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Medicine for Finals

Pre-Course Work

The aim of Medicine for Finals is to cover the essentials in a single day, allowing you to
organise your knowledge and refresh your memory of the common medical conditions
appearing in the final examination.

This pre-course material is designed to help you gain maximum benefit from the course
itself by giving you the opportunity to do some preparatory work on a few of the topics
which previous finalists have found challenging.

Please spend about an hour on the questions

You'll learn most if you test yourself first and then read the outline answers,
which are provided in short note format.

Topics Page Answers

Mitral stenosis 2 7
Signs of left ventricular failure 2 8
ECG 2 8
Optic neuropathy 3 9
Diagnosis of diabetes 3 10
Management of ketoacidosis 4 10
Data interpretation 5 11

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Medicine: Questions
Cardiology
1) List the physical signs of mitral stenosis. What would you be looking for when palpating for
the apex beat? What is the explanation for this physical sign?

2) What are the signs of left ventricular failure apart from basal crackles?

3) A 54 year-old man complains of chest pain. Report on his ECG taken in the emergency
department.

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Neurology

4) What are the signs of optic neuropathy?

Diabetes

5) A 50 year old man is referred to the diabetic clinic as a new patient referred for confirmation
of the diagnosis of type 2 diabetes mellitus.

What level of fasting venous plasma glucose confirms the diagnosis?

What level of venous plasma glucose two hours after a 75g glucose load would confirm
diabetes?

What level of HbA1c would confirm the diagnosis?

A diagnosis of type 2 diabetes is confirmed and you assess him for complications. His fundi
are abnormal.

6) Outline your classification of fundal abnormalities due to diabetes:

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The nurse in charge informs about a recently diagnosed type 1 diabetic who has been brought
in semi-conscious. The BM stix reading is between 22 and 44mmol/l and the urine contains
ketones ++.

7) Outline the management of diabetic ketoacidosis

Once the patient has been stabilised, your registrar gives you a quick tutorial on acidosis and
then asks you to interpret some data.

Acidosis
pH is tightly controlled between 7.38 and 7.42. pH is a negative logarithmic scale of
hydrogen ion concentration: a fall to pH 7.3 means a doubling of H+
Bicarbonate is the body's chief buffer system- the ratio of bicarbonate to pCO2 is the
main determinant of pH
Acidosis may be caused primarily by: respiratory problems (hypercapnia) or by
metabolic problems (lowering of bicarbonate)
Metabolic acidosis may be due either to loss of bicarbonate from the body (eg severe
diarrhoea, renal tubular acidosis, pancreatic fistula) or to addition of acids (eg
ketoacidosis, lactic acidosis, aspirin poisoning) when bicarbonate "mops up" the acid, is
converted to CO2 and excreted via the lungs
The difference between these is usually obvious clinically, but in cases of doubt the
anion gap can be measured
Normally there is a small difference between the sum of the two main cations (Na+K)
and the two main anions (Cl+HCO3). This is easily calculated from routine analysis of
venous blood. The anion gap of 12-18mmol/l is due to phosphate and some lactate
The gap increases when there is an "added acid" such as the ketone bodies:
acetoacetate and hydroxybutyrate

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Acidosis
Low pH

Acidosis

Check pCO2

Low High

Metabolic acidosis Respiratory acidosis

Acute Chronic

Bicarb low Bicarb normal Bicarb high

Added acid Loss of bicarbonate

High anion gap Normal anion gap

Data Interpretation

Interpret the arterial blood gases

8) Patient A
These are the results from the diabetic patient with ketoacidosis, on admission.
(Normal range)
pH 7.2 (7.38-7.42)
pCO2 2.8 (4.6-6.4 kPa)
HCO3 8.0 (22-28 mmol/l)
PO2 10.8 (>10.6 kPa)

Na 145 (135-145 mmol/l)

K 5 (3.5-5.0 mmol/l)
Cl 108 (95-105 mmol/l)

Lactate normal
Anion gap= (Na+K) - (HCO3+Cl) = 150 - 116= 34 (normal range 10-18).

What type of acidosis is this? Why?

Why is the pCO2 low?

What is the significance of the raised anion gap?

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9) Patient B
This is a patient with an exacerbation of COPD.

pH 7.2
pCO2 8.6
HCO3 34.0
PO2 4.8

What is the significance of the raised pCO2?

What is the significance of the raised bicarbonate?

How much oxygen would you give this patient?

10) Patient C
This is a young adult patient with acute asthma.

pH 7.2
pCO2 6.6
HCO3 26.0
PO2 8.0

Is the pCO2 level what you would expect in acute asthma?

What are the British Thoracic Society's signs of a severe and a life threatening attack?

How much oxygen would you give and why?

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Answers to Medicine Questions

Cardiology

1) List the physical signs of mitral stenosis. What would you be looking for when palpating for
the apex beat? What is the explanation for this physical sign?

Mitral stenosis
Malar flush
Atrial fibrillation
JVP not raised until late
Apex beat not displaced
Apex beat tapping in quality- due to a loud palpable first heart sound

Mitral stenosis is a left-sided heart lesion and in early uncomplicated cases, the JVP will be
normal. As the valve is narrowed, the pressure in the left atrium will be high and this is
transmitted backwards to the pulmonary veins, leading to pulmonary venous hypertension.
After some time, this may lead to pulmonary arterial hypertension, which after a further period
of time can lead to right ventricular hypertrophy. Only then will right-sided heart failure develop-
with a raised JVP.

The apex beat is not displaced in pure mitral stenosis as the narrow valve effectively protects
the ventricle, reducing the amount of blood that enters it. However the apex beat may be
tapping, which is due to a palpable first heart sound.

The first heart sound is palpable because it is loud and this is due to the high left atrial
pressure. Normally the mitral valve starts to glide shut towards the end of diastole and then, at
the start of ventricular systole, it closes causing the mitral component of the first heart sound. In
mitral stenosis, the high left atrial pressure keeps the valve open until right at the end of
diastole- so there is loss of the normal way in which the valve glides gently shut. Instead when
systole occurs, the valve is slammed shut from a more open position than normal.

Mitral stenosis: LUB de derrr

Loud first heart sound (high left atrial pressure keeps valve open until late in diastole; systole
then slams it shut)
Opening snap (high pitched sound just after second heart sound- best heard at lower left
sternal edge with diaphragm; may disappear if valve calcifies)
Low pitched rumbling diastolic murmur at the apex

Lub De Derrrr
LUB De Derrrr

ventricular systole diastole

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2) What are the signs of left ventricular failure apart from basal crackles?

Acute LVF: on inspection

Patient looks acutely unwell- pale and grey
Cold clammy peripheries ? cyanosis
Frothy blood stained sputum in sputum pot
Orthopnoeic using accessory muscles
May have wheeze (cardiac asthma)

Acute LVF
Sinus tachycardia or atrial fibrillation
Systolic hypotension
Signs of cardiomegaly (displaced apex, signs of valve disease)
Third and fourth heart sounds
Right sided or bilateral pleural effusions

3) Report on the ECG

Rate: 60/minute
Rhythm: sinus rhythm
Axis: normal
P waves: normal
QRS: ST elevation in 2, 3 and aVF; deep q wave in 3
T waves: inverted in 1 and V2-4 (reciprocal change)

This is likely to represent a myocardial infarct, which is full thickness as there is a q wave. This
is an inferior infarct as the main changes are in 2,3 and aVF.

Acute Myocardial Infarction

st elevation

q waves
imply a full thickness
transmural infarct;
without them:
subendocardial

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4) Optic neuropathy: signs

Pale disc
Loss of visual acuity
Loss of red colour vision
Central scotoma
Afferent pupillary defect- pupil dilates to light in the swinging torch test (Marcus Gunn pupil)

Swinging torch test

In the good eye, light causes constriction and this is consensual
Release of the stimulus from the good eye causes dilatation- this is also consensual
Light shone into the "bad" eye is a weak stimulus: there is a relative afferent defect
The release stimulus (moving the light away from the normal eye) acts consensually on the
pupil of the bad eye ie both eyes dilate
It competes with and beats the weak afferent stimulus as the light moves over to the
affected eye
The result is dilatation of the pupil on the affected side (Marcus Gunn Pupil)

Diabetes
5) A 50 year old man is referred to the diabetic clinic as a new patient referred for confirmation
of the diagnosis of diabetes mellitus. What level of fasting venous plasma glucose confirms the
diagnosis?
7.0 mmol/l

What level of venous plasma glucose two hours after a 75g glucose load would confirm
diabetes?
11.1 mmol/l

What level of HbA1c would confirm the diagnosis?

48mmol/mol

See also
https://www.diabetes.org.uk/Professionals/Position-statements-reports/Diagnosis-ongoing-
management-monitoring/New_diagnostic_criteria_for_diabetes/

A diagnosis of type 2 diabetes is confirmed and you assess him for complications.

His fundi are abnormal. Outline your classification of fundal abnormalities due to diabetes:

6) Retinopathy: summary
Background- micoraneurysms and hard exudates
Maculopathy- check acuity; reduction in acuity due either to cataracts or maculopathy
Pre-proliferative- cotton wool spots (an infarct of the nerve cell layer on surface of
retina); also venous beeding and looping; intra-retinal microvascular anbnormalities
Proliferative- new vessels
End-stage- scarring with white bands of scar tissue and retinal traction

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The nurse in charge informs you about a recently diagnosed type 1 diabetic who has been
brought in semi-conscious. The BM stix reading is between 22 and 44mmol/l and the urine
contains ketones ++.

Outline the management of diabetic ketoacidosis

7) Principles of treatment of diabetic ketoacidosis

Gastric aspiration (if the patient is drowsy or nauseous- to prevent inhalation)
Rehydation (as such patients are very dehydrated due to osmotic diuresis)
Insulin replacement
Potassium replacement (as total body potassium is always low)

The first hour: PANICS

P Potassium- measure hourly: omit if anuria suspected or serum level >5.5mmol/l
A Acidosis: check venous pH and ketone levels
N Normal saline: 500ml over 15 minutes if systolic <90mm; otherwise 1litre in first hour
I Insulin by infusion (weight based, fixed rate, soluble insulin: 0.1 units/kg/hour)
C Catheter and cultures; urine, blood etc
S Stomach aspiration if drowsy; endotracheal tube first if no gag reflex (see action 1 from
Diabetes UK guideline below)

Check BNF and Diabetes UK (2013) guideline: https://www.diabetes.org.uk/

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8) Patient A
These are the results from the diabetic patient with ketoacidosis, on admission.
(Normal range)
pH 7.2 (7.38-7.42)
pCO2 2.8 (4.6-6.4 kPa)
HCO3 8.0 (22-28 mmol/l)
PO2 10.8 (>10.6 kPa)

Na 145 (135-145 mmol/l)

K 5 (3.5-5.0 mmol/l)
Cl 108 (95-105 mmol/l)

Lactate normal
Anion gap= (Na+K) - (HCO3+Cl) = 150 - 116= 34 (normal range 10-18).

What type of acidosis is this? Why?

Metabolic acidosis as pH low and pCO2 low

Why is the pCO2 low?

The patient has deep sighing Kussmaul respiration in response to acidosis:
blowing off CO2 is the body's way of minimising the pH disturbance; pH depends
on the ratio of HCO3 and pCO2

What is the significance of the raised anion gap?

Confirms that this is a metabolic acidosis due to addition of acid rather than to
loss of bicarbonate from the body. The normal lactate excludes lactic acidosis. In
a diabetic, ketoacidosis is the most likely explanation- confirmed by high glucose
and ketonuria.

9) Patient B
This is a patient with an exacerbation of COPD.
pH 7.2
pCO2 8.6
HCO3 34.0
PO2 4.8

What is the significance of the raised pCO2?

Shows that this acidosis is respiratory in origin.

How much oxygen would you give this patient?

What is the significance of the raised bicarbonate?

Many would start with 24% oxygen as the raised bicarbonate suggests that renal
compensation has occurred: this implies a longstanding problem with an acute
exacerbation. If the patient has chronic hypercapnia, the respiratory drive may
well depend on hypoxia (unlike the normal person where it depends on pCO2).
Giving too much oxygen may "release the hypoxic respiratory drive", slow
respiration and precipitate CO2 narcosis. A simple clinical check is to measure
the respiratory rate before oxygen and 5 minutes after giving oxygen. You will
wish to check the gases again in any case to see if there has been an
improvement and particularly if there is any reduction in respiratory rate. A rising
pCO2 would indicate the need for ventilatory support.

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This is a controversial area. Some physicians argue that the danger of hypoxia is
actually greater than the danger of causing respiratory depression and that in a
critically ill patient, higher concentrations of oxygen should be used, with careful
monitoring of ABGs and then downward titration of oxygen concentrations, once
hypoxia has been corrected. The approach actually taken may depend on how ill
the patient is and how easy it will be to monitor ABGs and ventilate the patient if
necessary. The key point in answering the question is to make the examiner
aware that you recognise the risk and understand the mechanism by which
oxygen therapy could lead to deterioration in a patient with chronic hypercapnia.

Helpful reviews of oxygen therapy may be found at:

http://student.bmj.com/issues/04/02/education/56.php

and at

www.mcht.nhs.uk/documents/policies/Clinical/Oxygen%20Policy.pdf

10) Patient C
This is a patient with acute asthma.

pH 7.2
pCO2 6.6
HCO3 26.0
PO2 8.0

Is the pCO2 level what you would expect in acute asthma?

No; patients with asthma should have a low pCO2; if the level is normal,, or high,
as here, the patient is becoming exhausted and is very seriously ill

What are the British Thoracic Society's signs of a severe and a life threatening attack?

4 signs of severe asthma

Unable to complete sentences in one breath
Respiratory rate > 25
Heart rate > 110
PFR < 50% predicted (or best)

7 life threatening features: 33-92-chest

Less than 33% PFR
Less than or equal to 92% on pulse oximetry
C- cyanosis
H- hypotension
E- exhaustion or confusion
S- silent chest
T- tachycardia or bradycardia

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Blood gas markers of severity

SpO2 92% or less
Severe hypoxia (pO2<8kPa)
pCO2 normal - beware!- or high

Asthma leads to alveolar hypoventilation

This increases the respiratory drive
Low pCO2 normally results as it is easy to blow off CO2

How much oxygen would you give and why?

This patient is very ill with acute respiratory acidosis: the pCO2 should be low;
normal is worrying but high is a very serious sign. Call for senior help.

Give as much oxygen as possible while fast-bleeping the on-call anaesthetist as

an emergency and considering ventilation.

A non-rebreatheable oxygen delivery system would be ideal (trauma mask

Hudson mask), with a high flow rate of 15 l/min, together with a reservoir bag
and a valve to separate inspired from expired air, ensuring delivery of
approximately 80% oxygen. In addition, consider repeating any of the treatments
already given: eg salbutamol and ipratropium nebulisers, IV steroids.

Consider using IV magnesium sulphate after discussion with senior medial staff.
See SIGN/ BTS guidelines:

http://www.sign.ac.uk/guidelines/fulltext/63/index.html

http://www.sign.ac.uk/guidelines/fulltext/63/annex2.html

Repeat the arterial blood gases to monitor the effects of treatment and if no sign
if improvement, discuss the use of early ventilatory support.

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