstructive bronchitis.
  4. Cough/sputum are common-but breathlessness less so.

 

7. Q. Bronchial carcinomas usually arise in the major bronchi and spread into the lumen of the bronchus aswell as into the bronchial wall and surrounding tissues. What initial syndromes, therefore are patients likely to present with?

A.

  1. Haemoptysis (coughing up blood).
  2. Progressive breathlessness.
  3. Persistent respiratory infection.

 

8.Q. Name the type of hypersensitivity reaction in TB and briefly outline the sequence of events in the activation of this reaction.

A. Type IV cell mediated hypersensitivity reaction where T helper cells activate cytotoxic T cells.

 

9. Q. Post-primary TB is obviously a chronic inflammatory reaction. Describe the pathological features that you are likely to find.

A.

 

10. Q. State the clinical features of pulmonary infarction; comparisons with pulmonary oedema.

A. The clinical features of pulmonary infarction are sudden breathlessness followed by chest pain and haemoptysis (coughing up blood). There may be pain or swelling of a leg suggesting deep vein thrombosis. On examination there may be a pleural rub along with a fever and tachycardia.

Pulmonary oedema (the accumulation of extravascular fluid in the lung tissues and alveoli) is also characterised by breathlessness but usually at night then all day when severe. The patient will also exhibit wheezing, anxiety, profuse sweating and a productive cough which is copious, frothy, blood-tinged. Other clinical features include tachycardia, a raised venous pressure and a fast rhythm. Crackles will be heard upon examination.

 

 

 

PULMONARY INFARCTION

PULMONARY OEDEMA

 

CAUSES

Pulmonary embolism

Congestive heart failure

 

SYMPTOMS:

SPEED OF ONSET

MAIN SYMPTOMS

 

SPUTUM

 

Fast (if large)

SOB, dyspnoea, central cyanosis, haemoptysis

Reddish

 

Slow

Dyspnoea, orthopnoea, PND, cough

Pink and frothy

 

FEATURES ON GENERAL EXAMINATION

Decreased chest wall movement, dull percussion, maybe bronchial breathing on auscultation

‘99’ changes, dull percussion, crackles at lung base on auscultation, no pleural rub

 

11. Q. What are crackles and what is the underlying mechanism that gives rise to them?

A. Fine crackles are produced by small lower airways, where the airways snap open. Coarse crackles sound like a bubbling of fluid and indicate left heart failure.

 

12. Q. What causes pleural rubs and what do they sound like?

A. Pleural rubs are caused by the inflamed surfaces of the pleura rubbing together. Its sounds like new leather when it is bent. Pleural rubs are usually heard on both inspiration and expiration. Rubs are heard in all varieties of pleural inflammation such as in pneumonia (an acute inflammation of the lungs) and pulmonary embolism (a blockage of a pulmonary artery by a foreign matter).

 

13. Q. Which pathological processes in the lungs are associated with an increase and decrease in vocal fremitus and resonance? Name a disease that can cause this pathological change.

A.

Increase: Pneumonia (an acute inflammation of the lungs) (consolidation).

Decrease: Pleura becoming thicker; pneumothorax.

 

14. Q. List some important causes of haemoptysis (coughing up blood).

A. Tuberculosis, embolism or a pulmonary infarction.

 

15. Q. What questions would you ask in the history regarding shortness of breath?

A.

  1. Is the breathlessness recent or has it been present for sometime?
  2. Is it constant or does it come and go?
  3. What can’t you do because of the breathless?
  4. What makes the breathing worse?
  5. Does anything make it better?

 

16. Q. In addition to right heart failure, which lung conditions may cause a raised JVP?

A. Right pneumothorax (collapse of the right lung), pulmonary embolism (a blockage of a pulmonary artery by a foreign matter), hyper-inflated lung, chronic asthma and tumour on the supraclavicular.

 

17. Q. Many cases of asthma are said to be due to type I hypersensitivity reactions. Describe the mechanisms and features of this type of reaction.

A. Extrinsic (allergic) asthma is found mainly in children and only in a minority of adult patients. It is caused by the inhalation of pollen, animal dander, mould spores and feather dust. Exposure to these protein-containing allergens even in minute quantities will cause a type I inflammatory response. It is characterised by hypersensitivity of the tracheobronchial tree from external stimuli, leading to constriction of the airways caused by bronchospasm.

 

Asthma is initiated by a type I, IgE immune response. The mast cells of the bronchial tissues release chemical mediators, histamine, and slow reacting substance of anaphylaxis, eosinophil chemotatic factors, platelet-activating factors and prostaglandins. These produce bronchial smooth muscle spasm, vascular congestion, an increased vascular permeability, oedema, production of thick tenacious mucus and an impaired mucociliary function. When combined with the epithelial cell damage caused by eosinophil infiltration it results in hyper responsiveness of the airways. The obstruction of the airways by bronchospasm and excessive mucous production increases resistance to airflow especially expiratory. The continued trapped air within the lung increases intrapleural and alveolar gas pressure and causes decreased perfusion of the alveoli, with an uneven ventilation-perfusion relationship within the different segments of the lung. This causes early hypoxemia without CO? retention, which increases still further hyperventilation through the respiratory system, causing the partial pressure of carbon dioxide in the arterial blood (PaCO?) to decrease and pH to increase (respiratory alkalosis).

 

18. Q. Large cell tumours are undifferentiated. What does this term mean and consequently what are these tumours likely to do early on?

A. Large cell tumours constitute a heterogeneous group including giant cells and clear cell carcinomas, the cells of which show no evidence of maturation. They frequently arise centrally, invade the mediastinum and disseminate widely. They grow aggressively.

 

Nervous System:

1. Q. What are the clinical features of UMN disorders?

A.

  1. Drift of the upper limbs.
  2. Weakness with a characteristic distribution.
  3. Increase in tone of the spastic type.
  4. Exaggerated tendon reflexes.
  5. An extensor plantar response.
  6. Loss of abdominal reflexes.
  7. No muscle wasting.
  8. Normal electrical excitability of muscle.

 

2. Q. What are the clinical features of LMN disorders?

A.

  1. Weakness.
  2. Wasting.
  3. Hypotonia (diminished tone or tension).
  4. Reflex loss.
  5. Fasciculation (visible twitching of a muscle).
  6. Contractures of muscle.
  7. ‘Trophic’ changes in skin and nails.

 

3. Q. Review cranial nerves.

A.

Cranial nerves:

I (Olfactory):

II (Optic):

  • colour identification skills.
  • VISUAL ACUITY.
  • visual field.

III (Oculomotor), IV (Trochlear) and VI (Abducens):

  • EYE MOVEMENT.
  • NYSTAGMUS (rapid eye movement).
  • EYE CONVERGENCE. 
  • DIRECT PUPILLARY REFLEX.
  • CONSENSUAL REFLEX.

V (Trigeminal):

  • Ophthalmic, maxillary and mandibular.  
  • CORNEAL REFLEX.  
  • Chewing muscles.

VII (Facial):

  • Frown then raise your eyebrows, then close your eyes and I will try to open them, then smile and show your teeth, then blow your mouth up like this.

VIII (Vestibularcochlear):

  • HEARING.
  • Rinne’s Test.
  • WEBER’S TEST.

IX (Glossopharyngeal) and X (Vagus):

  • PALATAL MOVEMENT.
  • SWALLOWING.
  • gag test.
  • COUGH.

XI (Accessory):

  • HEAD AND SHOULDERS.

XII (Hypoglossal):

  • TONGUE.

 

4. Q. Compare UMN and LMN disorders.

A.

 

5. Q. What are the clinical features of trigeminal neuralgia?

A. Trigeminal neuralgia (facial nerve) is a sudden severe pain (like a hot needle) along the jaw and lasts seconds to minutes and may be followed by a dull aching pain. It occurs in bouts, often many times a day. It can be triggered by touch, movement or cold. It is usually caused by compression of the trigeminal nerve by a blood vessel.

 

Migrainous Neuralgia (cluster headaches)

Trigeminal Neuralgia

(affects Cranial Nerve V)

Post herpetic Neuralgia (affects Cranial Nerve V)

 

Commoner in males in 3rd and 4th decade

Occurs in bouts of weeks or months

Freedom of pain between attacks

Severe pain that wakes the patient at night

Lasts 15min-3 hours

Commoner in middle aged women

Short, sharp, shock-like paroxysms of pain

Freedom of pain between attacks

Unilateral

Provoked by trivial stimuli (cold, jaw movements)

Involves eye, maxillary and mandibular areas

Follows herpes zoster virus, lives in nerve roots, usually from chicken pox

Continuous burning pain

Involves eye, maxillary and mandibular areas

Unilateral

Depression is common

 

6. Q. List some common sources for emboli to the brain. List some common diseases and risk factors that may be associated with TIA’s.

A. TIA stands for Transient Ischaemic Attack. It is an episode of cerebrovascular insufficiency, usually associated with partial occlusion of an artery by an embolism.

There are various sources:

  1. Carotid arterial bruit (a murmur heard over the carotid artery in the neck, suggesting arterial narrowing).
  2. Dysrhythmia (abnormal rhythm) (AF).
  3. Heart disease, endocarditis (affects the endocardium and heart valves and is characterised by lesions),
  4. A recent MI,
  5. Differences in BP between the left and right brachial arteries.

The various risk factors that may be associated with TIA’s are:

  1. Hypertension,
  2. Smoking,
  3. High cholesterol,
  4. Oral contraception pill.
 

Carotid Involvement TIA (anterior)

Vertebrobasilar Involvement TIA (posterior)

 

Transient loss of vision in one eye due to emboli in the retinal artery

Aphasia (defected speech)

Hemiparesis (weakened one side)

Hemisensory loss

Hemianopia (loss of half of a visual field)

Affects the auditory + visual complex and cerebellum

Diplopia, vertigo, nausea

Choking and dysarthria (can’t speak due to poor muscle coordination)

Ataxia (unsteady gait)

Hemisensory loss

Hemianopia

Transient global amnesia

Tetraparesis

 

7. Q. Briefly describe the following gait disorders and state one cause of each.

A.

GAIT

DEFINITION

CAUSES

Spastic

Slow walking, stiff legs that may be dragging, weakness and stiffness of one leg if unilateral

Cerebrovascular Disorder (Stroke) or MS

Foot-Drop

Flexes leg at hip more than usual to prevent toes catching with stamping as foot hits the ground

Peripheral Neuropathy (weakness, sensory loss)

Ataxic

Unsteady when standing and adopts a broad base or lurches from side-to-side

Cerebellar Disease or MS

Waddling

Inability to tilt pelvis when swinging each leg through to take the next step with exaggerated lateral trunk movements

Proximal Muscle Disorder (Thyrotoxicosis)

Hypokinetic

Stopped posture with difficulty in initiating movement and small shuffling steps

Parkinson’s Disease

 

 

8. Q. Compare pyramidal and extra-pyramidal systems.

A.

Pyramidal system: refers to disorders affecting the cortex and corticospinal tract lesions. This leads to an increase in tone without muscle wasting or fasciculation. In the upper limbs, the flexor muscles remain stronger than the extensors and in the leg, the extensors muscles remain stronger than the flexors.

Extra-pyramidal system: refers to disorders produced by lesions affecting the basal ganglia. Diseases of the extra-pyramidal system may be divided into:

  1. The akinetic-rigid syndrome, such as Parkinson’s disease, which lead to a lack of movement with an increase in tone.
  2. The dyskinesias, in which occur involuntary movements.

 

PYRAMIDAL SYSTEM

EXTRAPYRAMIDAL SYSTEM

CEREBELLUM

 

Muscle Appearance

Gait (spastic, foot drop)

Tone

Muscle Power

Reflexes

Bradykinesia (reduced movement)

Involuntary movements (resting tremor)

Gait (Parkinsonian)

Speech (Dysarthria)

Balance and Coordination

Gait (ataxic)

Eye movements (nystagmus)

Tone

 

9. Q. Give one cause for a lower motor lesion and one cause of an upper motor lesion of the facial nerve. Draw a diagram to illustrate your answer.

A.

Upper (UMN): Parkinson’s disease.

Lower (LMN): Myasthenia gravis, where the deposition of antibody on the postsynaptic acetylcholine receptor site interrupts the function of the neuromuscular junction.

 

10. Q. Compare and contrast the clinical features of an upper motor neurone lesion and a lower motor neurone lesion in the lower limbs.

A.

 

 

LMN

UMN

Cerebellar

 

Muscle Bulk

Wasting

Normal

Normal

 

Tone

Decreased

Increased (Clasp Knife)

Decreased

 

Tremor

None

None

On Movement

 

Fasciculation

Yes

No

No

 

Power

Decreased

Decreased

Normal

 

Coordination

Normal

Impaired

Impaired

 

Limb Reflexes

Reduced/Absent

Increased (UMN cannot control LMN)

Not a good diagnostic test

 

Plantar

Flexor

Extensor

Extensor

 

Gait

Foot Drop

Spastic

Ataxic

 

11. Q. Define the term nystagmus and papilloedema.

A. Nystagmus is the rhythmic oscillation of the eyes. It is a sign of disease of either the ocular or the vestibular system and its connections.

Papilloedema is the swelling of the papilla – the optic disc. It is caused by various disorders: raised intracranial pressure, optic nerve disease, venous occlusion (a blockage in a canal, vessel or passage of the body), retinal vascular disease, metabolic causes and disc infiltration.

 

12. Q. State briefly the clinical features of tension headaches and migraines.

A. Tension headaches are the most common form of headache. The headache can be continuous or episodic and is described as pressure or a tight band around the head.

Migraine headaches are an episodic headache, associated with nausea and an aversion to light and sound. There may be an aura present, which occurs in a third of patients. The headache is usually unilateral, but bilateral in a third of cases. The pain is mainly over the temples but can affect the occipital regions. They are usually throbbing and may last for hours or even days. It is made worse with activity and relieved by sleep. Vomiting may also help.

 

 

TENSION HEADACHE

MIGRAINE

 

 

 

EPIDEMIOLOGY

Can effect anybody

Chronic recurrent problem

Recurrent headache usually associated with GI and visual disturbances

10% of population have had one

Commoner in females

 

 

 

 

PATHOGENESIS

Unknown

Precipitating factors:

Worry, noise, excess visual concentration, fumes, depression but not hypertension or sight problems

Precise mechanism unknown

Severe vasodilation around head and neck with oedema pressing on nerve endings which may release vaso-active substances

Associated factors:

Chocolate, cheese, puberty, menopause,

 

 

 

CLINICAL PATTERN

Tight band round head, tender temporal muscles, respond poorly to analgesics

Begins with a feeling of impending doom, starts unilaterally, visual disturbances, parasthesia, severe throbbing, nausea, vomiting, may last from hours to days, worsened by activity or movement, helped by sleep

 

13. Q. Describe the typical signs and symptoms of a severe (grand mal) epileptic seizure.

A.

Symptoms:

  1. Generalised stiffening (tonic).
  2. Repeated generalised jerking (clonic).
  3. Intermittent symmetrical jerks (myoclonic).
  4. Absence with no focal symptoms.
  5. Atonic drop attacks.

 

14. Q. List some common heart disorders that can lead to fainting.

A. Arythmia: sinos arrest, very tachycardia, AV block. Obstruction: stenosis (aortic, pulmonary, pulmonary hypertension) atrial thrombus.

 

15. Q. Give some reasons why hypoglycaemia may occur. Describe the typical features of a hypoglycaemic (low blood sugar level) attack.

A. Hepatic glucose output falls below the rate of uptake. Causes: inhibition of hepatic (liver cell) glycogenolysis (the breakdown of glycogen to glucose) and gluconeogenesis (the formation of glycogen from fatty acids and proteins) by insulin. Depletion of hepatic glycogen reserves by fasting, exercise and advanced liver disease. Clinical features include: diplopia (double vision), sweating, palpitations, weakness, confusion, abnormal behaviour, loss of consciousness and a grand mal seizure.

 

16. Q. Disorders of the left cortex cause aphasia (dysphasia), dysarthria, alexia (dyslexia) and agraphia. What do these terms mean?

A.

  1. Aphasia means the loss of the ability to swallow.
  2. Dysarthria means difficulty in speech articulation, resulting from interference in the control over the muscles of speech, usually caused by damage to a central or peripheral motor nerve.
  3. Alexia means an inability to comprehend written words.
  4. Agraphia means the loss of the ability to write, resulting from an injury to the language centre in the cerebral cortex.

 

17. Q. Bells palsy is a lower motor neurone disorder. Briefly describe the clinical features.

A.

  1. A loss of forehead furrowing.
  2. A loss of eye closure.
  3. A loss of mouth elevation.
  4. Pain behind the eye.
  5. Altered taste on one side of the tongue.

 

18. Q. With regard to tone, contrast the terms, spacticity and rigidity?

A. Spacticity is characterised by hesitant, jerky voluntary movements, increased muscle tone and hyperactive stretch reflexes (clasp knife).

Rigidity is where the tone is intermittent and feels like a ratchet.

 

19. Q. What are some causes of pins and needles?

A. Peripheral neuropathy (any functional or organic disorder of the peripheral nervous system), trauma, pregnancy, rheumatoid arthritis (a chronic inflammatory, destructive, deforming, collagen disease that has an autoimmune response), tumour, vitamin B12 deficiency, MS.

 

20. Q. List the main factors that are associated with or are known to cause seizures.

A. Genetic, abnormalities of neural development, trauma (surgery), children (high febrile conditions), intracranial legions/tumours, Alzheimer’s disease, encephalitis (an inflammatory condition of the brain), hypoglycaemia (low blood sugar level), infarct of the brain tissue, metabolic disorders (low calcium levels, low sodium levels), drugs and alcohol withdrawal, external audio or visual stimuli (TV), meningitis and either kidney or liver failure.

 

21. Q. What general features are likely to be found in a patient with bacterial meningitis?

A. Headache, stiff neck, fever, light sweating, light sensitivity, rash of meningococcal septicaemia called purpura (bleeding showing in the skin).

 

Abdominal System:

1. Q. What questions would you ask a patient with weight loss?

A.

  1. How much weight have you lost?
  2. How much over how long?
  3. When did it start?
  4. Have there been any changes in bowel habit?
  5. Have there been any changes in appetite?
  6. Has there been any vomiting or nausea?

 

2. Q. What are the common causes for nausea and vomiting?

A.

  1. Any gastrointestinal disease.
  2. Acute infections, i.e. influenza (a highly contagious infection of the respiratory tract) and pertussis (an acute highly contagious respiratory disease).
  3. Central nervous disease, i.e. raised intracranial pressure, meningitis, vestibular disturbances and migraines.
  4. Metabolic causes, i.e. uraemia (the presence of excessive amounts of urea and other nitrogenous waster products in the blood), diabetes and hypercalcaemia (greater than normal amounts of calcium in the blood).
  5. Drugs, i.e. digitalis toxicity, opiates and cytotoxins.
  6. Reflex, i.e. severe pain (MI).
  7. Psychogenesis (a disease caused by the mind).
  8. Pregnancy.
  9. Alcohol excess.

 

3. Q. What is melaena? State the causes with vomiting and without.

A. Melaena is dark black tarry stools resulting from bleeding in the gastrointestinal tract (GIT).

With vomiting is associated with the stomach, oesophagus or duodenum and is caused by peptic ulcers or carcinoma.

Without vomiting is associated with the jejunum, ileum or colon and is caused by Crohn’s disease or irritable bowel syndrome (IBS).

 

4. Q. What is Crohn’s disease? State its complications.

A. Crohn’s disease is a chronic inflammatory bowel disease of unknown origin, usually affecting the ileum, the colon or other parts of the GIT. The complications are:

  1. Acute colonic (toxic) dilatation.
  2. Sub acute small bowel obstruction.
  3. Fistula formation.
  4. Renal stones.
  5. Carcinoma of the colon.
  6. Amyloid.
  7. Perforation.
  8. Severe colonic haemorrhage.

 

 

5. Q. What are the causes of ulcerative colitis (a chronic, episodic, inflammatory disease of the large intestine and rectum)?

A. Unknown origin.

 

6. Q. State the causes of abdominal bleeding?

A.

  1. Oesophagus: carcinoma (a malignant epithelial neoplasm that tends to invade surrounding tissue and to metastasise to distant regions of the body), oesophagitis (inflammation of the mucosal lining of the oesophagus), peptic ulcers and varices (an enlarged artery).
  2. Stomach: peptic ulcer, carcinoma, acute erosions and acute gastritis (an inflammation of the lining of the stomach).
  3. Duodenum: peptic ulcer and duodenitis (an inflammation of the duodenum).
  4. Systemic causes: chronic renal failure.

 

7. Q. What are the causes of vomiting blood?

A.

  1. Chronic peptic ulcers.
  2. Cirrhosis.

 

8. Q. What are the causes and complications of chronic liver disease?

A.

Causes (common):

  1. Alcohol.
  2. Hepatitis B + D.
  3. Hepatitis C.

 

Complications:

  1. Portal hypertension (an increase in venous pressure in the portal circulation caused by compression) and gastrointestinal haemorrhage.
  2. Ascites.
  3. Porto systemic encephalopathy (a neuropsychiatric manifestation of extensive liver damage).
  4. Renal failure.
  5. Hepatocellular (injury to liver cells) carcinoma (a malignant epithelial neoplasm that tends to invade surrounding tissue and to metastasise to distant regions of the body).

 

9. Q. List the signs and symptoms of chronic liver disease.

A.

Symptoms:

1.      Oedema

2.      Bleeding:

3.      Pruritus (itchy skin from conjugated bilirubin)

4.      Cholestasis from cirrhosis of the primary biliary tract

5.      Confusion, drowsiness and other neuropsychiatric complications resulting from the failure of the liver in metabolising toxins

Signs:

1.      Hepatomegaly

2.      Clubbing,

3.      Yellow skin

4.      Ascites

5.      Ankle and sacral oedema,

6.      Palmar erythema,

7.      Spider naevi,

8.      Splenomegaly

9.      Breast swelling,

10.    Dupuytren’s Contracture

 

10. Q. What are the causes of distention?

A. Otherwise known as the five f’s:

  1. Fat
  2. Flatus
  3. Faeces
  4. Fluid
  5. Foetus

 

11. Q. What is meant by visceral, parietal and referred abdominal pain?

A.

  1. Visceral:
  2. Parietal:
  3. Referred:

 

12. Q. Define ascites.

A. Ascites is an abnormal intraperitoneal accumulation of a fluid containing large amounts of protein and electrolytes. It is only detectable when there is at least 500ml of fluid. The condition will be accompanied with general abdominal swelling, oedema and a decrease in urinary output. It is a complication of cirrhosis, congestive heart failure, nephrosis (abnormal condition of the kidney characterised by proteinuria (the presence of large amounts of protein, usually albumin), hypoalbuminemia and oedema) and peritonitis (inflammation of the peritoneum).

 

13. Q. How would you test for ascites in the abdominal examination?

A. With the patient lying on their back, percuss from the umbilicus to the flank. If a dull sound is noted then mark this and ask the patient to lie on their side. Wait a few minutes for the fluid to settle. This time percuss the patient from the flank to the other flank. If a dull note is found higher than the pervious marked area then this is diagnostic of ascites.

 

14. Q. Describe three clinical features of biliary obstruction in addition to dark urine and pale stools.

A.

 

15. Q. List the major signs and symptoms of cancer of the oesophagus.

A.

Symptoms:

  1. Dysphagia (initially solids then liquids then complete).
  2. Pain.
  3. Weight loss.
  4. Coughing.
  5. Acute gastrointestinal bleeding.
  6. Heartburn.
  7. Supaclavicular lymph node enlargement.

 

Signs:

  1. Weight loss.
  2. Anaemia.
  3. Enlarged cervical lymph nodes.
  4. Hepatomegaly (enlarged liver).

 

16. Q. State the major features of peptic ulcer pain.

A. Duodenal: tend to have epigastric pain which is worse when fasting, and better with antacids and food and the patient will wake at 2-4am. Gastric: epigastric pain is sometimes worse with food and relieved by vomiting.

 

17. Q. List the three major complications of peptic ulceration and describe their clinical presentations, indicating whether they are more likely to occur in gastric or duodenal ulceration.

A.

  1. Gastrointestinal bleeding (haemorrhage) - duodenal.
  2. Perforation – duodenal (gastric). Acute severe upper abdominal pain and circulatory collapse may rapidly occur.
  3. Pylonic stenosis (gastric outflow obstruction) – duodenal (gastric). Patients complain of vomiting food hours after having eaten it. A succussion splash may be heard many hours after the last meal.

 

18. Q. List the clinical features (non-abdominal) and abdominal of carcinoma of the stomach that may be found on examination.

A.

  1. Non-abdominal: jaundice, ascites, enlarged left supraclavicular node, acanthosis (diffuse thickening of the prickle cell layer of the skin), nigricans (pigmented rough thickening of the skin around the groin) and hepatomegaly (enlarged liver).
  2. Abdominal: epigastric masses.

 

19. Q. List the pathological differences of ulcerative colitis and Crohn’s disease.

A.

Ulcerative colitis:

  1. Affects only large bowels.
  2. Superficial mucosal ulcers.
  3. Plasma cell and neutrophil infiltration in Crypts of Liberkuhn.
  4. Crypts may break down to form crypt abscesses.

Crohn’s disease:

  1. Affects mouth to anus.
  2. Most common in terminal ileum then ascending colon.
  3. Thickened bowel.
  4. Transmural (entire thickness of the wall of an organ) ulcers.
  5. Granulomata (a chronic inflammatory lesion characterised by an accumulation of macrophages) (type IV).
  6. Local abscesses, fistulas (bowel to bowel, bowel to skin and bowel to bladder/vagina).

 

 

 

ULCERATIVE COLITIS

CROHN’S DISEASE

 

Epidemiology/Aetiology

Incidence

Age & Sex

Race

Familial/Genetic Factors

Smoking

Possible Infective Causes

Immunological Link

 

6-10 per 100, 000

Women, early adult life

Western

Possible

Relapses when stopped

No

Possible

 

3-6 per 100, 000

Equal amongst sexes

Western

Yes e.g. North European Jews

Aggravates

Mycobacterium, TB, measles

Type IV (CM) HS Reaction

 

Pathological Features

Large bowel only

Superficial mucosal ulcer

Plasma cell and neutrophil infiltration in Crypts of Lieberkuhn, which can break down to form abscesses

Mouth – Anus but common in terminal ileum and ascending colon

Bowel becomes thick with transmural ulcers and granulomata

Local abscesses + fistulas

 

Clinical Features

Frequent loose stools with blood and mucus

Mild: Up to 5 bowel movements per day

Moderate: Up to 10

Severe: More than 10 with fever, tachycardia

Ulceration + pseudopolyps

Iron deficiency, anaemia, hypoproteinaemia, oedema

Mild fever, malaise, anorexia, weight loss

Right-Sided: Steatorrhoea, colicky RIF pain

Left-Sided: Diarrhoea with blood

Urinary frequency dysuria due to inflamed bowel adjacent to urinary tract

Fistula formation

Nutritional deficiencies, anaemia, oedema etc.

 

20. Q. Define portal hypertension, variceal haemorrhage and ascites. Breifly describe their causes, mechanisms and clinical features.

A.

  1. Portal hypertension: an increase in venous pressure in the portal circulation caused by compression.
  2. Variceal haemorrhage:
  3. Ascites: is an abnormal intraperitoneal accumulation of a fluid containing large amounts of protein and electrolytes.

 

21. Q. What questions would you ask a patient with dysphagia?

A.

  1. Any difficulty in swallowing?
  2. Caused by pain or by sticking?
  3. What type of food?
  4. When does it happen?
  5. Does regurgitation occur?
  6. At what level did the food stick?
  7. Is it intermittent or progressive?
  8. Are both food and drink equally difficult to swallow?

 

22. Q. Which parts of the GIT are associated with darker red or maroon coloured blood per rectum?

A.

Bright red blood per rectum:

Associated with the rectum and sigmoid colon

Causes: Inflammatory Bowel Disease (Crohn’s and Ulcerative Colitis), haemorrhoids

Darker red or maroon blood per rectum:

Associated with the ascending, transverse and descending colons

Causes: Diverticular Disease, Ischaemic Colitis, Polyps (small tumour like growth projecting from a mucous membrane surface)

 

23. Q. What questions would you ask a patient with jaundice?

A.

  1. Have you travelled abroad recently?
  2. Is there any history of alcohol or IV abuse?
  3. Have you had a blood transfusion?
  4. Have you had any contact with anyone with jaundice?
  5. Is there any skin itching?
  6. Do you have any pain or weight loss?
  7. What are the colour of your stools and urine?
  8. Is there any family history of liver disease?
  9. Sexually activity.

 

24. Q. What questions would you ask a patient with abdominal pain?

A.

  1. Situation.
  2. Radiation.
  3. Associations.
  4. Effects of food.
  5. Effects of antacids.
  6. Effects of bowel movements.

 

25. Q. Which disorders causing constipation are associated with rectal bleeding and colicky pain?

A. Cancer, colonic strictures (a narrowing of a lumen or organ), diverticular disease (a pouch-like herniation through the muscular wall of a tubular organ).

 

26. Q. List the causes of splenomegaly (enlarged spleen).

A.

  1. Infective.
  2. Congestive.
  3. Related to blood disorders.
  4. Infiltrations.
  5. Enlarged kidneys.

Questions on this page are Copyright © 2003 by Attilio P. D’Alberto

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TCM CENTRAL • John R. Wahnish, MSTOM, L.Ac. • [TCMcentral.com] • Revised: Copyright © 2002 •  E-mail: tcmcentral@nyc.rr.com