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
|
- Pain radiates to the arm (commonly on
the left), and to the jaw and teeth.
|
- Chest pain and tightness.
- Breathlessness.
- Dizziness.
- Tiredness.
- Choking feeling in the throat.
- Discomfort after running, eating or in
the cold wind.
|
3.
Q. What questions would you ask a patient who presents
cardiac pain?
A.
- Do you get pain in your chest on
exertion?
- Whereabouts in the chest do you feel it?
- Is it worse in cold weather?
- Is it worse if you exercise after a big
meal?
- Is it bad enough to stop you from
exercising?
- Does is go away when you rest?
- Do you ever get similar pain if you get
excited or upset?
4.
Q. What are the causes of palpitations?
A.
- Extrasystoles.
- Paroxysmal atrial fibrillation.
- Paroxysmal supraventricular tachcardia.
- Thyrotoxicosis.
- Perimenopausal.
5.
Q. Compare the JVP and the carotid pulse.
A.
See the table below:
|
Jugular
Venous Pulse (JVP)
|
Carotid
Pulse
|
- The pulsation cannot be felt.
- Moves inside.
- See two movements for one heart beat.
- Increases when pressure is applied to
the liver.
- Pressure increased by deep
inspiration.
|
- The pulsation can be felt.
- Moves outside.
- Feel one movement for one heart beat.
- No change when pressure is applied to
the liver.
- Breathing has no effect on the pulse.
|
6.
Q. What is the major pathological reason for a general
increase in JVP?
A.
- Right cardiac failure.
- Obstruction superior to the vena cava.
- Tricuspid reflux and stenosis (an
abnormal narrowing of an opening or passageway in the
body).
- 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.
|
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
|
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.
- Do you have a respiratory illness? I.e.
asthma, pulmonary oedema, etc.
- How long have you had breathlessness?
- 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.
- Is there any pain and if so does it
move?
- Do you have any past history of
breathlessness?
- Is there any family history of
breathlessness?
14.
Q. What questions would you ask a patient who presents
palpitations?
A.
- Are they regular or irregular?
- Are you taking any medication?
- How long have you been experiencing
these palpitations?
- Are there any other (associated)
symptoms?
- How or when did it start?
- What is your diet, lifestyle (alcohol,
smoking)?
- Do you have any chest pain?
15.
Q. What questions related to family history would you ask
a patient presenting with heart disease?
A.
- Is there any heart disease in your
family?
- Are your parents still alive?
- Did they live to a good age?
- Do you know what they died from?
- Have you any brothers or sisters?
- 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.
- Cardiac output: a decrease lowers the
blood pressure whilst an increase raises blood
pressure.
- Blood volume: anything lowering the
volume such as haemorrhage, lowers blood pressure and
anything raising the volume such as water retention
increases blood pressure.
- 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.
- Cardiac enlargement: left or right
ventricle hypertrophy (an increase in the size of an
organ).
- Pneumothorax (collapse of a lung).
- 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.
- Anaemia (a decrease in blood levels).
- 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).
- Valves becoming rigid and calcified.
22.
Q. Name some common and physiological and pathological
situations which causes a softer first heart sound.
A.
- Heart failure.
- Mitral valve regurgitation (the back
flow of blood through a defective heart valve).
- Decreased output.
- 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:
- Reduced rib cage movement.
- Local lung fibrosis (the formation of
scar tissue in the connective tissue of the lungs as a
sequel to inflammation or irritation).
- Hyper-inflated lung (over inflated
lung).
- Myasthenia gravis.
Unilateral:
- Pneumothorax (collapse of the lung).
- Pleural effusion (an accumulation of
fluid in the spaces of the lungs).
- General lung fibrosis (the formation of
scar tissue in the connective tissue of the lungs as a
sequel to inflammation or irritation).
- Pneumonia (an acute inflammation of the
lungs) (consolidated).
3.
Q. What are dullness, resonance, hyper-resonance, collapse
and consolidation?
A.
- Dullness: a dull sound produced by
percussion of an organ or cavity of the body during a
physical examination.
- Resonance: an echo or other sound
produced by percussion of an organ or cavity of the
body during a physical examination.
- Hyper-resonance: a high noted sound
produced by percussion of an organ or cavity of the
body during a physical examination.
- Collapse: reduced size of the lung.
- 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.
- Congestion: fluids coming in.
- Red hepatisation: blood cells get in,
fibrin, lung has a reddish colour.
- Grey hepatisation: fibrin. B cells try
to be a grey colour.
- Resolution: Lungs become clean and
normal, or
- Organisation.
- Abscess.
6.
Q. State the differences between Type A (pink puffer) and
Type B (blue bloater).
A.
Type
A
|
Type
B
|
- Always breathless.
- Not cyanosed/are thin.
- Associated with emphysema.
- Cough sputum are less common.
- Carbon dioxide levels in the blood are
normal or low.
|
- Central cyanosed from hypoxia
(inadequate oxygen at the cellular level).
- Bloated from right sided heart
failure.
- Features of chronic obstructive
bronchitis.
- 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.
- Haemoptysis (coughing up blood).
- Progressive breathlessness.
- 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.
- Is the breathlessness recent or has it
been present for sometime?
- Is it constant or does it come and go?
- What can’t you do because of the
breathless?
- What makes the breathing worse?
- 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.
- Drift of the upper limbs.
- Weakness with a characteristic
distribution.
- Increase in tone of the spastic type.
- Exaggerated tendon reflexes.
- An extensor plantar response.
- Loss of abdominal reflexes.
- No muscle wasting.
- Normal electrical excitability of
muscle.
2.
Q. What are the clinical features of LMN disorders?
A.
- Weakness.
- Wasting.
- Hypotonia (diminished tone or tension).
- Reflex loss.
- Fasciculation (visible twitching of a
muscle).
- Contractures of muscle.
- ‘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):
XII
(Hypoglossal):
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:
- Carotid arterial bruit (a murmur heard
over the carotid artery in the neck, suggesting
arterial narrowing).
- Dysrhythmia (abnormal rhythm) (AF).
- Heart disease, endocarditis (affects the
endocardium and heart valves and is characterised by
lesions),
- A recent MI,
- Differences in BP between the left and
right brachial arteries.
The
various risk factors that may be associated with TIA’s
are:
- Hypertension,
- Smoking,
- High cholesterol,
- 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:
- The akinetic-rigid syndrome, such as
Parkinson’s disease, which lead to a lack of
movement with an increase in tone.
- 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:
- Generalised stiffening (tonic).
- Repeated generalised jerking (clonic).
- Intermittent symmetrical jerks (myoclonic).
- Absence with no focal symptoms.
- 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.
- Aphasia means the loss of the ability to
swallow.
- 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.
- Alexia means an inability to comprehend
written words.
- 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.
- A loss of forehead furrowing.
- A loss of eye closure.
- A loss of mouth elevation.
- Pain behind the eye.
- 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.
- How much weight have you lost?
- How much over how long?
- When did it start?
- Have there been any changes in bowel
habit?
- Have there been any changes in appetite?
- Has there been any vomiting or nausea?
2.
Q. What are the common causes for nausea and vomiting?
A.
- Any gastrointestinal disease.
- Acute infections, i.e. influenza (a
highly contagious infection of the respiratory tract)
and pertussis (an acute highly contagious respiratory
disease).
- Central nervous disease, i.e. raised
intracranial pressure, meningitis, vestibular
disturbances and migraines.
- 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).
- Drugs, i.e. digitalis toxicity, opiates
and cytotoxins.
- Reflex, i.e. severe pain (MI).
- Psychogenesis (a disease caused by the
mind).
- Pregnancy.
- 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:
- Acute colonic (toxic) dilatation.
- Sub acute small bowel obstruction.
- Fistula formation.
- Renal stones.
- Carcinoma of the colon.
- Amyloid.
- Perforation.
- 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.
- 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).
- Stomach: peptic ulcer, carcinoma, acute
erosions and acute gastritis (an inflammation of the
lining of the stomach).
- Duodenum: peptic ulcer and duodenitis
(an inflammation of the duodenum).
- Systemic causes: chronic renal failure.
7.
Q. What are the causes of vomiting blood?
A.
- Chronic peptic ulcers.
- Cirrhosis.
8.
Q. What are the causes and complications of chronic liver
disease?
A.
Causes
(common):
- Alcohol.
- Hepatitis B + D.
- Hepatitis C.
Complications:
- Portal hypertension (an increase in
venous pressure in the portal circulation caused by
compression) and gastrointestinal haemorrhage.
- Ascites.
- Porto systemic encephalopathy (a
neuropsychiatric manifestation of extensive liver
damage).
- Renal failure.
- 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:
- Fat
- Flatus
- Faeces
- Fluid
- Foetus
11.
Q. What is meant by visceral, parietal and referred
abdominal pain?
A.
- Visceral:
- Parietal:
- 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:
- Dysphagia (initially solids then liquids
then complete).
- Pain.
- Weight loss.
- Coughing.
- Acute gastrointestinal bleeding.
- Heartburn.
- Supaclavicular lymph node enlargement.
Signs:
- Weight loss.
- Anaemia.
- Enlarged cervical lymph nodes.
- 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.
- Gastrointestinal bleeding (haemorrhage)
- duodenal.
- Perforation – duodenal (gastric).
Acute severe upper abdominal pain and circulatory
collapse may rapidly occur.
- 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.
- 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).
- Abdominal: epigastric masses.
19.
Q. List the pathological differences of ulcerative colitis
and Crohn’s disease.
A.
Ulcerative
colitis:
- Affects only large bowels.
- Superficial mucosal ulcers.
- Plasma cell and neutrophil infiltration
in Crypts of Liberkuhn.
- Crypts may break down to form crypt
abscesses.
Crohn’s
disease:
- Affects mouth to anus.
- Most common in terminal ileum then
ascending colon.
- Thickened bowel.
- Transmural (entire thickness of the wall
of an organ) ulcers.
- Granulomata (a chronic inflammatory
lesion characterised by an accumulation of
macrophages) (type IV).
- 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.
- Portal hypertension: an increase in
venous pressure in the portal circulation caused by
compression.
- Variceal haemorrhage:
- 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.
- Any difficulty in swallowing?
- Caused by pain or by sticking?
- What type of food?
- When does it happen?
- Does regurgitation occur?
- At what level did the food stick?
- Is it intermittent or progressive?
- 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.
- Have you travelled abroad recently?
- Is there any history of alcohol or IV
abuse?
- Have you had a blood transfusion?
- Have you had any contact with anyone
with jaundice?
- Is there any skin itching?
- Do you have any pain or weight loss?
- What are the colour of your stools and
urine?
- Is there any family history of liver
disease?
- Sexually activity.
24.
Q. What questions would you ask a patient with abdominal
pain?
A.
- Situation.
- Radiation.
- Associations.
- Effects of food.
- Effects of antacids.
- 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.
- Infective.
- Congestive.
- Related to blood disorders.
- Infiltrations.
- Enlarged kidneys.
Questions
on this page are Copyright
© 2003 by Attilio
P. D’Alberto
|